Abba Martín C, Laguens Rubén M, Dulout Fernando N, Golijow Carlos D
Centro de Investigaciones en Genética Básica y Aplicada (CIGEBA), Facultad de Ciencias Veterinarias, Universidad Nacional de La Plata, Calle 60 y 118 s/n, B1900AVW, La Plata, Argentina.
Mutat Res. 2004 Feb 14;557(2):151-8. doi: 10.1016/j.mrgentox.2003.10.005.
Despite the prominent role for Human Papillomavirus (HPV) infection in the development of genital cancer, other genetic or environmental co-factors have also been involved. Studies of c-myc activation in cervical carcinomas have reported that gene over-expression (mainly gene amplification) are common in cervical squamous cell carcinomas and may correlate with the biologic behavior of the neoplasm. Using PCR based technology, DNAs from 79 normal cervical samples and 225 abnormal cervical tissue scrapes were analyzed for HPV detection and typing and for c-myc gene amplification. Significant differences were found between the different cyto/histology groups (P<0.0001) and also with HPV high-risk infected samples (P<0.0002). In this sense, we showed that the average c-myc copy number increased according to the histological grade of the lesion (OR=6.3, CI=2.1-18.8). Also, the results showed that the infection with HPV 16 was tightly associated with c-myc amplification (OR=10.6, CI=3.1-36). These results could indicate that oncogene amplification take place in pre-invasive stages of cervical disease and could cooperate not only in tumor progression but also in cell transformation. Moreover, the results strongly associate the c-myc gene amplification to the infection with the oncogenic HPV 16, showing that the pattern of virus infection and oncogene activation could be specific for different viral genotypes.
