Polymorphisms of estrogen receptor-alpha gene in Brazilian women with high breast density after menopause

Nenhuma Miniatura disponível
Citações na Scopus
3
Tipo de produção
article
Data de publicação
2013
Editora
INFORMA HEALTHCARE
Indexadores
Título da Revista
ISSN da Revista
Título do Volume
Autor de Grupo de pesquisa
Editores
Coordenadores
Organizadores
Citação
GYNECOLOGICAL ENDOCRINOLOGY, v.29, n.8, p.771-774, 2013
Projetos de Pesquisa
Unidades Organizacionais
Fascículo
Resumo
The association of genetic polymorphism in the estrogen receptor alpha (ER alpha) gene and risk for diseases including breast cancer (BC) has been the subject of great interest. Objective: Checking on women with high breast density after menopause, the frequency of the Pvull and Xbal polymorphisms of the ER alpha gene and the correlation between them and the known risk factors for breast cancer. Method: Observational study with 308 women between 45 and 65 years old with high breast density, without hormonal therapy, menstruation for a year or more, breast and ovarian cancer history. It was characterized in clinical history and physical examination: menarche, menopause, parity, family history of BC, smoking, alcohol intake and body mass index. Results: The allelic and genotypic frequencies for ER alpha-Pvull and Xbal: p = 43.99%; p = 56.01%; pp = 32.14%; Pp = 47.73% and PP = 20.13%; X = 41.56%; x = 58.44%; xx = 33.44%; Xx = 50.00% and XX = 16.56%, respectively. The most frequent risk factors for BC: menarche before 12 years old (35.38%), nulliparity or first child after 28 years old (41.66%), family history of BC (19.16%) and overweight/obesity (62.01%). Conclusion: Allelic and genotypic distribution similar to literature. The risk factors for BC were more prevalent in women with high breast density but without significant associations with these polymorphisms.
Palavras-chave
Breast neoplasms, estrogen receptors, genetic polymorphism, mammography, risk factors
Referências
  1. Allred DC, 2004, BREAST CANCER RES, V6, P240, DOI 10.1186/bcr938
  2. Barlow WE, 2006, J NATL CANCER I, V98, P1204, DOI 10.1093/jnci/djj331
  3. Cai QY, 2003, CANCER EPIDEM BIOMAR, V12, P853
  4. Gennari L, 2005, AM J EPIDEMIOL, V161, P307, DOI 10.1093/aje/kwi055
  5. Giacomazzi J., 2008, FATORES RISCO CANC M
  6. Gonzalez-Mancha R, 2008, MED SCI MONITOR, V14, P136
  7. Herrington DM, 2002, NEW ENGL J MED, V346, P967, DOI 10.1056/NEJMoa012952
  8. Hsieh PCH, 2007, NAT MED, V13, P970, DOI 10.1038/nm1618
  9. Hu Z, 2007, J CANCER RES CLIN, V133, P969, DOI 10.1007/s00432-007-0244-7
  10. Humphreys K, 2004, BREAST CANCER RES, V6, P437
  11. Javed S, 2011, MATURITAS, V69, P377, DOI 10.1016/j.maturitas.2011.05.008
  12. Jensen EV, 2003, CLIN CANCER RES, V9, P1980
  13. JEON JH, 2011, PUBMED CANC RES TREA, V43, P42, DOI 10.4143/CRT.2011.43.1.42
  14. Ma H, 2006, BREAST CANCER RES, V8, P43
  15. Martin LJ, 2008, BREAST CANCER RES, V10, P1
  16. Molvarec A, 2007, CLIN CHIM ACTA, V382, P100, DOI 10.1016/j.cca.2007.04.003
  17. Onland-Moret NC, 2005, CANCER CAUSE CONTROL, V16, P1195, DOI 10.1007/s10552-005-0307-5
  18. Pichard C, 2008, MATURITAS, V60, P19, DOI 10.1016/j.maturitas.2008.03.002
  19. Ramos EHD, 2009, CLIMACTERIC, V12, P490, DOI 10.3109/13697130902952585
  20. Shen YP, 2006, CANCER EPIDEM BIOMAR, V15, P342, DOI 10.1158/1055-9965.EPI-05-0485
  21. van Duijnhoven FJB, 2006, CANCER EPIDEM BIOMAR, V15, P462, DOI 10.1158/1055-9965.EPI-05-0754