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369 results on '"Begg, Colin B."'

3. Differences in Melanoma Between Canada and New South Wales, Australia: A Population-Based Genes, Environment, and Melanoma (GEM) Study

Author

Yardman-Frank, Joseph Michael, Glassheim, Elyssa, Kricker, Anne, Armstrong, Bruce K., Marrett, Loraine D., Luo, Li, Cust, Anne E., Busam, Klaus J., Orlow, Irene, Gallagher, Richard P., Gruber, Stephen B., Anton-Culver, Hoda, Rosso, Stefano, Zanetti, Roberto, Sacchetto, Lidia, Kanetsky, Peter A., Dwyer, Terence, Venn, Alison, Lee-Taylor, Julia, Begg, Colin B., Thomas, Nancy E., and Berwick, Marianne

Published
2021
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5. Inherited Genetic Variants Associated with Melanoma BRAF/NRAS Subtypes

Author

Berwick, Marianne, Begg, Colin, Orlow, Irene, Busam, Klaus J., Roy, Pampa, Reiner, Anne, Leong, Siok, Guerrero, Sergio Corrales, Sadeghi, Keimya, Luo, Li, Boyce, Tawny W., Cust, Anne E., Armstrong, Bruce K., Kricker, Anne, Venn, Alison, Dwyer, Terence, Tucker, Paul, Gallagher, Richard P., Marrett, Loraine D., From, Lynn, Zanetti, Roberto, Rosso, Stefano, Anton-Culver, Hoda, Gruber, Stephen B., Huang, Shu-Chen, Thomas, Nancy E., Conway, Kathleen, Ollila, David W., Groben, Pamela A., Edmiston, Sharon N., Hao, Honglin, Parrish, Eloise, Frank, Jill S., Gibbs, David C., Rebbeck, Timothy R., Kanetsky, Peter A., Lee Taylor, Julia, Madronich, Sasha, Parrish, Eloise A., Sacchetto, Lidia, and Begg, Colin B.

Published
2018
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8. Associations of MC1R Genotype and Patient Phenotypes with BRAF and NRAS Mutations in Melanoma

Author

Berwick, Marianne, Begg, Colin B., Orlow, Irene, Busam, Klaus J., Reiner, Anne S., Roy, Pampa, Patel, Himali, Luo, Li, Paine, Susan, Cust, Anne E., Armstrong, Bruce K., Kricker, Anne, Venn, Alison, Dwyer, Terence, Tucker, Paul, Gallagher, Richard P., Marrett, Loraine D., From, Lynn, Zanetti, Roberto, Rosso, Stefano, Anton-Culver, Hoda, Gruber, Stephen B., Huang, Shu-Chen, Thomas, Nancy E., Ollila, David W., Conway, Kathleen, Groben, Pamela A., Edmiston, Sharon N., Hao, Honglin, Parrish, Eloise, Frank, Jill S., Gibbs, David C., Bramson, Jennifer I., Rebbeck, Timothy R., Kanetsky, Peter A., Lee Taylor, Julia, Madronich, Sasha, Sacchetto, Lidia, and Parrish, Eloise A.

Published
2017
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12. Proceedings of the third international molecular pathological epidemiology (MPE) meeting

Author

Campbell, Peter T., Rebbeck, Timothy R., Nishihara, Reiko, Beck, Andrew H., Begg, Colin B., Bogdanov, Alexei A., Cao, Yin, Coleman, Helen G., Freeman, Gordon J., Heng, Yujing J., Huttenhower, Curtis, Irizarry, Rafael A., Kip, N. Sertac, Michor, Franziska, Nevo, Daniel, Peters, Ulrike, Phipps, Amanda I., Poole, Elizabeth M., Qian, Zhi Rong, Quackenbush, John, Robins, Harlan, Rogan, Peter K., Slattery, Martha L., Smith-Warner, Stephanie A., Song, Mingyang, VanderWeele, Tyler J., Xia, Daniel, Zabor, Emily C., Zhang, Xuehong, Wang, Molin, and Ogino, Shuji

