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• W2030026542 abstract "Adult T-cell leukemia (ATL) is a leukemia derived from mature CD4 + T cells and induced by human T-cell leukemia virus type 1 (HTLV-1) infection. Previous studies have revealed many possible molecular and cellular mechanisms of HTLV-1-induced leukemogenesis, but it still remains unknown how HTLV-1 transforms peripheral CD4 T cells in infected individuals. Given the fact that only 2–5% of infected individuals develop ATL, HTLV-1 infection alone is not sufficient for the transformation of infected cells. Host genetic and epigenetic abnormalities and host immunological status should be considered in attempting to understand the mechanism of the oncogenesis of ATL. Nonetheless, it is obvious that HTLV-1 infection dramatically increases the risk of leukemia generation from peripheral CD4 T-cells, in which the incidence of leukemia is quite low. Furthermore, the evidence that all ATL cases retain the HTLV-1 provirus, especially the <mml:math xmlns:mml=http://www.w3.org/1998/Math/MathML><mml:msup><mml:mn>3</mml:mn><mml:mo>′</mml:mo></mml:msup></mml:math> region, indicates that HTLV-1-encoded genes play a critical role in leukemogenesis. Since increasing evidence indicates that the HTLV-1 bZIP factor (HBZ) gene plays a significant role in the pathogenesis of HTLV-1, we will discuss the cellular and molecular mechanism of ATL generation from the virological point of view, particularly focusing on HBZ." @default.
• W2030026542 created "2016-06-24" @default.
• W2030026542 creator A5019527890 @default.
• W2030026542 creator A5080272176 @default.
• W2030026542 date "2012-11-24" @default.
• W2030026542 modified "2023-10-03" @default.
• W2030026542 title "Molecular and Cellular Mechanism of Leukemogenesis of ATL: Emergent Evidence of a Significant Role for HBZ in HTLV-1-Induced Pathogenesis" @default.
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• W2030026542 doi "https://doi.org/10.1155/2012/213653" @default.
• W2030026542 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/3504235" @default.
• W2030026542 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/23198153" @default.
• W2030026542 hasPublicationYear "2012" @default.
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