umu.sePublikationer
Ändra sökning
Avgränsa sökresultatet
1234 101 - 150 av 161
RefereraExporteraLänk till träfflistan
Permanent länk
Referera
Referensformat
  • apa
  • ieee
  • modern-language-association-8th-edition
  • vancouver
  • Annat format
Fler format
Språk
  • de-DE
  • en-GB
  • en-US
  • fi-FI
  • nn-NO
  • nn-NB
  • sv-SE
  • Annat språk
Fler språk
Utmatningsformat
  • html
  • text
  • asciidoc
  • rtf
Träffar per sida
  • 5
  • 10
  • 20
  • 50
  • 100
  • 250
Sortering
  • Standard (Relevans)
  • Författare A-Ö
  • Författare Ö-A
  • Titel A-Ö
  • Titel Ö-A
  • Publikationstyp A-Ö
  • Publikationstyp Ö-A
  • Äldst först
  • Nyast först
  • Skapad (Äldst först)
  • Skapad (Nyast först)
  • Senast uppdaterad (Äldst först)
  • Senast uppdaterad (Nyast först)
  • Disputationsdatum (tidigaste först)
  • Disputationsdatum (senaste först)
  • Standard (Relevans)
  • Författare A-Ö
  • Författare Ö-A
  • Titel A-Ö
  • Titel Ö-A
  • Publikationstyp A-Ö
  • Publikationstyp Ö-A
  • Äldst först
  • Nyast först
  • Skapad (Äldst först)
  • Skapad (Nyast först)
  • Senast uppdaterad (Äldst först)
  • Senast uppdaterad (Nyast först)
  • Disputationsdatum (tidigaste först)
  • Disputationsdatum (senaste först)
Markera
Maxantalet träffar du kan exportera från sökgränssnittet är 250. Vid större uttag använd dig av utsökningar.
  • 101. Ritte, Rebecca
    et al.
    Lukanova, Annekatrin
    Berrino, Franco
    Dossus, Laure
    Tjønneland, Anne
    Olsen, Anja
    Overvad, Thure Filskov
    Overvad, Kim
    Clavel-Chapelon, Françoise
    Fournier, Agnès
    Fagherazzi, Guy
    Rohrmann, Sabine
    Teucher, Birgit
    Boeing, Heiner
    Aleksandrova, Krasimira
    Trichopoulou, Antonia
    Lagiou, Pagona
    Trichopoulos, Dimitrios
    Palli, Domenico
    Sieri, Sabina
    Panico, Salvatore
    Tumino, Rosario
    Vineis, Paolo
    Quirós, José Ramón
    Buckland, Genevieve
    Sánchez, Maria-José
    Amiano, Pilar
    Chirlaque, María-Dolores
    Ardanaz, Eva
    Sund, Malin
    Umeå universitet, Medicinska fakulteten, Institutionen för kirurgisk och perioperativ vetenskap, Kirurgi.
    Lenner, Per
    Umeå universitet, Medicinska fakulteten, Institutionen för strålningsvetenskaper, Onkologi.
    Bueno-de-Mesquita, Bas
    van Gils, Carla H
    Peeters, Petra Hm
    Krum-Hansen, Sanda
    Gram, Inger Torhild
    Lund, Eiliv
    Khaw, Kay-Tee
    Wareham, Nick
    Allen, Naomi E
    Key, Timothy J
    Romieu, Isabelle
    Rinaldi, Sabina
    Siddiq, Afshan
    Cox, David
    Riboli, Elio
    Kaaks, Rudolf
    Adiposity, hormone replacement therapy use and breast cancer risk by age and hormone receptor status: a large prospective cohort study.2012Ingår i: Breast cancer research : BCR, ISSN 1465-542X, Vol. 14, nr 3, s. R76-Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    ABSTRACT: INTRODUCTION: Associations of hormone-receptor positive breast cancer with excess adiposity are reasonably well characterized; however, uncertainty remains regarding the association of body mass index (BMI) with hormone-receptor negative malignancies, and possible interactions by hormone replacement therapy (HRT) use. METHODS: Within the European EPIC cohort, Cox proportional hazards models were used to describe the relationship of BMI, waist and hip circumferences with risk of estrogen-receptor (ER) negative and progesterone-receptor (PR) negative (n = 1,021) and ER+PR+ (n = 3,586) breast tumors within five-year age bands. Among postmenopausal women, the joint effects of BMI and HRT use were analyzed. RESULTS: For risk of ER-PR- tumors, there was no association of BMI across the age bands. However, when analyses were restricted to postmenopausal HRT never users, a positive risk association with BMI (third versus first tertile HR = 1.47 (1.01 to 2.15)) was observed. BMI was inversely associated with ER+PR+ tumors among women aged ≤49 years (per 5 kg/m2 increase, HR = 0.79 (95%CI 0.68 to 0.91)), and positively associated with risk among women ≥65 years (HR = 1.25 (1.16 to 1.34)). Adjusting for BMI, waist and hip circumferences showed no further associations with risks of breast cancer subtypes. Current use of HRT was significantly associated with an increased risk of receptor-negative (HRT current use compared to HRT never use HR: 1.30 (1.05 to 1.62)) and positive tumors (HR: 1.74 (1.56 to 1.95)), although this risk increase was weaker for ER-PR- disease (Phet = 0.035). The association of HRT was significantly stronger in the leaner women (BMI ≤22.5 kg/m2) than for more overweight women (BMI ≥25.9 kg/m2) for, both, ER-PR- (HR: 1.74 (1.15 to 2.63)) and ER+PR+ (HR: 2.33 (1.84 to 2.92)) breast cancer and was not restricted to any particular HRT regime. CONCLUSIONS: An elevated BMI may be positively associated with risk of ER-PR- tumors among postmenopausal women who never used HRT. Furthermore, postmenopausal HRT users were at an increased risk of ER-PR- as well as ER+PR+ tumors, especially among leaner women. For hormone-receptor positive tumors, but not for hormone-receptor negative tumors, our study confirms an inverse association of risk with BMI among young women of premenopausal age. Our data provide evidence for a possible role of sex hormones in the etiology of hormone-receptor negative tumors.

  • 102. Ritte, Rebecca
    et al.
    Lukanova, Annekatrin
    Tjonneland, Anne
    Olsen, Anja
    Overvad, Kim
    Mesrine, Sylvie
    Fagherazzi, Guy
    Dossus, Laure
    Teucher, Birgit
    Steindorf, Karen
    Boeing, Heiner
    Aleksandrova, Krasimira
    Trichopoulou, Antonia
    Lagiou, Pagona
    Trichopoulos, Dimitrios
    Palli, Domenico
    Grioni, Sara
    Mattiello, Amalia
    Tumino, Rosario
    Sacerdote, Carlotta
    Ramon Quiros, Jose
    Buckland, Genevieve
    Molina-Montes, Esther
    Chirlaque, Maria-Dolores
    Ardanaz, Eva
    Amiano, Pilar
    Bueno-de-Mesquita, Bas
    van Duijnhoven, Franzel
    van Gils, Carla H.
    Peeters, Petra H. M.
    Wareham, Nick
    Khaw, Kay-Tee
    Key, Timothy J.
    Travis, Ruth C.
    Krum-Hansen, Sanda
    Gram, Inger Torhild
    Lund, Eiliv
    Sund, Malin
    Umeå universitet, Medicinska fakulteten, Institutionen för kirurgisk och perioperativ vetenskap, Kirurgi.
    Andersson, Anne
    Umeå universitet, Medicinska fakulteten, Institutionen för strålningsvetenskaper, Onkologi.
    Romieu, Isabelle
    Rinaldi, Sabina
    McCormack, Valerie
    Riboli, Elio
    Kaaks, Rudolf
    Height, age at menarche and risk of hormone receptor-positive and -negative breast cancer: A cohort study2013Ingår i: International Journal of Cancer, ISSN 0020-7136, E-ISSN 1097-0215, Vol. 132, nr 11, s. 2619-2629Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Associations of breast cancer overall with indicators of exposures during puberty are reasonably well characterized; however, uncertainty remains regarding the associations of height, leg length, sitting height and menarcheal age with hormone receptor-defined malignancies. Within the European Prospective Investigation into Cancer and Nutrition cohort, Cox proportional hazards models were used to describe the relationships of adult height, leg length and sitting height and age at menarche with risk of estrogen and progesterone receptor negative (ER-PR-) (n = 990) and ER+PR+ (n = 3,524) breast tumors. Height as a single risk factor was compared to a model combining leg length and sitting height. The possible interactions of height, leg length and sitting height with menarche were also analyzed. Risk of both ER-PR- and ER+PR+ malignancies was positively associated with standing height, leg length and sitting height and inversely associated with increasing age at menarche. For ER+PR+ disease, sitting height (hazard ratios: 1.14[95% confidence interval: 1.081.20]) had a stronger risk association than leg length (1.05[1.001.11]). In comparison, for ER-PR- disease, no distinct differences were observed between leg length and sitting height. Women who were tall and had an early menarche (13 years) showed an almost twofold increase in risk of ER+PR+ tumors but no such increase in risk was observed for ER-PR- disease. Indicators of exposures during rapid growth periods were associated with risks of both HR-defined breast cancers. Exposures during childhood promoting faster development may establish risk associations for both HR-positive and negative malignancies. The stronger associations of the components of height with ER+PR+ tumors among older women suggest possible hormonal links that could be specific for postmenopausal women.

  • 103. Ritte, Rebecca
    et al.
    Tikk, Kaja
    Lukanova, Annekatrin
    Tjonneland, Anne
    Olsen, Anja
    Overvad, Kim
    Dossus, Laure
    Fournier, Agnes
    Clavel-Chapelon, Francoise
    Grote, Verena
    Boeing, Heiner
    Aleksandrova, Krasimira
    Trichopoulou, Antonia
    Lagiou, Pagona
    Trichopoulos, Dimitrios
    Palli, Domenico
    Berrino, Franco
    Mattiello, Amalia
    Tumino, Rosario
    Sacerdote, Carlotta
    Ramon Quiros, Jose
    Buckland, Genevieve
    Molina-Montes, Esther
    Chirlaque, Maria-Dolores
    Ardanaz, Eva
    Amiano, Pilar
    Bueno-de-Mesquita, H. Bas
    van Gils, Carla H.
    Peeters, Petra H. M.
    Wareham, Nick
    Khaw, Kay-Tee
    Key, Timothy J.
    Travis, Ruth C.
    Weiderpass, Elisabete
    Dumeaux, Vanessa
    Lund, Eliv
    Sund, Malin
    Umeå universitet, Medicinska fakulteten, Institutionen för kirurgisk och perioperativ vetenskap, Kirurgi.
    Andersson, Anne
    Umeå universitet, Medicinska fakulteten, Institutionen för strålningsvetenskaper, Onkologi. Umeå universitet, Medicinska fakulteten, Institutionen för klinisk vetenskap, Professionell utveckling.
    Romieu, Isabelle
    Rinaldi, Sabina
    Vineis, Paulo
    Merritt, Melissa A.
    Riboli, Elio
    Kaaks, Rudolf
    Reproductive factors and risk of hormone receptor positive and negative breast cancer: a cohort study2013Ingår i: BMC Cancer, ISSN 1471-2407, E-ISSN 1471-2407, Vol. 13, s. Article Number: 584-Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Background: The association of reproductive factors with hormone receptor (HR)-negative breast tumors remains uncertain. Methods: Within the EPIC cohort, Cox proportional hazards models were used to describe the relationships of reproductive factors (menarcheal age, time between menarche and first pregnancy, parity, number of children, age at first and last pregnancies, time since last full-term childbirth, breastfeeding, age at menopause, ever having an abortion and use of oral contraceptives [OC]) with risk of ER-PR-(n = 998) and ER+PR+ (n = 3,567) breast tumors. Results: A later first full-term childbirth was associated with increased risk of ER+PR+ tumors but not with risk of ER-PR-tumors (= 35 vs. = 19 years HR: 1.47 [95% CI 1.15-1.88] p(trend) < 0.001 for ER+PR+ tumors; = 35 vs. = 19 years HR: 0.93 [95% CI 0.53-1.65] p(trend) = 0.96 for ER-PR-tumors; P-het = 0.03). The risk associations of menarcheal age, and time period between menarche and first full-term childbirth with ER-PR-tumors were in the similar direction with risk of ER+PR+ tumors (p(het) = 0.50), although weaker in magnitude and statistically only borderline significant. Other parity related factors such as ever a full-term birth, number of births, age-and time since last birth were associated only with ER+PR+ malignancies, however no statistical heterogeneity between breast cancer subtypes was observed. Breastfeeding and OC use were generally not associated with breast cancer subtype risk. Conclusion: Our study provides possible evidence that age at menarche, and time between menarche and first full-term childbirth may be associated with the etiology of both HR-negative and HR-positive malignancies, although the associations with HR-negative breast cancer were only borderline significant.

  • 104. Rohrmann, S
    et al.
    Grote, VA
    Becker, S
    Rinaldi, S
    Tjonneland, A
    Roswall, N
    Gronbaek, H
    Overvad, K
    Boutron-Ruault, MC
    Clavel-Chapelon, F
    Racine, A
    Teucher, B
    Boeing, H
    Drogan, D
    Dilis, V
    Lagiou, P
    Trichopoulou, A
    Palli, D
    Tagliabue, G
    Tumino, R
    Vineis, P
    Mattiello, A
    Rodriguez, L
    Duell, EJ
    Molina-Montes, E
    Dorronsoro, M
    Huerta, J-M
    Ardanaz, E
    Jeurnink, S
    Peeters, PHM
    Lindkvist, B
    Johansen, D
    Sund, Malin
    Umeå universitet, Medicinska fakulteten, Institutionen för kirurgisk och perioperativ vetenskap, Kirurgi.
    Ye, W
    Khaw, K-T
    Wareham, NJ
    Allen, NE
    Crowe, FL
    Fedirko, V
    Jenab, M
    Michaud, DS
    Norat, T
    Riboli, E
    Bueno-de-Mesquita, HB
    Kaaks, R
    Concentrations of IGF-I and IGFBP-3 and pancreatic cancer risk in the European Prospective Investigation into Cancer and Nutrition2012Ingår i: British Journal of Cancer, ISSN 0007-0920, E-ISSN 1532-1827, Vol. 106, nr 5, s. 1004-1010Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    BACKGROUND: Insulin-like growth factors (IGFs) and their binding proteins (BPs) regulate cell differentiation, proliferation and apoptosis, and may have a role in the aetiology of various cancers. Information on their role in pancreatic cancer is limited and was examined here in a case-control study nested within the European Prospective Investigation into Cancer and Nutrition.

    METHODS: Serum concentrations of IGF-I and IGFBP-3 were measured using enzyme-linked immunosorbent assays in 422 cases and 422 controls matched on age, sex, study centre, recruitment date, and time since last meal. Conditional logistic regression was used to compute odds ratios (OR) and 95% confidence intervals (CI) adjusted for confounding variables.

    RESULTS: Neither circulating levels of IGF-I (OR = 1.21, 95% CI 0.75-1.93 for top vs bottom quartile, P-trend 0.301), IGFBP-3 (OR = 1.00, 95% CI 0.66-1.51, P-trend 0.79), nor the molar IGF-I/IGFBP-3 ratio, an indicator of free IGF-I level (OR = 1.22, 95% CI 0.75-1.97, P-trend 0.27), were statistically significantly associated with the risk of pancreatic cancer. In a cross-classification, however, a high concentration of IGF-I with concurrently low levels of IGFBP-3 was related to an increased risk of pancreatic cancer (OR = 1.72, 95% CI 1.05-2.83; P-interaction = 0.154).

    CONCLUSION: On the basis of these results, circulating levels of components of the IGF axis do not appear to be the risk factors for pancreatic cancer. However, on the basis of the results of a subanalysis, it cannot be excluded that a relatively large amount of IGF-1 together with very low levels of IGFBP-3 might still be associated with an increase in pancreatic cancer risk.

    British Journal of Cancer (2012) 106, 1004-1010. doi:10.1038/bjc.2012.19 www.bjcancer.com Published online 7 February 2012 (C) 2012 Cancer Research UK

  • 105. Rohrmann, Sabine
    et al.
    Linseisen, Jakob
    Nöthlings, Ute
    Overvad, Kim
    Egeberg, Rikke
    Tjønneland, Anne
    Boutron-Ruault, Marie Christine
    Clavel-Chapelon, Françoise
    Cottet, Vanessa
    Pala, Valeria
    Tumino, Rosario
    Palli, Domenico
    Panico, Salvatore
    Vineis, Paolo
    Boeing, Heiner
    Pischon, Tobias
    Grote, Verena
    Teucher, Birigit
    Khaw, Kay-Tee
    Wareham, Nicholas J
    Crowe, Francesca L
    Goufa, Ioulia
    Orfanos, Philippos
    Trichopoulou, Antonia
    Jeurnink, Suzanne M
    Siersema, Peter D
    Peeters, Petra HM
    Brustad, Magritt
    Engeset, Dagrun
    Skeie, Guri
    Duell, Eric J
    Amiano, Pilar
    Barricarte, Aurelio
    Molina-Montes, Esther
    Rodríguez, Laudina
    Tormo, María-José
    Sund, Malin
    Umeå universitet, Medicinska fakulteten, Institutionen för kirurgisk och perioperativ vetenskap, Kirurgi.
    Ye, Weimin
    Lindkvist, Björn
    Johansen, Dorthe
    Ferrari, Pietro
    Jenab, Mazda
    Slimani, Nadia
    Ward, Heather
    Riboli, Elio
    Norat, Teresa
    Bueno-de-Mesquita, H Bas
    Meat and fish consumption and risk of pancreatic cancer: results from the European Prospective Investigation into Cancer and Nutrition2013Ingår i: International Journal of Cancer, ISSN 0020-7136, E-ISSN 1097-0215, Vol. 132, nr 3, s. 617-624Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Pancreatic cancer is the fourth most common cause of cancer death worldwide with large geographical variation, which implies the contribution of diet and lifestyle in its etiology. We examined the association of meat and fish consumption with risk of pancreatic cancer in the European Prospective Investigation into Cancer and Nutrition (EPIC). A total of 477,202 EPIC participants from 10 European countries recruited between 1992 and 2000 were included in our analysis. Until 2008, 865 nonendocrine pancreatic cancer cases have been observed. Calibrated relative risks (RRs) and 95% confidence intervals (CIs) were computed using multivariable-adjusted Cox hazard regression models. The consumption of red meat (RR per 50 g increase per day = 1.03, 95% CI = 0.93-1.14) and processed meat (RR per 50 g increase per day = 0.93, 95% CI = 0.71-1.23) were not associated with an increased pancreatic cancer risk. Poultry consumption tended to be associated with an increased pancreatic cancer risk (RR per 50 g increase per day = 1.72, 95% CI = 1.04-2.84); however, there was no association with fish consumption (RR per 50 g increase per day = 1.22, 95% CI = 0.92-1.62). Our results do not support the conclusion of the World Cancer Research Fund that red or processed meat consumption may possibly increase the risk of pancreatic cancer. The positive association of poultry consumption with pancreatic cancer might be a chance finding as it contradicts most previous findings.

