ALL-1 partial duplication in acute leukemia.

DOI Web Site 被引用文献11件
  • S A Schichman
    Jefferson Cancer Institute, Jefferson Cancer Center, Jefferson Medical College of Thomas Jefferson University, Philadelphia, PA 19107.
  • M A Caligiuri
    Jefferson Cancer Institute, Jefferson Cancer Center, Jefferson Medical College of Thomas Jefferson University, Philadelphia, PA 19107.
  • Y Gu
    Jefferson Cancer Institute, Jefferson Cancer Center, Jefferson Medical College of Thomas Jefferson University, Philadelphia, PA 19107.
  • M P Strout
    Jefferson Cancer Institute, Jefferson Cancer Center, Jefferson Medical College of Thomas Jefferson University, Philadelphia, PA 19107.
  • E Canaani
    Jefferson Cancer Institute, Jefferson Cancer Center, Jefferson Medical College of Thomas Jefferson University, Philadelphia, PA 19107.
  • C D Bloomfield
    Jefferson Cancer Institute, Jefferson Cancer Center, Jefferson Medical College of Thomas Jefferson University, Philadelphia, PA 19107.
  • C M Croce
    Jefferson Cancer Institute, Jefferson Cancer Center, Jefferson Medical College of Thomas Jefferson University, Philadelphia, PA 19107.

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<jats:p>The ALL-1 gene, located on chromosome band 11q23, is fused to a variety of other genes by reciprocal chromosomal translocations present in 5-10% of human acute leukemias. We have recently reported the detection by Southern blot of ALL-1 gene rearrangements in adult patients with acute myeloid leukemia lacking cytogenetic evidence of 11q23 translocations. These include 2 of 19 patients with normal karyotypes as well as 3 of 4 patients with trisomy 11. To characterize the abnormal ALL-1 genes, we cloned the ALL-1 rearrangements from two patients with trisomy 11. Characterization of the clones, together with Southern blot analysis, indicates that the ALL-1 rearrangement in both patients is the result of a direct tandem duplication of a portion of the ALL-1 gene spanning exons 2-6. The partial ALL-1 duplication is also detected by Southern blot analysis in a patient with a normal karyotype. RNA PCR and DNA sequence analysis show that the partially duplicated ALL-1 gene is transcribed into mRNA capable of encoding a partially duplicated protein. Partial duplication of ALL-1, in which a portion of a putative protooncogene is fused with itself, represents an additional genetic mechanism for leukemogenesis. Our findings suggest that the presence of trisomy in malignancy may sometimes indicate the partial duplication of a cellular protooncogene.</jats:p>

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