12 results on '"Rossing, M."'
Search Results
2. Menopausal hormone use and ovarian cancer risk : Individual participant meta-analysis of 52 epidemiological studies
- Author
-
Gapstur, S. M., Patel, A. V., Banks, E., Dal Maso, L., Talamini, R., Chetrit, A., Hirsh-Yechezkel, G., Lubin, F., Sadetzki, S., Beral, V., Bull, D., Cairns, B., Crossley, B., Gaitskell, K., Goodill, A., Green, J., Hermon, C., Key, T., Moser, K., Reeves, G., Sitas, F., Collins, R., Peto, R., Gonzalez, C. A., Lee, N., Marchbanks, P., Ory, H. W., Peterson, H. B., Wingo, P. A., Martin, N., Silpisornkosol, S., Theetranont, C., Boosiri, B., Chutivongse, S., Jimakorn, P., Virutamasen, P., Wongsrichanalai, C., Goodman, M. T., Lidegaard, O., Kjaer, S. K., Morch, L. S., Tjonneland, A., Byers, T., Rohan, T., Mosgaard, B., Vessey, M., Yeates, D., Freudenheim, J. L., Titus, L. J., Chang-Claude, J., Kaaks, R., Anderson, K. E., Lazovich, D., Robien, K., Hampton, J., Newcomb, P. A., Rossing, M. A., Thomas, D. B., Weiss, N. S., Lokkegaard, E., Riboli, E., Clavel-Chapelon, F., Cramer, D., Hankinson, S. E., Tamimi, R. M., Tworoger, S. S., Franceschi, S., La Vecchia, C., Negri, E., Adami, H. O., Magnusson, C., Riman, T., Weiderpass, E., Wolk, A., Schouten, L. J., van den Brandt, P. A., Chantarakul, N., Koetsawang, S., Rachawat, D., Palli, D., Black, A., Brinton, L. A., Freedman, D. M., Hartge, P., Hsing, A. W., Jnr, J. V. Lacey, Lissowska, J., Hoover, R. N., Schairer, C., Babb, C., Urban, M., Graff-Iversen, S., Selmer, R., Bain, C. J., Green, A. C., Purdie, D. M., Siskind, V., Webb, P. M., Moysich, K., McCann, S. E., Hannaford, P., Kay, C., Binns, C. W., Lee, A. H., Zhang, M., Ness, R. B., Nasca, P., Coogan, P. F., Palmer, J. R., Rosenberg, L., Whittemore, A., Katsouyanni, K., Trichopoulou, A., Trichopoulos, D., Tzonou, A., Dabancens, A., Martinez, L., Molina, R., Salas, O., Lurie, G., Carney, M. E., Wilkens, L. R., Werner Hartman, Linda, Manjer, Jonas, Olsson, Håkan, Kumle, M., Grisso, J. A., Morgan, M., Wheeler, J. E., Edwards, R. P., Kelley, J. L., Modugno, F., Onland-Moret, N. C., Peeters, P. H. M., Casagrande, J., Pike, M. C., Wu, A. H., Canfell, K., Miller, A. B., Gram, I. T., Lund, E., McGowan, L., Shu, X. O., Zheng, W., Farley, T. M. M., Holck, S., Meirik, O., Risch, H. A., S. M. Gapstur, A. V. Patel, E. Bank, L. Dal Maso, R. Talamini, A. Chetrit, G. Hirsh Yechezkel, F. Lubin, S. Sadetzki, V. Beral, D. Bull, B. Cairn, B. Crossley, K. Gaitskell, A. Goodill, J. Green, C. Hermon, T. Key, K. Moser, G. Reeve, F. Sita, R. Collin, R. Peto, C. A. Gonzalez, N. Lee, P. Marchbank, H. W. Ory, H. B. Peterson, P. A. Wingo, N. Martin, S. Silpisornkosol, C. Theetranont, B. Boosiri, S. Chutivongse, P. Jimakorn, P. Virutamasen, C. Wongsrichanalai, M. T. Goodman, O. Lidegaard, S. K. Kjaer, L. S. Morch, A. Tjonneland, T. Byer, T. Rohan, B. Mosgaard, M. Vessey, D. Yeate, J. L. Freudenheim, L. J. Titu, J. Chang Claude, R. Kaak, K. E. Anderson, D. Lazovich, K. Robien, J. Hampton, P. A. Newcomb, M. A. Rossing, D. B. Thoma, N. S. Wei, E. Lokkegaard, E. Riboli, F. Clavel Chapelon, D. Cramer, S. E. Hankinson, R. M. Tamimi, S. S. Tworoger, S. Franceschi, C. La Vecchia, E. Negri, H. O. Adami, C. Magnusson, T. Riman, E. Weiderpa, A. Wolk, L. J. Schouten, P. A. van den Brandt, N. Chantarakul, S. Koetsawang, D. Rachawat, D. Palli, A. Black, L. A. Brinton, D. M. Freedman, P. Hartge, A. W. Hsing, J. V. L. Jnr, J. Lissowska, R. N. Hoover, C. Schairer, C. Babb, M. Urban, S. Graff Iversen, R. Selmer, C. J. Bain, A. C. Green, D. M. Purdie, V. Siskind, P. M. Webb, K. Moysich, S. E. McCann, P. Hannaford, C. Kay, C. W. Binn, A. H. Lee, M. Zhang, R. B. Ne, P. Nasca, P. F. Coogan, J. R. Palmer, L. Rosenberg, A. Whittemore, K. Katsouyanni, A. Trichopoulou, D. Trichopoulo, A. Tzonou, A. Dabancen, L. Martinez, R. Molina, O. Sala, G. Lurie, M. E. Carney, L. R. Wilken, L. Hartman, J. Manjer, H. Olsson, M. Kumle, J. A. Grisso, M. Morgan, J. E. Wheeler, R. P. Edward, J. L. Kelley, F. Modugno, N. C. Onland Moret, P. H. M. Peeter, J. Casagrande, M. C. Pike, A. H. Wu, K. Canfell, A. B. Miller, I. T. Gram, E. Lund, L. McGowan, X. O. Shu, W. Zheng, T. M. M. Farley, S. Holck, O. Meirik, H. A. Risch, Epidemiologie, RS: CAPHRI School for Public Health and Primary Care, RS: CAPHRI - R3 - Functioning, Participating and Rehabilitation, RS: CAPHRI - R5 - Optimising Patient Care, RS: GROW - Oncology, and RS: GROW - R1 - Prevention
