Conference Publication Details
Mandatory Fields
Fernandes, RS,Gorman, AM,McGahon, A,Lawlor, M,McCann, S,Cotter, TG
The repression of apoptosis by activated abl oncogenes in chronic myelogenous leukaemia
LEUKEMIA
1996
June
Published
1
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Optional Fields
apoptosis abl leukaemia oncogenes CHRONIC MYELOID-LEUKEMIA CELL-DEATH C-MYC TYROSINE KINASE GENE PROTEIN RECOGNITION SUPPRESSION EXPRESSION RESISTANCE
17
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The formation of the unique fusion gene, bcr-abl, and the resultant increase in abl tyrosine kinase activity, is seen as the major driving force in the initiation of chronic myelogenous leukaemia (CML). The deregulation of abl tyrosine kinase activity, brought about by the binding of a portion of the Bcr molecule to the SH2 regulatory domain of abl, appears to play a role in promoting resistance to drug-induced apoptosis. Thus the large increase in mature myeloid cells seen in CML could be the direct result of the suppression of apoptosis by the bcr-abl fusion protein. The role and contribution of apoptosis in the progression of CML and the possible role of antisense oligonucleotides to the bcr-abl gene as therapeutic agents is discussed.
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