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  • 1. Belitskaya-Lévy, Ilana
    et al.
    Zeleniuch-Jacquotte, Anne
    Russo, Jose
    Russo, Irma H
    Bordás, Pal
    Ahman, Janet
    Afanasyeva, Yelena
    Johansson, Robert
    Umeå universitet, Medicinska fakulteten, Institutionen för strålningsvetenskaper, Onkologi.
    Lenner, Per
    Umeå universitet, Medicinska fakulteten, Institutionen för strålningsvetenskaper, Onkologi.
    Li, Xiaochun
    de Cicco, Ricardo López
    Peri, Suraj
    Ross, Eric
    Russo, Patricia A
    Santucci-Pereira, Julia
    Sheriff, Fathima S
    Slifker, Michael
    Hallmans, Göran
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin, Näringsforskning.
    Toniolo, Paolo
    Arslan, Alan A
    Characterization of a genomic signature of pregnancy identified in the breast2011Inngår i: Cancer Prevention Research, ISSN 1940-6207, E-ISSN 1940-6215, Vol. 4, nr 9, s. 1457-1464Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    The objective of this study was to comprehensively compare the genomic profiles in the breast of parous and nulliparous postmenopausal women to identify genes that permanently change their expression following pregnancy. The study was designed as a two-phase approach. In the discovery phase, we compared breast genomic profiles of 37 parous with 18 nulliparous postmenopausal women. In the validation phase, confirmation of the genomic patterns observed in the discovery phase was sought in an independent set of 30 parous and 22 nulliparous postmenopausal women. RNA was hybridized to Affymetrix HG_U133 Plus 2.0 oligonucleotide arrays containing probes to 54,675 transcripts, scanned and the images analyzed using Affymetrix GCOS software. Surrogate variable analysis, logistic regression, and significance analysis of microarrays were used to identify statistically significant differences in expression of genes. The false discovery rate (FDR) approach was used to control for multiple comparisons. We found that 208 genes (305 probe sets) were differentially expressed between parous and nulliparous women in both discovery and validation phases of the study at an FDR of 10% and with at least a 1.25-fold change. These genes are involved in regulation of transcription, centrosome organization, RNA splicing, cell-cycle control, adhesion, and differentiation. The results provide initial evidence that full-term pregnancy induces long-term genomic changes in the breast. The genomic signature of pregnancy could be used as an intermediate marker to assess potential chemopreventive interventions with hormones mimicking the effects of pregnancy for prevention of breast cancer.

  • 2. Duarte-Salles, Talita
    et al.
    Misra, Sandeep
    Stepien, Magdalena
    Plymoth, Amelie
    Muller, David
    Overvad, Kim
    Olsen, Anja
    Tjonneland, Anne
    Baglietto, Laura
    Severi, Gianluca
    Boutron-Ruault, Marie-Christine
    Turzanski-Fortner, Renee
    Kaaks, Rudolf
    Boeing, Heiner
    Aleksandrova, Krasimira
    Trichopoulou, Antonia
    Lagiou, Pagona
    Bamia, Christina
    Pala, Valeria
    Palli, Domenico
    Mattiello, Amalia
    Tumino, Rosario
    Naccarati, Alessio
    Bueno-de-Mesquita, H. B(as).
    Peeters, Petra H.
    Weiderpass, Elisabete
    Quiros, J. Ramon
    Agudo, Antonio
    Sanchez-Cantalejo, Emilio
    Ardanaz, Eva
    Gavrila, Diana
    Dorronsoro, Miren
    Werner, Mårten
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin, Medicin.
    Hemmingsson, Oskar
    Umeå universitet, Medicinska fakulteten, Institutionen för kirurgisk och perioperativ vetenskap, Kirurgi.
    Ohlsson, Bodil
    Sjoberg, Klas
    Wareham, Nicholas J.
    Khaw, Kay-Tee
    Bradbury, Kathryn E.
    Gunter, Marc J.
    Cross, Amanda J.
