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  • 1. Cramer, Daniel W.
    et al.
    Fichorova, Raina N.
    Terry, Kathryn L.
    Yamamoto, Hidemi
    Vitonis, Allison F.
    Ardanaz, Eva
    Aune, Dagfinn
    Boeing, Heiner
    Brändstedt, Jenny
    Boutron-Ruault, Marie-Christine
    Chirlaque, Maria-Dolores
    Dorronsoro, Miren
    Dossus, Laure
    Duell, Eric J.
    Gram, Inger T.
    Gunter, Marc
    Hansen, Louise
    Idahl, Annika
    Umeå University, Faculty of Medicine, Department of Clinical Sciences, Obstetrics and Gynecology.
    Johnson, Theron
    Khaw, Kay-Tee
    Krogh, Vittorio
    Kvaskoff, Marina
    Mattiello, Amalie
    Matullo, Giuseppe
    Merritt, Melissa A.
    Nodin, Björn
    Orfanos, Philippos
    Onland-Moret, N. Charlotte
    Palli, Domenico
    Peppa, Eleni
    Quirós, J. Ramón
    Sánchez-Perez, Maria-Jose
    Severi, Gianluca
    Tjønneland, Anne
    Travis, Ruth C.
    Trichopoulou, Antonia
    Tumino, Rosario
    Weiderpass, Elisabete
    Fortner, Renée T.
    Kaaks, Rudolf
    Anti-CA15.3 and Anti-CA125 Antibodies and Ovarian Cancer Risk: Results from the EPIC Cohort2018In: Cancer Epidemiology, Biomarkers and Prevention, ISSN 1055-9965, E-ISSN 1538-7755, Vol. 27, no 7, p. 790-804Article in journal (Refereed)
    Abstract [en]

    Background: Neoplastic and non-neoplastic events may raise levels of mucins, CA15.3, and CA125, and generate antibodies against them, but their impact on epithelial ovarian cancer (FOC) risk has not been fully defined.

    Methods: CA15.3, CA125, and IgC1 antibodies against them were measured in 806 women who developed FAN; and 1,927 matched controls from the European Prospective Investigation of Nutrition and Cancer. Associations between epidemiologic factors and anti-mucin antibodies were evaluated using generalized linear models; EOC risks associated with anti-mucin antibodies, by themselves or in combination with respective antigens, were evaluated using conditional logistic regression.

    Results: In controls, lower antibodies against both mucins were associated with current smoking; and, in postmenopausal women, higher levels with longer oral contraceptive use and later-age-at and shorter-interval-since last birth. Lower antiCA15.3 antibodies were associated with higher body mass and, in premenopausal women, more ovulatory cycles. Higher anti-CA15.3 and anti-CA In antibodies were associated with higher risk for mutinous IOC occurring >= 3 years from enrollment. Long-term risk for serous EOC was reduced in women with low CA125 and high anti-CA125 antibodies relative to women with low concentrations of both.

    Conclusions: We found general support for the hypothesis that anti-mucin antibody levels correlate with risk factors for EOC Antibodies alone or in combinations with their antigen may predict longer term risk of specific EOC types.

    Impact: Anti-CA125 and anti-CA15.3 antibodies alone or in perspective of antigens may be informative in the pathogenesis of EOC subtypes, but less useful for informing risk for all EOC.

