Angiogenesis inhibitors in gastric and gastroesophageal junction cancer

Giandomenico Roviello1, Roberto Petrioli2, Luigi Marano3

  • 1Medical Oncology Unit, University of Siena, Viale Bracci 11, 53100, Siena, Italy. giandomenicoroviello@hotmail.it.

Insights

Advanced gastric cancer prognosis remains poor despite chemotherapy. This review focuses on anti-angiogenic agents, highlighting the need for targeted therapies based on tumor molecular heterogeneity.

Area of Science:

  • Oncology
  • Gastroenterology
  • Pharmacology

Background:

  • Prognosis for advanced gastric and gastroesophageal junction adenocarcinoma remains poor despite chemotherapy advancements.
  • Tumor molecular heterogeneity necessitates classification by oncogenic pathways for targeted therapy development.
  • Limited clinical success of molecularly targeted agents in gastric cancer.

Purpose of the Study:

  • To review available data on anti-angiogenic agents for advanced or metastatic gastric cancer.
  • To discuss the potential of targeted therapies in managing gastric cancer.
  • To highlight the importance of understanding molecular drivers in gastric cancer treatment.

Main Methods:

  • Literature review of clinical studies and research on anti-angiogenic agents in advanced gastric cancer.
  • Analysis of data regarding efficacy and safety of targeted therapies.
  • Synthesis of current knowledge on molecular pathways in gastric adenocarcinoma.

Main Results:

  • Anti-angiogenic agents represent a key area of research for advanced gastric cancer.
  • Despite research, few targeted agents are currently clinically applicable.
  • Molecular classification is crucial for future therapeutic strategies.

Conclusions:

  • Targeted therapies, particularly anti-angiogenic agents, hold promise for improving outcomes in advanced gastric cancer.
  • Further research is needed to overcome challenges in clinical application.
  • Personalized medicine approaches are essential for treating this heterogeneous disease.

Related Concept Videos

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...
9.1K
Targeted Cancer Therapies02:57

Targeted Cancer Therapies

1.8K
Regulation of Angiogenesis and Blood Supply01:24

Regulation of Angiogenesis and Blood Supply

Rapidly dividing tumors, embryos, and wounded tissues require more oxygen than usual, lowering the oxygen concentration in the blood. At low oxygen or hypoxic conditions, an oxygen-sensitive transcription factor called the hypoxia-inducible factor 1 or HIF1 is activated. HIF1 is a dimeric protein of alpha (ɑ) and beta (β) subunits.  Under optimal oxygen conditions, HIF1β is present in the nucleus while HIF1ɑ remains in the cytosol. HIF1ɑ is hydroxylated by prolyl...
4.0K
Mechanism of Angiogenesis01:10

Mechanism of Angiogenesis

Blood vessel formation starts early during embryonic development, around day 7. In the extraembryonic yolk sac, mesodermal precursor cells called hemangioblast proliferate and differentiate into angioblast. Angioblasts express vascular endothelial growth factor receptor 2 or VEGFR2, which binds VEGF-A, a proangiogenic factor, guiding blood vessel formation. VEGF signaling promotes angioblasts to form a blood island in the developing embryo. Angioblasts further differentiate, giving rise to...
7.7K
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...
1.6K
Esophageal Varices-I: Introduction01:24

Esophageal Varices-I: Introduction

Esophageal varices are dilated, tortuous veins which are found mainly in the submucosa of the lower esophagus but which may also appear higher up or extend into the stomach. They develop due to increased pressure in the portal venous system, often as a result of liver cirrhosis. This condition scars and damages the liver, impeding normal blood flow through the portal vein. To compensate, blood seeks alternative pathways, forming fragile new vessels (varices) in the esophagus and stomach. These...
2.1K