    Riboli, Elio
    Jenab, Mazda
    Hainaut, Pierre
    Beretta, Laura
    Circulating Osteopontin and Prediction of Hepatocellular Carcinoma Development in a Large European Population2016Inngår i: Cancer Prevention Research, ISSN 1940-6207, E-ISSN 1940-6215, Vol. 9, nr 9, s. 758-765Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    We previously identified osteopontin (OPN) as a promising marker for the early detection of hepatocellular carcinoma (HCC). In this study, we investigated the association between prediagnostic circulating OPN levels and HCC incidence in a large population-based cohort. A nested case-control study was conducted within the European Prospective Investigation into Cancer and Nutrition (EPIC) cohort. During a mean follow-up of 4.8 years, 100 HCC cases were identified. Each case was matched to two controls and OPN levels were measured in baseline plasma samples. Viral hepatitis, liver function, and a-fetoprotein (AFP) tests were also conducted. Conditional logistic regression models were used to calculate multivariable odds ratio (OR) and 95% confidence intervals (95% CI) for OPN levels in relation to HCC. Receiver operating characteristics curves were constructed to determine the discriminatory accuracy of OPN alone or in combination with other liver biomarkers in the prediction of HCC. OPN levels were positively associated with HCC risk (per 10% increment, ORmultivariable = 1.30; 95% CI, 1.14-1.48). The association was stronger among cases diagnosed within 2 years of follow-up. Adding liver function tests to OPN improved the discriminatory performance for subjects who developed HCC (AUC = 0.86). For cases diagnosed within 2 years, the combination of OPN and AFP was best able to predict HCC risk (AUC = 0.88). The best predictive model for HCC in this low-risk population is OPN in combination with liver function tests. Within 2 years of diagnosis, the combination of OPN and AFP best predicted HCC development, suggesting that measuring OPN and AFP could identify high-risk groups independently of a liver disease diagnosis.

  • 3. Hoggart, Clive
    et al.
    Brennan, Paul
    Tjönneland, Anne
    Vogel, Ulla
    Overvad, Kim
    Nautrup Östergaard, Jane
    Kaaks, Rudolph
    Canzian, Federico
    Boeing, Heiner
    Steffen, Annika
    Trichopoulou, Antonia
    Bamia, Christina
    Trichopoulos, Dimitrios
    Johansson, Mattias
    Palli, Domenico
    Krogh, Vittorio
    Tumino, Rosario
    Sacerdote, Carlotta
    Panico, Salvatore
    Boshuizen, Hendriek C
    Bueno-de-Mesquita, H Bas
    Peeters, Petra H M
    Lund, Eiliv
    Gram, Inger Torhild
    Braaten, Tonje
    Rodríguez, Laudina
    Agudo, Antonio
    Sanchez-Cantalejo, Emilio
    Arriola, Larraitz
    Chirlaque, Maria-Dolores
    Barricarte, Aurelio
    Rasmuson, Torgny
    Umeå universitet, Medicinska fakulteten, Institutionen för strålningsvetenskaper, Onkologi.
    Khaw, Kay-Tee
    Wareham, Nicholas J
    Allen, Naomi E
    Riboli, Elio
    Vineis, Paolo
    A Risk Model for Lung Cancer Incidence2012Inngår i: Cancer Prevention Research, ISSN 1940-6207, E-ISSN 1940-6215, Vol. 5, nr 6, s. 834-846Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    Risk models for lung cancer incidence would be useful for prioritising individuals for screening and participation in clinical trials of chemoprevention. We present a risk model for lung cancer built using prospective cohort data from a general population which predicts individual incidence in a given time period.We build separate risk models for current and former smokers utilising 169,035 ever smokers from the multicentre European Prospective Investigation into Cancer and Nutrition (EPIC) and considered a model for never smokers. The data set was split into independent training and test sets. Lung cancer incidence was modelled using survival analysis, stratifying by age started smoking, and for former smokers, also smoking duration. Other risk factors considered were smoking intensity, ten occupational/environmental exposures previously implicated with lung cancer, and SNPs at two loci identified by genome-wide association studies of lung cancer. Individual risk in the test set was measured by the predicted probability of lung cancer incidence in the year preceding last follow-up time, predictive accuracy was measured by the area under the receiver operator characteristic curve (AUC).Utilising smoking information alone gave good predictive accuracy: the AUC and 95% confidence interval in ever smokers was 0.843 (0.810, 0.875), the Bach model applied to the same data gave an AUC of 0.775 (0.737, 0.813). Other risk factors had negligible effect on the AUC, including never smokers for whom prediction was poor.Our model is generalisable and straightforward to implement. Its accuracy can be attributed to its modelling of lifetime exposure to smoking.