  • 106. Sampson, Joshua N.
    et al.
    Wheeler, William A.
    Yeager, Meredith
    Panagiotou, Orestis
    Wang, Zhaoming
    Berndt, Sonja I.
    Lan, Qing
    Abnet, Christian C.
    Amundadottir, Laufey T.
    Figueroa, Jonine D.
    Landi, Maria Teresa
    Mirabello, Lisa
    Savage, Sharon A.
    Taylor, Philip R.
    De Vivo, Immaculata
    McGlynn, Katherine A.
    Purdue, Mark P.
    Rajaraman, Preetha
    Adami, Hans-Olov
    Ahlbom, Anders
    Albanes, Demetrius
    Amary, Maria Fernanda
    An, She-Juan
    Andersson, Ulrika
    Umeå universitet, Medicinska fakulteten, Institutionen för strålningsvetenskaper, Onkologi.
    Andriole, Gerald, Jr.
    Andrulis, Irene L.
    Angelucci, Emanuele
    Ansell, Stephen M.
    Arici, Cecilia
    Armstrong, Bruce K.
    Arslan, Alan A.
    Austin, Melissa A.
    Baris, Dalsu
    Barkauskas, Donald A.
    Bassig, Bryan A.
    Becker, Nikolaus
    Benavente, Yolanda
    Benhamou, Simone
    Berg, Christine
    Van Den Berg, David
    Bernstein, Leslie
    Bertrand, Kimberly A.
    Birmann, Brenda M.
    Black, Amanda
    Boeing, Heiner
    Boffetta, Paolo
    Boutron-Ruault, Marie-Christine
    Bracci, Paige M.
    Brinton, Louise
    Brooks-Wilson, Angela R.
    Bueno-de-Mesquita, H. Bas
    Burdett, Laurie
    Buring, Julie
    Butler, Mary Ann
    Cai, Qiuyin
    Cancel-Tassin, Geraldine
    Canzian, Federico
    Carrato, Alfredo
    Carreon, Tania
    Carta, Angela
    Chan, John K. C.
    Chang, Ellen T.
    Chang, Gee-Chen
    Chang, I-Shou
    Chang, Jiang
    Chang-Claude, Jenny
    Chen, Chien-Jen
    Chen, Chih-Yi
    Chen, Chu
    Chen, Chung-Hsing
    Chen, Constance
    Chen, Hongyan
    Chen, Kexin
    Chen, Kuan-Yu
    Chen, Kun-Chieh
    Chen, Ying
    Chen, Ying-Hsiang
    Chen, Yi-Song
    Chen, Yuh-Min
    Chien, Li-Hsin
    Chirlaque, Maria-Dolores
    Choi, Jin Eun
    Choi, Yi Young
    Chow, Wong-Ho
    Chung, Charles C.
    Clavel, Jacqueline
    Clavel-Chapelon, Franoise
    Cocco, Pierluigi
    Colt, Joanne S.
    Comperat, Eva
    Conde, Lucia
    Connors, Joseph M.
    Conti, David
    Cortessis, Victoria K.
    Cotterchio, Michelle
    Cozen, Wendy
    Crouch, Simon
    Crous-Bou, Marta
    Cussenot, Olivier
    Davis, Faith G.
    Ding, Ti
    Diver, W. Ryan
    Dorronsoro, Miren
    Dossus, Laure
    Duell, Eric J.
    Ennas, Maria Grazia
    Erickson, Ralph L.
    Feychting, Maria
    Flanagan, Adrienne M.
    Foretova, Lenka
    Fraumeni, Joseph F., Jr.
    Freedman, Neal D.
    Freeman, Laura E. Beane
    Fuchs, Charles
    Gago-Dominguez, Manuela
    Gallinger, Steven
    Gao, Yu-Tang
    Gapstur, Susan M.
    Garcia-Closas, Montserrat
    Garcia-Closas, Reina
    Gascoyne, Randy D.
    Gastier-Foster, Julie
    Gaudet, Mia M.
    Gaziano, J. Michael
    Giffen, Carol
    Giles, Graham G.
    Giovannucci, Edward
    Glimelius, Bengt
    Goggins, Michael
    Gokgoz, Nalan
    Goldstein, Alisa M.
    Gorlick, Richard
    Gross, Myron
    Grubb, Robert, III
    Gu, Jian
    Guan, Peng
    Gunter, Marc
    Guo, Huan
    Habermann, Thomas M.
    Haiman, Christopher A.
    Halai, Dina
    Hallmans, Göran
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin, Näringsforskning.
    Hassan, Manal
    Hattinger, Claudia
    He, Qincheng
    He, Xingzhou
    Helzlsouer, Kathy
    Henderson, Brian
    Henriksson, Roger
    Umeå universitet, Medicinska fakulteten, Institutionen för strålningsvetenskaper, Onkologi.
    Hjalgrim, Henrik
    Hoffman-Bolton, Judith
    Hohensee, Chancellor
    Holford, Theodore R.
    Holly, Elizabeth A.
    Hong, Yun-Chul
    Hoover, Robert N.
    Horn-Ross, Pamela L.
    Hosain, G. M. Monawar
    Hosgood, H. Dean, III
    Hsiao, Chin-Fu
    Hu, Nan
    Hu, Wei
    Hu, Zhibin
    Huang, Ming-Shyan
    Huerta, Jose-Maria
    Hung, Jen-Yu
    Hutchinson, Amy
    Inskip, Peter D.
    Jackson, Rebecca D.
    Jacobs, Eric J.
    Jenab, Mazda
    Jeon, Hyo-Sung
    Ji, Bu-Tian
    Jin, Guangfu
    Jin, Li
    Johansen, Christoffer
    Johnson, Alison
    Jung, Yoo Jin
    Kaaks, Rudolph
    Kamineni, Aruna
    Kane, Eleanor
    Kang, Chang Hyun
    Karagas, Margaret R.
    Kelly, Rachel S.
    Khaw, Kay-Tee
    Kim, Christopher
    Kim, Hee Nam
    Kim, Jin Hee
    Kim, Jun Suk
    Kim, Yeul Hong
    Kim, Young Tae
    Kim, Young-Chul
    Kitahara, Cari M.
    Klein, Alison P.
    Klein, Robert J.
    Kogevinas, Manolis
    Kohno, Takashi
    Kolonel, Laurence N.
    Kooperberg, Charles
    Kricker, Anne
    Krogh, Vittorio
    Kunitoh, Hideo
    Kurtz, Robert C.
    Kweon, Sun-Seog
    LaCroix, Andrea
    Lawrence, Charles
    Lecanda, Fernando
    Lee, Victor Ho Fun
    Li, Donghui
    Li, Haixin
    Li, Jihua
    Li, Yao-Jen
    Li, Yuqing
    Liao, Linda M.
    Liebow, Mark
    Lightfoot, Tracy
    Lim, Wei-Yen
    Lin, Chien-Chung
    Lin, Dongxin
    Lindstrom, Sara
    Linet, Martha S.
    Link, Brian K.
    Liu, Chenwei
    Liu, Jianjun
    Liu, Li
    Ljungberg, Börje
    Umeå universitet, Medicinska fakulteten, Institutionen för kirurgisk och perioperativ vetenskap, Urologi och andrologi.
    Lloreta, Josep
    Di Lollo, Simonetta
    Lu, Daru
    Lund, Eiluv
    Malats, Nuria
    Mannisto, Satu
    Le Marchand, Loic
    Marina, Neyssa
    Masala, Giovanna
    Mastrangelo, Giuseppe
    Matsuo, Keitaro
    Maynadie, Marc
    Mckay, James
    McKean-Cowdin, Roberta
    Melbye, Mads
    Melin, Beatrice S.
    Umeå universitet, Medicinska fakulteten, Institutionen för strålningsvetenskaper, Onkologi.
    Michaud, Dominique S.
    Mitsudomi, Tetsuya
    Monnereau, Alain
    Montalvan, Rebecca
    Moore, Lee E.
    Mortensen, Lotte Maxild
    Nieters, Alexandra
    North, Kari E.
    Novak, Anne J.
    Oberg, Ann L.
    Offit, Kenneth
    Oh, In-Jae
    Olson, Sara H.
    Palli, Domenico
    Pao, William
    Park, In Kyu
    Park, Jae Yong
    Park, Kyong Hwa
    Patino-Garcia, Ana
    Pavanello, Sofia
    Peeters, Petra H. M.
    Perng, Reury-Perng
    Peters, Ulrike
    Petersen, Gloria M.
    Picci, Piero
    Pike, Malcolm C.
    Porru, Stefano
    Prescott, Jennifer
    Prokunina-Olsson, Ludmila
    Qian, Biyun
    Qiao, You-Lin
    Rais, Marco
    Riboli, Elio
    Riby, Jacques
    Risch, Harvey A.
    Rizzato, Cosmeri
    Rodabough, Rebecca
    Roman, Eve
    Roupret, Morgan
    Ruder, Avima M.
    de Sanjose, Silvia
    Scelo, Ghislaine
    Schned, Alan
    Schumacher, Fredrick
    Schwartz, Kendra
    Schwenn, Molly
    Scotlandi, Katia
    Seow, Adeline
    Serra, Consol
    Serra, Massimo
    Sesso, Howard D.
    Setiawan, Veronica Wendy
    Severi, Gianluca
    Severson, Richard K.
    Shanafelt, Tait D.
    Shen, Hongbing
    Shen, Wei
    Shin, Min-Ho
    Shiraishi, Kouya
    Shu, Xiao-Ou
    Siddiq, Afshan
    Sierrasesumaga, Luis
    Sihoe, Alan Dart Loon
    Skibola, Christine F.
    Smith, Alex
    Smith, Martyn T.
    Southey, Melissa C.
    Spinelli, John J.
    Staines, Anthony
    Stampfer, Meir
    Stern, Marianna C.
    Stevens, Victoria L.
    Stolzenberg-Solomon, Rachael S.
    Su, Jian
    Su, Wu-Chou
    Sund, Malin
    Umeå universitet, Medicinska fakulteten, Institutionen för kirurgisk och perioperativ vetenskap, Kirurgi.
    Sung, Jae Sook
    Sung, Sook Whan
    Tan, Wen
    Tang, Wei
    Tardon, Adonina
    Thomas, David
    Thompson, Carrie A.
    Tinker, Lesley F.
    Tirabosco, Roberto
    Tjonneland, Anne
    Travis, Ruth C.
    Trichopoulos, Dimitrios
    Tsai, Fang-Yu
    Tsai, Ying-Huang
    Tucker, Margaret
    Turner, Jenny
    Vajdic, Claire M.
    Vermeulen, Roel C. H.
    Villano, Danylo J.
    Vineis, Paolo
    Virtamo, Jarmo
    Visvanathan, Kala
    Wactawski-Wende, Jean
    Wang, Chaoyu
    Wang, Chih-Liang
    Wang, Jiu-Cun
    Wang, Junwen
    Wei, Fusheng
    Weiderpass, Elisabete
    Weiner, George J.
    Weinstein, Stephanie
    Wentzensen, Nicolas
    White, Emily
    Witzig, Thomas E.
    Wolpin, Brian M.
    Wong, Maria Pik
    Wu, Chen
    Wu, Guoping
    Wu, Junjie
    Wu, Tangchun
    Wu, Wei
    Wu, Xifeng
    Wu, Yi-Long
    Wunder, Jay S.
    Xiang, Yong-Bing
    Xu, Jun
    Xu, Ping
    Yang, Pan-Chyr
    Yang, Tsung-Ying
    Ye, Yuanqing
    Yin, Zhihua
    Yokota, Jun
    Yoon, Ho-Il
    Yu, Chong-Jen
    Yu, Herbert
    Yu, Kai
    Yuan, Jian-Min
    Zelenetz, Andrew
    Zeleniuch-Jacquotte, Anne
    Zhang, Xu-Chao
    Zhang, Yawei
    Zhao, Xueying
    Zhao, Zhenhong
    Zheng, Hong
    Zheng, Tongzhang
    Zheng, Wei
    Zhou, Baosen
    Zhu, Meng
    Zucca, Mariagrazia
    Boca, Simina M.
    Cerhan, James R.
    Ferri, Giovanni M.
    Hartge, Patricia
    Hsiung, Chao Agnes
    Magnani, Corrado
    Miligi, Lucia
    Morton, Lindsay M.
    Smedby, Karin E.
    Teras, Lauren R.
    Vijai, Joseph
    Wang, Sophia S.
    Brennan, Paul
    Caporaso, Neil E.
    Hunter, David J.
    Kraft, Peter
    Rothman, Nathaniel
    Silverman, Debra T.
    Slager, Susan L.
    Chanock, Stephen J.
    Chatterjee, Nilanjan
    Analysis of Heritability and Shared Heritability Based on Genome-Wide Association Studies for 13 Cancer Types2015Ingår i: Journal of the National Cancer Institute, ISSN 0027-8874, E-ISSN 1460-2105, Vol. 107, nr 12, artikel-id djv279Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Background: Studies of related individuals have consistently demonstrated notable familial aggregation of cancer. We aim to estimate the heritability and genetic correlation attributable to the additive effects of common single-nucleotide polymorphisms (SNPs) for cancer at 13 anatomical sites.

    Methods: Between 2007 and 2014, the US National Cancer Institute has generated data from genome-wide association studies (GWAS) for 49 492 cancer case patients and 34 131 control patients. We apply novel mixed model methodology (GCTA) to this GWAS data to estimate the heritability of individual cancers, as well as the proportion of heritability attributable to cigarette smoking in smoking-related cancers, and the genetic correlation between pairs of cancers.

    Results: GWAS heritability was statistically significant at nearly all sites, with the estimates of array-based heritability, h(l)(2), on the liability threshold (LT) scale ranging from 0.05 to 0.38. Estimating the combined heritability of multiple smoking characteristics, we calculate that at least 24% (95% confidence interval [CI] = 14% to 37%) and 7% (95% CI = 4% to 11%) of the heritability for lung and bladder cancer, respectively, can be attributed to genetic determinants of smoking. Most pairs of cancers studied did not show evidence of strong genetic correlation. We found only four pairs of cancers with marginally statistically significant correlations, specifically kidney and testes (rho = 0.73, SE = 0.28), diffuse large B-cell lymphoma (DLBCL) and pediatric osteosarcoma (rho = 0.53, SE = 0.21), DLBCL and chronic lymphocytic leukemia (CLL) (rho = 0.51, SE = 0.18), and bladder and lung (rho = 0.35, SE = 0.14). Correlation analysis also indicates that the genetic architecture of lung cancer differs between a smoking population of European ancestry and a nonsmoking Asian population, allowing for the possibility that the genetic etiology for the same disease can vary by population and environmental exposures.

    Conclusion: Our results provide important insights into the genetic architecture of cancers and suggest new avenues for investigation.