- Subjects
medicine.medical_specialty ,medicine.medical_treatment ,Etiology - Endogenous Factors in the Origin and Cause of Cancer ,ovarian neoplasm ,THERAPY ,Medicine, General & Internal ,Internal medicine ,General & Internal Medicine ,Epidemiology ,middle aged ,medicine ,Cancer Type - Ovarian Cancer ,estrogen replacement therapy ,human ,Prospective cohort study ,medicine (all) ,Gynecology ,Science & Technology ,business.industry ,drug administration schedule ,WOMEN ,risk assessment ,Retrospective cohort study ,General Medicine ,11 Medical And Health Sciences ,medicine.disease ,postmenopause ,female ,Meta-analysis ,Relative risk ,Cancer and Oncology ,incidence ,Hormone therapy ,HEALTH ,Risk assessment ,Ovarian cancer ,business ,Life Sciences & Biomedicine - Abstract
SummaryBackgroundHalf the epidemiological studies with information about menopausal hormone therapy and ovarian cancer risk remain unpublished, and some retrospective studies could have been biased by selective participation or recall. We aimed to assess with minimal bias the effects of hormone therapy on ovarian cancer risk.MethodsIndividual participant datasets from 52 epidemiological studies were analysed centrally. The principal analyses involved the prospective studies (with last hormone therapy use extrapolated forwards for up to 4 years). Sensitivity analyses included the retrospective studies. Adjusted Poisson regressions yielded relative risks (RRs) versus never-use.FindingsDuring prospective follow-up, 12 110 postmenopausal women, 55% (6601) of whom had used hormone therapy, developed ovarian cancer. Among women last recorded as current users, risk was increased even with
- Published
- 2015
3. Obesity and survival among women with ovarian cancer: results from the Ovarian Cancer Association Consortium.
- Author
-
Nagle, C M, Dixon, S C, Jensen, A, Kjaer, S K, Modugno, F, deFazio, A, Fereday, S, Hung, J, Johnatty, S E, Fasching, P A, Beckmann, M W, Lambrechts, D, Vergote, I, Van Nieuwenhuysen, E, Lambrechts, S, Risch, H A, Rossing, M A, Doherty, J A, Wicklund, K G, and Chang-Claude, J
- Subjects
OVARIAN cancer treatment ,OVARIAN cancer ,CANCER complications ,OBESITY risk factors ,PROGRESSION-free survival ,BODY mass index ,CANCER risk factors - Abstract
Background:Observational studies have reported a modest association between obesity and risk of ovarian cancer; however, whether it is also associated with survival and whether this association varies for the different histologic subtypes are not clear. We undertook an international collaborative analysis to assess the association between body mass index (BMI), assessed shortly before diagnosis, progression-free survival (PFS), ovarian cancer-specific survival and overall survival (OS) among women with invasive ovarian cancer.Methods:We used original data from 21 studies, which included 12 390 women with ovarian carcinoma. We combined study-specific adjusted hazard ratios (HRs) using random-effects models to estimate pooled HRs (pHR). We further explored associations by histologic subtype.Results:Overall, 6715 (54%) deaths occurred during follow-up. A significant OS disadvantage was observed for women who were obese (BMI: 30-34.9, pHR: 1.10 (95% confidence intervals (CIs): 0.99-1.23); BMI: ⩾35, pHR: 1.12 (95% CI: 1.01-1.25)). Results were similar for PFS and ovarian cancer-specific survival. In analyses stratified by histologic subtype, associations were strongest for women with low-grade serous (pHR: 1.12 per 5 kg m
