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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.

Proteins function for anti-senescence and monoclonal proliferation of ATL cells