The SIGnaling Network
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Pathway ID: SIGNOR-AML-BCRABL

Description: The t(9;22)(q34;q11) reciprocal translocation (Philadelphia chromosome, Ph) is a molecular hallmark of chronic myeloid leukemia (CML). This translocation produces a protein that results from the fusion of BCR (chr. 22) to ABL1 (chr.9). The resulting chimeric proteins have different molecular weights: p190, associated to B-cell acute lymphoblastic leukemia (ALL), p210 (CML) or p230. The BCR-Abl protein is a constitutively activated tyrosine kinase, that triggers the RAS and Jun-kinase signaling playing a major role in transformation and proliferation. Inhibition of apoptosis is thought to result from the activation of the PI-3 kinase/AKT and RAS pathways, with induction of c-myc and BCL-2. BCR/ABL affects the JAK/ STAT signaling, which is constitutively active in BCR/ABL-positive cell lines and in primary cells from CML patients, probably contributing to the induction of cytokine independence.

Curated by: irozzo