  • 2. Fortner, Renee T.
    et al.
    Poole, Elizabeth M.
    Wentzensen, Nicolas A.
    Trabert, Britton
    White, Emily
    Arslan, Alan A.
    Patel, Alpa, V
    Setiawan, V. Wendy
    Visvanathan, Kala
    Weiderpass, Elisabete
    Adami, Hans-Olov
    Black, Amanda
    Bernstein, Leslie
    Brinton, Louise A.
    Buring, Julie
    Clendenen, Tess, V
    Fournier, Agnes
    Fraser, Gary
    Gapstur, Susan M.
    Gaudet, Mia M.
    Giles, Graham G.
    Gram, Inger T.
    Hartge, Patricia
    Hoffman-Bolton, Judith
    Idahl, Annika
    Umeå University, Faculty of Medicine, Department of Clinical Sciences, Obstetrics and Gynecology.
    Kaaks, Rudolf
    Kirsh, Victoria A.
    Knutsen, Synnove
    Koh, Woon-Puay
    Lacey, James V., Jr.
    Lee, I-Min
    Lundin, Eva
    Umeå University, Faculty of Medicine, Department of Medical Biosciences, Pathology.
    Merritt, Melissa A.
    Milne, Roger L.
    Onland-Moret, N. Charlotte
    Peters, Ulrike
    Poynter, Jenny N.
    Rinaldi, Sabina
    Robien, Kim
    Rohan, Thomas
    Sanchez, Maria-Jose
    Schairer, Catherine
    Schouten, Leo J.
    Tjonneland, Anne
    Townsend, Mary K.
    Travis, Ruth C.
    Trichopoulou, Antonia
    van den Brandt, Piet A.
    Vineis, Paolo
    Wilkens, Lynne
    Wolk, Alicja
    Yang, Hannah P.
    Zeleniuch-Jacquotte, Anne
    Tworoger, Shelley S.
    Ovarian cancer risk factors by tumor aggressiveness: an analysis from the Ovarian Cancer Cohort Consortium2019In: International Journal of Cancer, ISSN 0020-7136, E-ISSN 1097-0215, Vol. 145, no 1, p. 58-69Article in journal (Refereed)
    Abstract [en]

    Ovarian cancer risk factors differ by histotype; however, within subtype, there is substantial variability in outcomes. We hypothesized that risk factor profiles may influence tumor aggressiveness, defined by time between diagnosis and death, independent of histology. Among 1.3 million women from 21 prospective cohorts, 4,584 invasive epithelial ovarian cancers were identified and classified as highly aggressive (death in <1 year, n = 864), very aggressive (death in 1 to < 3 years, n = 1,390), moderately aggressive (death in 3 to < 5 years, n = 639), and less aggressive (lived 5+ years, n = 1,691). Using competing risks Cox proportional hazards regression, we assessed heterogeneity of associations by tumor aggressiveness for all cases and among serous and endometrioid/clear cell tumors. Associations between parity (phet = 0.01), family history of ovarian cancer (phet = 0.02), body mass index (BMI; phet ≤ 0.04) and smoking (phet < 0.01) and ovarian cancer risk differed by aggressiveness. A first/single pregnancy, relative to nulliparity, was inversely associated with highly aggressive disease (HR: 0.72; 95% CI [0.58–0.88]), no association was observed for subsequent pregnancies (per pregnancy, 0.97 [0.92–1.02]). In contrast, first and subsequent pregnancies were similarly associated with less aggressive disease (0.87 for both). Family history of ovarian cancer was only associated with risk of less aggressive disease (1.94 [1.47–2.55]). High BMI (≥35 vs. 20 to < 25 kg/m2, 1.93 [1.46–2.56] and current smoking (vs. never, 1.30 [1.07–1.57]) were associated with increased risk of highly aggressive disease. Results were similar within histotypes. Ovarian cancer risk factors may be directly associated with subtypes defined by tumor aggressiveness, rather than through differential effects on histology. Studies to assess biological pathways are warranted.

  • 3. Jung, Seungyoun
    et al.
    Allen, Naomi
    Arslan, Alan A.
    Baglietto, Laura
    Barricarte, Aurelio
    Brinton, Louise A.
    Egleston, Brian L.
    Falk, Roni T.
    Fortner, Renée T.
    Helzlsouer, Kathy J.
    Gao, Yutang
    Idahl, Annika
    Umeå University, Faculty of Medicine, Department of Clinical Sciences, Obstetrics and Gynecology.
    Kaaks, Rudolph
    Krogh, Vittorio
    Merritt, Melissa A.
    Lundin, Eva
    Umeå University, Faculty of Medicine, Department of Medical Biosciences, Pathology. Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Nutritional Research.
    Onland-Moret, N. Charlotte
    Rinaldi, Sabina
    Schock, Helena
    Shu, Xiao-Ou
    Sluss, Patrick M.
    Staats, Paul N.
    Sacerdote, Carlotta
    Travis, Ruth C.
    Tjønneland, Anne
    Trichopoulou, Antonia
    Tworoger, Shelley S.
    Visvanathan, Kala
    Weiderpass, Elisabete
    Zeleniuch-Jacquotte, Anne
    Dorgan, Joanne F.
    Anti‐Müllerian hormone and risk of ovarian cancer in nine cohorts2018In: International Journal of Cancer, ISSN 0020-7136, E-ISSN 1097-0215, Vol. 142, no 2, p. 262-270Article in journal (Refereed)
    Abstract [en]

