Identification of molecular variants of p210bcr-abl in chronic myelogenous leukemia. Blood 1987 Jul;70(1):233-6
Date
07/01/1987Pubmed ID
2885048DOI
10.1182/blood.v70.1.233.bloodjournal701233Scopus ID
2-s2.0-0023234119 (requires institutional sign-in at Scopus site) 56 CitationsAbstract
The aberrant abl protein product of a chronic myelogenous leukemia (CML) blast crisis cell line (K562) and of five Philadelphia chromosome-positive CML patients in blast crisis were analyzed by an immune complex kinase assay using two antipeptide sera generated against the hydrophilic domain of v-abl and a region within the third exon of the breakpoint cluster region (bcr) respectively. Both the anti-abl and anti-bcr sera detected a 210 kd band in extracts derived from K562 cells and from two CML patients with myeloid blast crisis. p210 was detected by the anti-abl but not the anti-bcr sera in three CML patients with myeloid (one patient) and lymphoid (two patients) blast crisis, indicating the absence of bcr exon 3 in this protein. Southern blot analysis on DNA derived from one of the patients in the latter group was consistent with the break on chromosome 22 occurring 5' to bcr exon 3. Our observations demonstrate that the Philadelphia translocation results in the generation of a chimeric bcr-abl protein with at least two molecular variants, both of which are enzymatically active as protein kinases.
Author List
Kurzrock R, Kloetzer WS, Talpaz M, Blick M, Walters R, Arlinghaus RB, Gutterman JUAuthor
Razelle Kurzrock MD Center Associate Director, Professor in the Medicine department at Medical College of WisconsinMESH terms used to index this publication - Major topics in bold
Blast CrisisCell Line
Chimera
Collodion
Electrophoresis, Polyacrylamide Gel
Exons
Humans
Leukemia, Experimental
Leukemia, Myeloid
Oncogenes
Philadelphia Chromosome
Polymorphism, Restriction Fragment Length
Protein Kinases
Translocation, Genetic