Expression profiles of acute lymphoblastic and myeloblastic leukemias with ALL-1 rearrangements
- T. Rozovskaiaa,
- O. Ravid-Amirb,
- S. Tillibc,d,
- G. Getzb,
- E. Feinsteine,
- H. Agrawalb,
- A. Naglerf,
- E. F. Rappaportg,
- I. Issaevaa,
- Y. Matsuoh,
- U. R. Keesi,
- T. Lapidotj,
- F. Lo Cocok,
- R. Foak,
- A. Mazoc,
- T. Nakamurac,
- C. M. Crocec,l,
- G. Ciminok,
- E. Domanyb,l, and
- E. Canaania,l
- Departments of aMolecular Cell Biology, bPhysics of Complex Systems, and jImmunology, Weizmann Institute of Science, Rehovot 76100, Israel; cKimmel Cancer Center, Jefferson Medical College, Philadelphia, PA 19107; dInstitute of Gene Biology, Russian Academy of Sciences, Moscow 119334, Russia; eQuark Biotech, Inc., Cleveland, OH 44106; fSheba Medical Center, Tel-Hashomer 52621, Israel; gChildren's Hospital, Philadelphia, PA 19104; hFujisaki Cell Center, Fujisaki, Okayama 702-8006, Japan; iInstitute for Child Health Research, Subiaco, Western Australia 6008, Australia; and kDepartment of Cellular Biotechnology and Hematology, University La Sapienza, 00161 Rome, Italy
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Contributed by C. M. Croce, April 10, 2003
Abstract
The ALL-1 gene is directly involved in 5–10% of acute lymphoblastic leukemias (ALLs) and acute myeloid leukemias (AMLs) by fusion to other genes or through internal rearrangements. DNA microarrays were used to determine expression profiles of ALLs and AMLs with ALL-1 rearrangements. These profiles distinguish those tumors from other ALLs and AMLs. The expression patterns of ALL-1-associated tumors, in particular ALLs, involve oncogenes, tumor suppressors, antiapoptotic genes, drug-resistance genes, etc., and correlate with the aggressive nature of the tumors. The genes whose expression differentiates between ALLs with and without ALL-1 rearrangement were further divided into several groups, enabling separation of ALL-1-associated ALLs into two subclasses. One of the groups included 43 genes that exhibited expression profiles closely linked to ALLs with ALL-1 rearrangements. Further, there were evident differences between the expression profiles of AMLs in which ALL-1 had undergone fusion to other genes and AMLs with partial duplication of ALL-1. The extensive analysis described here pinpointed genes that might have a direct role in pathogenesis.
Footnotes
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↵ l To whom correspondence may be addressed. E-mail: croce{at}calvin.jci.tju.edu, fedomany{at}wisemail.weizmann.ac.il, or eli.canaani{at}weizmann.ac.il.
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Abbreviations: ALL, acute lymphoblastic leukemia; AML, acute myeloblastic leukemia; FDR, false discovery rate.
- Copyright © 2003, The National Academy of Sciences
