TCL1 is overexpressed in patients affected by adult T-cell leukemias

Maria Grazia Narducci, Antonella Stoppacciaro, Kazunori Imada, Takashi Uchiyama, Laura Virgilio, Cristina Lazzeri, Carlo Maria Croce, Giandomenico Russo

Research output: Contribution to journalArticlepeer-review


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 distinctive etiopathogenetic features of this disease. However, unlike other acute transforming retroviruses, the human T-cell leukemia/lymphotropic virus type I lacks an oncogene within its genome. Other human postthymic leukemias, such as T-prolymphocytic leukemias, involve mostly the CD4 cellular subset and share many similarities to ATLs (aggressive course, cutaneous involvement, CD4+, CD29+, CD45RA- phenotype, and alpha-naphthyl-acetate esterase positivity). A chromosomal rearrangement at 14q32.1, involved in translocations or inversions with either the α/δ locus [t(14;14)(q11;q32.1), inv14(q11;q32.1)], or the β-chain locus of the T-cell receptor [t(7;14)(q35;q32.1)] is found. 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 CD8+ subpopulations. Here, using molecular and immunocytochemical analysis, we report that TCL1 is also overexpressed in 10 of 10 ATL specimens, indicating that this gene may play an important role in the pathogenesis of this disease.

Original languageEnglish
Pages (from-to)5452-5456
Number of pages5
JournalCancer Research
Issue number24
Publication statusPublished - Dec 15 1997

ASJC Scopus subject areas

  • Cancer Research
  • Oncology


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