−2 ) and endometrioid subtypes (pHR: 1.08 per 5 kg m−2 ), and more modest for the high-grade serous (pHR: 1.04 per 5 kg m−2 ) subtype, but only the association with high-grade serous cancers was significant.Conclusions:Higher BMI is associated with adverse survival among the majority of women with ovarian cancer. [ABSTRACT FROM AUTHOR]- Published
- 2015
- Full Text
- View/download PDF
4. Genome-Wide Meta-Analyses of Breast, Ovarian, and Prostate Cancer Association Studies Identify Multiple New Susceptibility Loci Shared by at Least Two Cancer Types
- Author
-
Kar, S. P., Beesley, J., Amin Al Olama, A., Michailidou, K., Tyrer, J., Kote-Jarai, Z., Lawrenson, K., Lindstrom, S., Ramus, S. J., Thompson, D. J., Kibel, Adam Stuart, Dansonka-Mieszkowska, A., Michael, A., Dieffenbach, A. K., Gentry-Maharaj, A., Whittemore, A. S., Wolk, A., Monteiro, A., Peixoto, A., Kierzek, A., Cox, A., Rudolph, A., Gonzalez-Neira, A., Wu, A. H., Lindblom, A., Swerdlow, A., Ziogas, A., Ekici, A. B., Burwinkel, B., Karlan, B. Y., Nordestgaard, B. G., Blomqvist, C., Phelan, C., McLean, C., Pearce, C. L., Vachon, C., Cybulski, C., Slavov, C., Stegmaier, C., Maier, C., Ambrosone, C. B., Hogdall, C. K., Teerlink, C. C., Kang, D., Tessier, D. C., Schaid, D. J., Stram, D. O., Cramer, Daniel William, Neal, D. E., Eccles, D., Flesch-Janys, D., Edwards, D. R. V., Wokozorczyk, D., Levine, D. A., Yannoukakos, D., Sawyer, E. J., Bandera, E. V., Poole, Elizabeth M., Goode, E. L., Khusnutdinova, E., Hogdall, E., Song, F, Bruinsma, F., Heitz, F., Modugno, F., Hamdy, F. C., Wiklund, F., Giles, G. G., Olsson, H., Wildiers, H., Ulmer, H.-U., Pandha, H., Risch, H. A., Darabi, H., Salvesen, H. B., Nevanlinna, H., Gronberg, H., Brenner, H., Brauch, H., Anton-Culver, H., Song, H., Lim, H.-Y., McNeish, I., Campbell, I., Vergote, I., Gronwald, J., Lubinski, J., Stanford, J. L., Benitez, J., Doherty, J. A., Permuth, J. B., Chang-Claude, J., Donovan, J. L., Dennis, J., Schildkraut, J. M., Schleutker, J., Hopper, J. L., Kupryjanczyk, J., Park, J. Y., Figueroa, J., Clements, J. A., Knight, J. A., Peto, J., Cunningham, J. M., Pow-Sang, J., Batra, J., Czene, K., Lu, K. H., Herkommer, K., Khaw, K.-T., Matsuo, K., Muir, K., Offitt, K., Chen, K., Moysich, K. B., Aittoma ki, K., Odunsi, K., Kiemeney, L. A., Massuger, L. F. A. G., Fitzgerald, L. M., Cook, L. S., Cannon-Albright, L., Hooning, M. J., Pike, M. C., Bolla, M. K., Luedeke, M., Teixeira, M. R., Goodman, M. T., Schmidt, M. K., Riggan, M., Aly, M., Rossing, M. A., Beckmann, M. W., Moisse, M., Sanderson, M., Southey, M. C., Jones, M., Lush, M., Hildebrandt, M. A. T., Hou, M.-F., Schoemaker, M. J., Garcia-Closas, M., Bogdanova, N., Rahman, N., Le, N. D., Orr, N., Wentzensen, N., Pashayan, N., Peterlongo, P., Guenel, P., Brennan, P., Paulo, P., Webb, P. M., Broberg, P., Fasching, P. A., Devilee, P., Wang, Q., Cai, Q., Li, Q., Kaneva, R., Butzow, R., Kopperud, R. K., Schmutzler, R. K., Stephenson, R. A., MacInnis, R. J., Hoover, R. N., Winqvist, R., Ness, R., Milne, R. L., Travis, R. C., Benlloch, S., Olson, S. H., McDonnell, S. K., Tworoger, Shelley Slate, Maia, S., Berndt, S., Lee, S. C., Teo, S.-H., Thibodeau, S. N., Bojesen, S. E., Gapstur, S. M., Kjaer, S. K., Pejovic, T., Tammela, T. L. J., Do rk, T., Bru ning, T., Wahlfors, T., Key, T. J., Edwards, T. L., Menon, U., Hamann, U., Mitev, V., Kosma, V.-M., Setiawan, V. W., Kristensen, V., Arndt, V., Vogel, W., Zheng, W., Sieh, W., Blot, W. J., Kluzniak, W., Shu, X.-O., Gao, Y.-T., Schumacher, F., Freedman, M. L., Berchuck, A., Dunning, A. M., Simard, J., Haiman, C. A., Spurdle, A., Sellers, T. A., Hunter, David J., Henderson, B. E., Kraft, Peter Elias, Chanock, S. J., Couch, F. J., Hall, P., Gayther, S. A., Easton, D. F., Chenevix-Trench, G., Eeles, R., Pharoah, P. D. P., Lambrechts, D., and undefined, undefined
- Subjects
breast cancer ,ovarian cancer ,prostate cancer ,genome-wide association studies ,pleiotropy - Abstract
