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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

Immunology Comes Full Circle in Melanoma While Specific Immunity Is Unleashed to Eliminate Metastatic Disease, Inflammatory Products of Innate Immunity Promote Resistance

Volumen 21, Edición 1-2, 2016, pp. 57-63
DOI: 10.1615/CritRevOncog.2016016901
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SINOPSIS

Melanoma and many other cancers often express cells and molecular features of inflammation. Intrinsic to melanoma is the expression of a continuous cycle of cytokines and oxidative stress markers. The oxidative stress of inflammation is proposed to drive a metastatic process, not only of DNA adducts and crosslinks, but also of posttranslational oxidative modifications to lipids and proteins that we argue support growth and survival. Fortunately, numerous antioxidant agents are available clinically and we further propose that the pharmacological attenuation of these inflammatory processes, particularly the reactive nitrogen species, will restore the cancer cells to an apoptosis-permissive and growth-inhibitory state. Experimental model data using a small-molecule arginine antagonist that prevents enzymatic production of nitric oxide supports this view directly. I propose that the recognition, measurement, and regulation of such carcinogenic inflammation be considered as part of the approach to the treatment of cancer.

PALABRAS CLAVE: nitric oxide, cytokines, MIF, CD74, iNOS
CITADO POR
  1. Surcel Mihaela, Constantin Carolina, Caruntu Constantin, Zurac Sabina, Neagu Monica, Inflammatory Cytokine Pattern Is Sex-Dependent in Mouse Cutaneous Melanoma Experimental Model, Journal of Immunology Research, 2017, 2017. Crossref

  2. Terzuoli Erika, Bellan Cristiana, Aversa Sara, Ciccone Valerio, Morbidelli Lucia, Giachetti Antonio, Donnini Sandra, Ziche Marina, ALDH3A1 Overexpression in Melanoma and Lung Tumors Drives Cancer Stem Cell Expansion, Impairing Immune Surveillance through Enhanced PD-L1 Output, Cancers, 11, 12, 2019. Crossref

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