TCL1 IS OVEREXPRESSED IN PATIENTS AFFECTED BY ADULT T-CELL LEUKEMIAS

Among mature postthymic T-cell leukemias, adult T-cell leukemia (ATL) has characteristic clinicopathological entities. The association with the human T-cell leukemia/lymphotropic virus type I is one of the dist inctive etiopathogenetic features of this disease, However, unlike oth er acute transforming retroviruses, the human T-cell leukemia/lymphotr opic virus type I lacks an oncogene within its genome. Other human pos tthymic leukemias, such as T-prolymphocytic leukemias, involve mostly the CD4 cellular subset and share many similarities to ATLs (aggressiv e course, cutaneous involvement, CD4(+), CD29(+), CD45RA(-) phenotype, and alphanaphthyl-acetate esterase positivity). A chromosomal rearran gement at 14q32.1, involved in translocations or inversions with eithe r the alpha/delta locus [t(14;14)(q11;q32.1), inv14(q11;q32.1)], or th e beta-chain locus of the T-cell receptor [t(7;14)(q35;q32.1)] is foun d, These rearrangements disregulate a gene, TCL1, located at the 14q32 .1 region, that we show is physiologically expressed in CD4/CD8 double -negative thymocyte cells, but not in more differentiated CD4(+) and C D8(+) subpopulations. Here, using molecular and immunocytochemical ana lysis, we report that TCL1 is also overexpressed in 10 of 10 ATL speci mens, indicating that this gene may play an important role in the path ogenesis of this disease.