Breast, ovarian, and prostate cancers are hormone-related and may have a shared genetic basis, but this has not been investigated systematically by genome-wide association (GWA) studies. Meta-analyses combining the largest GWA meta-analysis data sets for these cancers totaling 112,349 cases and 116,421 controls of European ancestry, all together and in pairs, identified at P < 10(-8) seven new cross-cancer loci: three associated with susceptibility to all three cancers (rs17041869/2q13/BCL2L11; rs7937840/11q12/INCENP; rs1469713/19p13/GATAD2A), two breast and ovarian cancer risk loci (rs200182588/9q31/SMC2; rs8037137/15q26/RCCD1), and two breast and prostate cancer risk loci (rs5013329/1p34/NSUN4; rs9375701/6q23/L3MBTL3). Index variants in five additional regions previously associated with only one cancer also showed clear association with a second cancer type. Cell-type-specific expression quantitative trait locus and enhancer-gene interaction annotations suggested target genes with potential cross-cancer roles at the new loci. Pathway analysis revealed significant enrichment of death receptor signaling genes near loci with P < 10(-5) in the three-cancer meta-analysis., Other Research Unit
- Published
- 2016
- Full Text
- View/download PDF
5. Tagging single-nucleotide polymorphisms in candidate oncogenes and susceptibility to ovarian cancer.
- Author
-
Quaye, L., Song, H., Ramus, S. J., Gentry-Maharaj, A., Høgdall, E., DiCioccio, R. A., McGuire, V., Wu, A. H., Van Den Berg, D. J., Pike, M. C., Wozniak, E., Doherty, J. A., Rossing, M. A., Ness, R. B., Moysich, K. B., Høgdall, C., Blaakaer, J., Easton, D. F., Ponder, B. A. J., and Jacobs, I. J.
- Subjects
NUCLEOTIDES ,GENETIC polymorphisms ,OVARIAN cancer ,CARCINOGENESIS ,DISEASE susceptibility ,COMPARATIVE studies ,GENES ,RESEARCH methodology ,MEDICAL cooperation ,ONCOGENES ,OVARIAN tumors ,PHOSPHOTRANSFERASES ,PROTEINS ,RESEARCH ,RESEARCH funding ,TRANSFERASES ,EVALUATION research ,HAPLOTYPES ,SIGNAL peptides ,GENOTYPES - Abstract
Low-moderate risk alleles that are relatively common in the population may explain a significant proportion of the excess familial risk of ovarian cancer (OC) not attributed to highly penetrant genes. In this study, we evaluated the risks of OC associated with common germline variants in five oncogenes (BRAF, ERBB2, KRAS, NMI and PIK3CA) known to be involved in OC development. Thirty-four tagging SNPs in these genes were genotyped in approximately 1800 invasive OC cases and 3000 controls from population-based studies in Denmark, the United Kingdom and the United States. We found no evidence of disease association for SNPs in BRAF, KRAS, ERBB2 and PIK3CA when OC was considered as a single disease phenotype; but after stratification by histological subtype, we found borderline evidence of association for SNPs in KRAS and BRAF with mucinous OC and in ERBB2 and PIK3CA with endometrioid OC. For NMI, we identified a SNP (rs11683487) that was associated with a decreased risk of OC (unadjusted P(dominant)=0.004). We then genotyped rs11683487 in another 1097 cases and 1792 controls from an additional three case-control studies from the United States. The combined odds ratio was 0.89 (95% confidence interval (CI): 0.80-0.99) and remained statistically significant (P(dominant)=0.032). We also identified two haplotypes in ERBB2 associated with an increased OC risk (P(global)=0.034) and a haplotype in BRAF that had a protective effect (P(global)=0.005). In conclusion, these data provide borderline evidence of association for common allelic variation in the NMI with risk of epithelial OC. [ABSTRACT FROM AUTHOR]
- Published
- 2009
- Full Text
- View/download PDF
6. Validating genetic risk associations for ovarian cancer through the international Ovarian Cancer Association Consortium.
- Author
-
Pearce, C. L., Near, A. M., Van Den Berg, D. J., Ramus, S. J., Gentry-Maharaj, A., Menon, U., Gayther, S. A., Anderson, A. R., Edlund, C. K., Wu, A. H., Chen, X., Beesley, J., Webb, P. M., Holt, S. K., Chen, C., Doherty, J. A., Rossing, M. A., Whittemore, A. S., McGuire, V., and DiCioccio, R. A.
