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Article
February 15, 1995

Self-fusion of the ALL 1 GeneA New Genetic Mechanism for Acute Leukemia

Author Affiliations

From the Jefferson Cancer Institute, Jefferson Cancer Center, and Department of Microbiology and Immunology, Jefferson Medical College of Thomas Jefferson University, Philadelphia, Pa (Drs Schichman and Croce), and the Department of Chemical Immunology, The Weizmann Institute, Rehovot, Israel (Dr Canaani).

JAMA. 1995;273(7):571-576. doi:10.1001/jama.1995.03520310069032
Abstract

LEUKEMIA is a clonal malignancy of blood cells that usually involves the myeloid or lymphoid lineages. The origin of leukemia, like other forms of cancer, lies in gene defects that alter the normal programs of cellular differentiation, proliferation, or apoptosis. Using chromosomal rearrangements as a guidepost to the location of genes involved in hematologic malignancy, researchers have identified and molecularly characterized many leukemia genes during the last decade.1 These studies have revealed some common genetic mechanisms for leukemogenesis, provided molecular tools for leukemia diagnosis and monitoring, and identified potential targets for a new generation of leukemia therapies.

One of the most significant of these genetic findings involves the ALL1 gene, which participates in acute leukemias in 5% to 10% of children and adults. Like other leukemia genes, ALL1 was discovered by its association with well-characterized chromosomal rearrangements. However, we have recently found that the ALL1 gene also participates in

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