  • 4. Klein, Robert J
    et al.
    Halldén, Christer
    Cronin, Angel M
    Ploner, Alexander
    Wiklund, Fredrik
    Bjartell, Anders S
    Stattin, Pär
    Umeå universitet, Medicinska fakulteten, Institutionen för kirurgisk och perioperativ vetenskap, Urologi och andrologi.
    Xu, Jianfeng
    Scardino, Peter T
    Offit, Kenneth
    Vickers, Andrew J
    Grönberg, Henrik
    Lilja, Hans
    Blood biomarker levels to aid discovery of cancer-related single-nucleotide polymorphisms: kallikreins and prostate cancer2010Inngår i: Cancer Prevention Research, ISSN 1940-6207, E-ISSN 1940-6215, Vol. 3, nr 5, s. 611-619Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    Polymorphisms associated with prostate cancer include those in three genes encoding major secretory products of the prostate: KLK2 (encoding kallikrein-related peptidase 2; hK2), KLK3 (encoding prostate-specific antigen; PSA), and MSMB (encoding beta-microseminoprotein). PSA and hK2, members of the kallikrein family, are elevated in sera of men with prostate cancer. In a comprehensive analysis that included sequencing of all coding, flanking, and 2 kb of putative promoter regions of all 15 kallikrein (KLK) genes spanning approximately 280 kb on chromosome 19q, we identified novel single-nucleotide polymorphisms (SNP) and genotyped 104 SNPs in 1,419 cancer cases and 736 controls in Cancer Prostate in Sweden 1, with independent replication in 1,267 cases and 901 controls in Cancer Prostate in Sweden 2. This verified prior associations of SNPs in KLK2 and in MSMB (but not in KLK3) with prostate cancer. Twelve SNPs in KLK2 and KLK3 were associated with levels of PSA forms or hK2 in plasma of control subjects. Based on our comprehensive approach, this is likely to represent all common KLK variants associated with these phenotypes. A T allele at rs198977 in KLK2 was associated with increased cancer risk and a striking decrease of hK2 levels in blood. We also found a strong interaction between rs198977 genotype and hK2 levels in blood in predicting cancer risk. Based on this strong association, we developed a model for predicting prostate cancer risk from standard biomarkers, rs198977 genotype, and rs198977 x hK2 interaction; this model had greater accuracy than did biomarkers alone (area under the receiver operating characteristic curve, 0.874 versus 0.866), providing proof in principle to clinical application for our findings.

  • 5. Michaud, Dominique S.
    et al.
    Bove, Gerald
    Gallo, Valentina
    Schlehofer, Brigitte
    Tjönneland, Anne
    Olsen, Anja
    Overvad, Kim
    Dahm, Christina C.
    Teucher, Brigit
    Boeing, Heiner
    Steffen, Annika
    Trichopoulou, Antonia
    Bamia, Christina
    Kyrozis, Andreas
    Sacerdote, Carlotta
    Agnoli, Claudia
    Palli, Domenico
    Tumino, Rosario
    Mattiello, Amalia
    Bueno-de-Mesquita, H. Bas
    Peeters, Petra H. M.
    May, Anne M.
    Barricarte, Aurelio
    Chirlaque, Maria-Dolores
    Dorronsoro, Miren
    Jose Sanchez, Maria
    Rodriguez, Laudina
    Duell, Eric J.
