Related Experiment Video

Updated: Mar 6, 2026

Oncogenic Gene Fusion Detection Using Anchored Multiplex Polymerase Chain Reaction Followed by Next Generation Sequencing
09:49

Oncogenic Gene Fusion Detection Using Anchored Multiplex Polymerase Chain Reaction Followed by Next Generation Sequencing

Published on: July 5, 2019

10.1K

FGFR rearrangements: oncogenic drivers and therapeutic targets

Julia Yemelyanenko1, Jos Jonkers1, Daniel Zingg2

  • 1Division of Molecular Pathology, Netherlands Cancer Institute, Amsterdam, The Netherlands; Oncode Institute, Utrecht, The Netherlands.

Trends in Cancer
|March 4, 2026
PubMed

Insights

Fibroblast growth factor receptor (FGFR) rearrangements, including fusions and truncations, are key drivers of cancer. Understanding these alterations is crucial for developing targeted therapies and advancing precision oncology.

Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Background:

  • Fibroblast growth factor receptors (FGFRs) are implicated in cancer through amplifications and mutations.
  • Emerging research identifies FGFR in-frame fusions and structural variants as significant oncogenic drivers.
  • FGFR2 exon 18 truncations represent a potent class of tumor driver alterations, influencing tumorigenesis.

Purpose of the Study:

  • To review the biological and clinical significance of FGFR rearrangements in cancer.
  • To explore the mechanisms by which FGFR alterations drive tumor development.
  • To discuss the role of FGFR rearrangements as biomarkers and therapeutic targets.

Main Methods:

  • Literature review of studies on FGFR rearrangements in human cancers.
  • Analysis of biological mechanisms underlying FGFR-driven tumorigenesis.
  • Evaluation of clinical implications, including treatment response and therapeutic strategies.

Main Results:

  • FGFR rearrangements, beyond mutations and amplifications, constitute a critical class of oncogenic drivers.
  • FGFR2 exon 18 truncations demonstrate potent oncogenic activity.
  • FGFR alterations have implications for predicting treatment response to FGFR-targeted agents.

Conclusions:

  • A comprehensive understanding of FGFR rearrangements is essential for advancing precision oncology.
  • Targeted therapies for FGFR alterations offer new avenues for cancer treatment.
  • Further research into FGFR rearrangements will improve patient outcomes and therapeutic strategies.
Keywords:
FGFRFGFR inhibitorsgene fusionsgene rearrangementstargeted therapy

More Related Videos

Next Generation Sequencing for the Detection of Actionable Mutations in Solid and Liquid Tumors11:15

Next Generation Sequencing for the Detection of Actionable Mutations in Solid and Liquid Tumors

Published on: September 20, 2016

25.2K
Mapping the Structure-Function Relationships of Disordered Oncogenic Transcription Factors Using Transcriptomic Analysis09:58

Mapping the Structure-Function Relationships of Disordered Oncogenic Transcription Factors Using Transcriptomic Analysis

Published on: June 27, 2020

3.2K

Related Concept Videos

Mitogens and the Cell Cycle02:38

Mitogens and the Cell Cycle

Mitogens and their receptors play a crucial role in controlling the progression of the cell cycle. However, the loss of mitogenic control over cell division leads to tumor formation. Therefore, mitogens and mitogen receptors play an important role in cancer research. For instance, the epidermal growth factor (EGF) - a type of mitogen and its transmembrane receptor (EGFR), decides the fate of the cell's proliferation. When EGF binds to EGFR, a member of the ErbB family of tyrosine kinase...
8.2K
Cancer-Critical Genes I: Proto-oncogenes01:33

Cancer-Critical Genes I: Proto-oncogenes

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...
11.7K
Targeted Cancer Therapies02:57

Targeted Cancer Therapies

The targeted cancer therapies, also known as “molecular targeted therapies,” take advantage of the molecular and genetic differences between the cancer cells and the normal cells. It needs a thorough understanding of the cancer cells to develop drugs that can target specific molecular aspects that drive the growth, progression, and spread of cancer cells without affecting the growth and survival of other normal cells in the body.
There are several types of targeted therapies against...
9.0K
Pharmacogenetics of Drug Targets: β₂-Adrenergic Receptors, Apo E, Thymidylate Synthase01:11

Pharmacogenetics of Drug Targets: β₂-Adrenergic Receptors, Apo E, Thymidylate Synthase

Genetic polymorphisms in drug targets have emerged as critical determinants of interindividual variability in drug response and toxicity. Pharmacogenomic investigations increasingly focus on identifying these variations to personalize and optimize therapeutic interventions. A drug target may be a receptor, enzyme, or signaling protein involved in pharmacologic responses or disease-related pathways. While early pharmacogenetic studies focused primarily on drug metabolism, current research...
56
Combination Therapies and Personalized Medicine02:50

Combination Therapies and Personalized Medicine

Combining two or more treatment methods increases the life span of cancer patients while reducing damage to vital organs or tissue from the overuse of a single treatment. Combination therapy also targets different cancer-inducing pathways, thus reducing the chances of developing resistance to treatment.
The combination of the drug acetazolamide and sulforaphane is a good example of combination therapy to treat cancer. The cells in the interior of a large tumor often die due to the hypoxic and...
6.3K
Abnormal Proliferation02:23

Abnormal Proliferation

Under normal conditions, most adult cells remain in a non-proliferative state unless stimulated by internal or external factors to replace lost cells. Abnormal cell proliferation is a condition in which the cell's growth exceeds and is uncoordinated with normal cells. In such situations, cell division persists in the same excessive manner even after cessation of the stimuli, leading to persistent tumors. The tumor arises from the damaged cells that replicate to pass the damage to the...
5.3K