Publications by authors named "Vladimir Pecenka"

Myeloblastosis-associated virus 2 (MAV-2) is a highly tumorigenic simple avian retrovirus. Chickens infected with MAV-2 develop tumors in the kidneys, lungs, and liver with a short latency, less than 8 weeks. Here we report the results of molecular analyses of MAV-2-induced liver tumors that fall into three classes: hepatic hemangiosarcomas (HHSs), intrahepatic cholangiocarcinomas (ICCs), and hepatocellular carcinomas (HCCs).

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A tumor cell is formed when a critical amount of endogenous and/or exogenous tumorigenic stimuli is exceeded. We have shown that the transient presence of nontumorigenic stray cells in tissues of experimental animals that contain cells with a subcritical set of genetic mutations can act as a tumor-promoting stimulus. To induce somatic mutations in all chicken tissues, we have used the MAV-2 retroviral insertion system that almost exclusively generates nephroblastomas.

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Gene deregulation is a frequent cause of malignant transformation. Alteration of the gene structure and/or expression leading to cellular transformation and tumor growth can be experimentally achieved by insertion of the retroviral genome into the host DNA. Retrovirus-containing host loci found repeatedly in clonal tumors are called common viral integration sites (cVIS).

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Article Synopsis
  • The study focused on kidney blastema cells in birds and identified the twist gene as a key player in tumor development after MAV2 retrovirus infection.
  • The MAV2 virus integrated into the twist gene, leading to significant overexpression, increasing transcription over 200 times in some cases, and also causing deletions at the 5' ends of proviruses.
  • The findings suggest that nephroblastoma in chickens may start from a single cell affected by the MAV2 retrovirus, which disrupts gene regulation, particularly that of the twist gene, contributing to tumor growth.
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