LEUKEMIA

Adrienne Gorman

LEUKEMIA

Adrienne Gorman

Cellular & Molecular Medicine

Research output: Chapter in Book or Conference Publication/Proceeding › Conference Publication › peer-review

Abstract

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.

Original language	English (Ireland)
Title of host publication	The repression of apoptosis by activated abl oncogenes in chronic myelogenous leukaemia
Number of pages	5
Volume	10
Publication status	Published - 1 Jun 1996

UN SDGs

This output contributes to the following UN Sustainable Development Goals (SDGs)

SDG 3 Good Health and Well-being

Authors (Note for portal: view the doc link for the full list of authors)

Authors
Fernandes, RS,Gorman, AM,McGahon, A,Lawlor, M,McCann, S,Cotter, TG

Cite this

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title = "LEUKEMIA",

abstract = "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.",

author = "Adrienne Gorman",

year = "1996",

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day = "1",

language = "English (Ireland)",

volume = "10",

booktitle = "The repression of apoptosis by activated abl oncogenes in chronic myelogenous leukaemia",

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TY - GEN

T1 - LEUKEMIA

AU - Gorman, Adrienne

PY - 1996/6/1

Y1 - 1996/6/1

N2 - 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.

AB - 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.

M3 - Conference Publication

VL - 10

BT - The repression of apoptosis by activated abl oncogenes in chronic myelogenous leukaemia

ER -

LEUKEMIA

Abstract

UN SDGs

Authors (Note for portal: view the doc link for the full list of authors)

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