Related Experiment Video

Updated: Jun 16, 2026

Multi-Gene Single Nucleotide Polymorphism Detection in Gastric Cancer Based on Ion Semiconductor Sequencing Platform
06:21

Multi-Gene Single Nucleotide Polymorphism Detection in Gastric Cancer Based on Ion Semiconductor Sequencing Platform

Published on: May 10, 2024

FGFR2 mutations are rare across histologic subtypes of ovarian cancer

Sara A Byron1, Michael G Gartside, Candice L Wellens

  • 1Cancer and Cell Biology Division, Translational Genomics Research Institute, Phoenix, AZ 85004, USA.

Gynecologic Oncology
|January 29, 2010
PubMed
Abstract

Insights

Activating Fibroblast Growth Factor Receptor 2 (FGFR2) mutations, found in endometrial cancer, were investigated in ovarian tumors. These rare mutations were detected in endometrioid and serous ovarian cancers, suggesting a potential role in tumorigenesis.

Area of Science:

  • Oncology
  • Molecular Genetics

Background:

  • Ovarian cancer is a leading cause of gynecologic cancer death.
  • Fibroblast growth factor receptor (FGFR) signaling is implicated in tumorigenesis.
  • FGFR2 mutations are common in endometrioid endometrial cancer.

Purpose of the Study:

  • To investigate the presence of activating FGFR2 mutations in ovarian tumors.
  • To explore the potential role of FGFR2 mutations in ovarian cancer development.

Main Methods:

  • Sequencing of six FGFR2 exons in 120 primary ovarian tumors.
  • Analysis of major ovarian cancer histologic subtypes.
  • Functional characterization of identified mutations.

Main Results:

  • FGFR2 mutations were detected at low frequency (2.2% in endometrioid, 2.4% in serous).
  • No mutations were found in other subtypes or cell lines.
  • Confirmed that identified mutations lead to FGFR2 receptor activation.

Conclusions:

  • Identified FGFR2 mutations (S252W, Y376C) overlap with those in endometrial tumors.
  • Activated FGFR2 may contribute to a small subset of ovarian cancer cases.
  • Suggests a potential therapeutic target for a subset of ovarian cancers.

More Related Videos

Testing Targeted Therapies in Cancer using Structural DNA Alteration Analysis and Patient-Derived Xenografts10:27

Testing Targeted Therapies in Cancer using Structural DNA Alteration Analysis and Patient-Derived Xenografts

Published on: July 25, 2020

Transplantation Into the Mouse Ovarian Fat Pad09:25

Transplantation Into the Mouse Ovarian Fat Pad

Published on: September 7, 2016

Related Concept Videos

The Retinoblastoma Gene01:20

The Retinoblastoma Gene

Tumor suppressor genes are normal genes that can slow down cell division, repair DNA mistakes, or program the cells for apoptosis in case of irreparable damage. Hence, they play an essential role in preventing the proliferation of damaged cells.
The first-ever tumor suppressor gene called Rb was identified in retinoblastoma - a rare eye tumor in children. In inherited forms of the disease, a child inherits one defective copy of the Rb gene, which predisposes them to retinoblastoma. However,...
Cancer-Critical Genes II: Tumor Suppressor Genes01:05

Cancer-Critical Genes II: Tumor Suppressor Genes

Genes usually encode proteins necessary for the proper functioning of a healthy cell. Mutations can often cause changes to the gene expression pattern, thereby altering the phenotype.
When the function of certain critical genes, especially those involved in cell cycle regulation and cell growth signaling cascades, gets disrupted, it upsets the cell cycle progression. Such cells with unchecked cell cycles start proliferating uncontrollably and eventually develop into tumors.
Such genes that act...
Cancer-Critical Genes II: Tumor Suppressor Genes01:05

Cancer-Critical Genes II: Tumor Suppressor Genes

Genes usually encode proteins necessary for the proper functioning of a healthy cell. Mutations can often cause changes to the gene expression pattern, thereby altering the phenotype.
When the function of certain critical genes, especially those involved in cell cycle regulation and cell growth signaling cascades, gets disrupted, it upsets the cell cycle progression. Such cells with unchecked cell cycles start proliferating uncontrollably and eventually develop into tumors.
Such genes that act...
Mutations01:39

Mutations

Overview
Cancers Originate from Somatic Mutations in a Single Cell02:21

Cancers Originate from Somatic Mutations in a Single Cell

Cancer arises from mutations in the critical genes that allow healthy cells to escape cell cycle regulation and acquire the ability to proliferate indefinitely. Though originating from a single mutation event in one of the originator cells, cancer progresses when the mutant cell lines continue to gain more and more mutations, and finally, become malignant. For example, chronic myelogenous leukemia (CML) develops initially as a non-lethal increase in white blood cells, which progressively...
Cancers Originate from Somatic Mutations in a Single Cell02:21

Cancers Originate from Somatic Mutations in a Single Cell

Cancer arises from mutations in the critical genes that allow healthy cells to escape cell cycle regulation and acquire the ability to proliferate indefinitely. Though originating from a single mutation event in one of the originator cells, cancer progresses when the mutant cell lines continue to gain more and more mutations, and finally, become malignant. For example, chronic myelogenous leukemia (CML) develops initially as a non-lethal increase in white blood cells, which progressively...