- Subjects
OVARIAN tumors ,CANCER genetics ,STEROID hormones ,SEX hormones ,DNA repair ,CELL cycle ,TUMOR risk factors ,CANCER invasiveness ,COMPARATIVE studies ,DISEASE susceptibility ,ENZYMES ,GENETIC polymorphisms ,LONGITUDINAL method ,RESEARCH methodology ,MEDICAL cooperation ,OXIDOREDUCTASES ,RESEARCH ,DNA-binding proteins ,EVALUATION research ,CASE-control method ,GENETIC carriers ,GENOTYPES - Abstract
The search for genetic variants associated with ovarian cancer risk has focused on pathways including sex steroid hormones, DNA repair, and cell cycle control. The Ovarian Cancer Association Consortium (OCAC) identified 10 single-nucleotide polymorphisms (SNPs) in genes in these pathways, which had been genotyped by Consortium members and a pooled analysis of these data was conducted. Three of the 10 SNPs showed evidence of an association with ovarian cancer at P< or =0.10 in a log-additive model: rs2740574 in CYP3A4 (P=0.011), rs1805386 in LIG4 (P=0.007), and rs3218536 in XRCC2 (P=0.095). Additional genotyping in other OCAC studies was undertaken and only the variant in CYP3A4, rs2740574, continued to show an association in the replication data among homozygous carriers: OR(homozygous(hom))=2.50 (95% CI 0.54-11.57, P=0.24) with 1406 cases and 2827 controls. Overall, in the combined data the odds ratio was 2.81 among carriers of two copies of the minor allele (95% CI 1.20-6.56, P=0.017, p(het) across studies=0.42) with 1969 cases and 3491 controls. There was no association among heterozygous carriers. CYP3A4 encodes a key enzyme in oestrogen metabolism and our finding between rs2740574 and risk of ovarian cancer suggests that this pathway may be involved in ovarian carcinogenesis. Additional follow-up is warranted. [ABSTRACT FROM AUTHOR]
- Published
- 2009
- Full Text
- View/download PDF
7. Network-Based Integration of GWAS and Gene Expression Identifies a HOX-Centric Network Associated with Serous Ovarian Cancer Risk
- Author
-
Kar, S. P., Tyrer, J. P., Li, Qiyuan, Lawrenson, K., Aben, K. K. H., Anton-Culver, H., Antonenkova, N., Chenevix-Trench, G., Baker, H., Bandera, E. V., Bean, Y. T., Beckmann, M. W., Berchuck, A., Bisogna, M., Bjorge, L., Bogdanova, N., Brinton, L., Brooks-Wilson, A., Butzow, R., Campbell, I., Carty, K., Chang-Claude, J., Chen, Y. A., Chen, Z., Cook, L. S., Cramer, Daniel William, Cunningham, J. M., Cybulski, C., Dansonka-Mieszkowska, A., Dennis, J., Dicks, E., Doherty, J. A., Dork, T., du Bois, A., Durst, M., Eccles, D., Easton, D. F., Edwards, R. P., Ekici, A. B., Fasching, P. A., Fridley, B. L., Gao, Y.-T., Gentry-Maharaj, A., Giles, G. G., Glasspool, R., Goode, E. L., Goodman, M. T., Grownwald, J., Harrington, P., Harter, P., Hein, A., Heitz, F., Hildebrandt, M. A. T., Hillemanns, P., Hogdall, E., Hogdall, C. K., Hosono, S., Iversen, E. S., Jakubowska, A., Paul, J., Jensen, A., Ji, B.-T., Karlan, B. Y., Kjaer, S. K., Kelemen, L. E., Kellar, M., Kelley, J., Kiemeney, L. A., Krakstad, C., Kupryjanczyk, J., Lambrechts, D., Lambrechts, S., Le, N. D., Lee, A. W., Lele, S., Leminen, A., Lester, J., Levine, D. A., Liang, D., Lissowska, J., Lu, K., Lubinski, J., Lundvall, L., Massuger, L., Matsuo, K., McGuire, V., McLaughlin, J. R., McNeish, I. A., Menon, U., Modugno, F., Moysich, K. B., Narod, S. A., Nedergaard, L., Ness, R. B., Nevanlinna, H., Odunsi, K., Olson, S. H., Orlow, I., Orsulic, S., Weber, R. P., Pearce, C. L., Pejovic, T., Pelttari, L. M., Permuth-Wey, J., Phelan, C. M., Pike, M. C., Poole, Elizabeth M., Ramus, S. J., Risch, H. A., Rosen, B., Rossing, M. A., Rothstein, J. H., Rudolph, A., Runnebaum, I. B., Rzepecka, I. K., Salvesen, H. B., Schildkraut, J. M., Schwaab, I., Shu, X.-O., Shvetsov, Y. B., Siddiqui, N., Sieh, W., Song, H., Southey, M. C., Sucheston-Campbell, L. E., Tangen, I. L., Teo, S.-H., Terry, Kathryn Lynne, Thompson, P. J., Timorek, A., Tsai, Y.-Y., Tworoger, Shelley Slate, van Altena, A. M., Van Nieuwenhuysen, E., Vergote, I., Vierkant, R. A., Wang-Gohrke, S., Walsh, C., Wentzensen, N., Whittemore, A. S., Wicklund, K. G., Wilkens, L. R., Woo, Y.-L., Wu, X., Wu, A., Yang, H., Zheng, W., Ziogas, A., Sellers, T. A., Monteiro, A. N. A., Freedman, M. L., Gayther, S. A., and Pharoah, P. D. P.
