Non-steroidal anti-inflammatory drugs and melanoma.

Curr Pharm Des

Dermatology Department, Hospital Universitario 12 de Octubre, Avenida de Córdoba s/n. 28026, Madrid, Spain.

Published: January 2013

AI Article Synopsis

  • Inflammation plays a key role in the development and progression of all cancers, fueled by inflammatory lipid metabolites like prostaglandins formed from arachidonic acid.
  • COX inhibitors, including NSAIDs, not only help reduce tumor growth but also alter gene expression independently, enhancing their anti-tumor effects.
  • Current research focuses on understanding the inflammatory mechanisms in malignant melanoma, which could lead to new therapeutic targets for this aggressive skin cancer.

Article Abstract

Inflammation is an important contributor to the development and progression of all human cancers. Inflammatory lipid metabolites, prostaglandins, formed from arachidonic acid by prostaglandin H synthases commonly called cyclooxygenases (COXs), bind to specific receptors that activate signaling pathways driving to the development and progression of tumors. Inhibitors of prostaglandin formation, COX inhibitors, including non-steroidal anti-inflammatory drugs (NSAIDs), are well documented agents that inhibit tumor growth and prevent tumor development specially due to long-term use. NSAIDs also alter gene expression independently of COX inhibition which also appear to contribute to the anti-tumorigenic activity of these drugs. In a dermatologic point of view, most investigations are oriented to improve the current knowledge related to the pathogenesis of malignant melanoma, a prevalent skin cancer characterized by a rapid progression with frequent metastases and a poor response to the different available treatments. In the present issue we review the role of inflammation in cutaneous malignant melanoma and its impact on cancer pathogenesis. This topic represents an exciting new area of research, and could potentially result in new targets for melanoma therapy in the future.

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Source
http://dx.doi.org/10.2174/138161212802083680DOI Listing

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