  • 107. Schlesinger, S
    et al.
    Aleksandrova, K
    Pischon, T
    Jenab, M
    Fedirko, V
    Trepo, E
    Overvad, K
    Roswall, N
    Tjønneland, A
    Boutron-Ruault, M C
    Fagherazzi, G
    Racine, A
    Kaaks, R
    Grote, V A
    Boeing, H
    Trichopoulou, A
    Pantzalis, M
    Kritikou, M
    Mattiello, A
    Sieri, S
    Sacerdote, C
    Palli, D
    Tumino, R
    Peeters, P H
    Bueno-de-Mesquita, H B
    Weiderpass, E
    Quirós, J R
    Zamora-Ros, R
    Sánchez, M J
    Arriola, L
    Ardanaz, E
    Tormo, M J
    Nilsson, P
    Lindkvist, B
    Sund, Malin
    Umeå universitet, Medicinska fakulteten, Institutionen för kirurgisk och perioperativ vetenskap, Kirurgi.
    Rolandsson, Olov
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin, Allmänmedicin.
    Khaw, K T
    Wareham, N
    Travis, R C
    Riboli, E
    Nöthlings, U
    Diabetes mellitus, insulin treatment, diabetes duration, and risk of biliary tract cancer and hepatocellular carcinoma in a European cohort2013Ingår i: Annals of Oncology, ISSN 0923-7534, E-ISSN 1569-8041, Vol. 24, nr 9, s. 2449-2455Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    BACKGROUND: Evidence on associations between self-reported diabetes mellitus, diabetes duration, age at diabetes diagnosis, insulin treatment, and risk of biliary tract cancer (BTC) and hepatocellular carcinoma (HCC), independent of general and abdominal obesity is scarce. PATIENTS AND METHODS: We conducted a prospective analysis in the EPIC-cohort study among 363 426 participants with self-reported diabetes data. Multivariable adjusted relative risks and 95% confidence intervals were estimated from Cox regression models. In a nested case-control subset, analyses were carried out in HCV/HBV-negative individuals. RESULTS: During 8.5 years of follow-up, 204 BTC cases [including 75 gallbladder cancer (GBC) cases], and 176 HCC cases were identified. Independent of body mass index and waist-to-height ratio diabetes status was associated with higher risk of BTC and HCC [1.77 (1.00-3.13) and 2.17 (1.36-3.47)]. For BTC, the risk seemed to be higher in participants with shorter diabetes duration and those not treated with insulin. Regarding cancer subsites, diabetes was only associated with GBC [2.72 (1.17-6.31)]. The risk for HCC was particularly higher in participants treated with insulin. The results were not appreciably different in HCV/HBV-negative individuals. CONCLUSION(S): This study supports the hypothesis that diabetes is a risk factor for BTC (particularly GBC) and HCC. Further research is required to establish whether diabetes treatment or duration is associated with these cancers.

  • 108. Schlesinger, Sabrina
    et al.
    Aleksandrova, Krasimira
    Pischon, Tobias
    Fedirko, Veronika
    Jenab, Mazda
    Trepo, Elisabeth
    Boffetta, Paolo
    Dahm, Christina C
    Overvad, Kim
    Tjønneland, Anne
    Halkjaer, Jytte
    Fagherazzi, Guy
    Boutron-Ruault, Marie-Christine
    Carbonnel, Franck
    Kaaks, Rudolf
    Lukanova, Annekatrin
    Boeing, Heiner
    Trichopoulou, Antonia
    Bamia, Christina
    Lagiou, Pagona
    Palli, Domenico
    Grioni, Sara
    Panico, Salvatore
    Tumino, Rosario
    Vineis, Paolo
    Bueno-de-Mesquita, HB
    van den Berg, Saskia
    Peeters, Petra HM
    Braaten, Tonje
    Weiderpass, Elisabete
    Quirós, J Ramón
    Travier, Noémie
    Sánchez, María-José
    Navarro, Carmen
    Barricarte, Aurelio
    Dorronsoro, Miren
    Lindkvist, Björn
    Regner, Sara
    Werner, Mårten
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin, Medicin.
    Sund, Malin
    Umeå universitet, Medicinska fakulteten, Institutionen för kirurgisk och perioperativ vetenskap, Kirurgi.
    Khaw, Kay-Tee
    Wareham, Nicholas
    Travis, Ruth C
    Norat, Teresa
    Wark, Petra A
    Riboli, Elio
    Nöthlings, Ute
    Abdominal obesity, weight gain during adulthood and risk of liver and biliary tract cancer in a European cohort2013Ingår i: International Journal of Cancer, ISSN 0020-7136, E-ISSN 1097-0215, Vol. 132, nr 3, s. 645-657Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    General obesity has been positively associated with risk of liver and probably with biliary tract cancer, but little is known about abdominal obesity or weight gain during adulthood. We used multivariable Cox proportional hazard models to investigate associations between weight, body mass index, waist and hip circumference, waist-to-hip and waist-to-height ratio (WHtR), weight change during adulthood and risk of hepatocellular carcinoma (HCC), intrahepatic (IBDC) and extrahepatic bile duct system cancer [EBDSC including gallbladder cancer (GBC)] among 359,525 men and women in the European Prospective Investigation into Cancer and Nutrition study. Hepatitis B and C virus status was measured in a nested case-control subset. During a mean follow-up of 8.6 years, 177 cases of HCC, 58 cases of IBDC and 210 cases of EBDSC, including 76 cases of GBC, occurred. All anthropometric measures were positively associated with risk of HCC and GBC. WHtR showed the strongest association with HCC [relative risk (RR) comparing extreme tertiles 3.51, 95% confidence interval (95% CI): 2.09-5.87; p(trend) < 0.0001] and with GBC (RR: 1.56, 95% CI: 1.12-2.16 for an increment of one unit in WHtR). Weight gain during adulthood was also positively associated with HCC when comparing extreme tertiles (RR: 2.48, 95% CI: 1.49-4.13; <0.001). No statistically significant association was observed between obesity and risk of IBDC and EBDSC. Our results provide evidence of an association between obesity, particularly abdominal obesity, and risk of HCC and GBC. Our findings support public health recommendations to reduce the prevalence of obesity and weight gain in adulthood for HCC and GBC prevention in Western populations.

  • 109. Schober, Marvin
    et al.
    Javed, Muhammad A.
    Beyer, G.
    Le, Nha
    Vinci, Alessio
    Sund, Malin
    Umeå universitet, Medicinska fakulteten, Institutionen för kirurgisk och perioperativ vetenskap, Kirurgi.
    Neesse, Albrecht
    Krug, Sebastian
    New Advances in the Treatment of Metastatic Pancreatic Cancer2015Ingår i: Digestion, ISSN 0012-2823, E-ISSN 1421-9867, Vol. 92, nr 3, s. 175-184Artikel, forskningsöversikt (Refereegranskat)
    Abstract [en]

    Background: Pancreatic ductal adenocarcinoma (PDAC) is characterised by an extremely poor overall survival (OS) compared to other solid tumours. As the incidence of the disease is rising and the treatment options are limited, PDAC is projected to be the 2nd leading cause of cancer-related deaths in the United States by 2030. A majority of patients are not eligible for curative resection at the time of diagnosis, and those that are resected will often relapse within the first few years after surgery. Summary: Until recently, the nucleoside analogue gemcitabine has been the standard of care for patients with non-resectable PDAC with only marginal effects on OS. In 2011, the gemcitabine-free FOLFIRINOX regimen (folinic acid, fluorouracil, irinotecan and oxaliplatin) showed a significant survival advantage for patients with metastatic PDAC in a phase III trial. In 2013, the Metastatic Pancreatic Adenocarcinoma Trial phase III trial with nano-formulated albumin-bound paclitaxel (nab-paclitaxel) in combination with gemcitabine also resulted in a significant survival extension compared to gemcitabine monotherapy. However, both intensified therapy regimens show a broad spectrum of side effects and patients need to be carefully selected for the most appropriate protocol. Key Message: In this study, recent advances in the chemotherapeutic options available to treat metastatic PDAC and their implications for today's treatment choices are reviewed.

  • 110. Schoemaker, Minouk J.
    et al.
    Nichols, Hazel B.
    Wright, Lauren B.
    Brook, Mark N.
    Jones, Michael E.
    O'Brien, Katie M.
    Adami, Hans-Olov
    Baglietto, Laura
    Bernstein, Leslie
    Bertrand, Kimberly A.
    Boutron-Ruault, Marie-Christine
    Braaten, Tonje
    Chen, Yu
    Connor, Avonne E.
    Dorronsoro, Miren
    Dossus, Laure
    Eliassen, A. Heather
    Giles, Graham G.
    Hankinson, Susan E.
    Kaaks, Rudolf
    Key, Timothy J.
    Kirsh, Victoria A.
    Kitahara, Cari M.
    Koh, Woon-Puay
    Larsson, Susanna C.
    Linet, Martha S.
    Ma, Huiyan
    Masala, Giovanna
    Merritt, Melissa A.
    Milne, Roger L.
    Overvad, Kim
    Ozasa, Kotaro
    Palmer, Julie R.
    Peeters, Petra H.
    Riboli, Elio
    Rohan, Thomas E.
    Sadakane, Atsuko
    Sund, Malin
    Umeå universitet, Medicinska fakulteten, Institutionen för kirurgisk och perioperativ vetenskap.
    Tamirni, Rulla M.
    Trichopoulou, Antonia
    Ursin, Giske
    Vatten, Lars
    Visvanathan, Kala
    Weiderpass, Elisabete
    Willett, Walter C.
    Wolk, Alicja
    Yuan, Jian-Min
    Zeleniuch-Jacquotte, Anne
    Sandler, Dale P.
    Swerdlow, Anthony J.
    Association of body mass index and age With subsequent breast cancer risk in premenopausal women2018Ingår i: JAMA Oncology, ISSN 2374-2437, E-ISSN 2374-2445, Vol. 4, nr 11, artikel-id e181771Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    IMPORTANCE The association between increasing body mass index (BMI; calculated as wei ght in kilograms divided by height in meters squared) and risk of breast cancer is unique in cancer epidemiology in that a crossover effect exists, with risk reduction before and risk increase after menopause. The inverse association with premenopausal breast cancer risk is poorly characterized but might be important in the understanding of breast cancer causation.

    OBJECTIVE To investigate the association of BMI with premenopausal breast cancer risk, in particular by age at BMI, attained age, risk factors for breast cancer, and tumor characteristics.

    DESIGN, SETTING, AND PARTICIPANTS This multicenter analysis used pooled individual-level data from 758 592 premenopausal women from 19 prospective cohorts to estimate hazard ratios (HRs) of premenopausal breast cancer in association with BMI from ages 18 through 54 years using Cox proportional hazards regression analysis. Median follow-up was 9.3 years (interquartile range, 4.9-13.5 years) per participant, with 13 082 incident cases of breast cancer. Participants were recruited from January 1,1963, through December 31, 2013, and data were analyzed from September 1.2013, through December 31, 2017.

    EXPOSURES Body mass index at ages 18 to 24, 25 to 34,35 to 44, and 45 to 54 years.

    MAIN OUTCOMES AND MEASURES Invasive or in situ premenopausal breast cancer.

    RESULTS Among the 758 592 premenopausal women (median age, 40.6 years; interquartile range, 35.2-45.5 years) included in the analysis, inverse linear associations of BMI with breast cancer risk were found that were stronger for BMI at ages 18 to 24 years (HR per 5 kg/m(2) [5.0-U] difference, 0.77; 95% CI, 0.73-0.80) than for BMI at ages 45 to 54 years (HR per 5.0-U difference, 0.88; 95% CI, 0.86-0.91). The inverse associations were observed even among nonoverweight women. There was a 4.2-fold risk gradient between the highest and lowest BMI categories (BMI >= 35.0 vs <17.0) at ages 18 to 24 years (HR, 0.24; 95% CI, 0.14-0.40). Hazard ratios did not appreciably vary by attained age or between strata of other breast cancer risk factors. Associations were stronger for estrogen receptor-positive and/or progesterone receptor-positive than for hormone receptor-negative breast cancer for BMI at every age group (eg, for BMI at age 18 to 24 years: HR per 5.0-U difference for estrogen receptor-positive and progesterone receptor-positive tumors, 0.76 [95% CI, 0.70-0.81] vs hormone receptor-negative tumors, 0.85 [95% CI: 0.76-0.95]); BMI at ages 25 to 54 years was not consistently associated with triple-negative or hormone receptor-negative breast cancer overall.

    CONCLUSIONS AND RELEVANCE The results of this study suggest that increased adiposity is associated with a reduced risk of premenopausal breast cancer at a greater magnitude than previously shown and across the entire distribution of BMI. The strongest associations of risk were observed for BMI in early adulthood. Understanding the biological mechanisms underlying these associations could have important preventive potential.

  • 111. Siddiq, Afshan
    et al.
    Couch, Fergus J.
    Chen, Gary K.
    Lindstrom, Sara
    Eccles, Diana
    Millikan, Robert C.
    Michailidou, Kyriaki
    Stram, Daniel O.
    Beckmann, Lars
    Rhie, Suhn Kyong
    Ambrosone, Christine B.
    Aittomaki, Kristiina
    Amiano, Pilar
    Apicella, Carmel
    Baglietto, Laura
    Bandera, Elisa V.
    Beckmann, Matthias W.
    Berg, Christine D.
    Bernstein, Leslie
    Blomqvist, Carl
    Brauch, Hiltrud
    Brinton, Louise
    Bui, Quang M.
    Buring, Julie E.
    Buys, Saundra S.
    Campa, Daniele
    Carpenter, Jane E.
    Chasman, Daniel I.
    Chang-Claude, Jenny
    Chen, Constance
    Clavel-Chapelon, Francoise
    Cox, Angela
    Cross, Simon S.
    Czene, Kamila
    Deming, Sandra L.
    Diasio, Robert B.
    Diver, W. Ryan
    Dunning, Alison M.
    Durcan, Lorraine
    Ekici, Arif B.
    Fasching, Peter A.
    Feigelson, Heather Spencer
    Fejerman, Laura
    Figueroa, Jonine D.
    Fletcher, Olivia
    Flesch-Janys, Dieter
    Gaudet, Mia M.
    Gerty, Susan M.
    Rodriguez-Gil, Jorge L.
    Giles, Graham G.
    van Gils, Carla H.
    Godwin, Andrew K.
    Graham, Nikki
    Greco, Dario
    Hall, Per
    Hankinson, Susan E.
    Hartmann, Arndt
    Hein, Rebecca
    Heinz, Judith
    Hoover, Robert N.
    Hopper, John L.
    Hu, Jennifer J.
    Huntsman, Scott
    Ingles, Sue A.
    Irwanto, Astrid
    Isaacs, Claudine
    Jacobs, Kevin B.
    John, Esther M.
    Justenhoven, Christina
    Kaaks, Rudolf
    Kolonel, Laurence N.
    Coetzee, Gerhard A.
    Lathrop, Mark
    Le Marchand, Loic
    Lee, Adam M.
    Lee, I-Min
    Lesnick, Timothy
    Lichtner, Peter
    Liu, Jianjun
    Lund, Eiliv
    Makalic, Enes
    Martin, Nicholas G.
    McLean, Catriona A.
    Meijers-Heijboer, Hanne
    Meindl, Alfons
    Miron, Penelope
    Monroe, Kristine R.
    Montgomery, Grant W.
    Mueller-Myhsok, Bertram
    Nickels, Stefan
    Nyante, Sarah J.
    Olswold, Curtis
    Overvad, Kim
    Palli, Domenico
    Park, Daniel J.
    Palmer, Julie R.
    Pathak, Harsh
    Peto, Julian
    Pharoah, Paul
    Rahman, Nazneen
    Rivadeneira, Fernando
    Schmidt, Daniel F.
    Schmutzler, Rita K.
    Slager, Susan
    Southey, Melissa C.
    Stevens, Kristen N.
    Sinn, Hans-Peter
    Press, Michael F.
    Ross, Eric
    Riboli, Elio
    Ridker, Paul M.
    Schumacher, Fredrick R.
    Severi, Gianluca
    Silva, Isabel dos Santos
    Stone, Jennifer
    Sund, Malin
    Umeå universitet, Medicinska fakulteten, Institutionen för kirurgisk och perioperativ vetenskap, Kirurgi.
    Tapper, William J.
    Thun, Michael J.
    Travis, Ruth C.
    Turnbull, Clare
    Uitterlinden, Andre G.
    Waisfisz, Quinten
    Wang, Xianshu
    Wang, Zhaoming
    Weaver, JoEllen
    Schulz-Wendtland, Ruediger
    Wilkens, Lynne R.
    Van Den Berg, David
    Zheng, Wei
    Ziegler, Regina G.
    Ziv, Elad
    Nevanlinna, Heli
    Easton, Douglas F.
    Hunter, David J.
    Henderson, Brian E.
    Chanock, Stephen J.
    Garcia-Closas, Montserrat
    Kraft, Peter
    Haiman, Christopher A.
    Vachon, Celine M.
    A meta-analysis of genome-wide association studies of breast cancer identifies two novel susceptibility loci at 6q14 and 20q112012Ingår i: Human Molecular Genetics, ISSN 0964-6906, E-ISSN 1460-2083, Vol. 21, nr 24, s. 5373-5384Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Genome-wide association studies (GWAS) of breast cancer defined by hormone receptor status have revealed loci contributing to susceptibility of estrogen receptor (ER)-negative subtypes. To identify additional genetic variants for ER-negative breast cancer, we conducted the largest meta-analysis of ER-negative disease to date, comprising 4754 ER-negative cases and 31 663 controls from three GWAS: NCI Breast and Prostate Cancer Cohort Consortium (BPC3) (2188 ER-negative cases; 25 519 controls of European ancestry), Triple Negative Breast Cancer Consortium (TNBCC) (1562 triple negative cases; 3399 controls of European ancestry) and African American Breast Cancer Consortium (AABC) (1004 ER-negative cases; 2745 controls). We performed in silico replication of 86 SNPs at P 1 10(-5) in an additional 11 209 breast cancer cases (946 with ER-negative disease) and 16 057 controls of Japanese, Latino and European ancestry. We identified two novel loci for breast cancer at 20q11 and 6q14. SNP rs2284378 at 20q11 was associated with ER-negative breast cancer (combined two-stage OR 1.16; P 1.1 10(8)) but showed a weaker association with overall breast cancer (OR 1.08, P 1.3 10(6)) based on 17 869 cases and 43 745 controls and no association with ER-positive disease (OR 1.01, P 0.67) based on 9965 cases and 22 902 controls. Similarly, rs17530068 at 6q14 was associated with breast cancer (OR 1.12; P 1.1 10(9)), and with both ER-positive (OR 1.09; P 1.5 10(5)) and ER-negative (OR 1.16, P 2.5 10(7)) disease. We also confirmed three known loci associated with ER-negative (19p13) and both ER-negative and ER-positive breast cancer (6q25 and 12p11). Our results highlight the value of large-scale collaborative studies to identify novel breast cancer risk loci.