- Subjects
ovarian cancer ,network analysis ,GWAS ,gene expression ,transcription factors - Abstract
BACKGROUND: Genome-wide association studies (GWAS) have so far reported 12 loci associated with serous epithelial ovarian cancer (EOC) risk. We hypothesized that some of these loci function through nearby transcription factor (TF) genes and that putative target genes of these TFs as identified by coexpression may also be enriched for additional EOC risk associations. METHODS: We selected TF genes within 1 Mb of the top signal at the 12 genome-wide significant risk loci. Mutual information, a form of correlation, was used to build networks of genes strongly coexpressed with each selected TF gene in the unified microarray dataset of 489 serous EOC tumors from The Cancer Genome Atlas. Genes represented in this dataset were subsequently ranked using a gene-level test based on results for germline SNPs from a serous EOC GWAS meta-analysis (2,196 cases/4,396 controls). RESULTS: Gene set enrichment analysis identified six networks centered on TF genes (HOXB2, HOXB5, HOXB6, HOXB7 at 17q21.32 and HOXD1, HOXD3 at 2q31) that were significantly enriched for genes from the risk-associated end of the ranked list (P < 0.05 and FDR < 0.05). These results were replicated (P < 0.05) using an independent association study (7,035 cases/21,693 controls). Genes underlying enrichment in the six networks were pooled into a combined network. CONCLUSION: We identified a HOX-centric network associated with serous EOC risk containing several genes with known or emerging roles in serous EOC development. IMPACT: Network analysis integrating large, context-specific datasets has the potential to offer mechanistic insights into cancer susceptibility and prioritize genes for experimental characterization.
- Published
- 2015
- Full Text
- View/download PDF
8. Tubal ligation and risk of ovarian cancer subtypes: a pooled analysis of case-control studies
- Author
-
Sieh, W., Salvador, S., McGuire, V., Weber, R. P., Terry, Kathryn Lynne, Rossing, M. A., Risch, H., Wu, A. H., Webb, P. M., Moysich, K., Doherty, J. A., Felberg, A., Miller, D., Jordan, S. J., Goodman, M. T., Lurie, G., Chang-Claude, J., Rudolph, A., Kjaer, S. K., Jensen, A., Hogdall, E., Bandera, E. V., Olson, S. H., King, M. G., Rodriguez-Rodriguez, L., Kiemeney, L. A., Marees, T., Massuger, L. F., van Altena, A. M., Ness, R. B., Cramer, Daniel William, Pike, M. C., Pearce, C. L., Berchuck, A., Schildkraut, J. M., and Whittemore, A. S.
- Subjects
Ovarian cancer ,tubal ligation ,sterilization - Abstract
Background Tubal ligation is a protective factor for ovarian cancer, but it is unknown whether this protection extends to all invasive histological subtypes or borderline tumors. We undertook an international collaborative study to examine the association between tubal ligation and ovarian cancer subtypes. Methods We pooled primary data from 13 population-based case-control studies, including 10 157 patients with ovarian cancer (7942 invasive; 2215 borderline) and 13 904 control women. Invasive cases were analysed by histological type, grade and stage, and borderline cases were analysed by histological type. Pooled odds ratios were estimated using conditional logistic regression to match on site, race/ethnicity and age categories, and to adjust for age, oral contraceptive use duration and number of full-term births. Results Tubal ligation was associated with significantly reduced risks of invasive serous (OR, 0.81; 95% CI, 0.74-0.89; P < 0.001), endometrioid (OR, 0.48; 95% CI, 0.40-0.59; P < 0.001), clear cell (OR, 0.52; 95% CI, 0.40-0.67; P < 0.001) and mucinous (OR, 0.68; 95% CI, 0.52-0.89; P = 0.005) cancers. The magnitude of risk reduction was significantly greater for invasive endometrioid (P < 0.0001) and clear cell (P = 0.0018) than for serous cancer. No significant associations were found with borderline serous or mucinous tumours. Conclusions We found that the protective effects of tubal ligation on ovarian cancer risk were subtype-specific. These findings provide insights into distinct aetiologies of ovarian cancer subtypes and mechanisms underlying the protective effects of tubal ligation.
- Published
- 2013
- Full Text
- View/download PDF
9. Obesity and risk of ovarian cancer subtypes: evidence from the Ovarian Cancer Association Consortium
- Author
-
Olsen, C. M., Nagle, C. M., Whiteman, D. C., Ness, R., Pearce, C. L., Pike, M. C., Rossing, M. A., Terry, Kathryn Lynne, Wu, A. H., Risch, H. A., Yu, H., Doherty, J. A., Chang-Claude, J., Hein, R., Nickels, S., Wang-Gohrke, S., Goodman, M. T., Carney, M. E., Matsuno, R. K., Lurie, G., Moysich, K., Kjaer, S. K., Jensen, A., Hogdall, E., Goode, E. L., Fridley, B. L., Vierkant, R. A., Larson, M. C., Schildkraut, J., Hoyo, C., Moorman, P., Weber, R. P., Cramer, Daniel William, Vitonis, A. F., Bandera, E. V., Olson, S. H., Rodriguez-Rodriguez, L., King, M., Brinton, L. A., Yang, H., Garcia-Closas, M., Lissowska, J., Anton-Culver, H., Ziogas, A., Gayther, S. A., Ramus, S. J., Menon, U., Gentry-Maharaj, A., and Webb, P. M.
