TEL-AML1, expressed from t(12;21) in human acute lymphocytic leukemia, induces acute leukemia in mice

Florence Bernardin, Yandan Yang, Rebecca Cleaves, Marianna Zahurak, Linzhao Cheng, Curt I. Civin, Alan D. Friedman

Research output: Contribution to journalArticle

Abstract

TEL-AML1 is expressed from the t(12;21) chromosomal translocation in B-precursor acute lymphocytic leukemia (ALL). Creation of the TEL-AML1 fusion disrupts one copy of the TEL and AML1 genes, and loss of TEL or AML1 is also associated with cases of acute leukemia without TEL-AML1. To determine whether TEL-AML1 can contribute to leukemogenesis, we transduced marrow from C57BL/6 mice with a retroviral vector expressing TEL-AML1 or with a control vector. Transduced cells were introduced into irradiated syngeneic recipients. Two of 9 TEL-AML1 mice developed ALL (one T-lineage ALL and one B-precursor ALL), whereas 0 of 20 control mice developed leukemia. The B-precursor ALL was retransplantable and expressed TEL-AML1. We similarly transduced marrow from C57BL/6 mice lacking the overlapping p16INK4ap19ARF genes and transplanted the cells into wild-type recipients. No control mice died, but six of eight TEL-AML1/p16p19 mice died with leukemia. Overall, these findings indicate that TEL-AML1 contributes to leukemogenesis and may cooperate with loss of p16INK4ap14ARF to transform lymphoid progenitors.

Original languageEnglish (US)
Pages (from-to)3904-3908
Number of pages5
JournalCancer Research
Volume62
Issue number14
StatePublished - Jul 15 2002

ASJC Scopus subject areas

  • Oncology
  • Cancer Research

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