  • 112. Sieri, Sabina
    et al.
    Chiodini, Paolo
    Agnoli, Claudia
    Pala, Valeria
    Berrino, Franco
    Trichopoulou, Antonia
    Benetou, Vassiliki
    Vasilopoulou, Effie
    Sánchez, María-José
    Chirlaque, Maria-Dolores
    Amiano, Pilar
    Quirós, J Ramón
    Ardanaz, Eva
    Buckland, Genevieve
    Masala, Giovanna
    Panico, Salvatore
    Grioni, Sara
    Sacerdote, Carlotta
    Tumino, Rosario
    Boutron-Ruault, Marie-Christine
    Clavel-Chapelon, Françoise
    Fagherazzi, Guy
    Peeters, Petra H M
    van Gils, Carla H
    Bueno-de-Mesquita, H Bas
    van Kranen, Henk J
    Key, Timothy J
    Travis, Ruth C
    Khaw, Kay Tee
    Wareham, Nicholas J
    Kaaks, Rudolf
    Lukanova, Annekatrin
    Boeing, Heiner
    Schütze, Madlen
    Sonestedt, Emily
    Wirfält, Elisabeth
    Sund, Malin
    Umeå universitet, Medicinska fakulteten, Institutionen för kirurgisk och perioperativ vetenskap, Kirurgi.
    Andersson, Anne
    Umeå universitet, Medicinska fakulteten, Institutionen för strålningsvetenskaper, Onkologi.
    Chajes, Veronique
    Rinaldi, Sabina
    Romieu, Isabelle
    Weiderpass, Elisabete
    Skeie, Guri
    Dagrun, Engeset
    Tjønneland, Anne
    Halkjær, Jytte
    Overvard, Kim
    Merritt, Melissa A
    Cox, David
    Riboli, Elio
    Krogh, Vittorio
    Dietary fat intake and development of specific breast cancer subtypes2014Ingår i: Journal of the National Cancer Institute, ISSN 0027-8874, E-ISSN 1460-2105, Vol. 106, nr 5, s. dju068-Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    We prospectively evaluated fat intake as predictor of developing breast cancer (BC) subtypes defined by estrogen receptor (ER), progesterone receptor (PR), and human epidermal growth factor 2 receptor (HER2), in a large (n = 337327) heterogeneous cohort of women, with 10062 BC case patients after 11.5 years, estimating BC hazard ratios (HRs) by Cox proportional hazard modeling. High total and saturated fat were associated with greater risk of ER(+)PR(+) disease (HR = 1.20, 95% confidence interval [CI] = 1.00 to 1.45; HR = 1.28, 95% CI = 1.09 to 1.52; highest vs lowest quintiles) but not ER(-)PR(-) disease. High saturated fat was statistically significantly associated with greater risk of HER2(-) disease. High saturated fat intake particularly increases risk of receptor-positive disease, suggesting saturated fat involvement in the etiology of this BC subtype.

  • 113. Soreide, K.
    et al.
    Sund, Malin
    Umeå universitet, Medicinska fakulteten, Institutionen för kirurgisk och perioperativ vetenskap, Kirurgi.
    Translational research in surgical oncology2017Ingår i: British Journal of Surgery, ISSN 0007-1323, E-ISSN 1365-2168, Vol. 104, nr 5, s. 491-492Artikel i tidskrift (Refereegranskat)
  • 114. Steindorf, Karen
    et al.
    Ritte, Rebecca
    Eomois, Piia-Piret
    Lukanova, Annekatrin
    Tjonneland, Anne
    Johnsen, Nina Fons
    Overvad, Kim
    Ostergaard, Jane Nautrup
    Clavel-Chapelon, Francoise
    Fournier, Agnes
    Dossus, Laure
    Teucher, Birgit
    Rohrmann, Sabine
    Boeing, Heiner
    Wientzek, Angelika
    Trichopoulou, Antonia
    Karapetyan, Tina
    Trichopoulos, Dimitrios
    Masala, Giovanna
    Berrino, Franco
    Mattiello, Amalia
    Tumino, Rosario
    Ricceri, Fulvio
    Ramon Quiros, J.
    Travier, Noemie
    Sanchez, Maria-Jose
    Navarro, Carmen
    Ardanaz, Eva
    Amiano, Pilar
    Bueno-de-Mesquita, H. B. (as).
    van Duijnhoven, Franzel
    Monninkhof, Evelyn
    May, Anne M.
    Khaw, Kay-Tee
    Wareham, Nick
    Key, Tim J.
    Travis, Ruth C.
    Borch, Kristin Benjaminsen
    Sund, Malin
    Umeå universitet, Medicinska fakulteten, Institutionen för kirurgisk och perioperativ vetenskap, Kirurgi.
    Andersson, Anne
    Umeå universitet, Medicinska fakulteten, Institutionen för strålningsvetenskaper, Onkologi.
    Fedirko, Veronika
    Rinaldi, Sabina
    Romieu, Isabelle
    Wahrendorf, Juergen
    Riboli, Elio
    Kaaks, Rudolf
    Physical activity and risk of breast cancer overall and by hormone receptor status: The European prospective investigation into cancer and nutrition2013Ingår i: International Journal of Cancer, ISSN 0020-7136, E-ISSN 1097-0215, Vol. 132, nr 7, s. 1667-1678Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Physical activity is associated with reduced risks of invasive breast cancer. However, whether this holds true for breast cancer subtypes defined by the estrogen receptor (ER) and the progesterone receptor (PR) status is controversial. The study included 257,805 women from the multinational EPIC-cohort study with detailed information on occupational, recreational and household physical activity and important cofactors assessed at baseline. During 11.6 years of median follow-up, 8,034 incident invasive breast cancer cases were identified. Data on ER, PR and combined ER/PR expression were available for 6,007 (67.6%), 4,814 (54.2%) and 4,798 (53.9%) cases, respectively. Adjusted hazard ratios (HR) were estimated by proportional hazards models. Breast cancer risk was inversely associated with moderate and high levels of total physical activity (HR = 0.92, 95% confidence interval (CI): 0.860.99, HR = 0.87, 95%-CI: 0.790.97, respectively; p-trend = 0.002), compared to the lowest quartile. Among women diagnosed with breast cancer after age 50, the largest risk reduction was found with highest activity (HR = 0.86, 95%-CI: 0.770.97), whereas for cancers diagnosed before age 50 strongest associations were found for moderate total physical activity (HR = 0.78, 95%-CI: 0.640.94). Analyses by hormone receptor status suggested differential associations for total physical activity (p-heterogeneity = 0.04), with a somewhat stronger inverse relationship for ER+/PR+ breast tumors, primarily driven by PR+ tumors (p-heterogeneity < 0.01). Household physical activity was inversely associated with ER/PR tumors. The results of this largest prospective study on the protective effects of physical activity indicate that moderate and high physical activity are associated with modest decreased breast cancer risk. Heterogeneities by receptor status indicate hormone-related mechanisms.

  • 115. Stepien, Magdalena
    et al.
    Duarte-Salles, Talita
    Fedirko, Veronika
    Floegel, Anne
    Barupal, Dinesh Kumar
    Rinaldi, Sabina
    Achaintre, David
    Assi, Nada
    Tjønneland, Anne
    Overvad, Kim
    Bastide, Nadia
    Boutron-Ruault, Marie-Christine
    Severi, Gianluca
    Kühn, Tilman
    Kaaks, Rudolf
    Aleksandrova, Krasimira
    Boeing, Heiner
    Trichopoulou, Antonia
    Bamia, Christina
    Lagiou, Pagona
    Saieva, Calogero
    Agnoli, Claudia
    Panico, Salvatore
    Tumino, Rosario
    Naccarati, Alessio
    Bueno-de-Mesquita, H Bas
    Peeters, Petra H
    Weiderpass, Elisabete
    Quirós, J Ramón
    Agudo, Antonio
    Sánchez, María-José
    Dorronsoro, Miren
    Gavrila, Diana
    Barricarte, Aurelio
    Ohlsson, Bodil
    Sjöberg, Klas
    Werner, Mårten
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin, Medicin.
    Sund, Malin
    Umeå universitet, Medicinska fakulteten, Institutionen för kirurgisk och perioperativ vetenskap, Kirurgi.
    Wareham, Nick
    Khaw, Kay-Tee
    Travis, Ruth C
    Schmidt, Julie A
    Gunter, Marc
    Cross, Amanda
    Vineis, Paolo
    Romieu, Isabelle
    Scalbert, Augustin
    Jenab, Mazda
    Alteration of amino acid and biogenic amine metabolism in hepatobiliary cancers: findings from a prospective cohort study2016Ingår i: International Journal of Cancer, ISSN 0020-7136, E-ISSN 1097-0215, Vol. 138, nr 2, s. 348-360Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Perturbations in levels of amino acids (AA) and their derivatives are observed in hepatocellular carcinoma (HCC). Yet, it is unclear whether these alterations precede or are a consequence of the disease, nor whether they pertain to anatomically related cancers of the intrahepatic bile duct (IHBC), and gallbladder and extrahepatic biliary tract (GBTC). Circulating standard AA, biogenic amines and hexoses were measured (Biocrates AbsoluteIDQ-p180Kit) in a case-control study nested within a large prospective cohort (147 HCC, 43 IHBC and 134 GBTC cases). Liver function and hepatitis status biomarkers were determined separately. Multivariable conditional logistic regression was used to calculate odds ratios and 95% confidence intervals (OR; 95%CI) for log-transformed standardised (mean = 0, SD = 1) serum metabolite levels and relevant ratios in relation to HCC, IHBC or GBTC risk. Fourteen metabolites were significantly associated with HCC risk, of which seven metabolites and four ratios were the strongest predictors in continuous models. Leucine, lysine, glutamine and the ratio of branched chain to aromatic AA (Fischer's ratio) were inversely, while phenylalanine, tyrosine and their ratio, glutamate, glutamate/glutamine ratio, kynurenine and its ratio to tryptophan were positively associated with HCC risk. Confounding by hepatitis status and liver enzyme levels was observed. For the other cancers no significant associations were observed. In conclusion, imbalances of specific AA and biogenic amines may be involved in HCC development.

  • 116.
    Stylianidis, Giorgios
    et al.
    Umeå universitet, Medicinska fakulteten, Institutionen för kirurgisk och perioperativ vetenskap, Kirurgi.
    Haapamäki, Markku
    Umeå universitet, Medicinska fakulteten, Institutionen för kirurgisk och perioperativ vetenskap, Kirurgi.
    Sund, Malin
    Umeå universitet, Medicinska fakulteten, Institutionen för kirurgisk och perioperativ vetenskap, Kirurgi.
    Nilsson, Erik
    Umeå universitet, Medicinska fakulteten, Institutionen för kirurgisk och perioperativ vetenskap, Kirurgi.
    Nordin, Pär
    Umeå universitet, Medicinska fakulteten, Institutionen för kirurgisk och perioperativ vetenskap, Kirurgi.
    Management of the hernial sac in inguinal hernia repair.2010Ingår i: British Journal of Surgery, ISSN 0007-1323, E-ISSN 1365-2168, Vol. 97, nr 3, s. 415-419Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    BACKGROUND: There is no consensus on the best management of the indirect hernial sac in groin hernia surgery. The aim of this study was to investigate to what extent different management options are associated with reoperation for recurrence. METHODS: This study used data from the Swedish Hernia Register. Surgeons registered whether the indirect hernial sac was managed by division (leaving the distal part in place), excision or invagination. RESULTS: An indirect hernia was found in 48 433 operations; the sac was excised in 49.5 per cent, invaginated in 37.6 per cent and divided in 12.9 per cent of operations. The 5-year cumulative reoperation incidence was 1.7 per cent for hernial sac excision, 1.7 per cent for division and 2.7 per cent for invagination. For indirect hernia repair, the relative risk of reoperation for recurrence was 0.63 (95 per cent confidence interval 0.51 to 0.79) for excision of the sac and 0.72 (0.53 to 0.99) for division compared with invagination. Lichtenstein repair combined with hernial sac excision had a 5-year cumulative reoperation incidence of only 1.0 per cent. CONCLUSION: Excision of the indirect hernial sac in inguinal hernia repair is associated with a lower risk of hernia recurrence than division or invagination.

  • 117. Sugimoto, Hikaru
    et al.
    Mundel, Thomas M
    Sund, Malin
    Umeå universitet, Medicinsk fakultet, Kirurgisk och perioperativ vetenskap, Kirurgi.
    Xie, Liang
    Cosgrove, Dominic
    Kalluri, Raghu
    Bone-marrow-derived stem cells repair basement membrane collagen defects and reverse genetic kidney disease.2006Ingår i: Proc Natl Acad Sci U S A, ISSN 0027-8424, Vol. 103, nr 19, s. 7321-6Artikel i tidskrift (Refereegranskat)
  • 118.
    Sund, Malin
    Umeå universitet, Medicinska fakulteten, Institutionen för kirurgisk och perioperativ vetenskap, Kirurgi.
    Effects of tirapazamine on experimental colorectal liver metastases after radiofrequency ablation (Br J Surg 2012; 99567-575)2012Ingår i: British Journal of Surgery, ISSN 0007-1323, E-ISSN 1365-2168, Vol. 99, nr 4, s. 576-576Artikel i tidskrift (Övrigt vetenskapligt)
  • 119.
    Sund, Malin
    et al.
    Umeå universitet, Medicinsk fakultet, Kirurgisk och perioperativ vetenskap, Kirurgi.
    Hamano, Yuki
    Sugimoto, Hikaru
    Sudhakar, Akulapalli
    Soubasakos, Mary
    Yerramalla, Udaya
    Benjamin, Laura E
    Lawler, Jack
    Kieran, Mark
    Shah, Amish
    Kalluri, Raghu
    Function of endogenous inhibitors of angiogenesis as endothelium-specific tumor suppressors.2005Ingår i: Proc Natl Acad Sci U S A, ISSN 0027-8424, Vol. 102, nr 8, s. 2934-9Artikel i tidskrift (Refereegranskat)
  • 120.
    Sund, Malin
    et al.
    Umeå universitet, Medicinska fakulteten, Institutionen för kirurgisk och perioperativ vetenskap, Kirurgi.
    Kalluri, Raghu
    Tumor stroma derived biomarkers in cancer2009Ingår i: Cancer Metastasis Review, ISSN 0167-7659, E-ISSN 1573-7233, Vol. 28, nr 1-2, s. 177-183Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    In recent years the importance of the tumor stroma for the development, promotion and invasion of cancer is becoming increasingly clear. Besides a malignantly transformed cancer cell, tumors also contains many other cell types, including endothelial cells, fibroblasts and cells of the immune system. These cells together with the cancer cells produce the sum extracellular matrix (ECM) of the tumor. The ECM and the non-malignant cells of the tumor are defined as the "tumor stroma". Just as the malignant cell itself can be the source of substances that can be used as biomarkers of cancer, the tumor stroma contains factors that potentially can be used as biomarkers when treating patients with cancer. In this review we will discuss the role of the tumor stroma as a source of new cancer biomarkers. This concept highlights a novel view of cancer and treats them as organized organs. Additionally, this further stresses the importance of including factors related to the tumor stroma into the diagnostic and therapeutic equation of cancer.

  • 121.
    Sund, Malin
    et al.
    Umeå universitet, Medicinsk fakultet, Kirurgisk och perioperativ vetenskap, Kirurgi.
    Maeshima, Yohei
    Kalluri, Raghu
    Bifunctional promoter of type IV collagen COL4A5 and COL4A6 genes regulates the expression of alpha5 and alpha6 chains in a distinct cell-specific fashion.2005Ingår i: Biochem J, ISSN 1470-8728, Vol. 387, nr Pt 3, s. 755-61Artikel i tidskrift (Refereegranskat)
  • 122.
    Sund, Malin
    et al.
    Umeå universitet, Medicinska fakulteten, Institutionen för kirurgisk och perioperativ vetenskap, Kirurgi.
    Nyberg, Pia
    Eikesdal, Hans Petter
    Endogenous matrix-derived inhibitors of angiogenesis2010Ingår i: Pharmaceuticals, Vol. 3, s. 3021-3039Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Endogenous inhibitors of angiogenesis are proteins or fragments of proteins that are formed in the body, which can inhibit the angiogenic process. These molecules can be found both in the circulation and sequestered in the extracellular matrix (ECM) surrounding cells. Many matrix-derived inhibitors of angiogenesis, such as endostatin, tumstatin, canstatin and arresten, are bioactive fragments of larger ECM molecules. These substances become released upon proteolysis of the ECM and the vascular basement membrane (VBM) by enzymes of the tumor microenvironment. Although the role of matrix-derived angiogenesis inhibitors is well studied in animal models of cancer, their role in human cancers is less established. In this review we discuss the current knowledge about these molecules and their potential use as cancer therapeutics and biomarkers.