    Hallmans, Göran
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin, Näringsforskning.
    Melin, Beatrice S.
    Umeå universitet, Medicinska fakulteten, Institutionen för strålningsvetenskaper, Onkologi.
    Manjer, Jonas
    Borgquist, Signe
    Khaw, Kay-Tee
    Wareham, Nick
    Allen, Naomi E.
    Travis, Ruth C.
    Romieu, Isabelle
    Vineis, Paolo
    Riboli, Elio
    Anthropometric Measures, Physical Activity, and Risk of Glioma and Meningioma in a Large Prospective Cohort Study2011Inngår i: Cancer Prevention Research, ISSN 1940-6207, E-ISSN 1940-6215, Vol. 4, nr 9, s. 1385-1392Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    Body fatness has been associated with increased risk of a number of hormone-dependent cancers. Recent studies suggest that body mass index (BMI) may be related to meningiomas, which are more common in women than men, and for which estrogens are believed to play a role. Using data from a large European propective cohort, 203 incident cases of meningioma and 340 cases of glioma were included in the analysis for measures of body fat, height, and physical activity among 380,775 participants. All analyses were conducted using Cox proportional hazards model and controlling for age, sex, country, and education. A 71% increase in risk of meningioma was observed among men and women in the top quartile of waist circumference (HR = 1.71, 95% CI = 1.08-2.73, P(trend) = 0.01). A positive association was also observed for BMI and meningioma (HR = 1.48, 95% CI = 0.98-2.23, for BMI >= 30 compared with a BMI of 20-24.9, P(trend) = 0.05). An association with height and meningioma was also suggestive (HR = 1.24, 95% 0.96-1.51, for each 10 cm increase). In contrast, no associations were observed for height and different measures of body fat and risk of glioma. Physical activity was not related to either type of brain tumors. Results from this study support an increase in risk of meningioma with higher body fatness among both men and women. No association was observed between anthropometric measures and risk of glioma. Cancer Prev Res; 4(9); 1385-92. (C) 2011 AACR.

  • 6.
    Plym Forshell, Tacha Zi
    et al.
    Umeå universitet, Teknisk-naturvetenskapliga fakulteten, Institutionen för molekylärbiologi (Teknisk-naturvetenskaplig fakultet).
    Rimpi, Sara
    Umeå universitet, Teknisk-naturvetenskapliga fakulteten, Institutionen för molekylärbiologi (Teknisk-naturvetenskaplig fakultet).
    Nilsson, Jonas A
    Umeå universitet, Teknisk-naturvetenskapliga fakulteten, Institutionen för molekylärbiologi (Teknisk-naturvetenskaplig fakultet).
    Chemoprevention of B-cell lymphomas by inhibition of the Myc target spermidine synthase2010Inngår i: Cancer Prevention Research, ISSN 1940-6207, E-ISSN 1940-6215, Vol. 3, nr 2, s. 140-147Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    The oncogenic transcription factor c-Myc (Myc) is frequently overexpressed in human cancers. Myc is known to induce or repress a large set of genes involved in cell growth and proliferation, explaining the selection for mutations in cancer that deregulate Myc expression. Inhibition of ornithine decarboxylase, an enzyme of the polyamine biosynthetic pathway and a Myc target, has been shown to be chemopreventive. In the present study, we have dissected the role of another enzyme in the polyamine biosynthetic pathway, spermidine synthase (Srm), in Myc-induced cancer. We find that Srm is encoded by a Myc target gene containing perfect E-boxes and that it is induced by Myc in a direct manner. RNA interference against Srm shows that it is important for Myc-induced proliferation of mouse fibroblasts but to a lesser extent for transformation. Using the compound trans-4-methylcyclohexylamine, we show that Srm inhibition can delay the onset of B-cell lymphoma development in λ-Myc transgenic mice. We therefore suggest that inhibition of Srm is an additional chemopreventive strategy that warrants further consideration.

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