Related Experiment Video

Updated: Aug 11, 2026

Sample Extraction and Simultaneous Chromatographic Quantitation of Doxorubicin and Mitomycin C Following Drug Combination Delivery in Nanoparticles to Tumor-bearing Mice
08:57

Sample Extraction and Simultaneous Chromatographic Quantitation of Doxorubicin and Mitomycin C Following Drug Combination Delivery in Nanoparticles to Tumor-bearing Mice

Published on: October 5, 2017

[Cyclooxygenase 2 inhibitors and urologic and gynaecologic cancers]

Pascal Eschwege1

  • 1Service d'Urologie, Hôpital Bicêtre, Faculté de Médecine Paris-Sud Département de Chirurgie, Institut Gustave-Roussy, avenue Camille-Desmoulins, 94805 Villejuif.

Bulletin Du Cancer
|July 9, 2004
PubMed

Insights

Prostaglandin E2 (PGE2), elevated in epithelial cancers, is produced by cyclooxygenase 2 (Cox2). Cox2 inhibitors show anticancer effects, with clinical trials ongoing for bladder, prostate, and uterine cancers.

Area of Science:

  • Biochemistry
  • Oncology
  • Pharmacology

Context:

  • Prostaglandin E2 (PGE2) is a key mediator in oncogenesis.
  • Elevated PGE2 levels are observed in various epithelial cancers.
  • Cyclooxygenase 2 (Cox2) is the enzyme responsible for PGE2 synthesis in urologic and gynecologic cancers.

Purpose:

  • To investigate the role of PGE2 and Cox2 in cancer development.
  • To explore the potential of Cox2 inhibitors as anticancer agents.

Summary:

  • PGE2 is significantly implicated in the development of cancer.
  • High concentrations of PGE2 are prevalent in most epithelial cancers.
  • The enzyme cyclooxygenase 2 (Cox2), responsible for PGE2 production, is expressed in urologic and gynecologic cancers.
  • Cox2 inhibitors have demonstrated anticancer properties in preclinical studies.
  • Clinical trials are evaluating Cox2 inhibitors for bladder, prostate, and uterine carcinomas.

Impact:

  • Cox2 inhibitors represent a promising therapeutic strategy for epithelial cancers.
  • Further research and clinical trials are warranted to establish the efficacy of Cox2 inhibitors in human cancer treatment.

More Related Videos

Analysis of Combinatorial miRNA Treatments to Regulate Cell Cycle and Angiogenesis11:44

Analysis of Combinatorial miRNA Treatments to Regulate Cell Cycle and Angiogenesis

Published on: March 30, 2019

Structure-Guided Design and Development of Novel Cyclophilin A Inhibitors and Ganoderiol-F Derivatives: An In-Silico Approach10:01

Structure-Guided Design and Development of Novel Cyclophilin A Inhibitors and Ganoderiol-F Derivatives: An In-Silico Approach

Published on: June 23, 2026

Related Concept Videos

Cancer Therapies02:49

Cancer Therapies

Cancer therapies are various modes of treatment, such as surgery, radiation therapy, and chemotherapy that are administered to cancer patients.
However, cancer treatments can pose several challenges, as therapies used to kill cancer cells are generally also toxic to normal cells. Moreover, cancer cells mutate rapidly and can develop resistance to chemical agents or radiation therapy. Besides, all types of cancer cells may not respond to the same therapy. Some cancer cells respond to one...
Targeted Cancer Therapies02:57

Targeted Cancer Therapies

The targeted cancer therapies, also known as “molecular targeted therapies,” take advantage of the molecular and genetic differences between the cancer cells and the normal cells. It needs a thorough understanding of the cancer cells to develop drugs that can target specific molecular aspects that drive the growth, progression, and spread of cancer cells without affecting the growth and survival of other normal cells in the body.
There are several types of targeted therapies against specific...
Targeted Cancer Therapies02:57

Targeted Cancer Therapies

The targeted cancer therapies, also known as “molecular targeted therapies,” take advantage of the molecular and genetic differences between the cancer cells and the normal cells. It needs a thorough understanding of the cancer cells to develop drugs that can target specific molecular aspects that drive the growth, progression, and spread of cancer cells without affecting the growth and survival of other normal cells in the body.
There are several types of targeted therapies against specific...
Antiplatelet Drugs: Prostaglandin Synthesis, P2Y12 and Glycoprotein IIb/IIIa Inhibitors01:20

Antiplatelet Drugs: Prostaglandin Synthesis, P2Y12 and Glycoprotein IIb/IIIa Inhibitors

Antiplatelet drugs emerge as frontline defenders against the insidious threat of thromboembolic diseases, where abnormal clots obstruct vital blood vessels. These drugs stand as bulwarks, inhibiting platelet aggregation and clot formation, thereby mitigating the risk of life-threatening conditions like myocardial infarction, coronary artery disease, and thrombotic strokes.
Prostaglandin synthesis inhibitors, exemplified by the widely known aspirin, wield their power by irreversibly acetylating...
Treatment for Pulmonary Arterial Hypertension: Prostacyclin Receptor Agonists01:23

Treatment for Pulmonary Arterial Hypertension: Prostacyclin Receptor Agonists

Prostacyclin receptor agonists are a class of therapeutic agents integral to managing pulmonary arterial hypertension (PAH). These drugs operate by mimicking the action of prostaglandin I2, or PGI2, a naturally occurring compound in the body.
These agonists bind to the IPR receptor situated on the plasma membrane of the pulmonary artery smooth muscle cells. This binding triggers a cascade of reactions known as the GS-AC-cAMP-PKA pathway. This pathway results in the relaxation of smooth muscle...
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...