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ABL proteins in Philadelphia‐positive acute leukaemias and chronic myelogenous leukaemia blast crises
Author(s) -
Ponzetto Carola,
Guerrasio Angelo,
Rosso Claudia,
Avanzi Giancarlo,
Tassinari Angela,
Zaccaria Alfonso,
LoCoco Francesco,
Foa Robin,
Basso Giuseppe,
Abate Maria Lorena,
Comoglio Paolo M.,
Saglio Giuseppe
Publication year - 1990
Publication title -
british journal of haematology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.907
H-Index - 186
eISSN - 1365-2141
pISSN - 0007-1048
DOI - 10.1111/j.1365-2141.1990.tb07834.x
Subject(s) - philadelphia chromosome , chromosomal translocation , chronic myelogenous leukemia , abl , cancer research , breakpoint cluster region , acute myeloblastic leukemia , biology , gene rearrangement , leukemia , microbiology and biotechnology , immunology , gene , genetics , receptor , tyrosine kinase
S ummary . The Philadelphia chromosome (Ph 1 ) is present in 95% of chronic myelogenous leukaemias (CML) and 15% of acute lymphoblastic leukaemias (ALL). This cytogenetic marker is due to a t(9;22) translocation, which causes a rearrangement of the ABL oncogene. In order to better define the relationship between type of genomic rearrangement, variant ABL protein expressed and haematological phenotype, a series of Ph l ‐positive acute leukaemias, both myeloblastic (AML) and lymphoblastic, and several CML lymphoid blast crises have been analysed at the DNA and protein level. The results confirm the presence of the ABL protein P210 in all cases of CML, ALL and AML positive for rearrangement in the bcr region of chromosome 22, and, surprisingly, in one AML case apparently negative for bcr rearrangement. The ABL protein P190 was found to be present only in cases of ALL negative for bcr rearrangement. Polymerase chain reaction (PCR) analysis of the types of 9/22 junctions present in the mRNA of CML lymphoid blast crises showed no evidence of‘ALL‐type’transcripts.