%0 Journal Article
%T Chromosome Aberrations in Cells Infected with Bovine Papillomavirus: Comparing Cutaneous Papilloma, Esophagus Papilloma, and Urinary Bladder Lesion Cells
%A S. R. C. Campos
%A T. C. Melo
%A S. Assaf
%A R. P. Araldi
%A J. Mazzuchelli-de-Souza
%A M. P. Sircili
%A R. F. Carvalho
%A F. Roperto
%A W. Be£żak
%A R. C. Stocco
%J ISRN Oncology
%D 2013
%R 10.1155/2013/910849
%X The majority of malignant cells present genetic instability with chromosome number changes plus segmental defects: these changes involve intact chromosomes and breakage-induced alterations. Some pathways of chromosomal instability have been proposed as random breakage, telomere fusion, and centromere fission. Chromosome alterations in tumor cells have been described in animal models and in vitro experiments. One important question is about possible discrepancies between animal models, in vitro studies, and the real events in cancer cells in vivo. Papillomaviruses are relevant agents in oncogenic processes related to action on host genome. Recently, many reports have discussed the presence of virus DNA in peripheral blood, in humans and in animals infected by papillomaviruses. The meaning of this event is of controversy: possible product of apoptosis occurring in cancer cells, metastasized cancer cells, or active DNA sequences circulating in bloodstream. This study compares chromosome aberrations detected in bovine cells, in peripheral blood cells, and in BPV lesion cells: the literature is poor in this type of study. Comparing chromosome aberrations described in the different cells, a common mechanism in their origin, can be suggested. Furthermore blood cells can be evaluated as an effective way of virus transmission. 1. Introduction The papillomaviruses (PVs) are viruses that require the environment of a differentiating epithelium for their replication cycle [1]. PVs infect mammals, including man, and are related to development of benign lesions that can progress to cancer [2]. Uterine cervical cancer, the second most frequently occurring cancer in women worldwide, is causal related to human papillomavirus infection (HPV) [3, 4]. The Papillomavirus genome comprises three regions: LCR, Ħ°long control regionĦħ responsible for genome transcription control, L region, encoding the capsid major and minor proteins (L1 and L2, resp.), presenting late transcription in virus replication cycle, and E region, with early transcription in virus cycle, which codifies the proteins related to carcinogenic action [5, 6]. The virus transmission is recognized as occurring through direct contact: the abrasion of the skin or sexual intercourse leads to PV infection [7]. PV oncoproteins are the source for the alterations related to carcinogenesis: they interfere with the host cell cycle control, through interactions with specific proteins, as p53, p RB, p21, and p27 [8]. As examples of viral oncoprotein actions, E6 induces accelerated degradation of p53 [9]. E7 binds and
%U http://www.hindawi.com/journals/isrn.oncology/2013/910849/