Exposure to wood smoke, HPV infection, and genetic susceptibility for cervical neoplasia among women in Colombia

Cervical cancer is the second leading cause of death from cancer among women in Colombia (16/100,000). Infection with high‐risk human papillomavirus (HPV) plays a major role in the etiology of high‐grade squamous intraepithelial lesions (HSILs). Exposure to chemical agents may be a cofactor for tumo...

Full description

Saved in:
Bibliographic Details
Published inEnvironmental and molecular mutagenesis Vol. 47; no. 7; pp. 553 - 561
Main Authors Sierra-Torres, Carlos H., Arboleda-Moreno, Yexania Y., Orejuela-Aristizabal, Leonora
Format Journal Article
LanguageEnglish
Published Hoboken Wiley Subscription Services, Inc., A Wiley Company 01.08.2006
Wiley-Liss
Subjects
Online AccessGet full text

Cover

Loading…
More Information
Summary:Cervical cancer is the second leading cause of death from cancer among women in Colombia (16/100,000). Infection with high‐risk human papillomavirus (HPV) plays a major role in the etiology of high‐grade squamous intraepithelial lesions (HSILs). Exposure to chemical agents may be a cofactor for tumor induction, and individual genetic differences in the metabolism of these chemical agents may affect the susceptibility of individuals towards the development of HSIL. In this case–control study, a total of 91 cases with HSIL and 92 healthy controls, frequency‐matched by age and place of origin, were recruited, and their frequencies of CYP2E1, GSTM1, and GSTT1 polymorphism were determined. We then evaluated the association of these polymorphisms, by themselves and in combination with wood smoke exposure and HPV‐infection status, with the risk of HSIL. The results indicate that GSTM1 and GSTT1 polymorphism were not associated with HSIL, although a small increase in risk was observed for individuals who were GSTT1 null (OR = 1.4, 95% CI = 0.57–3.44). Contrary to other investigations, the c2/c2 variant of the CYP2E1 gene was associated with a significant increase in risk after adjusting for wood smoke exposure (OR = 6.3, 95% CI = 1.10–36.38) or wood smoke exposure and HPV‐infection status (OR = 10.7, 95% CI = 1.76–65.58). Wood smoke exposure also increased the risk of HSIL among CYP2E1 c2/c2 HPV‐positive women (OR = 3.3, CI = 0.50–22.50); however, the increase did not achieve statistical significance. Our study provides tantalizing evidence that genetic differences in the metabolism of wood smoke carcinogens, particularly metabolism by CYP2E1, may confer susceptibility for HSIL development. Further investigations with larger populations will be needed to confirm this association, which may provide important information for improving cervical cancer prevention programs. Environ. Mol. Mutagen., 2006. © 2006 Wiley‐Liss, Inc.
Bibliography:Colciencias, Observatorio Colombiano de Ciencia y Tecnología - No. 1103-04-11087
ark:/67375/WNG-KQ4N6J95-N
istex:DAF46965740AB22BFD396DA0EE54D10E1804BAD6
ArticleID:EM20228
Presented at the 9th International Conference on Environmental Mutagens and 36th Annual Meeting of the Environmental Mutagen Society, San Francisco, CA, September 3-8, 2005.
Presented at the 9th International Conference on Environmental Mutagens and 36th Annual Meeting of the Environmental Mutagen Society, San Francisco, CA, September 3–8, 2005.
ObjectType-Article-1
SourceType-Scholarly Journals-1
ObjectType-Feature-2
content type line 23
ISSN:0893-6692
1098-2280
DOI:10.1002/em.20228