Related Experiment Video

Updated: Mar 11, 2026

Comet Assay to Quantify DNA Damage in FLT3 Mutant-expressing 32D Cells after Exposure to Type I and Type II FLT3 Inhibitors
04:36

Comet Assay to Quantify DNA Damage in FLT3 Mutant-expressing 32D Cells after Exposure to Type I and Type II FLT3 Inhibitors

Published on: October 17, 2025

1.0K

The implication of FLT3 amplification for FLT targeted therapeutics in solid tumors

Sung Hee Lim1, Sun-Young Kim1, Kyung Kim2

  • 1Division of Hematology-Oncology, Department of Medicine, Samsung Medical Center, Sungkyunkwan University School of Medicine, Seoul, Korea.

Oncotarget
|December 2, 2016
PubMed

Insights

Fms-like tyrosine kinase 3 (FLT3) amplification in solid tumors is rare and may not predict response to FLT3 inhibitors. Further research is needed to determine its clinical significance.

Area of Science:

  • Oncology
  • Genetics
  • Pharmacology

Background:

  • Fms-like tyrosine kinase 3 (FLT3) amplification is an uncommon genetic alteration in solid cancers.
  • Understanding the role of FLT3 amplification in solid tumors is crucial for developing targeted therapies.

Purpose of the Study:

  • To investigate the presence and clinical relevance of FLT3 amplification in solid cancer patients.
  • To evaluate the efficacy of FLT3 inhibitors in preclinical models of FLT3-amplified solid tumors.

Main Methods:

  • Targeted sequencing and FISH assay were used to identify FLT3 amplification in tumor tissues.
  • FLT3-amplified patient-derived cells (PDCs) were generated for drug sensitivity testing.
  • In vitro assays assessed the response to FLT3 inhibitors (regorafenib, sorafenib) and combination therapies.

Main Results:

  • A patient with metastatic colon cancer and FLT3 amplification showed a partial response to regorafenib.
  • FLT3-amplified PDCs exhibited increased FLT3 mRNA expression but were not significantly inhibited by regorafenib or sorafenib.
  • Combination therapy with an mTOR inhibitor did not improve cell proliferation inhibition.

Conclusions:

  • FLT3 amplification is infrequently detected in solid cancers via targeted genomic profiling.
  • FLT3 amplification does not appear to be a reliable actionable target or biomarker for FLT3 inhibitor sensitivity in solid tumors.
Keywords:
FLT3 amplificationregorafenibsolid tumors

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
Experimental Melanoma Immunotherapy Model Using Tumor Vaccination with a Hematopoietic Cytokine09:15

Experimental Melanoma Immunotherapy Model Using Tumor Vaccination with a Hematopoietic Cytokine

Published on: February 24, 2023

4.1K

Related Concept Videos

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...
60
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
Tumor Immunotherapy01:27

Tumor Immunotherapy

Immunotherapy is a treatment that boosts or manipulates the immune system to fight diseases, including cancer. For instance, by stimulating an immune response through vaccinations against viruses that cause cancers, like hepatitis B virus and human papillomavirus, these diseases can be prevented. Nonetheless, some cancer cells can avoid the immune system due to their rapid mutation and division. The immune response to many cancers involves three phases: elimination, equilibrium, and escape.
2.1K