    Animal and experimental data suggest that anti‐Müllerian hormone (AMH) serves as a marker of ovarian reserve and inhibits the growth of ovarian tumors. However, few epidemiologic studies have examined the association between AMH and ovarian cancer risk. We conducted a nested case‐control study of 302 ovarian cancer cases and 336 matched controls from nine cohorts. Prediagnostic blood samples of premenopausal women were assayed for AMH using a picoAMH enzyme‐linked immunosorbent assay. Odds ratios (ORs) and 95% confidence intervals (CIs) were calculated using multivariable‐adjusted conditional logistic regression. AMH concentration was not associated with overall ovarian cancer risk. The multivariable‐adjusted OR (95% CI), comparing the highest to the lowest quartile of AMH, was 0.99 (0.59–1.67) (Ptrend: 0.91). The association did not differ by age at blood draw or oral contraceptive use (all Pheterogeneity: ≥0.26). There also was no evidence for heterogeneity of risk for tumors defined by histologic developmental pathway, stage, and grade, and by age at diagnosis and time between blood draw and diagnosis (all Pheterogeneity: ≥0.39). In conclusion, this analysis of mostly late premenopausal women from nine cohorts does not support the hypothesized inverse association between prediagnostic circulating levels of AMH and risk of ovarian cancer.

  • 4. Kaaks, Rudolf
    et al.
    Fortner, Renée Turzanski
    Hüsing, Anika
    Barrdahl, Myrto
    Hopper, Marika
    Johnson, Theron
    Tjønneland, Anne
    Hansen, Louise
    Overvad, Kim
    Fournier, Agnès
    Boutron-Ruault, Marie-Christine
    Kvaskoff, Marina
    Dossus, Laure
    Johansson, Mattias
    Boeing, Heiner
    Trichopoulou, Antonia
    Benetou, Vassiliki
    La Vecchia, Carlo
    Sieri, Sabina
    Mattiello, Amalia
    Palli, Domenico
    Tumino, Rosario
    Matullo, Giuseppe
    Onland-Moret, N. Charlotte
    Gram, Inger T.
    Weiderpass, Elisabete
    Sánchez, Maria-Jose
    Navarro Sanchez, Carmen
    Duell, Eric J.
    Ardanaz, Eva
    Larranaga, Nerea
    Lundin, Eva
    Umeå University, Faculty of Medicine, Department of Medical Biosciences, Pathology.
    Idahl, Annika
    Umeå University, Faculty of Medicine, Department of Clinical Sciences, Obstetrics and Gynecology.
    Jirström, Karin
    Nodin, Björn
    Travis, Ruth C.
    Riboli, Elio
    Merritt, Melissa
    Aune, Dagfinn
    Terry, Kathryn
    Cramer, Daniel W.
    Anderson, Karen S.
    Tumor-associated autoantibodies as early detection markers for ovarian cancer?: A prospective evaluation2018In: International Journal of Cancer, ISSN 0020-7136, E-ISSN 1097-0215, Vol. 143, no 3, p. 515-526Article in journal (Refereed)
    Abstract [en]

    Immuno-proteomic screening has identified several tumor-associated autoantibodies (AAb) that may have diagnostic capacity for invasive epithelial ovarian cancer, with AAbs to P53 proteins and cancer-testis antigens (CTAGs) as prominent examples. However, the early detection potential of these AAbs has been insufficiently explored in prospective studies. We performed ELISA measurements of AAbs to CTAG1A, CTAG2, P53 and NUDT11 proteins, for 194 patients with ovarian cancer and 705 matched controls from the European EPIC cohort, using serum samples collected up to 36 months prior to diagnosis under usual care. CA125 was measured using electrochemo-luminiscence. Diagnostic discrimination statistics were calculated by strata of lead-time between blood collection and diagnosis. With lead times 6 months, ovarian cancer detection sensitivity at 0.98 specificity (SE98) varied from 0.19 [95% CI 0.08-0.40] for CTAG1A, CTAG2 and NUDT1 to 0.23 [0.10-0.44] for P53 (0.33 [0.11-0.68] for high-grade serous tumors). However, at longer lead-times, the ability of these AAb markers to distinguish future ovarian cancer cases from controls declined rapidly; at lead times >1 year, SE98 estimates were close to zero (all invasive cases, range: 0.01-0.11). Compared to CA125 alone, combined logistic regression scores of AAbs and CA125 did not improve detection sensitivity at equal level of specificity. The added value of these selected AAbs as markers for ovarian cancer beyond CA125 for early detection is therefore limited. What's new? Could autoantibodies against tumor antigens provide an early warning system for ovarian cancer? These authors tested how well certain antibodies detected ovarian cancer. They selected four candidate antibodies, to p53, CTAG1A, CTAG2 and NUDT11 proteins, which appear in elevated levels in cancer patients. None of them performed well as a herald of burgeoning cancer. They did not perform any better than the best currently available biomarker, CA125, and as lead times increased past 6 months prediagnosis, the effectiveness diminished. Surprisingly, elevated antibodies appeared in quite a few of the control samples, suggesting they might not be as cancer-specific as expected.