  • 123.
    Sund, Malin
    et al.
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin. Umeå universitet, Medicinska fakulteten, Institutionen för kirurgisk och perioperativ vetenskap, Kirurgi.
    Xu, Li Li
    Rahman, Arman
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin.
    Qian, Bi-Feng
    Hammarström, Marie-Louise
    Umeå universitet, Medicinska fakulteten, Institutionen för klinisk mikrobiologi, Immunologi/immunkemi.
    Danielsson, Åke
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin.
    Reduced susceptibility to dextran sulphate sodium-induced colitis in the interleukin-2 heterozygous (IL-2) mouse.2005Ingår i: Immunology, ISSN 0019-2805, E-ISSN 1365-2567, Vol. 114, nr 4, s. 554-564Artikel i tidskrift (Refereegranskat)
  • 124.
    Sund, Malin
    et al.
    Umeå universitet, Medicinsk fakultet, Kirurgisk och perioperativ vetenskap, Kirurgi.
    Zeisberg, Michael
    Kalluri, Raghu
    Endogenous stimulators and inhibitors of angiogenesis in gastrointestinal cancers: basic science to clinical application.2005Ingår i: Gastroenterology, ISSN 0016-5085, Vol. 129, nr 6, s. 2076-91Artikel i tidskrift (Refereegranskat)
  • 125. Søreide, Kjetil
    et al.
    Sund, Malin
    Umeå universitet, Medicinska fakulteten, Institutionen för kirurgisk och perioperativ vetenskap, Kirurgi.
    Epidemiological-molecular evidence of metabolic reprogramming on proliferation, autophagy and cell signaling in pancreas cancer2015Ingår i: Cancer Letters, ISSN 0304-3835, E-ISSN 1872-7980, Vol. 356, nr 2, s. 281-288Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Pancreatic cancer remains one of the deadliest human cancers with little progress made in survival over the past decades, and 5-year survival usually below 5%. Despite this dismal scenario, progresses have been made in understanding of the underlying tumor biology through among other definition of precursor lesions, delineation of molecular pathways, and advances in genome-wide technology. Further, exploring the relationship between epidemiological risk factors involving metabolic features to that of an altered cancer metabolism may provide the foundation for new therapies. Here we explore how nutrients and caloric intake may influence the KRAS-driven ductal carcinogenesis through mediators of metabolic stress, including autophagy in presence of TP53, advanced glycation end products (AGE) and the receptors (RAGE) and ligands (HMGB1), as well as glutamine pathways, among others. Effective understanding the cancer metabolism mechanisms in pancreatic cancer may propose new ways of prevention and treatment.

  • 126. Tahkola, Jenni
    et al.
    Räsänen, Juha
    Sund, Malin
    Mäkikallio, Kaarin
    Autio-Harmainen, Helena
    Pihlajaniemi, Taina
    Cardiac dysfunction in transgenic mouse fetuses overexpressing shortened type XIII collagen2008Ingår i: Cell and Tissue Research, ISSN 0302-766X, E-ISSN 1432-0878, Vol. 333, nr 1, s. 61-69Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Overexpression of type XIII collagen molecules with an 83-amino-acid residue in-frame deletion of part of the ectodomain leads to fetal lethality in Col13a1COL2del transgenic mice. We characterize here the functional disturbances in the cardiovascular system of mouse fetuses overexpressing mutant type XIII collagen. Doppler ultrasonography was performed at 12.5 days of gestation on 33 fetuses resulting from heterozygous matings of seven female mice and on 16 fetuses from two matings between heterozygous and wild-type mice. Nine fetuses had atrioventricular valve regurgitation (AVVR), and all of them were transgene-positive. The fetuses with AVVR had a lower outflow mean velocity (Vmean; P<0.005) and a greater proportion of isovolumetric relaxation time (IRT%) in the cardiac cycle (P<0.0001) than those without AVVR, and their ductus venosus pulsatility indices for veins (DV PIV) and the umbilical artery pulsatility indices were increased. A positive correlation was found between IRT% and DV PIV, and a negative correlation was seen between outflow V(mean) and DV PIV. Morphological analysis of the heart revealed no differences between the two groups of fetuses, but histological analysis showed the trabeculation of the ventricles to be reduced and the myocardium to be thinner in the fetuses with AVVR. Based on in situ hybridization, type XIII collagen mRNAs were normal constituents of these structures. Moreover, a positive correlation was found between outflow Vmean and myocardial thickness. IRT% and DV PIV correlated negatively with myocardial thickness. Thus, overexpression of mutant type XIII collagen results in mid-gestation cardiac dysfunction in mouse fetuses, and these disturbances in cardiac function may lead to death in utero.

  • 127. Tang, Hongwei
    et al.
    Wei, Peng
    Duell, Eric J
    Risch, Harvey A
    Olson, Sara H
    Bueno-de-Mesquita, H Bas
    Gallinger, Steven
    Holly, Elizabeth A
    Petersen, Gloria
    Bracci, Paige M
    McWilliams, Robert R
    Jenab, Mazda
    Riboli, Elio
    Tjønneland, Anne
    Boutron-Ruault, Marie Christine
    Kaaks, Rudolph
    Trichopoulos, Dimitrios
    Panico, Salvatore
    Sund, Malin
    Umeå universitet, Medicinska fakulteten, Institutionen för kirurgisk och perioperativ vetenskap, Kirurgi.
    Peeters, Petra H M
    Khaw, Kay-Tee
    Amos, Christopher I
    Li, Donghui
    Axonal guidance signaling pathway interacting with smoking in modifying the risk of pancreatic cancer: a gene- and pathway-based interaction analysis of GWAS data2014Ingår i: Carcinogenesis, ISSN 0143-3334, E-ISSN 1460-2180, Vol. 35, nr 5, s. 1039-1045Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Cigarette smoking is the best established modifiable risk factor for pancreatic cancer. Genetic factors that underlie smoking-related pancreatic cancer have previously not been examined at the genome-wide level. Taking advantage of the existing Genome-wide association study (GWAS) genotype and risk factor data from the Pancreatic Cancer Case Control Consortium, we conducted a discovery study in 2028 cases and 2109 controls to examine gene-smoking interactions at pathway/gene/single nucleotide polymorphism (SNP) level. Using the likelihood ratio test nested in logistic regression models and ingenuity pathway analysis (IPA), we examined 172 KEGG (Kyoto Encyclopedia of Genes and Genomes) pathways, 3 manually curated gene sets, 3 nicotine dependency gene ontology pathways, 17 912 genes and 468 114 SNPs. None of the individual pathway/gene/SNP showed significant interaction with smoking after adjusting for multiple comparisons. Six KEGG pathways showed nominal interactions (P < 0.05) with smoking, and the top two are the pancreatic secretion and salivary secretion pathways (major contributing genes: RAB8A, PLCB and CTRB1). Nine genes, i.e. ZBED2, EXO1, PSG2, SLC36A1, CLSTN1, MTHFSD, FAT2, IL10RB and ATXN2 had P interaction < 0.0005. Five intergenic region SNPs and two SNPs of the EVC and KCNIP4 genes had P interaction < 0.00003. In IPA analysis of genes with nominal interactions with smoking, axonal guidance signaling $$\left(P=2.12\times 1{0}^{-7}\right)$$ and α-adrenergic signaling $$\left(P=2.52\times 1{0}^{-5}\right)$$ genes were significantly overrepresented canonical pathways. Genes contributing to the axon guidance signaling pathway included the SLIT/ROBO signaling genes that were frequently altered in pancreatic cancer. These observations need to be confirmed in additional data set. Once confirmed, it will open a new avenue to unveiling the etiology of smoking-associated pancreatic cancer.

  • 128. Tang, Hongwei
    et al.
    Wei, Peng
    Duell, Eric J
    Risch, Harvey A
    Olson, Sara H
    Bueno-de-Mesquita, H Bas
    Gallinger, Steven
    Holly, Elizabeth A
    Petersen, Gloria M
    Bracci, Paige M
    McWilliams, Robert R
    Jenab, Mazda
    Riboli, Elio
    Tjønneland, Anne
    Boutron-Ruault, Marie Christine
    Kaaks, Rudolf
    Trichopoulos, Dimitrios
    Panico, Salvatore
    Sund, Malin
    Umeå universitet, Medicinska fakulteten, Institutionen för kirurgisk och perioperativ vetenskap, Kirurgi.
    Peeters, Petra H M
    Khaw, Kay-Tee
    Amos, Christopher I
    Li, Donghui
    Genes-environment interactions in obesity- and diabetes-associated pancreatic cancer: a GWAS data analysis2014Ingår i: Cancer Epidemiology, Biomarkers and Prevention, ISSN 1055-9965, E-ISSN 1538-7755, Vol. 23, nr 1, s. 98-106Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    BACKGROUND: Obesity and diabetes are potentially alterable risk factors for pancreatic cancer. Genetic factors that modify the associations of obesity and diabetes with pancreatic cancer have previously not been examined at the genome-wide level. METHODS: Using genome-wide association studies (GWAS) genotype and risk factor data from the Pancreatic Cancer Case Control Consortium, we conducted a discovery study of 2,028 cases and 2,109 controls to examine gene-obesity and gene-diabetes interactions in relation to pancreatic cancer risk by using the likelihood-ratio test nested in logistic regression models and Ingenuity Pathway Analysis (IPA). RESULTS: After adjusting for multiple comparisons, a significant interaction of the chemokine signaling pathway with obesity (P = 3.29 × 10(-6)) and a near significant interaction of calcium signaling pathway with diabetes (P = 1.57 × 10(-4)) in modifying the risk of pancreatic cancer were observed. These findings were supported by results from IPA analysis of the top genes with nominal interactions. The major contributing genes to the two top pathways include GNGT2, RELA, TIAM1, and GNAS. None of the individual genes or single-nucleotide polymorphism (SNP) except one SNP remained significant after adjusting for multiple testing. Notably, SNP rs10818684 of the PTGS1 gene showed an interaction with diabetes (P = 7.91 × 10(-7)) at a false discovery rate of 6%. CONCLUSIONS: Genetic variations in inflammatory response and insulin resistance may affect the risk of obesity- and diabetes-related pancreatic cancer. These observations should be replicated in additional large datasets. IMPACT: A gene-environment interaction analysis may provide new insights into the genetic susceptibility and molecular mechanisms of obesity- and diabetes-related pancreatic cancer.

  • 129. Thomas, Hanna S.
    et al.
    Sund, Malin
    Umeå universitet, Medicinska fakulteten, Enheten för biobanksforskning. Umeå universitet, Medicinska fakulteten, Institutionen för kirurgisk och perioperativ vetenskap.
    Andersson, Linda
    Umeå universitet, Medicinska fakulteten, Institutionen för kirurgisk och perioperativ vetenskap.
    Gunnarsson, Ulf
    Umeå universitet, Medicinska fakulteten, Institutionen för kirurgisk och perioperativ vetenskap.
    Blanco, R.
    Pooled analysis of WHO Surgical Safety Checklist use and mortality after emergency laparotomy2019Ingår i: British Journal of Surgery, ISSN 0007-1323, E-ISSN 1365-2168, Vol. 106, nr 2, s. E103-E112Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Background: The World Health Organization (WHO) Surgical Safety Checklist has fostered safe practice for 10 years, yet its place in emergency surgery has not been assessed on a global scale. The aim of this study was to evaluate reported checklist use in emergency settings and examine the relationship with perioperative mortality in patients who had emergency laparotomy.

    Methods: In two multinational cohort studies, adults undergoing emergency laparotomy were compared with those having elective gastrointestinal surgery. Relationships between reported checklist use and mortality were determined using multivariable logistic regression and bootstrapped simulation.

    Results: Of 12 296 patients included from 76 countries, 4843 underwent emergency laparotomy. After adjusting for patient and disease factors, checklist use before emergency laparotomy was more common in countries with a high Human Development Index (HDI) (2455 of 2741, 89⋅6 per cent) compared with that in countries with a middle (753 of 1242, 60⋅6 per cent; odds ratio (OR) 0⋅17, 95 per cent c.i. 0⋅14 to 0⋅21, P < 0⋅001) or low (363 of 860, 42⋅2 per cent; OR 0⋅08, 0⋅07 to 0⋅10, P < 0⋅001) HDI. Checklist use was less common in elective surgery than for emergency laparotomy in high-HDI countries (risk difference −9⋅4 (95 per cent c.i. −11⋅9 to −6⋅9) per cent; P < 0⋅001), but the relationship was reversed in low-HDI countries (+12⋅1 (+7⋅0 to +17⋅3) per cent; P < 0⋅001). In multivariable models, checklist use was associated with a lower 30-day perioperative mortality (OR 0⋅60, 0⋅50 to 0⋅73; P < 0⋅001). The greatest absolute benefit was seen for emergency surgery in low- and middle-HDI countries.

    Conclusion: Checklist use in emergency laparotomy was associated with a significantly lower perioperative mortality rate. Checklist use in low-HDI countries was half that in high-HDI countries.

  • 130. Tikk, Kaja
    et al.
    Sookthai, Disorn
    Fortner, Renee T.
    Johnson, Theron
    Rinaldi, Sabina
    Romieu, Isabelle
    Tjonneland, Anne
    Olsen, Anja
    Overvad, Kim
    Clavel-Chapelon, Francoise
    Baglietto, Laura
    Boeing, Heiner
    Trichopoulou, Antonia
    Lagiou, Pagona
    Trichopoulos, Dimitrios
    Masala, Giovanna
    Krogh, Vittorio
    Tumino, Rosario
    Ricceri, Fulvio
    Mattiello, Amalia
    Agudo, Antonio
    Menendez, Virginia
    Sanchez, Maria-Jose
    Amiano, Pilar
    Chirlaque, Maria-Dolores
    Barricarte, Aurelio
    Bueno-de-Mesquita, HBas
    Monninkhof, Evelyn M.
    Onland-Moret, N. Charlotte
    Andresson, Anne
    Umeå universitet, Medicinska fakulteten, Institutionen för strålningsvetenskaper.
    Sund, Malin
    Umeå universitet, Medicinska fakulteten, Institutionen för kirurgisk och perioperativ vetenskap, Kirurgi.
    Weiderpass, Elisabete
    Khaw, Kay-Tee
    Key, Timothy J.
    Travis, Ruth C.
    Merritt, Melissa A.
    Riboli, Elio
    Dossus, Laure
    Kaaks, Rudolf
    Circulating prolactin and in situ breast cancer risk in the European EPIC cohort: a case-control study2015Ingår i: Breast Cancer Research, ISSN 1465-5411, E-ISSN 1465-542X, Vol. 17, artikel-id 49Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Introduction The relationship between circulating prolactin and invasive breast cancer has been investigated previously, but the association between prolactin levels and in situ breast cancer risk has received less attention.

    Methods We analysed the relationship between pre-diagnostic prolactin levels and the risk of in situ breast cancer overall, and by menopausal status and use of postmenopausal hormone therapy (HT) at blood donation. Conditional logistic regression was used to assess this association in a case-control study nested within the European Prospective Investigation into Cancer and Nutrition (EPIC) cohort, including 307 in situ breast cancer cases and their matched control subjects.

    Results We found a significant positive association between higher circulating prolactin levels and risk of in situ breast cancer among all women [pre-and postmenopausal combined, ORlog2 = 1.35 (95% CI 1.04-1.76), P-trend = 0.03]. No statistically significant heterogeneity was found between prolactin levels and in situ cancer risk by menopausal status (P-het = 0.98) or baseline HT use (P-het = 0.20), although the observed association was more pronounced among postmenopausal women using HT compared to non-users (P-trend = 0.06 vs P-trend = 0.35). In subgroup analyses, the observed positive association was strongest in women diagnosed with in situ breast tumors <4 years compared to >= 4 years after blood donation (P-trend = 0.01 vs P-trend = 0.63; P-het = 0.04) and among nulliparous women compared to parous women (P-trend = 0.03 vs P-trend = 0.15; P-het = 0.07).

    Conclusions Our data extends prior research linking prolactin and invasive breast cancer to the outcome of in situ breast tumours and shows that higher circulating prolactin is associated with increased risk of in situ breast cancer.The relationship between circulating prolactin and invasive breast cancer has been investigated previously, but the association between prolactin levels and in situ breast cancer risk has received less attention.

  • 131. Tikk, Kaja
    et al.
    Sookthai, Disorn
    Johnson, Theron
    Rinaldi, Sabina
    Romieu, Isabelle
    Tjønneland, Anne
    Olsen, Anja
    Overvad, Kim
    Clavel-Chapelon, Francoise
    Baglietto, Laura
    Boeing, Heiner
    Trichopoulou, Antonia
    Lagiou, Pagona
    Trichopoulos, Dimitrios
    Palli, Domenico
    Pala, V
    Tumino, Rosario
    Rosso, S
    Panico, Salvatore
    Agudo, A
    Menéndez, Virginia
    Sánchez, Maria-Jose
    Amiano, Pilar
    Castaño, J M Huerta
    Ardanaz, Eva
    Bas Bueno-de-Mesquita, H
    Monninkhof, Evelyn
    Onland-Moret, C
    Andersson, Anne
    Umeå universitet, Medicinska fakulteten, Institutionen för strålningsvetenskaper, Onkologi.
    Sund, Malin
    Umeå universitet, Medicinska fakulteten, Institutionen för kirurgisk och perioperativ vetenskap, Kirurgi.
    Weiderpass, Elisabete
    Khaw, Kay-Tee
    Key, Timothy J
    Travis, Ruth C
    Gunter, Marc J
    Riboli, Elio
    Dossus, Laure
    Kaaks, Rudolf
    Circulating prolactin and breast cancer risk among pre- and postmenopausal women in the EPIC cohort2014Ingår i: Annals of Oncology, ISSN 0923-7534, E-ISSN 1569-8041, Vol. 25, nr 7, s. 1422-1428Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    BACKGROUND: Experimental and epidemiological evidence suggests that prolactin might play a role in the etiology of breast cancer. We analyzed the relationship of pre-diagnostic circulating prolactin levels with the risk of breast cancer by menopausal status, use of postmenopausal hormone replacement therapy (HRT) at blood donation, and by estrogen and progesterone receptor-status of the breast tumors. METHODS: Conditional logistic regression was used to analyze the data from a case-control study nested within the prospective European EPIC cohort, including 2250 invasive breast cancer and their matched control subjects. RESULTS: Statistically significant heterogeneity in the association of prolactin levels with breast cancer risk between women who were either pre- or postmenopausal at the time of blood donation was observed (Phet=0.04). Higher serum levels of prolactin were associated with significant increase in risk of breast cancer among postmenopausal women (ORQ4-Q1=1.29 [95%CI 1.05-1.58], Ptrend=0.09); however this increase in risk seemed to be confined to women who used postmenopausal HRT at blood donation (ORQ4-Q1=1.45 [95%CI 1.08-1.95], Ptrend=0.01), whereas no statistically significant association was found for the non-users of HRT (ORQ4-Q1 =1.11 [95%CI 0.83-1.49], Ptrend=0.80) (Phet=0.08). Among premenopausal women, a statistically non-significant inverse association was observed (ORQ4-Q1 =0.70 [95%CI 0.48-1.03], Ptrend=0.16). There was no heterogeneity in the prolactin-breast cancer association by hormone receptor status of the tumor. CONCLUSION: Our study indicates that higher circulating levels of prolactin among the postmenopausal HRT users at baseline may be associated with increased breast cancer risk.

