Related Experiment Video

Updated: Mar 24, 2026

Synthesis and Characterization of an Aspirin-fumarate Prodrug that Inhibits NFκB Activity and Breast Cancer Stem Cells
13:38

Synthesis and Characterization of an Aspirin-fumarate Prodrug that Inhibits NFκB Activity and Breast Cancer Stem Cells

Published on: January 18, 2017

12.8K

Mechanisms of nonsteroidal anti-inflammatory drugs in cancer prevention

Asad Umar1, Vernon E Steele1, David G Menter2

  • 1Division of Cancer Prevention, National Cancer Institute, National Institutes of Health, Bethesda, MD, USA.

Seminars in Oncology
|March 13, 2016
PubMed

Insights

Nonsteroidal anti-inflammatory drugs (NSAIDs) like aspirin and COXIBs show promise in cancer prevention by targeting eicosanoid metabolism. Emerging research suggests these drugs may involve additional molecular targets, expanding our understanding of their anti-cancer mechanisms.

Area of Science:

  • Oncology
  • Pharmacology
  • Molecular Biology

Background:

  • Clinical and epidemiologic studies indicate nonsteroidal anti-inflammatory drugs (NSAIDs) possess cancer-preventive properties.
  • Established mechanisms involve the inhibition of eicosanoid metabolism by NSAIDs, including aspirin and cyclooxygenase inhibitors (COXIBs).

Purpose of the Study:

  • To review recent advancements and emerging molecular targets associated with NSAID-mediated cancer prevention.
  • To synthesize current knowledge on the broader biological impact of NSAIDs beyond eicosanoid pathways.

Main Methods:

  • Literature review of recent clinical, epidemiologic, and molecular studies.
  • Analysis of emerging research on novel drug targets and biological pathways.
  • Synthesis of findings to provide a comprehensive overview.

Main Results:

  • NSAIDs, such as aspirin and COXIBs, are linked to cancer prevention.
  • Eicosanoid metabolism is a primary target, but additional molecular targets are increasingly recognized.
  • New research highlights expanded mechanisms of action for NSAIDs in cancer prevention.

Conclusions:

  • The role of NSAIDs in cancer prevention extends beyond their known effects on eicosanoid metabolism.
  • Further investigation into novel molecular targets may reveal new therapeutic strategies.
  • Understanding these expanded mechanisms is crucial for optimizing NSAID use in oncology.
Keywords:
AspirinCancer preventionInflammationNon-steroidal anti-inflammatory drugs (NSAID)

More Related Videos

Using Mouse Mammary Tumor Cells to Teach Core Biology Concepts: A Simple Lab Module10:39

Using Mouse Mammary Tumor Cells to Teach Core Biology Concepts: A Simple Lab Module

Published on: June 18, 2015

13.9K
Author Spotlight: Exploring Salidroside's Molecular Mechanisms in Breast Cancer Treatment11:13

Author Spotlight: Exploring Salidroside's Molecular Mechanisms in Breast Cancer Treatment

Published on: June 9, 2023

2.5K

Related Concept Videos

Cancer Prevention02:59

Cancer Prevention

Several factors can increase the risk of cancer in an individual. About 50% of cancer cases can be prevented by adopting a healthy lifestyle, regular exercise, eating healthy, and following a modest cancer prevention diet. Epidemiological studies have consistently shown that populations with vegetable and fruit-rich diets have reduced the incidence of cancer. On the other hand, populations who have a diet rich in animal fat, red meat, junk food, or high calories are predisposed to cancer.
Some...
8.7K
Cancer Prevention02:59

Cancer Prevention

3.0K
Drugs for Peptic Ulcer Disease: Prostaglandin Analogs as Mucosal Protective Agents01:20

Drugs for Peptic Ulcer Disease: Prostaglandin Analogs as Mucosal Protective Agents

The gastric mucosa produces prostaglandins E2 (PGE2) and prostacyclin (PGI2), crucial in maintaining gastric health. They exert cytoprotective effects, including increasing bicarbonate secretion, releasing protective mucin, reducing gastric acid output, and preventing harmful vasoconstriction. These effects are mediated through various receptors, such as EP1, EP2, EP3, and EP4.
Non-steroidal anti-inflammatory drugs (NSAIDs) can induce peptic ulcers by inhibiting cyclooxygenase, decreasing...
1.5K
Inhibition of Cdk Activity02:34

Inhibition of Cdk Activity

The orderly progression of the cell cycle depends on the activation of Cdk protein by binding to its cyclin partner. However, the cell cycle must be restricted when undergoing abnormal changes. Most cancers correlate to the deregulated cell cycle, and since Cdks are a central component of the cell cycle, Cdk inhibitors are extensively studied to develop anticancer agents. For instance, cyclin D associates with several Cdks, such as Cdk 4/6, to form an active complex. The cyclin D-Cdk4/6 complex...
6.2K
Chemotherapy-Induced Nausea and Vomiting: Neurokinin-1 Receptor Antagonists01:28

Chemotherapy-Induced Nausea and Vomiting: Neurokinin-1 Receptor Antagonists

Neurokinin 1 (NK1) receptors are distributed across the GI tract, vagal afferents, and key CNS regions including the central vomiting center and chemoreceptor trigger zone (CTZ) Chemotherapy agents stimulate enterochromaffin cells in the gastrointestinal (GI) tract to release large amounts of substance P (SP). SP is a neuropeptide released by specific sensory nerves in response to many different stressors, including those in the GI mucosa affected by chemotherapy.  SP binds and activates...
735
Adaptive Mechanisms in Cancer Cells02:53

Adaptive Mechanisms in Cancer Cells

4.2K