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An Orthotopic Endometrial Cancer Model with Retroperitoneal Lymphadenopathy Made From In Vivo Propagated and Cultured VX2 Cells
Published on: September 12, 2019
The molecular biology of endometrial cancers and the implications for pathogenesis, classification, and targeted
Nisha Bansal1, Vimala Yendluri, Robert M Wenham
1Gynecologic Oncology Program, H. Lee Moffitt Cancer Center & Research Institute, Tampa, FL 33612, USA.
Background:
Understanding and identifying molecular biology and genetics of endometrial cancer are central to the development of novel therapies. This article reviews the molecular basis for genesis of endometrial cancer with regard to pathogenesis, classification, and implications for targeted therapies.
Methods:
Genes and cellular pathways that may have an important role in endometrial cancers, both endometrioid and nonendometrioid cancers, are identified. Recently studied drugs and potential future drugs that target some of these genes and pathways are reviewed.
Results:
The most frequent genetic alteration of endometrioid endometrial cancer is PTEN. PI3CA and K-ras mutations are less common but are often associated with PTEN. Alterations in MLH1 and MSH6 are documented with microsatellite instability. Beta-catenin has a minor but significant association. Conversely, p53 mutation is more often associated with nonendometrioid cancer; others being inactivation of p16 and/or overexpression of HER-2/neu. Absence of E-cadherin is more often than not present in nonendometrioid cancers and is associated with poor prognosis. Novel agents that target the AKT-PI3K-mTOR pathway and those that inhibit epidermal growth factor receptor (EGFR), vascular endothelial growth factors (VEGF), fibroblast growth factor receptor 2 (FGFR2), and folate receptors are currently being investigated.
Conclusions:
Novel targeted agents, either alone or in combination with cytotoxic agents, may result in superior treatment for patients.
Insights
Identifying molecular targets in endometrial cancer is key for new treatments. This review covers genetic alterations and therapies for endometrioid and non-endometrioid cancers.
Area of Science:
- Oncology
- Molecular Biology
- Genetics
Background:
- Understanding endometrial cancer's molecular basis is crucial for developing new therapies.
- This review focuses on the molecular pathogenesis and classification of endometrial cancer.
- Identifying genetic drivers informs targeted treatment strategies.
Purpose of the Study:
- To review the molecular basis of endometrial cancer genesis.
- To identify key genes and pathways involved in both endometrioid and non-endometrioid endometrial cancers.
- To discuss current and future targeted therapies.
Main Methods:
- Literature review of genes and cellular pathways implicated in endometrial cancer.
- Identification of genetic alterations in endometrioid and non-endometrioid subtypes.
- Review of existing and investigational drugs targeting these molecular pathways.
Main Results:
- PTEN alterations are frequent in endometrioid cancer; PI3KCA and K-ras mutations are less common. MLH1/MSH6 alterations are linked to microsatellite instability.
- Non-endometrioid cancers show frequent p53 mutations, p16 inactivation, HER-2/neu overexpression, and E-cadherin loss, associated with poor prognosis.
- Targeted agents for AKT-PI3K-mTOR, EGFR, VEGF, FGFR2, and folate receptors are under investigation.
Conclusions:
- Novel targeted agents offer potential for improved endometrial cancer treatment, alone or combined with cytotoxic therapies.
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