期刊
BLOOD REVIEWS
卷 31, 期 2, 页码 77-92出版社
CHURCHILL LIVINGSTONE
DOI: 10.1016/j.blre.2016.10.001
关键词
NF-kappa B pathway; B-cell lymphoma; Apoptosis; MiRNA; Tumor microenvironment; EBV
类别
资金
- National Cancer Institute/National Institutes of Health [R01CA138688, 1RC1CA146299, P50CA136411, P50CA142509]
- hematology/oncology scholarship award
- University of Texas MD Anderson Cancer Center Lymphoma Moonshot Program
- Institutional Research and Development Fund
- Institutional Research Grant Award
- MD Anderson Cancer Center Lymphoma Specialized Programs on Research Excellence (SPORE) Research Development Program Award
- MD Anderson Cancer Center Myeloma SPORE Research Development Program Award
- Gunderson Lutheran Medical Foundation Award
- MD Anderson's Cancer Center Support Grant [CA016672]
- University Cancer Foundation via the Sister Institution Network Fund at The University of Texas MD Anderson Cancer Center
The NF-kappa B pathway, a critical regulator of apoptosis, plays a key role in many normal cellular functions. Genetic alterations and other mechanisms leading to constitutive activation of the NF-kappa B pathway contribute to cancer development, progression and therapy resistance by activation of downstream anti-apoptotic pathways, unfavorable microenvironment interactions, and gene dysregulation. Not surprisingly, given its importance to normal and cancer cell function, the NF-kappa B pathway has emerged as a target for therapy. In the review, we present the physiologic role of the NF-kappa B pathway and recent advances in better understanding of the pathologic roles of the NF-kappa B pathway in major types of lymphoid neoplasms. We also provide an update of clinical trials that use NF-kappa B pathway inhibitors. These trials are exploring the clinical efficiency of combining NF-kappa B pathway inhibitors with various agents that target diverse mechanisms of action with the goal being to optimize novel therapeutic opportunities for targeting oncogenic pathways to eradicate cancer cells. (C) 2016 Elsevier Ltd. All rights reserved.
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