The BCR-ABL/NF-κB signal transduction network: a long lasting relationship in Philadelphia positive Leukemias

Giovanna Carrà, Davide Torti, Sabrina Crivellaro, Cristina Panuzzo, Riccardo Taulli, Daniela Cilloni, Angelo Guerrasio, Giuseppe Saglio and Alessandro Morotti _

PDF  |  HTML  |  How to cite

Oncotarget. 2016; 7:66287-66298. https://doi.org/10.18632/oncotarget.11507

Metrics: PDF 2146 views  |   HTML 2724 views  |   ?  


Giovanna Carrà1, Davide Torti1, Sabrina Crivellaro1, Cristina Panuzzo1, Riccardo Taulli2, Daniela Cilloni1, Angelo Guerrasio1, Giuseppe Saglio1 and Alessandro Morotti1

1 Department of Clinical and Biological Sciences, University of Turin, Orbassano, Italy

2 Department of Oncology, University of Turin, Orbassano, Italy

Correspondence to:

Alessandro Morotti, email:

Keywords: BCR-ABL; NF-κB; IκB-α; NFKBIA; CML

Received: April 17, 2016 Accepted: August 10, 2016 Published: August 22, 2016


The Nuclear Factor-kappa B (NF-κB) family of transcription factors plays a key role in cancer pathogenesis due to the ability to promote cellular proliferation and survival, to induce resistance to chemotherapy and to mediate invasion and metastasis. NF-κB is recruited through different mechanisms involving either canonical (RelA/p50) or non-canonical pathways (RelB/p50 or RelB/p52), which transduce the signals originated from growth-factors, cytokines, oncogenic stress and DNA damage, bacterial and viral products or other stimuli. The pharmacological inhibition of the NF-κB pathway has clearly been associated with significant clinical activity in different cancers. Almost 20 years ago, NF-κB was described as an essential modulator of BCR-ABL signaling in Chronic Myeloid Leukemia and Philadelphia-positive Acute Lymphoblastic Leukemia. This review summarizes the role of NF-κB in BCR-ABL-mediated leukemogenesis and provides new insights on the long lasting BCR-ABL/NF-κB connection.

Creative Commons License All site content, except where otherwise noted, is licensed under a Creative Commons Attribution 4.0 License.
PII: 11507