- Subjects
ovarian cancer ,obesity ,body mass index - Abstract
Whilst previous studies have reported that higher body-mass index (BMI) increases a woman’s risk of developing ovarian cancer, associations for the different histological subtypes have not been well defined. As the prevalence of obesity has increased dramatically, and classification of ovarian histology has improved in the last decade, we sought to examine the association in a pooled analysis of recent studies participating in the Ovarian Cancer Association Consortium. We evaluated the association between BMI (recent, maximum, and in young adulthood) and ovarian cancer risk using original data from 15 case-control studies (13,548 cases, 17,913 controls). We combined study-specific adjusted odds ratios (ORs) using a random–effects model. We further examined the associations by histological subtype, menopausal status and post-menopausal hormone use. High BMI (all time-points) was associated with increased risk. This was most pronounced for borderline serous (recent BMI: pooled OR=1.24 per 5kg/m2; 95%CI 1.18–1.30), invasive endometrioid (1.17; 1.11–1.23) and invasive mucinous (1.19; 1.06–1.32) tumours. There was no association with serous invasive cancer overall (0.98; 0.94–1.02), but increased risks for low grade serous invasive tumours (1.13, 1.03–1.25) and in pre-menopausal women (1.11; 1.04–1.18). Among post–menopausal women, the associations did not differ between HRT users and non–users. Whilst obesity appears to increase risk of the less common histological subtypes of ovarian cancer, it does not increase risk of high grade invasive serous cancers, and reducing BMI is therefore unlikely to prevent the majority of ovarian cancer deaths. Other modifiable factors must be identified to control this disease.
- Published
- 2013
- Full Text
- View/download PDF
10. Prostate Cancer Susceptibility Polymorphism rs2660753 Is Not Associated with Invasive Ovarian Cancer
- Author
-
Amankwah, E. K., Kelemen, L. E., Wang, Q., Song, H., Chenevix-Trench, G., Beesley, J., Webb, P. M., Pearce, C. L., Wu, A. H., Pike, M. C., Stram, D. O., Chang-Claude, J., Wang-Gohrke, S., Ness, R. B., Goode, E. L., Cunningham, J. M., Fridley, B. L., Vierkant, R. A., Tworoger, Shelley Slate, Whittemore, A. S., McGuire, V., Sieh, W., Gayther, S. A., Gentry-Maharaj, A., Menon, U., Ramus, S. J., Rossing, M. A., Doherty, J. A., Goodman, M. T., Carney, M. E., Lurie, G., Wilkens, L. R., Kruger Kjaer, S., Hogdall, E., Cramer, Daniel William, Terry, Kathryn Lynne, Garcia-Closas, M., Yang, H., Lissowska, J., Anton-Culver, H., Ziogas, A., Schildkraut, J. M., Berchuck, A., and Pharoah, P. D. P.
- Subjects
chromosome 3p ,SNP ,ovarian cancer ,risk factors - Abstract
Background We previously reported an association between rs2660753, a prostate cancer susceptibility polymorphism, and invasive epithelial ovarian cancer (EOC) [odds ratio (OR)=1.2, 95% confidence interval (CI)=1.0-1.4, Ptrend=0.01] that showed a stronger association with the serous histological subtype (OR=1.3, 95% CI=1.1-1.5, Ptrend=0.003). Methods We sought to replicate this association in 12 other studies comprising 4,482 cases and 6,894 controls of white non-Hispanic ancestry in the Ovarian Cancer Association Consortium. Results No evidence for an association with all cancers or serous cancers was observed in a combined analysis of data from the replication studies (all: OR=1.0, 95% CI=0.9-1.1, Ptrend=0.61; serous: OR=1.0, 95% CI=0.9-1.1, Ptrend=0.85) or from the combined analysis of discovery and replication studies (all: OR=1.0, 95% CI=1.0-1.1, Ptrend= 0.28; serous: OR=1.1, 95% CI=1.0-1.2, Ptrend=0.11). There was no evidence for statistical heterogeneity in ORs across the studies. Conclusions Although rs2660753 is a strong a prostate cancer susceptibility polymorphism, the association with another hormonally related cancer, invasive EOC, is not supported by this replication study. Impact Our findings, based on a larger sample size, emphasize the importance of replicating potentially promising genetic risk associations.