Published
2017

18. Association of functional, inherited vitamin D–binding protein variants with melanoma-specific death.

Author

Gibbs, David Corley, Thomas, Nancy E, Kanetsky, Peter A, Luo, Li, Busam, Klaus J, Cust, Anne E, Anton-Culver, Hoda, Gallagher, Richard P, Zanetti, Roberto, Rosso, Stefano, Sacchetto, Lidia, Edmiston, Sharon N, Conway, Kathleen, Ollila, David W, Begg, Colin B, Berwick, Marianne, Ward, Sarah V, and Orlow, Irene

Abstract

Background It is unclear whether genetic variants affecting vitamin D metabolism are associated with melanoma prognosis. Two functional missense variants in the vitamin D–binding protein gene (GC), rs7041 and rs4588, determine 3 common haplotypes, Gc1s, Gc1f, and Gc2, of which Gc1f may be associated with decreased all-cause death among melanoma patients based on results of a prior study, but the association of Gc1f with melanoma-specific death is unclear. Methods We investigated the association of the Gc1s, Gc1f, and Gc2 haplotypes with melanoma-specific and all-cause death among 4490 individuals with incident, invasive primary melanoma in 2 population-based studies using multivariable Cox-proportional hazards regression. Results In the pooled analysis of both datasets, the patients with the Gc1f haplotype had a 37% lower risk of melanoma-specific death than the patients without Gc1f (hazard ratio [HR] = 0.63, 95% confidence interval [CI] = 0.47 to 0.83, P  =  .001), with adjustments for age, sex, study center, first- or higher-order primary melanoma, tumor site, pigmentary phenotypes, and Breslow thickness. Associations were similar in both studies. In pooled analyses stratified by Breslow thickness, the corresponding melanoma-specific death HRs for those patients with the Gc1f haplotype compared with those without Gc1f were 0.89 (95% CI = 0.63 to 1.27) among participants with tumor Breslow thickness equal to or less than 2.0 mm and 0.40 (95% CI = 0.25 to 0.63) among participants with tumor Breslow thickness greater than 2.0 mm (P interaction   =  .003). Conclusions Our findings suggest that individuals with the GC haplotype Gc1f may have a lower risk of dying from melanoma—specifically from thicker, higher-risk melanoma—than individuals without this Gc1f haplotype. [ABSTRACT FROM AUTHOR]

Published
2023
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28. Proceedings of the second international molecular pathological epidemiology (MPE) meeting

Author

Ogino, Shuji, Campbell, Peter T., Nishihara, Reiko, Phipps, Amanda I., Beck, Andrew H., Sherman, Mark E., Chan, Andrew T., Troester, Melissa A., Bass, Adam J., Fitzgerald, Kathryn C., Irizarry, Rafael A., Kelsey, Karl T., Nan, Hongmei, Peters, Ulrike, Poole, Elizabeth M., Qian, Zhi Rong, Tamimi, Rulla M., Tchetgen, Eric J. Tchetgen, Tworoger, Shelley S., Zhang, Xuehong, Giovannucci, Edward L., van den Brandt, Piet A., Rosner, Bernard A., Wang, Molin, Chatterjee, Nilanjan, and Begg, Colin B.

Published
2015

29. The interaction between vitamin D receptor polymorphisms and sun exposure around time of diagnosis influences melanoma survival

Author

Orlow, Irene, Shi, Yang, Kanetsky, Peter A., Thomas, Nancy E., Luo, Li, Corrales‐Guerrero, Sergio, Cust, Anne E., Sacchetto, Lidia, Zanetti, Roberto, Rosso, Stefano, Armstrong, Bruce K., Dwyer, Terence, Venn, Alison, Gallagher, Richard P., Gruber, Stephen B., Marrett, Loraine D., Anton‐Culver, Hoda, Busam, Klaus, Begg, Colin B., Berwick, Marianne, Roy, Pampa, Patel, Himali, Yoo, Sarah, Reiner, Anne, Paine, Susan, Kricker, Anne, Tucker, Paul, From, Lynn, Ollila, David W., Groben, Pamela A., Rebbeck, Timothy R., Taylor, Julia Lee, and Madronich, Sasha

Published
2018
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30. Contralateral breast cancers: Independent cancers or metastases?

