B3/A3 rearrangement in a patient with chronic myeloid leukemia.
The role of BCR/ABL isoforms and their relationships to leukemia phenotype are discussed continuously because of the variety of information reported. Here we describe a man with CML an atypical b3/a3 rearrangement, who had a good response to INFalpha treatment. This may be due to a deletion of the ABL exon 2 sequences, which are an essential part of the ABL SH3 domain inducing STAT5 expression, which is indeed crucial for the BCR/ABL leukemogenesis; because of its role in anti-apoptotic activity and cell cycle progress.
Paz-Y-Miño
César
C
Arévalo
Melissa
M
Leone
Paola E
PE
D000368:Aged; D005091:Exons; D016044:Fusion Proteins, bcr-abl / Q000235:genetics*; D015321:Gene Rearrangement; D006801:Humans; D016898:Interferon-alpha / Q000627:therapeutic use; D015464:Leukemia, Myelogenous, Chronic, BCR-ABL Positive / Q000235:genetics*; D008297:Male; D020033:Protein Isoforms / Q000235:genetics; D017384:Sequence Deletion
D016898:Interferon-alpha; D020033:Protein Isoforms; D016044:Fusion Proteins, bcr-abl