Promising molecular targets in ovarian cancer

Curr Opin Oncol. 2009 Sep;21(5):412-9. doi: 10.1097/CCO.0b013e32832eab1f.

Abstract

Purpose of review: Clinically and on a molecular level, ovarian cancer is a unique and complex disease. The explosion in potential molecular targets over the last decade has led to the arrival of many novel therapies into oncology. In the present article, we review the most promising of these agents in ovarian cancer.

Recent findings: Targeted therapies, such as epidermal growth factor receptor inhibitors, that have worked well in other cancers have shown only moderate success in ovarian cancer, whereas other treatment approaches have yielded surprisingly positive outcomes. An example is anti-vascular endothelial growth factor and proapoptotic strategies, which are effective in both primary and relapsed ovarian cancer. Use of poly (ADP-ribose)-polymerase inhibitors has shown that targeting one form of DNA repair profoundly affects cell survival in those with a hereditary failure to mend DNA damage using another mechanism. This can be extrapolated to patients with sporadic ovarian cancers, with or without the 'BRCAness' phenotype.

Summary: Using targeted agents in ovarian cancer, we are discovering not only how these novel therapies work but are also unveiling the complex 'wiring' of the disease itself, and the interconnections between what were previously believed to be distinct molecular pathways. The addition of targeted agents to our therapeutic armoury is likely to significantly and positively impact on patient survival.

Publication types

  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Antineoplastic Agents / therapeutic use*
  • Female
  • Humans
  • Ovarian Neoplasms / drug therapy*
  • Ovarian Neoplasms / metabolism
  • Ovarian Neoplasms / pathology
  • Phosphatidylinositol 3-Kinases / metabolism
  • Poly(ADP-ribose) Polymerase Inhibitors*
  • Poly(ADP-ribose) Polymerases / metabolism
  • Protein Kinases / metabolism
  • Proto-Oncogene Proteins c-akt / metabolism
  • Signal Transduction / drug effects
  • TOR Serine-Threonine Kinases
  • Vascular Endothelial Growth Factor A / antagonists & inhibitors*
  • Vascular Endothelial Growth Factor A / metabolism

Substances

  • Antineoplastic Agents
  • Poly(ADP-ribose) Polymerase Inhibitors
  • Vascular Endothelial Growth Factor A
  • Poly(ADP-ribose) Polymerases
  • Protein Kinases
  • MTOR protein, human
  • Proto-Oncogene Proteins c-akt
  • TOR Serine-Threonine Kinases