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1. 11q13 is a susceptibility locus for hormone receptor positive breast cancer

Author

Lambrechts, D, Truong, T, Justenhoven, C, Humphreys, MK, Wang, J, Hopper, JL, Dite, GS, Apicella, C, Southey, MC, Schmidt, MK, Broeks, A, Cornelissen, S, van Hien, R, Sawyer, E, Tomlinson, I, Kerin, M, Miller, N, Milne, RL, Pilar Zamora, M, Arias Perez, JI, Benitez, J, Hamann, U, Ko, Y-D, Bruening, T, Chang-Claude, J, Eilber, U, Hein, R, Nickels, S, Flesch-Janys, D, Wang-Gohrke, S, John, EM, Miron, A, Winqvist, R, Pylkas, K, Jukkola-Vuorinen, A, Grip, M, Chenevix-Trench, G, Beesley, J, Chen, X, Menegaux, F, Cordina-Duverger, E, Shen, C-Y, Yu, J-C, Wu, P-E, Hou, M-F, Andrulis, IL, Selander, T, Glendon, G, Mulligan, AM, Anton-Culver, H, Ziogas, A, Muir, KR, Lophatananon, A, Rattanamongkongul, S, Puttawibul, P, Jones, M, Orr, N, Ashworth, A, Swerdlow, A, Severi, G, Baglietto, L, Giles, G, Southey, M, Marme, F, Schneeweiss, A, Sohn, C, Burwinkel, B, Yesilyurt, BT, Neven, P, Paridaens, R, Wildiers, H, Brenner, H, Mueller, H, Arndt, V, Stegmaier, C, Meindl, A, Schott, S, Bartram, CR, Schmutzler, RK, Cox, A, Brock, IW, Elliott, G, Cross, SS, Fasching, PA, Schulz-Wendtland, R, Ekici, AB, Beckmann, MW, Fletcher, O, Johnson, N, Silva, IDS, Peto, J, Nevanlinna, H, Muranen, TA, Aittomaki, K, Blomqvist, C, Doerk, T, Schuermann, P, Bremer, M, Hillemanns, P, Bogdanova, NV, Antonenkova, NN, Rogov, YI, Karstens, JH, Khusnutdinova, E, Bermisheva, M, Prokofieva, D, Gancev, S, Jakubowska, A, Lubinski, J, Jaworska, K, Durda, K, Nordestgaard, BG, Bojesen, SE, Lanng, C, Mannermaa, A, Kataja, V, Kosma, V-M, Hartikainen, JM, Radice, P, Peterlongo, P, Manoukian, S, Bernard, L, Couch, FJ, Olson, JE, Wang, X, Fredericksen, Z, Alnaes, GG, Kristensen, V, Borresen-Dale, A-L, Devilee, P, Tollenaar, RAEM, Seynaeve, CM, Hooning, MJ, Garcia-Closas, M, Chanock, SJ, Lissowska, J, Sherman, ME, Hall, P, Liu, J, Czene, K, Kang, D, Yoo, K-Y, Noh, D-Y, Lindblom, A, Margolin, S, Dunning, AM, Pharoah, PDP, Easton, DF, Guenel, P, Brauch, H, Lambrechts, D, Truong, T, Justenhoven, C, Humphreys, MK, Wang, J, Hopper, JL, Dite, GS, Apicella, C, Southey, MC, Schmidt, MK, Broeks, A, Cornelissen, S, van Hien, R, Sawyer, E, Tomlinson, I, Kerin, M, Miller, N, Milne, RL, Pilar Zamora, M, Arias Perez, JI, Benitez, J, Hamann, U, Ko, Y-D, Bruening, T, Chang-Claude, J, Eilber, U, Hein, R, Nickels, S, Flesch-Janys, D, Wang-Gohrke, S, John, EM, Miron, A, Winqvist, R, Pylkas, K, Jukkola-Vuorinen, A, Grip, M, Chenevix-Trench, G, Beesley, J, Chen, X, Menegaux, F, Cordina-Duverger, E, Shen, C-Y, Yu, J-C, Wu, P-E, Hou, M-F, Andrulis, IL, Selander, T, Glendon, G, Mulligan, AM, Anton-Culver, H, Ziogas, A, Muir, KR, Lophatananon, A, Rattanamongkongul, S, Puttawibul, P, Jones, M, Orr, N, Ashworth, A, Swerdlow, A, Severi, G, Baglietto, L, Giles, G, Southey, M, Marme, F, Schneeweiss, A, Sohn, C, Burwinkel, B, Yesilyurt, BT, Neven, P, Paridaens, R, Wildiers, H, Brenner, H, Mueller, H, Arndt, V, Stegmaier, C, Meindl, A, Schott, S, Bartram, CR, Schmutzler, RK, Cox, A, Brock, IW, Elliott, G, Cross, SS, Fasching, PA, Schulz-Wendtland, R, Ekici, AB, Beckmann, MW, Fletcher, O, Johnson, N, Silva, IDS, Peto, J, Nevanlinna, H, Muranen, TA, Aittomaki, K, Blomqvist, C, Doerk, T, Schuermann, P, Bremer, M, Hillemanns, P, Bogdanova, NV, Antonenkova, NN, Rogov, YI, Karstens, JH, Khusnutdinova, E, Bermisheva, M, Prokofieva, D, Gancev, S, Jakubowska, A, Lubinski, J, Jaworska, K, Durda, K, Nordestgaard, BG, Bojesen, SE, Lanng, C, Mannermaa, A, Kataja, V, Kosma, V-M, Hartikainen, JM, Radice, P, Peterlongo, P, Manoukian, S, Bernard, L, Couch, FJ, Olson, JE, Wang, X, Fredericksen, Z, Alnaes, GG, Kristensen, V, Borresen-Dale, A-L, Devilee, P, Tollenaar, RAEM, Seynaeve, CM, Hooning, MJ, Garcia-Closas, M, Chanock, SJ, Lissowska, J, Sherman, ME, Hall, P, Liu, J, Czene, K, Kang, D, Yoo, K-Y, Noh, D-Y, Lindblom, A, Margolin, S, Dunning, AM, Pharoah, PDP, Easton, DF, Guenel, P, and Brauch, H

