Untitled

Abstract

Adult T-cell leukemia/lymphoma (ATL) is a distinct clinicopathological entity, i.e., peripheral T-lymphocytic malignancy caused by human T-lymphotropic virus type I (HTLV-1) with diverse clinical features. High frequency of genetic instability (GIN) in both aggressive and indolent ATL was detected by comparative genomic hybridization (CGH). Among GIN, chromosomal instability, i.e., ancuploidy, in indolent ATL was as frequent but less complex and dynamic as compared to those in aggressive ATL. Some of the CGH alterations, including gain of 14q32, appear to be rather ATL specific. Clonal instability of HTLV-1-infected T cells. i.e., emergence of distinct clone, was detected in about one forth of acute crisis from indolent ATL by CGH and Southern blotting for HTLV-1. Taking together with the previous reports of frequent subtle mutations in several tumor suppressor genes in aggressive ATL, GIN in multistep leukemogenesis of ATL is diverse including clonal, chromosomal, and nucleotide levels.

Expression profiles of adult T-cell leukemia–lymphoma and associations with clinical responses to zidovudine and interferon α

“…The primary leukemic cells analyzed in this study harbored genetic aberrations similar to aberrations previously reported in the literature and included frequent chromosomal gains of chromosomal regions 3p, 7q, 1q, 2q, 3q, 8p, 8q, 9q, 18q, and 19p, in addition to losses at chromosomal regions 6q, 2q, 4q, 5q, 10p, 10q, 12p, 18p, and chromosome 13 [47,48]. Analyses of correlation between chromosomal changes and alteration in gene expression of chromosomes located in the chromosomal aberration regions demonstrated relatively poor correlation, similar to our observations in transformed follicular lymphoma specimens [49].…”