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Published on: September 12, 2019

Molecular target therapies in endometrial cancer: from the basic research to the clinic

Angiolo Gadducci1, Roberta Tana, Stefania Cosio

  • 1Department of Procreative Medicine, Division of Gynecology and Obstetrics, University of Pisa, Pisa, Italy. a.gadducci@obgyn.med.unipi.it

Gynecological Endocrinology : the Official Journal of the International Society of Gynecological Endocrinology
|June 24, 2008
PubMed

Insights

Molecular targeted therapies show promise for endometrial cancer. Targeting the PI3K-AKT-mTOR pathway in endometrioid carcinomas and ErbB-2 in uterine papillary serous carcinomas offers new treatment avenues.

Area of Science:

  • Oncology
  • Pharmacology
  • Molecular Biology

Background:

  • Endometrial cancer, particularly endometrioid-type and uterine papillary serous carcinoma (UPSC), presents therapeutic challenges.
  • Dysregulation of signaling pathways like PI3K-AKT-mTOR (due to PTEN loss) and overexpression of ErbB-2 are common in these subtypes.
  • Existing treatments have limitations, necessitating novel therapeutic strategies.

Purpose of the Study:

  • To explore the potential of molecular targeted therapies for endometrial cancer.
  • To investigate the role of mTOR inhibition in endometrioid-type endometrial carcinomas.
  • To evaluate ErbB-2 as a target in UPSC and explore novel CPE-mediated therapies.

Main Methods:

  • Review of existing research on molecular targeted therapies in endometrial cancer.
  • Analysis of signaling pathway dysregulation (PTEN/PI3K/AKT/mTOR) in endometrioid carcinomas.
  • Examination of ErbB-2 and claudin-3/4 expression in UPSC and potential therapeutic targets.

Main Results:

  • mTOR inhibitors (e.g., AP-23573, CCI-799) have shown clinical benefit and response rates in endometrioid-type endometrial carcinoma.
  • ErbB-2 overexpression in UPSC supports the use of targeted agents like trastuzumab.
  • Claudin-3/4 overexpression in UPSC suggests potential for Clostridium perfringens enterotoxin (CPE)-mediated therapy.

Conclusions:

  • Targeting the PI3K-AKT-mTOR pathway is a viable strategy for endometrioid-type endometrial carcinoma.
  • ErbB-2 and CPE-mediated therapies represent promising avenues for UPSC treatment.
  • Further understanding of dysregulated pathways will drive the development of novel molecular targeted therapies for endometrial cancer.

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