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