  • 132. Tuomisto, Anne
    et al.
    Sund, Malin
    Tahkola, Jenni
    Latvanlehto, Anne
    Savolainen, Eeva-Riitta
    Autio-Harmainen, Helena
    Liakka, Annikki
    Sormunen, Raija
    Vuoristo, Jussi
    West, Anne
    Lahesmaa, Riitta
    Morse, Herbert C
    Pihlajaniemi, Taina
    A mutant collagen XIII alters intestinal expression of immune response genes and predisposes transgenic mice to develop B-cell lymphomas2008Ingår i: Cancer Research, ISSN 0008-5472, E-ISSN 1538-7445, Vol. 68, nr 24, s. 10324-10332Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Epithelial cells of mucosal surfaces are critical for maintaining immune homeostasis by aiding in the discrimination of pathogenic and commensal microorganisms and modulating the activities of antigen-presenting cells and lymphocytes. Functional breakdowns resulting in chronic infection and inflammation are associated with the development of hematologic and solid neoplasms for which detailed pathogenetic mechanisms are poorly understood. Mice heterozygous for a transgene Col13a1(del) expressing a mutant collagen XIII developed clonal mature B-cell lineage lymphomas originating in mesenteric lymph nodes (MLN). The tumors were associated with T cells and macrophages. The incidence of disease was reduced 2-fold in transgenic mice raised under specific pathogen-free conditions, suggesting a role for infectious agents. The lymphomas did not express the mutant collagen XIII, indicating that its influence on tumorigenesis was B-cell extrinsic and likely to be associated with collagen XIII-positive tissues drained by the MLN. Studies of the small intestines of transgenic mice showed that the subepithelial basement membranes (BM) were highly abnormal and that they exhibited heightened expression of genes involved in immune responses. These results define collagen XIII-dependent maintenance of the intestinal BM as a previously unappreciated component of immune responses and a critical determinant of cancer susceptibility.

  • 133. Valachis, Antonis
    et al.
    Garmo, Hans
    Weinman, John
    Fredriksson, Irma
    Ahlgren, Johan
    Sund, Malin
    Umeå universitet, Medicinska fakulteten, Institutionen för kirurgisk och perioperativ vetenskap, Kirurgi.
    Holmberg, Lars
    Effect of selective serotonin reuptake inhibitors use on endocrine therapy adherence and breast cancer mortality: a population-based study2016Ingår i: Breast Cancer Research and Treatment, ISSN 0167-6806, E-ISSN 1573-7217, Vol. 159, nr 2, s. 293-303Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    The purpose of the study was to investigate whether the concomitant use of selective serotonin reuptake inhibitors (SSRI) with tamoxifen influences the risk of death due to breast cancer, and we also investigated the association between SSRI use and adherence to oral endocrine therapy (ET). We analyzed data from BCBaSe Sweden, which is a database created by the data linkage of Registries from three different regions of Sweden. To investigate the association between ET adherence and SSRI use, we included all women who were diagnosed with non-distant metastatic ER-positive invasive breast cancer from July 2007 to July 2011 and had at least one dispensed prescription of oral tamoxifen or aromatase inhibitor. To investigate the role of concurrent administration of SSRI and tamoxifen on breast cancer prognosis, we performed a nested case-control study. In the adherence cohort, 9104 women were included in the analyses. Women who received SSRI, either before or after breast cancer diagnosis, were at higher risk for low adherence to ET. However, when the overlapping period between SSRI use and ET was > 50 %, no excess risk for low adherence was observed. Non-adherence (< 80 %) to ET was significantly associated with worse breast cancer survival (OR 4.07; 95 % CI 3.27-5.06). In the case-control study, 445 cases and 11125 controls were included. The concomitant administration of SSRI and tamoxifen did not influence breast cancer survival, neither in short-term (OR 1.41; 95 % CI 0.74-2.68) nor in long-term SSRI users (OR 0.85; 95 % CI 0.35-2.08). Concomitant SSRI and tamoxifen use does not seem to increase risk for death due to breast cancer. Given the positive association between continuing antidepressive pharmacotherapy for a longer period of time and adherence to ET, it is essential to capture and treat depression in breast cancer patients to secure adherence to ET.

  • 134. van Boeckel, Petra G A
    et al.
    Boshuizen, Hendriek C
    Siersema, Peter D
    Vrieling, Alina
    Kunst, Anton E
    Ye, Weimin
    Sund, Malin
    Dept. of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
    Michaud, Dominique S
    Gallo, Valentina
    Spencer, Elizabeth A
    Trichopoulou, Antonia
    Benetou, Vasiliki
    Orfanos, Philippos
    Cirera, Lluis
    Duell, Eric J
    Rohrmann, Sabine
    Hemann, Silke
    Masala, Giovanni
    Manjer, Jonas
    Mattiello, Amalia
    Lindkvist, Bjorn
    Sánchez, María-José
    Pala, Valeria
    Peeters, Petra H M
    Braaten, Tonje
    Tjonneland, Anne
    Dalton, Susanne Oksbjerg
    Larranaga, Nerea
    Dorronsoro, Miren
    Overvad, Kim
    Illner, Anne-Kathrin
    Ardanaz, Eva
    Marron, M
    Straif, K
    Riboli, E
    Bueno-de-Mesquita, B
    No association between educational level and pancreatic cancer incidence in the European Prospective Investigation into Cancer and Nutrition2010Ingår i: Cancer Epidemiology, ISSN 1877-7821, E-ISSN 1877-783X, Vol. 34, nr 6, s. 696-701Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    INTRODUCTION: Until now, studies examining the relationship between socioeconomic status and pancreatic cancer incidence have been inconclusive.

    AIM: To prospectively investigate to what extent pancreatic cancer incidence varies according to educational level within the European Prospective Investigation into Cancer and Nutrition (EPIC) study.

    METHODS: In the EPIC study, socioeconomic status at baseline was measured using the highest level of education attained. Hazard ratios by educational level and a summary index, the relative indices of inequality (RII), were estimated using Cox regression models stratified by age, gender, and center and adjusted for known risk factors. In addition, we conducted separate analyses by age, gender and geographical region.

    RESULTS: Within the source population of 407, 944 individuals at baseline, 490 first incident primary pancreatic adenocarcinoma cases were identified in 9 European countries. The crude difference in risk of pancreatic cancer according to level of education was small and not statistically significant (RII=1.14, 95% CI 0.80-1.62). Adjustment for known risk factors reduced the inequality estimates to only a small extent. In addition, no statistically significant associations were observed for age groups (adjusted RII(≤ 60 years)=0.85, 95% CI 0.44-1.64, adjusted RII(>60 years)=1.18, 95% CI 0.73-1.90), gender (adjusted RII(male)=1.20, 95% CI 0.68-2.10, adjusted RII(female)=0.96, 95% CI 0.56-1.62) or geographical region (adjusted RII(Northern Europe)=1.14, 95% CI 0.81-1.61, adjusted RII(Middle Europe)=1.72, 95% CI 0.93-3.19, adjusted RII(Southern Europe)=0.75, 95% CI 0.32-1.80).

    CONCLUSION: Despite large educational inequalities in many risk factors within the EPIC study, we found no evidence for an association between educational level and the risk of developing pancreatic cancer in this European cohort.

  • 135. Vrieling, Alina
    et al.
    Bueno-de-Mesquita, H Bas
    Boshuizen, Hendriek C
    Michaud, Dominique S
    Severinsen, Marianne T
    Overvad, Kim
    Olsen, Anja
    Tjønneland, Anne
    Clavel-Chapelon, Françoise
    Boutron-Ruault, Marie-Christine
    Kaaks, Rudolf
    Rohrmann, Sabine
    Boeing, Heiner
    Nöthlings, Ute
    Trichopoulou, Antonia
    Moutsiou, Eftihia
    Dilis, Vardis
    Palli, Domenico
    Krogh, Vittorio
    Panico, Salvatore
    Tumino, Rosario
    Vineis, Paolo
    van Gils, Carla H
    Peeters, Petra H M
    Lund, Eiliv
    Gram, Inger T
    Rodríguez, Laudina
    Agudo, Antonio
    Larrañaga, Nerea
    Sánchez, María-José
    Navarro, Carmen
    Barricarte, Aurelio
    Manjer, Jonas
    Lindkvist, Björn
    Sund, Malin
    Umeå universitet, Medicinska fakulteten, Institutionen för kirurgisk och perioperativ vetenskap, Kirurgi.
    Ye, Weimin
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin, Näringsforskning.
    Bingham, Sheila
    Khaw, Kay-Tee
    Roddam, Andrew
    Key, Tim
    Boffetta, Paolo
    Duell, Eric J
    Jenab, Mazda
    Gallo, Valentina
    Riboli, Elio
    Cigarette smoking, environmental tobacco smoke exposure and pancreatic cancer risk in the European Prospective Investigation into Cancer and Nutrition.2010Ingår i: International Journal of Cancer, ISSN 0020-7136, E-ISSN 1097-0215, Vol. 126, nr 10, s. 2394-2403Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Cigarette smoking is an established risk factor for pancreatic cancer. However, prospective data for most European countries are lacking, and epidemiologic studies on exposure to environmental tobacco smoke (ETS) in relation to pancreatic cancer risk are scarce. We examined the association of cigarette smoking and exposure to ETS with pancreatic cancer risk within the European Prospective Investigation into Cancer and Nutrition (EPIC). This analysis was based on 465,910 participants, including 524 first incident pancreatic cancer cases diagnosed after a median follow-up of 8.9 years. Estimates of risk were obtained by Cox proportional hazard models and adjusted for weight, height, and history of diabetes mellitus. An increased risk of pancreatic cancer was found for current cigarette smokers compared with never smokers (HR = 1.71, 95% CI = 1.36-2.15), and risk increased with greater intensity and pack-years. Former cigarette smokers who quit for less than 5 years were at increased risk of pancreatic cancer (HR = 1.78, 95% CI = 1.23-2.56), but risk was comparable to never smokers after quitting for 5 years or more. Pancreatic cancer risk was increased among never smokers daily exposed to ETS (for many hours) during childhood (HR = 2.61, 95% CI = 0.96-7.10) and exposed to ETS at home and/or work (HR = 1.54, 95% CI = 1.00-2.39). These results suggest that both active cigarette smoking, as well as exposure to ETS, is associated with increased risk of pancreatic cancer and that risk is reduced to levels of never smokers within 5 years of quitting.

  • 136. Wadsten, C.
    et al.
    Heyman, H.
    Holmqvist, M.
    Ahlgren, J.
    Lambe, M.
    Sund, Malin
    Umeå universitet.
    Warnberg, F.
    Treatment and prognosis of DCIS during twenty years. A population-based register study from a Swedish cohort2016Ingår i: Cancer Research, ISSN 0008-5472, E-ISSN 1538-7445, Vol. 76Artikel i tidskrift (Övrigt vetenskapligt)
  • 137.
    Wadsten, Charlotta
    et al.
    Umeå universitet, Medicinska fakulteten, Institutionen för kirurgisk och perioperativ vetenskap, Kirurgi.
    Garmo, H.
    Umeå universitet.
    Fredriksson, I.
    Sund, Malin
    Umeå universitet, Medicinska fakulteten, Institutionen för kirurgisk och perioperativ vetenskap, Kirurgi.
    Warnberg, F.
    DCIS and the risk of breast cancer death: a case control study2017Ingår i: Cancer Research, ISSN 0008-5472, E-ISSN 1538-7445, Vol. 77Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Introduction: The risk of breast cancer death after a primary ductal carcinoma in situ (DCIS) is less than 2 % after 10 years. Whereas in situ recurrences do not influence survival, a 17-fold elevated risk of breast cancer specific mortality has been shown for invasive recurrences. Adjuvant radiotherapy (RT) effectively reduces recurrences after breast conserving surgery (BCS) for DCIS, but no studies have been able to demonstrate a survival benefit from adjuvant RT treatment or from choosing mastectomy instead of BCS. Here patient and tumour related risk factors for breast cancer death in women with a pure primary DCIS were studied.

    Patients and methods: Women registered with a primary DCIS, between 1992-2012 in three of Sweden´s health care regions with a population of approximately 5.2 million, were enrolled in a nested case-control study. Out of 6,964 women with DCIS, 96 patients who later died from breast cancer were identified. Four controls per case (n=318) were randomly selected by incidence density sampling. We retrieved medical records and pathology reports and calculated OR with 95% CIs for various variables using conditional logistic regression.

    Results: Of the 96 cases, 10 patients developed distant metastasis without a known local recurrence. In 56 patients death was preceded by an invasive ipsilateral recurrence and in 3 patients by a recurrent ipsilateral DCIS. Seven patients had invasive breast events in both the ipsilateral and the contralateral breast. Seventeen patients had contralateral invasive breast cancer and 3 patients contralateral DCIS.

    Multifocality and tumour size over 25mm (OR 2.6 (1.6 to 4.2)), positive or uncertain margin status (OR 2.8 (1.6 to 4.9)) and detection outside screening (OR 2.1 (1.2 to 3.9)) increased the risk of breast cancer death in univariate analysis, when adjusted for age and year of diagnosis. Suspicion of micro-invasion and nuclear grade 3 was associated with a nonsignificant increased risk, OR 1.8 (0.6 to 5.0) and 2.6 (0.9-6.5), respectively. The risk was not affected by age or treatment. Tumour size and margin status remained significant in the multivariable analysis, when adjusted for treatment and for contralateral breast cancer (OR 2.0 (1.2 to 3.7)).

    Conclusion: In the present study, large tumours and positive or uncertain margin status were significant risk factors for later breast cancer death after a primary DCIS. More extensive treatment was not related to a lower risk. The significance of tumour biology and nuclear grade will be further examined and evaluated.

  • 138.
    Wadsten, Charlotta
    et al.
    Umeå universitet, Medicinska fakulteten, Institutionen för kirurgisk och perioperativ vetenskap. Department of Surgery, Sundsvall Hospital, Sundsvall ; Department of Surgical Sciences, Uppsala University.
    Garmo, H.
    Fredriksson, I.
    Sund, Malin
    Umeå universitet, Medicinska fakulteten, Institutionen för kirurgisk och perioperativ vetenskap.
    Warnberg, F.
    Risk of death from breast cancer after treatment for ductal carcinoma in situ2017Ingår i: British Journal of Surgery, ISSN 0007-1323, E-ISSN 1365-2168, Vol. 104, nr 11, s. 1506-1513Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Background Studies to date have failed to demonstrate any survival benefit from preventing local recurrence after treatment for ductal breast carcinoma in situ (DCIS). Patient- and tumour-related risk factors for death from breast cancer in women with a primary DCIS were analysed here in a large case-control study.

    Methods A nested case-control study was conducted in a population-based cohort of women with primary DCIS between 1992 and 2012. Women who later died from breast cancer were identified. Four controls per case were selected randomly by incidence density sampling. Medical records and pathology reports were retrieved. Conditional logistic regression was used to calculate odds ratios (ORs) and 95 per cent confidence intervals for risk of death from breast cancer.

    Results From a cohort of 6964 women, 96 who died from breast cancer were identified and these were compared with a group of 318 controls. Tumour size over 25mm or multifocal DCIS (OR 255, 95 per cent c.i. 153 to 425), a positive or uncertain margin status (OR 391, 159 to 961) and detection outside the screening programme (OR 212, 116 to 386) increased the risk of death from breast cancer. The risks were not affected by age or type of treatment. In the multivariable analysis, tumour size (OR 195, 106 to 367) and margin status (OR 269, 115 to 711) remained significant.

    Conclusion In the present study, large tumour size and positive or uncertain margin status were associated with a higher risk of death from breast cancer after treatment for primary DCIS. More extensive treatment was not associated with lower risk, which may be due to confounding by indication, or indicate that some DCIS has an inherent potential for metastatic spread. Rare, but worse for large tumours and uncertain margins.