Abstract

A recent two-stage genome-wide association study (GWAS) identified five novel breast cancer susceptibility loci on chromosomes 9, 10, and 11. To provide more reliable estimates of the relative risk associated with these loci and investigate possible heterogeneity by subtype of breast cancer, we genotyped the variants rs2380205, rs1011970, rs704010, rs614367, and rs10995190 in 39 studies from the Breast Cancer Association Consortium (BCAC), involving 49,608 cases and 48,772 controls of predominantly European ancestry. Four of the variants showed clear evidence of association (P ≤ 3 × 10(-9) ) and weak evidence was observed for rs2380205 (P = 0.06). The strongest evidence was obtained for rs614367, located on 11q13 (per-allele odds ratio 1.21, P = 4 × 10(-39) ). The association for rs614367 was specific to estrogen receptor (ER)-positive disease and strongest for ER plus progesterone receptor (PR)-positive breast cancer, whereas the associations for the other three loci did not differ by tumor subtype.

Published
2012

2. A polymorphism in the coding sequence of WT1 is an independent prognostic marker in 1,101 patients with lobular breast cancer.

Author

Heuser, M., primary, Damm, F., additional, Schuermann, P., additional, Zucknick, M., additional, Shah, M., additional, Harrington, P., additional, Pharoah, P., additional, Schmidt, M., additional, Broeks, A., additional, van Hien, R., additional, Tollenaar, R. A., additional, Nevanlinna, H., additional, Heikkinen, T., additional, Aittomaki, K., additional, Blomqvist, C., additional, Krauter, J., additional, Hillemanns, P., additional, Ganser, A., additional, Park-Simon, T., additional, and Dork, T., additional

Published
2011
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3. Age- and Tumor Subtype-Specific Breast Cancer Risk Estimates for CHEK2*1100delC Carriers

