Abstract
The demonstration of the BCR-ABL fusion gene in patients with chronic granulocytic leukaemia and t(9;22)(q34;q11) represents the first recognition, in a human neoplasm, of a translocation leading to formation of an oncogenic fusion gene. Since this initial observation, this leukaemogenic mechanism has been increasingly recognized in chronic myeloid leukaemias. The fusion gene has often incorporated part of a gene encoding a receptor or cytoplasmic tyrosine kinase, particularly ABL, PDGFRB and FGFR1. This contrasts with the frequent involvement of genes encoding transcription factors or other nuclear proteins in acute myeloid leukaemia. Nevertheless, genes encoding tyrosine kinases have also been implicated in some cases of acute leukaemia. With the exception of the BCR-ABL fusion gene in chronic granulocytic leukaemia, all these fusion genes are uncommon or rare among cases of chronic myeloid leukaemia. The molecular mechanisms underlying the great majority of cases of Philadelphia-negative chronic myeloid leukaemia remain to be discovered.
Citations
Jun 28, 2005·Leukemia Research·Maria Cristina RapanottiGiulio De Rossi
Aug 30, 2008·Leukemia·J T Reilly
Jul 7, 2007·Leukemia & Lymphoma·Sook Young BaeIn Keun Choi
Dec 3, 2005·Leukemia & Lymphoma·Angela DispenzieriThomas E Witzig
May 27, 2004·Expert Review of Anticancer Therapy·Francesco Piazza, Gianpietro Semenzato
Dec 3, 2011·Blood Cells, Molecules & Diseases·Douglas VivonaElvira M Guerra-Shinohara
Jul 9, 2003·British Journal of Haematology·Barbara J Bain
May 6, 2016·Expert Opinion on Drug Metabolism & Toxicology·Gloria RavegniniPatrizia Hrelia
Dec 14, 2011·Acta Haematologica·Aylin Canbolat AyhanMuferet Erguven
Aug 12, 2003·Cancer·Rosemarie E SchmandtDavid M Gershenson
Apr 9, 2004·Blood·Jason GotlibSteven E Coutré
Nov 25, 2003·Blood·Jan CoolsD Gary Gilliland
Jul 17, 2009·American Journal of Clinical Pathology·Juergen Thiele