Curbing tumorigenesis and malignant progression through the pharmacological control of the wound healing process.

Abstract

The prevention of cancer development and its progression is an urgent unmet medical need. Novel knowledge on the biology of cancer has evidenced that genetic changes occurring within cancer cells contribute, but are not sufficient, for tumor promotion and progression. The results of clinical studies and experimental animal models have suggested pursuing new avenues for the prevention of cancer development in the early stages, by using drugs that modulate platelet responses and those interfering with the synthesis and action of the mediators of inflammation. In fact, malignant tumors often develop at sites of chronic injury associated with platelet activation and chronic inflammation. In this review, we cover the evidence supporting this hypothesis and the rationale for the pharmacological treatment with antiplatelet agents, including low-dose aspirin, and antiinflammatory drugs to curb tumorigenesis and malignant progression. The evidence for a chemopreventive effect of low-dose aspirin against colorectal cancer (CRC) has been recently found appropriate by the U.S. Preventive Services Task Force, which recommends the use of the drug for primary prevention of cardiovascular disease and CRC.

• Authors: Melania Dovizio, Angela Sacco, Paola Patrignani
• Journal: Vascular pharmacology (Vascul Pharmacol) Vol. 89 Pg. 1-11 (02 2017) ISSN: 1879-3649 [Electronic] United States
• PMID: 28089842 (Publication Type: Journal Article, Review, Research Support, Non-U.S. Gov't)
• Copyright: Copyright © 2017 Elsevier Inc. All rights reserved.

Chemical References

• Anti-Inflammatory Agents
• Anticarcinogenic Agents
• Platelet Aggregation Inhibitors

Topics

• Animals
• Anti-Inflammatory Agents (therapeutic use)
• Anticarcinogenic Agents (therapeutic use)
• Carcinogenesis (drug effects, metabolism, pathology)
• Cell Transformation, Neoplastic (drug effects, metabolism, pathology)
• Colorectal Neoplasms (blood, etiology, pathology, prevention & control)
• Humans
• Inflammation (blood, complications, drug therapy, pathology)
• Platelet Activation (drug effects)
• Platelet Aggregation Inhibitors (therapeutic use)
• Risk Factors
• Signal Transduction (drug effects)
• Stromal Cells (drug effects, metabolism, pathology)
• Tumor Microenvironment
• Wound Healing (drug effects)