- Published
- 2011
- Full Text
- View/download PDF
11. Evaluation of candidate stromal epithelial cross-talk genes identifies association between risk of serous ovarian cancer and TERT, a cancer susceptibility 'hot-spot'
- Author
-
Johnatty, S. E., Beesley, J., Chen, X., Macgregor, S., Duffy, D. L., Spurdle, A. B., Defazio, A., Gava, N., Penelope Webb, Rossing, M. A., Doherty, J. A., Goodman, M. T., Lurie, G., Thompson, P. J., Wilkens, L. R., Ness, R. B., Moysich, K. B., Chang-Claude, J., Wang-Gohrke, S., Cramer, D. W., Terry, K. L., Hankinson, S. E., Tworoger, S. S., Garcia-Closas, M., Yang, H., Lissowska, J., Chanock, S. J., Pharoah, P. D., Song, H., Whitemore, A. S., Pearce, C. L., Stram, D. O., Wu, A. H., Pike, M. C., Gayther, S. A., Ramus, S. J., Menon, U., Gentry-Maharaj, A., Anton-Culver, H., Ziogas, A., Hogdall, E., Kjaer, S. K., Hogdall, C., Berchuck, A., Schildkraut, J. M., Iversen, E. S., Moorman, P. G., Phelan, C. M., Sellers, T. A., Cunningham, J. M., Vierkant, R. A., Rider, D. N., Goode, E. L., Haviv, I., Chenevix-Trench, G., Ovarian Cancer Association Consortium, Australian Ovarian Cancer Study Group, and Australian Cancer Study (Ovarian Cancer)
- Subjects
Cancer Research ,Genotype ,lcsh:QH426-470 ,Colorectal cancer ,Locus (genetics) ,Genome-wide association study ,Single-nucleotide polymorphism ,Genetics and Genomics/Complex Traits ,Biology ,Polymorphism, Single Nucleotide ,White People ,03 medical and health sciences ,0302 clinical medicine ,Genetics ,medicine ,Humans ,Genetic Predisposition to Disease ,Telomerase reverse transcriptase ,Genetics and Genomics/Cancer Genetics ,Telomerase ,Molecular Biology ,Genetics and Genomics/Genetics of Disease ,Genetics (clinical) ,Ecology, Evolution, Behavior and Systematics ,030304 developmental biology ,Ovarian Neoplasms ,0303 health sciences ,Epithelial Cells ,medicine.disease ,3. Good health ,lcsh:Genetics ,Serous fluid ,Case-Control Studies ,030220 oncology & carcinogenesis ,Cancer research ,Chromosomes, Human, Pair 5 ,Female ,Public Health and Epidemiology/Epidemiology ,Stromal Cells ,Ovarian cancer ,Research Article - Abstract
We hypothesized that variants in genes expressed as a consequence of interactions between ovarian cancer cells and the host micro-environment could contribute to cancer susceptibility. We therefore used a two-stage approach to evaluate common single nucleotide polymorphisms (SNPs) in 173 genes involved in stromal epithelial interactions in the Ovarian Cancer Association Consortium (OCAC). In the discovery stage, cases with epithelial ovarian cancer (n = 675) and controls (n = 1,162) were genotyped at 1,536 SNPs using an Illumina GoldenGate assay. Based on Positive Predictive Value estimates, three SNPs—PODXL rs1013368, ITGA6 rs13027811, and MMP3 rs522616—were selected for replication using TaqMan genotyping in up to 3,059 serous invasive cases and 8,905 controls from 16 OCAC case-control studies. An additional 18 SNPs with P per-allele, Author Summary In this article, we report the findings from a large-scale analysis of common variation in genes that are expressed as a consequence of interactions between ovarian cancer cells and their host micro-environment that could influence serous ovarian cancer risk. We evaluated 1,302 common variants within or near 173 genes in two large case-control studies from the Ovarian Cancer Association Consortium (OCAC) and selected three variants for further evaluation in sixteen OCAC studies and an additional 18 for evaluation in five OCAC studies. We observed a significantly increased risk of serous ovarian cancer associated with a variant in the telomerase reverse transcriptase (TERT) gene. Although TERT variants have not been previously shown to contribute to ovarian cancer risk, several studies have recently reported associations between TERT variants and other forms of cancer, including gliomas, lung cancer, adenocarcinoma, basal cell carcinoma, prostate cancer, and multiple other cancers. TERT encodes a protein that is essential for the replication and maintenance of chromosomal integrity during cell division. In cancer cells, TERT has been linked to genomic instability and tumour cell proliferation. Further studies are necessary to confirm our findings and to investigate the mechanisms for the observed association.
12. 755P Beyond HRD status: Unraveling genetic variants impacting PARP inhibitor sensitivity in advanced ovarian cancer.
- Author
-
Kjeldsen, M.K., Grønseth, D.B.S., Nyvang, G-B., Haslund, C.A., Malander, S., Anttila, M.A., Lindahl, G., Mäenpää, J., Dimoula, M., Werner, T., Iversen, T.Z., Hietanen, S., Fokdal, L., Dahlstrand, H., Bjorge, L., Rossing, M., and Mirza, M.R.
- Subjects
- *
GENETIC variation , *OVARIAN cancer , *POLY(ADP-ribose) polymerase - Published
- 2024
- Full Text
- View/download PDF
Catalog
Discovery Service for Jio Institute Digital Library
For full access to our library's resources, please sign in.