Damaged DNA and miscounted chromosomes: human T cell leukemia virus type I tax oncoprotein and genetic lesions in transformed cells.

Susan J Marriott, Francene J Lemoine, Kuan-Teh Jeang

Journal: Journal of biomedical science 2003;9(4):292-8

PMID: 12145525

Abstract

Genetic instability is a recurring theme in human cancers. Although the molecular mechanisms mediating this effect commonly observed in transformed cells are not completely understood, it has been proposed to involve either the loss of DNA repair capabilities or the loss of chromosomal stability. The transforming retrovirus human T cell leukemia virus type I (HTLV-I) encodes a viral oncoprotein Tax, which is believed to cause the genomic instability characteristic of HTLV-I-infected cells. This review focuses on the ability of HTLV-I Tax to disrupt the cellular processes of DNA repair and chromosomal segregation. The consequences of these effects as well as the evolutionary advantage this may provide to HTLV-I are discussed.

Address: Department of Molecular Virology and Microbiology, Baylor College of Medicine, Houston, TX 77030, USA. [email protected]

DOI: 10.1007/BF02256583

MeSH Terms: Aneuploidy, Calcium-Binding Proteins, Cell Cycle Proteins, Cell Transformation, Neoplastic, Chromosome Aberrations, DNA Damage, DNA Repair, Gene Products, tax, Human T-lymphotropic virus 1, Humans, Mad2 Proteins, Neoplasms, Nuclear Proteins, Phosphoproteins, Repressor Proteins