Telomere Disfunction Is Not An Early Genetic Event in Adult T-Cell Leukemia/Lymphoma

Adult T-cell leukemia/lymphoma (ATL) is a mature T-cell neoplasm of post-thymic lymphocytes linked to human T-cell lymphotropic virus type I (HTLV-I). ATL develops in 3–5% of HTLV-I carriers after a long period of clinical latency and presents chromosomes abnormalities resulting in aneuploidy usually seem in telomere dysfunction disease. We were interested whether the abnormalities of the telomere regulation in ATL and if its abnormalities are correlated with ATL pathogenesis. The telomere length of TCD4 and TCD8 lymphocytes in samples from HTLV-I carriers (n= 52) with median age of 49.5 years (18–71 years) and ATL patients (n= 6) with median of 39 years (18–59 years) were assessed by fluorescence in situ hybridization and flow cytometry (Flow-FISH) and compared with healthy subjects (n = 58) matched for gender and age. We did not detected significant difference the telomere length of the TCD4 and TCD8 lymphocytes between HTLV-I carriers and health subjects. However we showed an accentuated loss in telomere length of the malignant T lymphocyte in ATL disease and values closed to those ageexpected in non-malignant T lymphocyte in ATL disease. We concluded that these results do not support a major role of telomere disfunction as an early event in pathogenesis of the ATL.