Author

Schmidt, MK, Hogervorst, F, Van Hien, R, Cornelissen, S, Broeks, A, Adank, MA, Meijers, H, Waisfisz, Q, Hollestelle, A, Schutte, M, Van Den Ouweland, A, Hooning, M, Andrulis, IL, Anton-Culver, H, Antonenkova, NN, Antoniou, AC, Arndt, V, Bermisheva, M, Bogdanova, NV, Bolla, MK, Brauch, H, Brenner, H, Brüning, T, Burwinkel, B, Chang-Claude, J, Chenevix-Trench, G, Couch, FJ, Cox, A, Cross, SS, Czene, K, Dunning, AM, Fasching, PA, Figueroa, J, Fletcher, O, Flyger, H, Galle, E, García-Closas, M, Giles, GG, Haeberle, L, Hall, P, Hillemanns, P, Hopper, JL, Jakubowska, A, John, EM, Jones, M, Khusnutdinova, E, Knight, JA, Kosma, V-M, Kristensen, V, Lee, A, Lindblom, A, Lubinski, J, Mannermaa, A, Margolin, S, Meindl, A, Milne, RL, Muranen, TA, Newcomb, PA, Offit, K, Park-Simon, T-W, Peto, J, Pharoah, PDP, Robson, M, Rudolph, A, Sawyer, EJ, Schmutzler, RK, Seynaeve, C, Soens, J, Southey, MC, Spurdle, AB, Surowy, H, Swerdlow, A, Tollenaar, RAEM, Tomlinson, I, Trentham-Dietz, A, Vachon, C, Wang, Q, Whittemore, AS, Ziogas, A, Van Der Kolk, L, Nevanlinna, H, Dörk, T, Bojesen, S, and Easton, DF

Subjects
Adult, Aged, 80 and over, Heterozygote, Homozygote, Age Factors, Breast Neoplasms, Middle Aged, Risk Assessment, 3. Good health, Checkpoint Kinase 2, Receptors, Estrogen, Case-Control Studies, Odds Ratio, Humans, Female, Genetic Predisposition to Disease, skin and connective tissue diseases, Receptors, Progesterone, Aged, Sequence Deletion
Abstract

PURPOSE: CHEK2*1100delC is a well-established breast cancer risk variant that is most prevalent in European populations; however, there are limited data on risk of breast cancer by age and tumor subtype, which limits its usefulness in breast cancer risk prediction. We aimed to generate tumor subtype- and age-specific risk estimates by using data from the Breast Cancer Association Consortium, including 44,777 patients with breast cancer and 42,997 controls from 33 studies genotyped for CHEK2*1100delC. PATIENTS AND METHODS: CHEK2*1100delC genotyping was mostly done by a custom Taqman assay. Breast cancer odds ratios (ORs) for CHEK2*1100delC carriers versus noncarriers were estimated by using logistic regression and adjusted for study (categorical) and age. Main analyses included patients with invasive breast cancer from population- and hospital-based studies. RESULTS: Proportions of heterozygous CHEK2*1100delC carriers in controls, in patients with breast cancer from population- and hospital-based studies, and in patients with breast cancer from familial- and clinical genetics center-based studies were 0.5%, 1.3%, and 3.0%, respectively. The estimated OR for invasive breast cancer was 2.26 (95%CI, 1.90 to 2.69; P = 2.3 × 10(-20)). The OR was higher for estrogen receptor (ER)-positive disease (2.55 [95%CI, 2.10 to 3.10; P = 4.9 × 10(-21)]) than it was for ER-negative disease (1.32 [95%CI, 0.93 to 1.88; P = .12]; P interaction = 9.9 × 10(-4)). The OR significantly declined with attained age for breast cancer overall (P = .001) and for ER-positive tumors (P = .001). Estimated cumulative risks for development of ER-positive and ER-negative tumors by age 80 in CHEK2*1100delC carriers were 20% and 3%, respectively, compared with 9% and 2%, respectively, in the general population of the United Kingdom. CONCLUSION: These CHEK2*1100delC breast cancer risk estimates provide a basis for incorporating CHEK2*1100delC into breast cancer risk prediction models and into guidelines for intensified screening and follow-up.

4. Age- and Tumor Subtype-Specific Breast Cancer Risk Estimates for CHEK2*1100delC Carriers.

Author

Schmidt MK, Hogervorst F, van Hien R, Cornelissen S, Broeks A, Adank MA, Meijers H, Waisfisz Q, Hollestelle A, Schutte M, van den Ouweland A, Hooning M, Andrulis IL, Anton-Culver H, Antonenkova NN, Antoniou AC, Arndt V, Bermisheva M, Bogdanova NV, Bolla MK, Brauch H, Brenner H, Brüning T, Burwinkel B, Chang-Claude J, Chenevix-Trench G, Couch FJ, Cox A, Cross SS, Czene K, Dunning AM, Fasching PA, Figueroa J, Fletcher O, Flyger H, Galle E, García-Closas M, Giles GG, Haeberle L, Hall P, Hillemanns P, Hopper JL, Jakubowska A, John EM, Jones M, Khusnutdinova E, Knight JA, Kosma VM, Kristensen V, Lee A, Lindblom A, Lubinski J, Mannermaa A, Margolin S, Meindl A, Milne RL, Muranen TA, Newcomb PA, Offit K, Park-Simon TW, Peto J, Pharoah PD, Robson M, Rudolph A, Sawyer EJ, Schmutzler RK, Seynaeve C, Soens J, Southey MC, Spurdle AB, Surowy H, Swerdlow A, Tollenaar RA, Tomlinson I, Trentham-Dietz A, Vachon C, Wang Q, Whittemore AS, Ziogas A, van der Kolk L, Nevanlinna H, Dörk T, Bojesen S, and Easton DF