Author

Begg, Colin B., Ostrovnaya, Irina, Geyer, Felipe C., Papanastasiou, Anastasios D., Ng, Charlotte K.Y., Sakr, Rita A., Bernstein, Jonine L., Burke, Kathleen A., King, Tari A., Piscuoglio, Salvatore, Mauguen, Audrey, Orlow, Irene, Weigelt, Britta, Seshan, Venkatraman E., Morrow, Monica, and Reis‐Filho, Jorge S.

Published
2018
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31. Sex-Specific Associations of MDM2 and MDM4 Variants with Risk of Multiple Primary Melanomas and Melanoma Survival in Non-Hispanic Whites.

Author

Ward, Sarah V., Autuori, Isidora, Luo, Li, LaPilla, Emily, Yoo, Sarah, Sharma, Ajay, Busam, Klaus J., Olilla, David W., Dwyer, Terence, Anton-Culver, Hoda, Zanetti, Roberto, Sacchetto, Lidia, Cust, Anne E., Gallagher, Richard P., Kanetsky, Peter A., Rosso, Stefano, Begg, Colin B., Berwick, Marianne, Thomas, Nancy E., and Orlow, Irene

Subjects
PROTEINS, CONFIDENCE intervals, MELANOMA, HISPANIC Americans, LI-Fraumeni syndrome, GENETIC polymorphisms, QUANTITATIVE research, SEX distribution, GENE expression, ESTROGEN receptors, TUMOR suppressor genes, RESEARCH funding, PROGRESSION-free survival, WHITE people, ODDS ratio, LOGISTIC regression analysis, LONGITUDINAL method, PROPORTIONAL hazards models, DISEASE risk factors, EVALUATION
Abstract

Simple Summary: Melanoma is the most severe type of skin cancer, and the risk of developing melanoma and of dying of melanoma varies between women and men. This study investigated whether widely studied genetic single nucleotide polymorphisms (SNPs) in two oncogenes known to promote cell proliferation explain these sex differences by testing such variants in a large cohort of 3663 melanoma patients. Formal analyses demonstrated that females, but not males, who carried the variant MDM4-rs4245739*C were more likely to develop a new primary melanoma, and those with the variant MDM2-rs2279744*G were less likely to succumb to the disease. We also identified a number of additional variants, often co-inherited with the tested SNPs, which modify how these and other genes work locally in the skin, as well as in distal organs where melanoma tends to spread or invade during the progression of the disease. MDM2-SNP309 (rs2279744), a common genetic modifier of cancer incidence in Li-Fraumeni syndrome, modifies risk, age of onset, or prognosis in a variety of cancers. Melanoma incidence and outcomes vary by sex, and although SNP309 exerts an effect on the estrogen receptor, no consensus exists on its effect on melanoma. MDM2 and MDM4 restrain p53-mediated tumor suppression, independently or together. We investigated SNP309, an a priori MDM4-rs4245739, and two coinherited variants, in a population-based cohort of 3663 primary incident melanomas. Per-allele and per-haplotype (MDM2_SNP309-SNP285; MDM4_rs4245739-rs1563828) odds ratios (OR) for multiple-melanoma were estimated with logistic regression models. Hazard ratios (HR) for melanoma death were estimated with Cox proportional hazards models. In analyses adjusted for covariates, females carrying MDM4-rs4245739*C were more likely to develop multiple melanomas (ORper-allele = 1.25, 95% CI 1.03–1.51, and Ptrend = 0.03), while MDM2-rs2279744*G was inversely associated with melanoma-death (HRper-allele = 0.63, 95% CI 0.42–0.95, and Ptrend = 0.03). We identified 16 coinherited expression quantitative loci that control the expression of MDM2, MDM4, and other genes in the skin, brain, and lungs. Our results suggest that MDM4/MDM2 variants are associated with the development of subsequent primaries and with the death of melanoma in a sex-dependent manner. Further investigations of the complex MDM2/MDM4 motif, and its contribution to the tumor microenvironment and observed associations, are warranted. [ABSTRACT FROM AUTHOR]

Published
2023
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32. Pathway Alterations in Stage II/III Primary Melanoma.

