The molecular mechanisms involved in JCPyV oncogenesis have been extensively studied: the main oncogenic viral protein is the large tumor antigen (T-Ag), that is able to bind, among other cellular factors, both Retinoblastoma protein (pRb) and p53 and to dysregulate the cell cycle, but also the early proteins small tumor antigen (t-Ag) and Agnoprotein appear to cooperate in the process of cell transformation.
Dysfunction of T cells, such as exhaustion under the persistent presence of tumor antigen, compromise host anti-tumor immunity resulting in oncogenesis.
Detection of BKV sequences in urinary tract neoplasms has led to the postulate that this virus may induce human oncogenesis through the function of its large tumor antigen (TAg).
The higher PR and catD concentrations in diffuse adenocarcinomas, and the overexpression of TAG-72 in the intestinal type, support the existence of two modes of gastric carcinogenesis.
Since we have mapped the low-oncogenic or nononcogenic Ad12 cyt mutants within the 19-kd tumor antigen-coding region, our results further indicate that the 19-kd tumor antigen also directly or indirectly plays an important role in tumorigenesis of Ad12.