  • 5. Sasamoto, Naoko
    et al.
    Babic, Ana
    Rosner, Bernard A.
    Fortner, Renee T.
    Vitonis, Allison F.
    Yamamoto, Hidemi
    Fichorova, Raina N.
    Tjonneland, Anne
    Hansen, Louise
    Overvad, Kim
    Kvaskoff, Marina
    Fournier, Agnes
    Mancini, Francesca Romana
    Boeing, Heiner
    Trichopoulou, Antonia
    Peppa, Eleni
    Karakatsani, Anna
    Palli, Domenico
    Pala, Valeria
    Mattiello, Amalia
    Tumino, Rosario
    Grasso, Chiara C.
    Onland-Moret, N. Charlotte
    Weiderpass, Elisabete
    Ramon Quiros, J.
    Lujan-Barroso, Leila
    Rodriguez-Barranco, Miguel
    Colorado-Yohar, Sandra
    Barricarte, Aurelio
    Dorronsoro, Miren
    Idahl, Annika
    Umeå University, Faculty of Medicine, Department of Clinical Sciences, Obstetrics and Gynecology. Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Nutritional Research.
    Lundin, Eva
    Umeå University, Faculty of Medicine, Department of Medical Biosciences, Pathology.
    Sartor, Hanna
    Khaw, Kay-Tee
    Key, Timothy J.
    Muller, David
    Riboli, Elio
    Gunter, Marc J.
    Dossus, Laure
    Kaaks, Rudolf
    Cramer, Daniel W.
    Tworoger, Shelley S.
    Terry, Kathryn L.
    Predicting Circulating CA125 Levels among Healthy Premenopausal Women2019In: Cancer Epidemiology, Biomarkers and Prevention, ISSN 1055-9965, E-ISSN 1538-7755, Vol. 28, no 6, p. 1076-1085Article in journal (Refereed)
    Abstract [en]

    Background: Cancer antigen 125 (CA125) is the most promising ovarian cancer screening biomarker to date. Multiple studies reported CA125 levels vary by personal characteristics, which could inform personalized CA125 thresholds. However, this has not been well described in premenopausal women. Methods: We evaluated predictors of CA125 levels among 815 premenopausal women from the New England Case Control Study (NEC). We developed linear and dichotomous (>= 35 U/mL) CA125 prediction models and externally validated an abridged model restricting to available predictors among 473 premenopausal women in the European Prospective Investigation into Cancer and Nutrition Study (EPIC). Results: The final linear CA125 prediction model included age, race, tubal ligation, endometriosis, menstrual phase at blood draw, and fibroids, which explained 7% of the total variance of CA125. The correlation between observed and predicted CA125 levels based on the abridged model (including age, race, and menstrual phase at blood draw) had similar correlation coefficients in NEC (r = 0.22) and in EPIC (r = 0.22). The dichotomous CA125 prediction model included age, tubal ligation, endometriosis, prior personal cancer diagnosis, family history of ovarian cancer, number of miscarriages, menstrual phase at blood draw, and smoking status with AUC of 0.83. The abridged dichotomous model (including age, number of miscarriages, menstrual phase at blood draw, and smoking status) showed similar AUCs in NEC (0.73) and in EPIC (0.78). Conclusions: We identified a combination of factors associated with CA125 levels in premenopausal women. Impact: Our model could be valuable in identifying healthy women likely to have elevated CA125 and consequently improve its specificity for ovarian cancer screening.

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