Author

Kostrzewa, Caroline E., Luo, Li, Arora, Arshi, Seshan, Venkatraman E., Ernstoff, Marc S., Edmiston, Sharon N., Conway, Kathleen, Gorlov, Ivan, Busam, Klaus, Orlow, Irene, Hernando-Monge, Eva, Thomas, Nancy E., Berwick, Marianne, Begg, Colin B., and Shen, Ronglai

Subjects
SOMATIC mutation, NUCLEOTIDE sequencing, CELL cycle, CONSORTIA, BRAF genes, MELANOMA
Abstract

PURPOSE: Genomic classification of melanoma has thus far focused on the mutational status of BRAF , NRAS , and NF1. The clinical utility of this classification remains limited, and the landscape of alterations in other oncogenic signaling pathways is underexplored. METHODS: Using primary samples from the InterMEL study, a retrospective cohort of cases with specimens collected from an international consortium with participating institutions throughout the United States and Australia, with oversampling of cases who ultimately died of melanoma, we examined mutual exclusivity and co-occurrence of genomic alterations in 495 stage II/III primary melanomas across 11 cancer pathways. Somatic mutation and copy number alterations were analyzed from next-generation sequencing using a clinical sequencing panel. RESULTS: Mutations in the RTK-RAS pathway were observed in 81% of cases. Other frequently occurring pathways were TP53 (31%), Cell Cycle (30%), and PI3K (18%). These frequencies are generally lower than was observed in The Cancer Genome Atlas, where the specimens analyzed were predominantly obtained from metastases. Overall, 81% of the cases had at least one targetable mutation. The RTK-RAS pathway was the only pathway that demonstrated strong and statistically significant mutual exclusivity. However, this strong mutual exclusivity signal was evident only for the three common genes in the pathway (BRAF , NRAS , and NF1). Analysis of co-occurrence of different pathways exhibited no positive significant trends. However, interestingly, a high frequency of cases with none of these pathways represented was observed, 8.4% of cases versus 4.0% expected (P <.001). A higher frequency of RTK-RAS singletons (with no other pathway alteration) was observed compared with The Cancer Genome Atlas. Clonality analyses suggest strongly that both the cell cycle and RTK-RAS pathways represent early events in melanogenesis. CONCLUSION: Our results confirm the dominance of mutations in the RTK-RAS pathway. The presence of many mutations in several well-known, actionable pathways suggests potential avenues for targeted therapy in these early-stage cases. [ABSTRACT FROM AUTHOR]

Published
2023
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39. Ambient UV, Personal Sun Exposure and Risk of Multiple Primary Melanomas

Author

GEM Study Group, Kricker, Anne, Armstrong, Bruce K., Goumas, Chris, Litchfield, Melisa, Begg, Colin B., Hummer, Amanda J., Marrett, Loraine D., Theis, Beth, Millikan, Robert C., Thomas, Nancy, Culver, Hoda Anton, Gallagher, Richard P., Dwyer, Terence, Rebbeck, Timothy R., Kanetsky, Peter A., Busam, Klaus, From, Lynn, Mujumdar, Urvi, Zanetti, Roberto, and Berwick, Marianne

Published
2007
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42. Association Between NRAS and BRAF Mutational Status and Melanoma-Specific Survival Among Patients With Higher-Risk Primary Melanoma

Author

Thomas, Nancy E., Edmiston, Sharon N., Alexander, Audrey, Groben, Pamela A., Parrish, Eloise, Kricker, Anne, Armstrong, Bruce K., Anton-Culver, Hoda, Gruber, Stephen B., From, Lynn, Busam, Klaus J., Hao, Honglin, Orlow, Irene, Kanetsky, Peter A., Luo, Li, Reiner, Anne S., Paine, Susan, Frank, Jill S., Bramson, Jennifer I., Marrett, Lorraine D., Gallagher, Richard P., Zanetti, Roberto, Rosso, Stefano, Dwyer, Terence, Cust, Anne E., Ollila, David W., Begg, Colin B., Berwick, Marianne, and Conway, Kathleen

Published
2015
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