ABSTRACT
Las evidencias epidemiológicas, virológicas y clínicas demuestran que hay una estrecha asociación entre tipos específicos de HPV y cáncer cervicouterino. La infección por HPV precede el desarrollo de la enfermedad cervical. Los HPV están presentes en las lesiones precursoras. La infección por HPV es una condición necesaria pero no suficiente, se requiere de factores que participan en la oncogénesis cervical. No se conoce la función que ejercen algunos factores asociados. Una pequeña proporción de las infecciones por HPV de alto riesgo desarrollan una neoplasia maligna.
Subject(s)
Humans , Female , Papillomavirus Infections/complications , Papillomavirus Infections/epidemiology , Papillomavirus Infections/virology , Uterine Cervical Neoplasms/etiology , Uterine Cervical Neoplasms/prevention & control , Oncogenes/physiology , Oncogenes/genetics , PapillomaviridaeABSTRACT
Storey et al. (1998) implicated the proline/argine polymorphism of the codon 72 of the tumor-suppressor gene p53 in the development of cervical cancer (CC) with the observation that the p53 protein is more efficiently inactivated by the E6 oncoprotein of human papillomavirus in p53 arginine as compared with its proline isoform. These authors further noted that in the United Kingdom, individuals homozygous for the arginine allele were several times more susceptible to HPV-associated tumorigenesis that proline/arginine heterozygotes. Subsequent studies in different countries failed to unanimously confirm this association. Motivated by the high incidence of CC in Chile, we undertook a case control study obtaining the following frequencies for genotypes PP, AP and AA in 60 ICC cases and 53 carefully selected controls: 0.067, 0.250, 0.683 and 0.075, 0.453, 0.472 respectively. A significant difference (X2 = 3.19 p < 0.02) and an odds ratio of 2.62 supported Storey et al (1998)'s results. In addition, rejecting previous hypotheses about the world distribution of the p53 codon 72 polymorphism, we conclude that this distribution most likely represents ancient human dispersal routes. Several methodological and biological explanations for the results obtained in previous negative association studies are briefly discussed