Abstract
Background ATL is a highly aggressive leukemia/lymphoma which was first proposed as a new disease entity in 1977. The long clinical latency and low incidence of ATL indicate that some genetic changes are involved in malignant transformation and monoclonal expansion of HTLV-1infected cells. Monoclonal proliferation of HTLV-1infected cells is observed in a part of the virus carriers, who are considered to be the high risk group for development of ATL [1]. We reviewed the process of senescence and how proteins allow the monoclonal proliferation of ATL cells.
Highlights
ATL is a highly aggressive leukemia/lymphoma which was first proposed as a new disease entity in 1977
We reviewed the process of senescence and how proteins allow the monoclonal proliferation of ATL cells
Constitutive activation of STAT as well as functional impairment and stabilization of p53 protein found in the PBMCs of ATL patients are supposed to be one base for ATL development [2,3]
Summary
ATL is a highly aggressive leukemia/lymphoma which was first proposed as a new disease entity in 1977. We reviewed the process of senescence and how proteins allow the monoclonal proliferation of ATL cells.
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