A remarkABL new fusion oncogene in T-cell ALL

Blood

Volumn 105, Issue 12, 2005, Pages 4547-4548

  Van Etten, Richard A ^a  

^a TUFTS MEDICAL CENTER   (United States)

Author keywords

[No Author keywords available]

Indexed keywords

ABELSON KINASE; BCR ABL PROTEIN; ECHINODERM MICROTUBULE ASSOCIATED PROTEIN 1; HOMEODOMAIN PROTEIN; IMATINIB; INTERLEUKIN 3; MITOGEN ACTIVATED PROTEIN KINASE; PROTEIN; STAT5 PROTEIN; UNCLASSIFIED DRUG;

ACUTE LYMPHOBLASTIC LEUKEMIA; AMINO TERMINAL SEQUENCE; ARTICLE; AUTOPHOSPHORYLATION; CHROMOSOME 14; ENZYME ACTIVITY; FUSION GENE; GENE AMPLIFICATION; GENE DELETION; HUMAN; OLIGOMERIZATION; ONCOGENE; PRIORITY JOURNAL; SIGNAL TRANSDUCTION; T LYMPHOCYTE;

EID: 20444401129     PISSN: 00064971     EISSN: None     Source Type: Journal    
DOI: 10.1182/blood-2005-03-1302     Document Type: Article

References (6)

1. Barber KE, Martineau M, Harewood L, et al. Amplification of the ABL gene in T-cell acute lymphoblastic leukemia. Leukemia. 2004;18:1153-1156.
2. Graux C, Cools J, Melotte C, et al. Fusion of NUP214 to ABL1 on amplified episomes in T-cell acute lymphoblastic leukemia. Nat Genet. 2004;36:1084-1089.
3. Smith KM, Yacobi R, Van Etten RA. Autoinhibition of Bcr-Abl through its SH3 domain. Mol Cell. 2003; 12:27-37.
4. Ferrando AA, Neuberg DS, Staunton J, et al. Gene expression signatures define novel oncoganic pathways in T cell acute lymphoblastic leukemia. Cancer Cell. 2002;1:75-37.
5. Gorre ME, Mohammed M, Ellwood K, et al. Clinical resistance to STI-571 cancer therapy caused by BCR-ABL gene mutation or amplification. Science. 2001; 293:876-880.
6. Van Etten RA, Debnath J, Zhou H, Casasnovas JM. Introduction of a loss-of-function point mutation from the SH3 region of the Caenorhabditis elegans sem-5 gene activates the transforming ability of c-abl in vivo and abolishes binding of proline-rich ligands in vitro. Oncogene. 1995;10: 1977-1988.