Abstract
Putative oncogenic viruses: Some data on Brazilian subjects
Highlights
Despite some controversies, it is the common sense that cancer is a multifactorial event mainly determined by aging, as the cellular biochemical machinery, along the years, gathers nucleotide sequences coding for altered or non-functional proteins playing pivotal roles at different stages of the cell cycle [1]
Cervix uterine cancer patients exhibited relatively elevated Human T-cell lymphotropic virus (HTLV)-1 prevalence [67,69], but scarce data confirmed our results, as published by Du et al [71] assessing the potential association of HTLV-1 to endometrial carcinoma; in the Yucatan peninsula, Góngorra-Bianchi et al [72] showed that Mexican Mayan descendants with high incidence of cervix uterine cancer, yielded HTLV-2 positivity, in both cancer and healthy women, as expected; as well, in Japan and Jamaica, HTLV-1 markers were detected among cervix uterine cancer patients [73,74]
Cervix uterine cancer is etiologically linked to Human Papillomavirus (HPV) persistent infection but, both HTLV-1/2 and HPV are mainly sexually transmitted, and mostly by promiscuous behavior, despite HTLV-1/2 infection be usually circumscribed to nuclear families
Summary
It is the common sense that cancer is a multifactorial event mainly determined by aging, as the cellular biochemical machinery, along the years, gathers nucleotide sequences coding for altered or non-functional proteins playing pivotal roles at different stages of the cell cycle [1]. Cancer seems to be an unsuccessful event for the host, that winds up with abnormal cells metabolism and growth in a chaotic genomic and tissue organization [2,3,4,5]. It is understandable and well-known that isolated events do not play any significative role in cancer etiology and evolution but, integrated and orchestrated molecular events, even in distorted physiological processes, have been well-characterized and proved to participate in the tumorigenesis and cancerization. How do proteins coded by virus genomes could participate or contribute to the genesis of the genomic chaos in the host cell?
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