Subjects
Adult, Age Factors, Aged, Aged, 80 and over, Breast Neoplasms chemistry, Case-Control Studies, Female, Heterozygote, Homozygote, Humans, Middle Aged, Odds Ratio, Receptors, Estrogen analysis, Receptors, Progesterone analysis, Risk Assessment, Sequence Deletion, Breast Neoplasms epidemiology, Breast Neoplasms genetics, Checkpoint Kinase 2 genetics, Genetic Predisposition to Disease genetics
Abstract

Purpose: CHEK2*1100delC is a well-established breast cancer risk variant that is most prevalent in European populations; however, there are limited data on risk of breast cancer by age and tumor subtype, which limits its usefulness in breast cancer risk prediction. We aimed to generate tumor subtype- and age-specific risk estimates by using data from the Breast Cancer Association Consortium, including 44,777 patients with breast cancer and 42,997 controls from 33 studies genotyped for CHEK2*1100delC., Patients and Methods: CHEK2*1100delC genotyping was mostly done by a custom Taqman assay. Breast cancer odds ratios (ORs) for CHEK2*1100delC carriers versus noncarriers were estimated by using logistic regression and adjusted for study (categorical) and age. Main analyses included patients with invasive breast cancer from population- and hospital-based studies., Results: Proportions of heterozygous CHEK2*1100delC carriers in controls, in patients with breast cancer from population- and hospital-based studies, and in patients with breast cancer from familial- and clinical genetics center-based studies were 0.5%, 1.3%, and 3.0%, respectively. The estimated OR for invasive breast cancer was 2.26 (95%CI, 1.90 to 2.69; P = 2.3 × 10(-20)). The OR was higher for estrogen receptor (ER)-positive disease (2.55 [95%CI, 2.10 to 3.10; P = 4.9 × 10(-21)]) than it was for ER-negative disease (1.32 [95%CI, 0.93 to 1.88; P = .12]; P interaction = 9.9 × 10(-4)). The OR significantly declined with attained age for breast cancer overall (P = .001) and for ER-positive tumors (P = .001). Estimated cumulative risks for development of ER-positive and ER-negative tumors by age 80 in CHEK2*1100delC carriers were 20% and 3%, respectively, compared with 9% and 2%, respectively, in the general population of the United Kingdom., Conclusion: These CHEK2*1100delC breast cancer risk estimates provide a basis for incorporating CHEK2*1100delC into breast cancer risk prediction models and into guidelines for intensified screening and follow-up., Competing Interests: Authors’ disclosures of potential conflicts of interest are found in the article online at www.jco.org. Author contributions are found at the end of this article., (© 2016 by American Society of Clinical Oncology.)

Published
2016
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5. CHEK2*1100delC heterozygosity in women with breast cancer associated with early death, breast cancer-specific death, and increased risk of a second breast cancer.

Author

Weischer M, Nordestgaard BG, Pharoah P, Bolla MK, Nevanlinna H, Van't Veer LJ, Garcia-Closas M, Hopper JL, Hall P, Andrulis IL, Devilee P, Fasching PA, Anton-Culver H, Lambrechts D, Hooning M, Cox A, Giles GG, Burwinkel B, Lindblom A, Couch FJ, Mannermaa A, Grenaker Alnæs G, John EM, Dörk T, Flyger H, Dunning AM, Wang Q, Muranen TA, van Hien R, Figueroa J, Southey MC, Czene K, Knight JA, Tollenaar RA, Beckmann MW, Ziogas A, Christiaens MR, Collée JM, Reed MW, Severi G, Marme F, Margolin S, Olson JE, Kosma VM, Kristensen VN, Miron A, Bogdanova N, Shah M, Blomqvist C, Broeks A, Sherman M, Phillips KA, Li J, Liu J, Glendon G, Seynaeve C, Ekici AB, Leunen K, Kriege M, Cross SS, Baglietto L, Sohn C, Wang X, Kataja V, Børresen-Dale AL, Meyer A, Easton DF, Schmidt MK, and Bojesen SE