  • 139.
    Wadsten, Charlotta
    et al.
    Umeå universitet, Medicinska fakulteten, Institutionen för kirurgisk och perioperativ vetenskap, Kirurgi.
    Heyman, Hanna
    Holmqvist, Marit
    Ahlgren, Johan
    Lambe, Mats
    Sund, Malin
    Umeå universitet, Medicinska fakulteten, Institutionen för kirurgisk och perioperativ vetenskap, Kirurgi.
    Warnberg, Fredrik
    A validation of DCIS registration in a population-based breast cancer quality register and a study of treatment and prognosis for DCIS during 20 years: Two decades of DCIS in Sweden2016Ingår i: Acta Oncologica, ISSN 0284-186X, E-ISSN 1651-226X, Vol. 55, nr 11, s. 1338-1343Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Aims: Sweden has a long history of population-based cancer registration. The aim of our study was to assess the validity of DCIS registration in a regional Breast Cancer Quality Register (BCQR) and to analyze trends in incidence, treatment and outcome of DCIS, over a 20-year period.Material and methods: All patients with a diagnosis of primary DCIS reported in the BCQR of the Uppsala-orebro healthcare region in Sweden 1992-2012 were included. Three hundred women were randomly selected and their medical records were compared to register data. The study period was divided into four time periods.Results: A total of 2952 women were registered with a DCIS diagnosis. In the final validation cohort of 295 patients, 23 were found to have either recurrent DCIS or invasive breast cancer and eight had LCIS. The completeness and validity of key variables were 91-99%. Twenty of 31 local recurrences were registered (65%).The proportion of DCIS to all breast cancers was 9.5%. Tumor size increased over time. The frequency of mastectomy increased from 23.0% to 39.0%. The proportion of patients receiving radiotherapy after breast conserving surgery increased from 30.1% to 67.6%. The reported local recurrence rate was 9.7% after 10 years. Reported recurrences after BCS and mastectomy were 12.0 and 7.0%, respectively. The recurrence rate did not differ between women undergoing BCS with or without radiotherapy.Conclusion: Only 89.5% of reported DCIS was a primary pure DCIS. The completeness of primary treatment and tumor data was high. The proportion of reported local recurrences was disappointingly low, 65%. The proportion of DCIS was stable over time with a trend towards more intensified treatment. The reported recurrence rate was low independent of treatment and can reflect adequate patient selection, but also over treatment. Our results address the necessity to validate register data on a regular basis.

  • 140.
    Wadsten, Charlotta
    et al.
    Umeå universitet, Medicinska fakulteten, Institutionen för kirurgisk och perioperativ vetenskap.
    Wennstig, A. K.
    Garmo, H.
    Nilsson, G.
    Blomqvist, C.
    Holmberg, L.
    Fredriksson, I.
    Wärnberg, Fredrik
    Sund, Malin
    Umeå universitet, Medicinska fakulteten, Enheten för biobanksforskning. Umeå universitet, Medicinska fakulteten, Institutionen för kirurgisk och perioperativ vetenskap.
    Biomarkers in DCIS associated with breast cancer related deathManuskript (preprint) (Övrig (populärvetenskap, debatt, mm))
  • 141.
    Wadsten, Charlotta
    et al.
    Umeå universitet, Medicinska fakulteten, Institutionen för kirurgisk och perioperativ vetenskap. Department of Surgical Sciences, Uppsala University, Uppsala, Sweden; Department of Surgery, Sundsvall Hospital, Sundsvall, Sweden.
    Wennstig, A.-K
    Garmo, H.
    Nilsson, Greger
    Blomqvist, Carl
    Holmberg, Lars
    Fredriksson, Irma
    Wärnberg, F.
    Sund, Malin
    Umeå universitet, Medicinska fakulteten, Institutionen för kirurgisk och perioperativ vetenskap.
    Risk of ischemic heart disease after radiotherapy for ductal carcinoma in situ2018Ingår i: Breast Cancer Research and Treatment, ISSN 0167-6806, E-ISSN 1573-7217, Vol. 171, nr 1, s. 95-101Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Purpose: The use of adjuvant radiotherapy (RT) in the management of ductal carcinoma in situ (DCIS) is increasing. Left-sided breast irradiation may involve exposure of the heart to ionising radiation, increasing the risk of ischemic heart disease (IHD). We examined the incidence of IHD in a population-based cohort of women with DCIS.

    Methods: The Breast Cancer DataBase Sweden (BCBase) cohort includes women registered with invasive and in situ breast cancers 1992-2012 and age-matched women without a history of breast cancer. In this analysis, 6270 women with DCIS and a comparison cohort of 31,257 women were included. Through linkage with population-based registers, data on comorbidity, socioeconomic status and incidence of IHD was obtained. Hazard ratios (HR) for IHD with 95% confidence intervals (CI) were analysed.

    Results: Median follow-up time was 8.8 years. The risk of IHD was not increased for women with DCIS versus women in the comparison cohort (HR 0.93; 95% CI 0.82-1.06), after treatment with radiotherapy versus surgery alone (HR 0.77; 95% CI 0.60-0.98) or when analysing RT by laterality (HR 0.85; 95% CI 0.53-1.37 for left-sided versus right-sided RT).

    Conclusions: The risk of IHD was lower for women with DCIS allocated to RT compared to non-irradiated women and to the comparison cohort, probably due to patient selection. Comparison of RT by laterality did not show any over-risk for irradiation of the left breast.

  • 142. Walsh, Naomi
    et al.
    Zhang, Han
    Hyland, Paula L
    Yang, Qi
    Mocci, Evelina
    Zhang, Mingfeng
    Childs, Erica J
    Collins, Irene
    Wang, Zhaoming
    Arslan, Alan A
    Beane-Freeman, Laura
    Bracci, Paige M
    Brennan, Paul
    Canzian, Federico
    Duell, Eric J
    Gallinger, Steven
    Giles, Graham G
    Goggins, Michael
    Goodman, Gary E
    Goodman, Phyllis J
    Hung, Rayjean J
    Kooperberg, Charles
    Kurtz, Robert C
    Malats, Núria
    LeMarchand, Loic
    Neale, Rachel E
    Olson, Sara H
    Scelo, Ghislaine
    Shu, Xiao O
    Van Den Eeden, Stephen K
    Visvanathan, Kala
    White, Emily
    Zheng, Wei
    Albanes, Demetrius
    Andreotti, Gabriella
    Babic, Ana
    Bamlet, William R
    Berndt, Sonja I
    Borgida, Ayelet
    Boutron-Ruault, Marie-Christine
    Brais, Lauren
    Brennan, Paul
    Bueno-de-Mesquita, Bas
    Buring, Julie
    Chaffee, Kari G
    Chanock, Stephen
    Cleary, Sean
    Cotterchio, Michelle
    Foretova, Lenka
    Fuchs, Charles
    M Gaziano, J Michael
    Giovannucci, Edward
    Goggins, Michael
    Hackert, Thilo
    Haiman, Christopher
    Hartge, Patricia
    Hasan, Manal
    Helzlsouer, Kathy J
    Herman, Joseph
    Holcatova, Ivana
    Holly, Elizabeth A
    Hoover, Robert
    Hung, Rayjean J
    Janout, Vladimir
    Klein, Eric A
    Kurtz, Robert C
    Laheru, Daniel
    Lee, I-Min
    Lu, Lingeng
    Malats, Núria
    Mannisto, Satu
    Milne, Roger L
    Oberg, Ann L
    Orlow, Irene
    Patel, Alpa V
    Peters, Ulrike
    Porta, Miquel
    Real, Francisco X
    Rothman, Nathaniel
    Sesso, Howard D
    Severi, Gianluca
    Silverman, Debra
    Strobel, Oliver
    Sund, Malin
    Umeå universitet, Medicinska fakulteten, Institutionen för kirurgisk och perioperativ vetenskap.
    Thornquist, Mark D
    Tobias, Geoffrey S
    Wactawski-Wende, Jean
    Wareham, Nick
    Weiderpass, Elisabete
    Wentzensen, Nicolas
    Wheeler, William
    Yu, Herbert
    Zeleniuch-Jacquotte, Anne
    Kraft, Peter
    Li, Donghui
    Jacobs, Eric J
    Petersen, Gloria M
    Wolpin, Brian M
    Risch, Harvey A
    Amundadottir, Laufey T
    Yu, Kai
    Klein, Alison P
    Stolzenberg-Solomon, Rachael Z
    Agnostic Pathway/Gene Set Analysis of Genome-Wide Association Data Identifies Associations for Pancreatic Cancer2019Ingår i: Journal of the National Cancer Institute, ISSN 0027-8874, E-ISSN 1460-2105, Vol. 111, nr 6, artikel-id djy155Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Background: Genome-wide association studies (GWAS) identify associations of individual single-nucleotide polymorphisms (SNPs) with cancer risk but usually only explain a fraction of the inherited variability. Pathway analysis of genetic variants is a powerful tool to identify networks of susceptibility genes.

    Methods: We conducted a large agnostic pathway-based meta-analysis of GWAS data using the summary-based adaptive rank truncated product method to identify gene sets and pathways associated with pancreatic ductal adenocarcinoma (PDAC) in 9040 cases and 12 496 controls. We performed expression quantitative trait loci (eQTL) analysis and functional annotation of the top SNPs in genes contributing to the top associated pathways and gene sets. All statistical tests were two-sided.

    Results: We identified 14 pathways and gene sets associated with PDAC at a false discovery rate of less than 0.05. After Bonferroni correction (P ≤ 1.3 × 10-5), the strongest associations were detected in five pathways and gene sets, including maturity-onset diabetes of the young, regulation of beta-cell development, role of epidermal growth factor (EGF) receptor transactivation by G protein-coupled receptors in cardiac hypertrophy pathways, and the Nikolsky breast cancer chr17q11-q21 amplicon and Pujana ATM Pearson correlation coefficient (PCC) network gene sets. We identified and validated rs876493 and three correlating SNPs (PGAP3) and rs3124737 (CASP7) from the Pujana ATM PCC gene set as eQTLs in two normal derived pancreas tissue datasets.

    Conclusion: Our agnostic pathway and gene set analysis integrated with functional annotation and eQTL analysis provides insight into genes and pathways that may be biologically relevant for risk of PDAC, including those not previously identified.

  • 143. Wang, Zhaoming
    et al.
    Zhu, Bin
    Zhang, Mingfeng
    Parikh, Hemang
    Jia, Jinping
    Chung, Charles C
    Sampson, Joshua N
    Hoskins, Jason W
    Hutchinson, Amy
    Burdette, Laurie
    Ibrahim, Abdisamad
    Hautman, Christopher
    Raj, Preethi S
    Abnet, Christian C
    Adjei, Andrew A
    Ahlbom, Anders
    Albanes, Demetrius
    Allen, Naomi E
    Ambrosone, Christine B
    Aldrich, Melinda
    Amiano, Pilar
    Amos, Christopher
    Andersson, Ulrika
    Umeå universitet, Medicinska fakulteten, Institutionen för strålningsvetenskaper, Onkologi.
    Andriole, Gerald
    Andrulis, Irene L
    Arici, Cecilia
    Arslan, Alan A
    Austin, Melissa A
    Baris, Dalsu
    Barkauskas, Donald A
    Bassig, Bryan A
    Beane Freeman, Laura E
    Berg, Christine D
    Berndt, Sonja I
    Bertazzi, Pier Alberto
    Biritwum, Richard B
    Black, Amanda
    Blot, William
    Boeing, Heiner
    Boffetta, Paolo
    Bolton, Kelly
    Boutron-Ruault, Marie-Christine
    Bracci, Paige M
    Brennan, Paul
    Brinton, Louise A
    Brotzman, Michelle
    Bueno-de-Mesquita, H Bas
    Buring, Julie E
    Butler, Mary Ann
    Cai, Qiuyin
    Cancel-Tassin, Geraldine
    Canzian, Federico
    Cao, Guangwen
    Caporaso, Neil E
    Carrato, Alfredo
    Carreon, Tania
    Carta, Angela
    Chang, Gee-Chen
    Chang, I-Shou
    Chang-Claude, Jenny
    Che, Xu
    Chen, Chien-Jen
    Chen, Chih-Yi
    Chen, Chung-Hsing
    Chen, Constance
    Chen, Kuan-Yu
    Chen, Yuh-Min
    Chokkalingam, Anand P
    Chu, Lisa W
    Clavel-Chapelon, Francoise
    Colditz, Graham A
    Colt, Joanne S
    Conti, David
    Cook, Michael B
    Cortessis, Victoria K
    Crawford, E David
    Cussenot, Olivier
    Davis, Faith G
    De Vivo, Immaculata
    Deng, Xiang
    Ding, Ti
    Dinney, Colin P
    Di Stefano, Anna Luisa
    Diver, W Ryan
    Duell, Eric J
    Elena, Joanne W
    Fan, Jin-Hu
    Feigelson, Heather Spencer
    Feychting, Maria
    Figueroa, Jonine D
    Flanagan, Adrienne M
    Fraumeni, Joseph F
    Freedman, Neal D
    Fridley, Brooke L
    Fuchs, Charles S
    Gago-Dominguez, Manuela
    Gallinger, Steven
    Gao, Yu-Tang
    Gapstur, Susan M
    Garcia-Closas, Montserrat
    Garcia-Closas, Reina
    Gastier-Foster, Julie M
    Gaziano, J Michael
    Gerhard, Daniela S
    Giffen, Carol A
    Giles, Graham G
    Gillanders, Elizabeth M
    Giovannucci, Edward L
    Goggins, Michael
    Gokgoz, Nalan
    Goldstein, Alisa M
    Gonzalez, Carlos
    Gorlick, Richard
    Greene, Mark H
    Gross, Myron
    Grossman, H Barton
    Grubb, Robert
    Gu, Jian
    Guan, Peng
    Haiman, Christopher A
    Hallmans, Göran
    Umeå universitet, Medicinska fakulteten, Enheten för biobanksforskning. Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin, Näringsforskning.
    Hankinson, Susan E
    Harris, Curtis C
    Hartge, Patricia
    Hattinger, Claudia
    Hayes, Richard B
    He, Qincheng
    Helman, Lee
    Henderson, Brian E
    Henriksson, Roger
    Umeå universitet, Medicinska fakulteten, Institutionen för strålningsvetenskaper, Onkologi.
    Hoffman-Bolton, Judith
    Hohensee, Chancellor
    Holly, Elizabeth A
    Hong, Yun-Chul
    Hoover, Robert N
    Hosgood, H Dean
    Hsiao, Chin-Fu
    Hsing, Ann W
    Hsiung, Chao Agnes
    Hu, Nan
    Hu, Wei
    Hu, Zhibin
    Huang, Ming-Shyan
    Hunter, David J
    Inskip, Peter D
    Ito, Hidemi
    Jacobs, Eric J
    Jacobs, Kevin B
    Jenab, Mazda
    Ji, Bu-Tian
    Johansen, Christoffer
    Johansson, Mattias
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin. International Agency for Research on Cancer (IARC-WHO), Lyon, France.
    Johnson, Alison
    Kaaks, Rudolf
    Kamat, Ashish M
    Kamineni, Aruna
    Karagas, Margaret
    Khanna, Chand
    Khaw, Kay-Tee
    Kim, Christopher
    Kim, In-Sam
    Kim, Jin Hee
    Kim, Yeul Hong
    Kim, Young-Chul
    Kim, Young Tae
    Kang, Chang Hyun
    Jung, Yoo Jin
    Kitahara, Cari M
    Klein, Alison P
    Klein, Robert
    Kogevinas, Manolis
    Koh, Woon-Puay
    Kohno, Takashi
    Kolonel, Laurence N
    Kooperberg, Charles
    Kratz, Christian P
    Krogh, Vittorio
    Kunitoh, Hideo
    Kurtz, Robert C
    Kurucu, Nilgun
    Lan, Qing
    Lathrop, Mark
    Lau, Ching C
    Lecanda, Fernando
    Lee, Kyoung-Mu
    Lee, Maxwell P
    Le Marchand, Loic
    Lerner, Seth P
    Li, Donghui
    Liao, Linda M
    Lim, Wei-Yen
    Lin, Dongxin
    Lin, Jie
    Lindstrom, Sara
    Linet, Martha S
    Lissowska, Jolanta
    Liu, Jianjun
    Ljungberg, Börje
    Umeå universitet, Medicinska fakulteten, Institutionen för kirurgisk och perioperativ vetenskap, Urologi och andrologi.
    Lloreta, Josep
    Lu, Daru
    Ma, Jing
    Malats, Nuria
    Mannisto, Satu
    Marina, Neyssa
    Mastrangelo, Giuseppe
    Matsuo, Keitaro
    McGlynn, Katherine A
    McKean-Cowdin, Roberta
    McNeill, Lorna H
    McWilliams, Robert R
    Melin, Beatrice S
    Umeå universitet, Medicinska fakulteten, Institutionen för strålningsvetenskaper, Onkologi.
    Meltzer, Paul S
    Mensah, James E
    Miao, Xiaoping
    Michaud, Dominique S
    Mondul, Alison M
    Moore, Lee E
    Muir, Kenneth
    Niwa, Shelley
    Olson, Sara H
    Orr, Nick
    Panico, Salvatore
    Park, Jae Yong
    Patel, Alpa V
    Patino-Garcia, Ana
    Pavanello, Sofia
    Peeters, Petra H M
    Peplonska, Beata
    Peters, Ulrike
    Petersen, Gloria M
    Picci, Piero
    Pike, Malcolm C
    Porru, Stefano
    Prescott, Jennifer
    Pu, Xia
    Purdue, Mark P
    Qiao, You-Lin
    Rajaraman, Preetha
    Riboli, Elio
    Risch, Harvey A
    Rodabough, Rebecca J
    Rothman, Nathaniel
    Ruder, Avima M
    Ryu, Jeong-Seon
    Sanson, Marc
    Schned, Alan
    Schumacher, Fredrick R
    Schwartz, Ann G
    Schwartz, Kendra L
    Schwenn, Molly
    Scotlandi, Katia
    Seow, Adeline
    Serra, Consol
    Serra, Massimo
    Sesso, Howard D
    Severi, Gianluca
    Shen, Hongbing
    Shen, Min
    Shete, Sanjay
    Shiraishi, Kouya
    Shu, Xiao-Ou
    Siddiq, Afshan
    Sierrasesumaga, Luis
    Sierri, Sabina
    Loon Sihoe, Alan Dart
    Silverman, Debra T
    Simon, Matthias
    Southey, Melissa C
    Spector, Logan
    Spitz, Margaret
    Stampfer, Meir
    Stattin, Pär
    Umeå universitet, Medicinska fakulteten, Institutionen för kirurgisk och perioperativ vetenskap, Urologi och andrologi.
    Stern, Mariana C
    Stevens, Victoria L
    Stolzenberg-Solomon, Rachael Z
    Stram, Daniel O
    Strom, Sara S
    Su, Wu-Chou
    Sund, Malin
    Umeå universitet, Medicinska fakulteten, Institutionen för kirurgisk och perioperativ vetenskap, Kirurgi.
    Sung, Sook Whan
    Swerdlow, Anthony
    Tan, Wen
    Tanaka, Hideo
    Tang, Wei
    Tang, Ze-Zhang
    Tardon, Adonina
    Tay, Evelyn
    Taylor, Philip R
    Tettey, Yao
    Thomas, David M
    Tirabosco, Roberto
    Tjonneland, Anne
    Tobias, Geoffrey S
    Toro, Jorge R
    Travis, Ruth C
    Trichopoulos, Dimitrios
    Troisi, Rebecca
    Truelove, Ann
    Tsai, Ying-Huang
    Tucker, Margaret A
    Tumino, Rosario
    Van Den Berg, David
    Van Den Eeden, Stephen K
    Vermeulen, Roel
    Vineis, Paolo
    Visvanathan, Kala
    Vogel, Ulla
    Wang, Chaoyu
    Wang, Chengfeng
    Wang, Junwen
    Wang, Sophia S
    Weiderpass, Elisabete
    Weinstein, Stephanie J
    Wentzensen, Nicolas
    Wheeler, William
    White, Emily
    Wiencke, John K
    Wolk, Alicja
    Wolpin, Brian M
    Wong, Maria Pik
    Wrensch, Margaret
    Wu, Chen
    Wu, Tangchun
    Wu, Xifeng
    Wu, Yi-Long
    Wunder, Jay S
    Xiang, Yong-Bing
    Xu, Jun
    Yang, Hannah P
    Yang, Pan-Chyr
    Yatabe, Yasushi
    Ye, Yuanqing
    Yeboah, Edward D
    Yin, Zhihua
    Ying, Chen
    Yu, Chong-Jen
    Yu, Kai
    Yuan, Jian-Min
    Zanetti, Krista A
    Zeleniuch-Jacquotte, Anne
    Zheng, Wei
    Zhou, Baosen
    Mirabello, Lisa
    Savage, Sharon A
    Kraft, Peter
    Chanock, Stephen J
    Yeager, Meredith
    Landi, Maria Terese
    Shi, Jianxin
    Chatterjee, Nilanjan
    Amundadottir, Laufey T
    Imputation and subset-based association analysis across different cancer types identifies multiple independent risk loci in the TERT-CLPTM1L region on chromosome 5p15.332014Ingår i: Human Molecular Genetics, ISSN 0964-6906, E-ISSN 1460-2083, Vol. 23, nr 24, s. 6616-6633Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Genome-wide association studies (GWAS) have mapped risk alleles for at least 10 distinct cancers to a small region of 63 000 bp on chromosome 5p15.33. This region harbors the TERT and CLPTM1L genes; the former encodes the catalytic subunit of telomerase reverse transcriptase and the latter may play a role in apoptosis. To investigate further the genetic architecture of common susceptibility alleles in this region, we conducted an agnostic subset-based meta-analysis (association analysis based on subsets) across six distinct cancers in 34 248 cases and 45 036 controls. Based on sequential conditional analysis, we identified as many as six independent risk loci marked by common single-nucleotide polymorphisms: five in the TERT gene (Region 1: rs7726159, P = 2.10 × 10(-39); Region 3: rs2853677, P = 3.30 × 10(-36) and PConditional = 2.36 × 10(-8); Region 4: rs2736098, P = 3.87 × 10(-12) and PConditional = 5.19 × 10(-6), Region 5: rs13172201, P = 0.041 and PConditional = 2.04 × 10(-6); and Region 6: rs10069690, P = 7.49 × 10(-15) and PConditional = 5.35 × 10(-7)) and one in the neighboring CLPTM1L gene (Region 2: rs451360; P = 1.90 × 10(-18) and PConditional = 7.06 × 10(-16)). Between three and five cancers mapped to each independent locus with both risk-enhancing and protective effects. Allele-specific effects on DNA methylation were seen for a subset of risk loci, indicating that methylation and subsequent effects on gene expression may contribute to the biology of risk variants on 5p15.33. Our results provide strong support for extensive pleiotropy across this region of 5p15.33, to an extent not previously observed in other cancer susceptibility loci.

