Tumor Suppressor Inactivation in the Pathogenesis of Adult T-Cell Leukemia

Tumor suppressor functions are essential to control cellular proliferation, to activate the apoptosis or senescence pathway to eliminate unwanted cells, to link DNA damage signals to cell cycle arrest checkpoints, to activate appropriate DNA repair pathways, and to prevent the loss of adhesion to in...

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Bibliographic Details
Published in:Journal of Oncology 2015-01, Vol.2015 (2015), p.213-223
Main Author: Nicot, Christophe
Format: Article
Language:English
Subjects:
Cell cycle
Cloning
Cyclin-dependent kinases
Development and progression
Epigenetics
Gene expression
Genetic aspects
Kinases
Leukemia
Lymphoma
Medical prognosis
MicroRNAs
Mutation
Non-Hodgkin's lymphomas
Patients
Physiological aspects
Proteins
Review
T cells
Tumor suppressor genes
Viral infections
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Summary:Tumor suppressor functions are essential to control cellular proliferation, to activate the apoptosis or senescence pathway to eliminate unwanted cells, to link DNA damage signals to cell cycle arrest checkpoints, to activate appropriate DNA repair pathways, and to prevent the loss of adhesion to inhibit initiation of metastases. Therefore, tumor suppressor genes are indispensable to maintaining genetic and genomic integrity. Consequently, inactivation of tumor suppressors by somatic mutations or epigenetic mechanisms is frequently associated with tumor initiation and development. In contrast, reactivation of tumor suppressor functions can effectively reverse the transformed phenotype and lead to cell cycle arrest or death of cancerous cells and be used as a therapeutic strategy. Adult T-cell leukemia/lymphoma (ATLL) is an aggressive lymphoproliferative disease associated with infection of CD4 T cells by the Human T-cell Leukemia Virus Type 1 (HTLV-I). HTLV-I-associated T-cell transformation is the result of a multistep oncogenic process in which the virus initially induces chronic T-cell proliferation and alters cellular pathways resulting in the accumulation of genetic defects and the deregulated growth of virally infected cells. This review will focus on the current knowledge of the genetic and epigenetic mechanisms regulating the inactivation of tumor suppressors in the pathogenesis of HTLV-I.
ISSN:1687-8450
1687-8450
DOI:10.1155/2015/183590