Subjects
Case-Control Studies, Checkpoint Kinase 2, Female, Genetic Predisposition to Disease, Genotype, Heterozygote, Humans, Middle Aged, Prognosis, Prospective Studies, Breast Neoplasms enzymology, Breast Neoplasms genetics, Germ-Line Mutation, Neoplasms, Second Primary enzymology, Neoplasms, Second Primary genetics, Protein Serine-Threonine Kinases genetics
Abstract

Purpose: We tested the hypotheses that CHEK2*1100delC heterozygosity is associated with increased risk of early death, breast cancer-specific death, and risk of a second breast cancer in women with a first breast cancer., Patients and Methods: From 22 studies participating in the Breast Cancer Association Consortium, 25,571 white women with invasive breast cancer were genotyped for CHEK2*1100delC and observed for up to 20 years (median, 6.6 years). We examined risk of early death and breast cancer-specific death by estrogen receptor status and risk of a second breast cancer after a first breast cancer in prospective studies., Results: CHEK2*1100delC heterozygosity was found in 459 patients (1.8%). In women with estrogen receptor-positive breast cancer, multifactorially adjusted hazard ratios for heterozygotes versus noncarriers were 1.43 (95% CI, 1.12 to 1.82; log-rank P = .004) for early death and 1.63 (95% CI, 1.24 to 2.15; log-rank P < .001) for breast cancer-specific death. In all women, hazard ratio for a second breast cancer was 2.77 (95% CI, 2.00 to 3.83; log-rank P < .001) increasing to 3.52 (95% CI, 2.35 to 5.27; log-rank P < .001) in women with estrogen receptor-positive first breast cancer only., Conclusion: Among women with estrogen receptor-positive breast cancer, CHEK2*1100delC heterozygosity was associated with a 1.4-fold risk of early death, a 1.6-fold risk of breast cancer-specific death, and a 3.5-fold risk of a second breast cancer. This is one of the few examples of a genetic factor that influences long-term prognosis being documented in an extensive series of women with breast cancer.

Published
2012
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6. 11q13 is a susceptibility locus for hormone receptor positive breast cancer.

Author

Lambrechts D, Truong T, Justenhoven C, Humphreys MK, Wang J, Hopper JL, Dite GS, Apicella C, Southey MC, Schmidt MK, Broeks A, Cornelissen S, van Hien R, Sawyer E, Tomlinson I, Kerin M, Miller N, Milne RL, Zamora MP, Pérez JI, Benítez J, Hamann U, Ko YD, Brüning T, Chang-Claude J, Eilber U, Hein R, Nickels S, Flesch-Janys D, Wang-Gohrke S, John EM, Miron A, Winqvist R, Pylkäs K, Jukkola-Vuorinen A, Grip M, Chenevix-Trench G, Beesley J, Chen X, Menegaux F, Cordina-Duverger E, Shen CY, Yu JC, Wu PE, Hou MF, Andrulis IL, Selander T, Glendon G, Mulligan AM, Anton-Culver H, Ziogas A, Muir KR, Lophatananon A, Rattanamongkongul S, Puttawibul P, Jones M, Orr N, Ashworth A, Swerdlow A, Severi G, Baglietto L, Giles G, Southey M, Marmé F, Schneeweiss A, Sohn C, Burwinkel B, Yesilyurt BT, Neven P, Paridaens R, Wildiers H, Brenner H, Müller H, Arndt V, Stegmaier C, Meindl A, Schott S, Bartram CR, Schmutzler RK, Cox A, Brock IW, Elliott G, Cross SS, Fasching PA, Schulz-Wendtland R, Ekici AB, Beckmann MW, Fletcher O, Johnson N, Silva Idos S, Peto J, Nevanlinna H, Muranen TA, Aittomäki K, Blomqvist C, Dörk T, Schürmann P, Bremer M, Hillemanns P, Bogdanova NV, Antonenkova NN, Rogov YI, Karstens JH, Khusnutdinova E, Bermisheva M, Prokofieva D, Gancev S, Jakubowska A, Lubinski J, Jaworska K, Durda K, Nordestgaard BG, Bojesen SE, Lanng C, Mannermaa A, Kataja V, Kosma VM, Hartikainen JM, Radice P, Peterlongo P, Manoukian S, Bernard L, Couch FJ, Olson JE, Wang X, Fredericksen Z, Alnaes GG, Kristensen V, Børresen-Dale AL, Devilee P, Tollenaar RA, Seynaeve CM, Hooning MJ, García-Closas M, Chanock SJ, Lissowska J, Sherman ME, Hall P, Liu J, Czene K, Kang D, Yoo KY, Noh DY, Lindblom A, Margolin S, Dunning AM, Pharoah PD, Easton DF, Guénel P, and Brauch H

