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Critical Reviews™ in Oncogenesis

Publicado 4 números por año

ISSN Imprimir: 0893-9675

ISSN En Línea: 2162-6448

SJR: 0.395 SNIP: 0.322 CiteScore™:: 2.5 H-Index: 54

Indexed in

Nuclear Factor-κB Signaling: A Contributor in Leukemogenesis and a Target for Pharmacological Intervention in Human Acute Myelogenous Leukemia

Volumen 15, Edición 1-2, 2009, pp. 1-41
DOI: 10.1615/CritRevOncog.v15.i1-2.10
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SINOPSIS

Acute myeloid leukemia (AML) is an aggressive malignancy with only 40%-50% long-term survival even for younger patients who can receive the most aggressive therapy. For elderly patients who only receive palliative treatment, the median survival is only 2-3 months. Inhibition of the nuclear factor-κB (NF-κB) transcription factor family is one of the therapeutic strategies that are considered in AML. NF-κB is an important regulator of several biological processes that are involved in leukemogenesis, including proliferation, differentiation, autophagy, and apoptosis. Constitutive NF-κB activation has been detected in AML cells and NF-κB inhibition is therefore a possible therapeutic strategy in AML. Multiple pharmacological agents have shown inhibitory effects against NF-κB signaling pathways, including proteasome inhibitors as well as the more-specific agents that are directed against various steps of this signaling pathway. Recent studies strongly suggest that primary human AML cells (including AML stem cells) are susceptible to NF-κB inhibition, but this therapeutic approach should possibly be combined with other therapeutic agents to achieve a combined effect both on NF-κB transcriptional activity, tumor suppressor-induced signaling, and stress-induced pathways. The clinical documentation with regard to the efficiency and safety of NF-κB inhibition is still limited, but experimental evidence strongly suggests that NF-κB inhibition should be further investigated in human AML.

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