  • 144. Weniger, M.
    et al.
    Moir, J.
    Damm, M.
    Maggino, L.
    Kordes, M.
    Rosendahl, J.
    Ceyhan, G.
    Schorn, S.
    Schmid, D.
    D'Haese, J. G.
    Boeck, S.
    Kruger, S.
    Haas, M.
    Roeder, F.
    del Chiaro, M.
    Lohr, M.
    Tamburrino, D.
    Westermark, S.
    Umeå universitet, Medicinska fakulteten, Institutionen för kirurgisk och perioperativ vetenskap.
    Sund, Malin
    Umeå universitet, Medicinska fakulteten, Institutionen för kirurgisk och perioperativ vetenskap.
    Masini, G.
    Maisonneuve, P.
    Malleo, G.
    Salvia, R.
    Charnley, R. M.
    RESPECT- A Multicenter REtrospective Study on PrEoperative ChemoTherapy With FOLFIRINOX in Locally Advanced and Borderline Respectable Pancreatic Cancer2018Ingår i: Pancreas, ISSN 0885-3177, E-ISSN 1536-4828, Vol. 47, nr 10, s. 1433-1433Artikel i tidskrift (Övrigt vetenskapligt)
  • 145.
    Wennstig, A. K.
    et al.
    Umeå universitet, Medicinska fakulteten, Institutionen för kirurgisk och perioperativ vetenskap, Kirurgi. Department of Oncology, Sundsvall Hospital, Sundsvall, Sweden.
    Garmo, H.
    Isacsson, U.
    Gagliardi, G.
    Rintelä, N.
    Lagerqvist, B.
    Holmberg, L.
    Blomqvist, C.
    Sund, Malin
    Umeå universitet, Medicinska fakulteten, Institutionen för kirurgisk och perioperativ vetenskap, Kirurgi.
    Nilsson, G.
    The relationship between radiation doses to coronary arteries and later intervention requiring coronary stenosis in breast cancer2018Ingår i: European Journal of Cancer, ISSN 0959-8049, E-ISSN 1879-0852, Vol. 92, s. S61-S62Artikel i tidskrift (Övrigt vetenskapligt)
  • 146.
    Wennstig, Anna-Karin
    et al.
    Umeå universitet, Medicinska fakulteten, Institutionen för kirurgisk och perioperativ vetenskap, Kirurgi. Department of Oncology, Sundsvall Hospital, Sweden.
    Garmo, Hans
    Hållström, Per
    Witt Nyström, Petra
    Edlund, Per
    Blomqvist, Carl
    Sund, Malin
    Umeå universitet, Medicinska fakulteten, Institutionen för kirurgisk och perioperativ vetenskap, Kirurgi.
    Nilsson, Greger
    Inter-observer variation in delineating the coronary arteries as organs at risk2017Ingår i: Radiotherapy and Oncology, ISSN 0167-8140, E-ISSN 1879-0887, Vol. 122, nr 1, s. 72-78Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    PURPOSE: To determine the inter-observer variation in delineating the coronary arteries as organs at risk (OAR) in breast cancer (BC) radiotherapy (RT) and how this variation affects the estimated coronary artery radiation dose.

    METHOD: Delineation of the left main and the left anterior descending coronary artery (LMCA and LAD), and the right coronary artery (RCA), by using the heart atlas by Feng et al., was performed by three radiation oncologists in 32 women who had received adjuvant RT for BC. Centres of the arteries were calculated and distances between artery centres were measured and the artery radiation doses were estimated. The intraclass correlation coefficient (ICC) was used to quantify the variability in doses.

    RESULTS: Along the extent of RCA, the median distance between centres of arteries varied from 2 to 9mm with similar patterns over pairs of oncologists. For the LMCA-LAD the median distance varied from 1 to 4mm. The estimated maximum radiation doses showed an ICC variation from 0.82 to 0.97.

    CONCLUSION: The coronary arteries can be reliably identified and delineated as OARs in BC RT. The spatial variance is limited and the total variation in radiation dose is almost completely determined by the between patient variation.

  • 147.
    Wennstig, Anna-Karin
    et al.
    Umeå universitet, Medicinska fakulteten, Institutionen för kirurgisk och perioperativ vetenskap, Kirurgi. Department of Oncology, Sundsvall Hospital, Sundsvall, Sweden.
    Garmo, Hans
    Isacsson, Ulf
    Gagliardi, Giovanna
    Rintelae, Niina
    Lagerqvist, Bo
    Holmberg, Lars
    Blomqvist, Carl
    Sund, Malin
    Umeå universitet, Medicinska fakulteten, Institutionen för kirurgisk och perioperativ vetenskap, Kirurgi.
    Nilsson, Greger
    The relationship between radiation doses to coronary arteries and location of coronary stenosis requiring intervention in breast cancer survivors2019Ingår i: Radiation Oncology, ISSN 1748-717X, E-ISSN 1748-717X, Vol. 14, artikel-id 40Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    BackgroundTo assess the relationship between radiation doses to the coronary arteries (CAs) and location of a coronary stenosis that required intervention after three-dimensional conformal radiotherapy (3DCRT) for breast cancer (BC).MethodsThe study population consisted of 182 women treated for BC in Sweden between 1992 and 2012. All women received 3DCRT and subsequently underwent coronary angiography due to a suspected coronary event. CA segments were delineated in the patient's original planning-CT and radiation doses were recalculated based on the dose distribution of the original radiotherapy (RT) plan. The location of the CA stenosis that required intervention was identified from the Swedish Coronary Angiography and Angioplasty Registry (SCAAR). Logistic regression analysis was used to assess the relationship between CA radiation doses and risk of a later coronary intervention at this specific location.ResultsThe odds ratio (OR) varied by radiation dose to the mid left anterior descending artery (LAD) (p=0.005). Women receiving mean doses of 1-5 Gray (Gy) to the mid LAD had an adjusted OR of 0.90 (95% CI 0.47-1.74) for a later coronary intervention compared to women receiving mean doses of 0-1Gy to the mid LAD. In women receiving mean doses of 5-20Gy to the mid LAD, an adjusted OR of 1.24 (95% CI 0.52-2.95) was observed, which increased to an OR of 5.23 (95% CI 2.01-13.6) for mean doses over 20Gy, when compared to women receiving mean doses of 0-1Gy to the mid LAD.ConclusionsIn women receiving conventional 3DCRT for BC between 1992 and 2012, radiation doses to the LAD remained high and were associated with an increased requirement of coronary intervention in mid LAD. The results support that the LAD radiation dose should be considered in RT treatment planning and that the dose should be kept as low as possible. Minimising the dose to LAD is expected to diminish the risk of later radiation-induced stenosis.

  • 148. Winter, D C
    et al.
    Sund, Malin
    Umeå universitet, Medicinska fakulteten, Institutionen för kirurgisk och perioperativ vetenskap.
    Cancer surgery in the genomic era2018Ingår i: British Journal of Surgery, ISSN 0007-1323, E-ISSN 1365-2168, Vol. 105, nr 2, s. e12-e13Artikel i tidskrift (Refereegranskat)
  • 149. Wolpin, Brian M.
    et al.
    Rizzato, Cosmeri
    Kraft, Peter
    Kooperberg, Charles
    Petersen, Gloria M.
    Wang, Zhaoming
    Arslan, Alan A.
    Beane-Freeman, Laura
    Bracci, Paige M.
    Buring, Julie
    Canzian, Federico
    Duell, Eric J.
    Gallinger, Steven
    Giles, Graham G.
    Goodman, Gary E.
    Goodman, Phyllis J.
    Jacobs, Eric J.
    Kamineni, Aruna
    Klein, Alison P.
    Kolonel, Laurence N.
    Kulke, Matthew H.
    Li, Donghui
    Malats, Nuria
    Olson, Sara H.
    Risch, Harvey A.
    Sesso, Howard D.
    Visvanathan, Kala
    White, Emily
    Zheng, Wei
    Abnet, Christian C.
    Albanes, Demetrius
    Andreotti, Gabriella
    Austin, Melissa A.
    Barfield, Richard
    Basso, Daniela
    Berndt, Sonja I.
    Boutron-Ruault, Marie-Christine
    Brotzman, Michelle
    Buechler, Markus W.
    Bueno-de-Mesquita, H. Bas
    Bugert, Peter
    Burdette, Laurie
    Campa, Daniele
    Caporaso, Neil E.
    Capurso, Gabriele
    Chung, Charles
    Cotterchio, Michelle
    Costello, Eithne
    Elena, Joanne
    Funel, Niccola
    Gaziano, J. Michael
    Giese, Nathalia A.
    Goggins, Michael
    Gorman, Megan J.
    Gross, Myron
    Haiman, Christopher A.
    Hassan, Manal
    Helzlsouer, Kathy J.
    Henderson, Brian E.
    Holly, Elizabeth A.
    Hu, Nan
    Hunter, David J.
    Innocenti, Federico
    Jenab, Mazda
    Kaaks, Rudolf
    Key, Timothy J.
    Khaw, Kay-Tee
    Klein, Eric A.
    Kogevinas, Manolis
    Krogh, Vittorio
    Kupcinskas, Juozas
    Kurtz, Robert C.
    LaCroix, Andrea
    Landi, Maria T.
    Landi, Stefano
    Le Marchand, Loic
    Mambrini, Andrea
    Mannisto, Satu
    Milne, Roger L.
    Nakamura, Yusuke
    Oberg, Ann L.
    Owzar, Kouros
    Patel, Alpa V.
    Peeters, Petra H. M.
    Peters, Ulrike
    Pezzilli, Raffaele
    Piepoli, Ada
    Porta, Miquel
    Real, Francisco X.
    Riboli, Elio
    Rothman, Nathaniel
    Scarpa, Aldo
    Shu, Xiao-Ou
    Silverman, Debra T.
    Soucek, Pavel
    Sund, Malin
    Umeå universitet, Medicinska fakulteten, Institutionen för kirurgisk och perioperativ vetenskap.
    Talar-Wojnarowska, Renata
    Taylor, Philip R.
    Theodoropoulos, George E.
    Thornquist, Mark
    Tjonneland, Anne
    Tobias, Geoffrey S.
    Trichopoulos, Dimitrios
    Vodicka, Pavel
    Wactawski-Wende, Jean
    Wentzensen, Nicolas
    Wu, Chen
    Yu, Herbert
    Yu, Kai
    Zeleniuch-Jacquotte, Anne
    Hoover, Robert
    Hartge, Patricia
    Fuchs, Charles
    Chanock, Stephen J.
    Stolzenberg-Solomon, Rachael S.
    Amundadottir, Laufey T.
    Genome-wide association study identifies multiple susceptibility loci for pancreatic cancer2014Ingår i: Nature Genetics, ISSN 1061-4036, E-ISSN 1546-1718, Vol. 46, nr 9, s. 994-+Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    We performed a multistage genome-wide association study including 7,683 individuals with pancreatic cancer and 14,397 controls of European descent. Four new loci reached genome-wide significance: rs6971499 at 7q32.3 (LINC-PINT, per-allele odds ratio (OR) = 0.79, 95% confidence interval (CI) 0.74-0.84, P = 3.0 x 10(-12)), rs7190458 at 16q23.1 (BCAR1/CTRB1/CTRB2, OR = 1.46, 95% CI 1.30-1.65, P = 1.1 x 10(-10)), rs9581943 at 13q12.2 (PDX1, OR = 1.15, 95% CI 1.10-1.20, P = 2.4 x 10(-9)) and rs16986825 at 22q12.1 (ZNRF3, OR = 1.18, 95% CI 1.12-1.25, P = 1.2 x 10(-8)). We identified an independent signal in exon 2 of TERT at the established region 5p15.33 (rs2736098, OR = 0.80, 95% CI 0.76-0.85, P = 9.8 x 10(-14)). We also identified a locus at 8q24.21 (rs1561927, P = 1.3 x 10(-7)) that approached genome-wide significance located 455 kb telomeric of PVT1. Our study identified multiple new susceptibility alleles for pancreatic cancer that are worthy of follow-up studies.

  • 150. Ylönen, Riikka
    et al.
    Kyrönlahti, Tuomo
    Sund, Malin
    Umeå universitet, Medicinsk fakultet, Kirurgisk och perioperativ vetenskap, Kirurgi.
    Ilves, Mika
    Lehenkari, Petri
    Tuukkanen, Juha
    Pihlajaniemi, Taina
    Type XIII collagen strongly affects bone formation in transgenic mice.2005Ingår i: J Bone Miner Res, ISSN 0884-0431, Vol. 20, nr 8, s. 1381-93Artikel i tidskrift (Refereegranskat)
1234 101 - 150 av 161
RefereraExporteraLänk till träfflistan
Permanent länk
Referera
Referensformat
  • apa
  • ieee
  • modern-language-association-8th-edition
  • vancouver
  • Annat format
Fler format
Språk
  • de-DE
  • en-GB
  • en-US
  • fi-FI
  • nn-NO
  • nn-NB
  • sv-SE
  • Annat språk
Fler språk
Utmatningsformat
  • html
  • text
  • asciidoc
  • rtf