Molecular pathologic aspects of endometrial cancer: An update

Paulette Mhawech-Fauceglia, Elham Pakzamir, Helena Hwang, Yvonne G. Lin

Research output: Chapter in Book/Report/Conference proceedingChapter

Abstract

Endometrial cancer is the common gynecologic malignancies in the western countries. Understanding its genetic fingerprints and its genetic pathways would be a major step toward more tailored therapy to patients who are affected by this cancer. Type I (endometrioid and mucinous) and type II (serous and clear cell) endometrial cancer have different genetic alterations such as PTEN gene mutation and defects of DNA mismatch repair gene for the former and p53 and Her-2 mutation for the latter. In this review, we summarized genes/proteins that it has been found to be involved in endometrial cancer tumorigenesis, disease prognosis and patients outcomes. We will discuss genes involved in cell proliferation such as aldolase C, HIF1a, Pax8, TGFß, GRP78, 14-3-3s, in cell migration including TFF3, PSMA, TGFß, 14-3-3s and finally those involved in angiogenesis such as TTF3, HIF1a, PSMA and TGFß. Also, we will discuss novel agents that target these genes by specific inhibitors antibodies, CpG methylation silencing or other mechanisms. Future investigations into the molecular pathways of endometrial cancer could increase our knowledge of this malignancy and will lead to novel targeted therapy more tailored to each individual patient.

Original languageEnglish (US)
Title of host publicationEndometrial Cancer
Subtitle of host publicationCurrent Epidemiology, Detection and Management
PublisherNova Science Publishers, Inc.
Pages37-63
Number of pages27
ISBN (Electronic)9781634631945
ISBN (Print)9781634631631
StatePublished - Oct 1 2014

ASJC Scopus subject areas

  • Medicine(all)

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    Mhawech-Fauceglia, P., Pakzamir, E., Hwang, H., & Lin, Y. G. (2014). Molecular pathologic aspects of endometrial cancer: An update. In Endometrial Cancer: Current Epidemiology, Detection and Management (pp. 37-63). Nova Science Publishers, Inc..