Subjects
Female, Genetic Predisposition to Disease genetics, Genome-Wide Association Study, Genotype, Humans, Polymorphism, Single Nucleotide genetics, Risk Factors, White People, Breast Neoplasms genetics, Chromosomes, Human, Pair 11 genetics, Receptors, Estrogen genetics, Receptors, Progesterone genetics
Abstract

A recent two-stage genome-wide association study (GWAS) identified five novel breast cancer susceptibility loci on chromosomes 9, 10, and 11. To provide more reliable estimates of the relative risk associated with these loci and investigate possible heterogeneity by subtype of breast cancer, we genotyped the variants rs2380205, rs1011970, rs704010, rs614367, and rs10995190 in 39 studies from the Breast Cancer Association Consortium (BCAC), involving 49,608 cases and 48,772 controls of predominantly European ancestry. Four of the variants showed clear evidence of association (P ≤ 3 × 10(-9) ) and weak evidence was observed for rs2380205 (P = 0.06). The strongest evidence was obtained for rs614367, located on 11q13 (per-allele odds ratio 1.21, P = 4 × 10(-39) ). The association for rs614367 was specific to estrogen receptor (ER)-positive disease and strongest for ER plus progesterone receptor (PR)-positive breast cancer, whereas the associations for the other three loci did not differ by tumor subtype., (© 2012 Wiley Periodicals, Inc.)

Published
2012
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7. Genetic variants in TGFβ-1 and PAI-1 as possible risk factors for cardiovascular disease after radiotherapy for breast cancer.

Author

Hilbers FS, Boekel NB, van den Broek AJ, van Hien R, Cornelissen S, Aleman BM, van 't Veer LJ, van Leeuwen FE, and Schmidt MK

Subjects
Aged, Female, Follow-Up Studies, Genetic Variation, Genotype, Humans, Middle Aged, Proportional Hazards Models, Real-Time Polymerase Chain Reaction, Retrospective Studies, Risk Factors, Survival Rate, Breast Neoplasms genetics, Breast Neoplasms radiotherapy, Cardiovascular Diseases etiology, Cardiovascular Diseases genetics, Cardiovascular System radiation effects, Plasminogen Activator Inhibitor 1 genetics, Polymorphism, Genetic, Transforming Growth Factor beta1 genetics
Abstract

Background and Purpose: It has been established that radiotherapy can increase cardiovascular disease (CVD) risk. Genetic variants, which play a role in the tissue, damage response and angiogenesis regulating TGFβ pathway might give us insight into the mechanisms underlying radiation-induced CVD. We examined the effects of two polymorphisms, TGFβ1 29C>T and PAI-1 5G>4G, on CVD incidence., Materials and Methods: This retrospective cohort study included 422 10-year breast cancer survivors, aged <50 years at diagnosis, treated between 1977 and 1995. We collected information on treatment, oncological follow-up, CVD, CVD risk factors and genotypes., Results: During a mean follow-up of 19.4 years, 61 patients developed CVD. Internal mammary chain (IMC) irradiation, exposing a part of the heart to radiation, was associated with a hazard ratio of 2.36 (95% CI: 1.27-4.37, p=0.01) compared to no IMC irradiation. Compared to the C/C+C/T genotype, the T/T genotype of the TGFβ1 polymorphism was associated with hazard ratios of 1.79 (0.99-3.26, p=0.06) and 1.74 (0.90-3.34, p=0.10) in the total and IMC-irradiated group, respectively. We found no evidence for an association between PAI-1 5G>4G and CVD risk., Conclusion: Our study suggests there might be an association between the TGFβ1 29C>T polymorphism and CVD risk in long-term breast cancer survivors., (Copyright © 2011 Elsevier Ireland Ltd. All rights reserved.)

Published
2012
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