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Related Concept Videos

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Cancer is the second leading cause of death in the United States. A cancer cell is genetically unstable and hence can mutate faster. They can also modify their microenvironment and escape immune surveillance. The difficulties in treating cancer are further compounded by the emergence of rapid resistance to anticancer drugs. The most common ways to attain resistance in cancer cells include alteration in drug transport and metabolism, modification of drug target, elevated DNA damage response, or...
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Updated: Apr 30, 2026

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

David F Heigener1, Martin Reck

  • 1Department of Thoracic Oncology, LungenClinic Grosshansdorf, Grosshansdorf, Germany, D.heigener@lungenclinic.de.

Recent Results in Cancer Research. Fortschritte Der Krebsforschung. Progres Dans Les Recherches Sur Le Cancer
|April 24, 2014
PubMed
Summary
This summary is machine-generated.

Crizotinib effectively treats non-small-cell lung cancer (NSCLC) with ALK or ROS1 rearrangements. Molecular typing is crucial for identifying patients who will benefit from this targeted therapy.

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Area of Science:

  • Oncology
  • Pharmacology
  • Molecular Biology

Background:

  • Crizotinib targets receptor tyrosine kinases (RTKs) including anaplastic lymphoma kinase (ALK), ROS1, and c-Met.
  • Non-small-cell lung cancer (NSCLC) with EML4-ALK rearrangements shows high response rates to crizotinib.
  • ALK and ROS1 rearrangements are present in a small percentage of NSCLC cases (3-5% and ~1%, respectively).

Purpose of the Study:

  • To evaluate the efficacy of crizotinib in NSCLC patients with specific genetic alterations.
  • To determine the clinical utility of molecular profiling in NSCLC treatment selection.
  • To assess the role of crizotinib in c-Met altered cancers.

Main Methods:

  • Clinical evidence review for crizotinib effectiveness in ALK-rearranged NSCLC.
  • Analysis of response rates in NSCLC with ROS1 rearrangements.
  • Investigation into the diagnostic role of Fluorescence In Situ Hybridization (FISH) for ALK rearrangements.

Main Results:

  • Crizotinib demonstrates impressive response rates in NSCLC harboring EML4-ALK rearrangements.
  • Similar efficacy is observed in NSCLC with ROS1 rearrangements.
  • FISH testing on tumor tissue is essential for predicting crizotinib efficacy in ALK-positive NSCLC.

Conclusions:

  • Crizotinib is an effective targeted therapy for ALK- and ROS1-positive NSCLC.
  • Molecular typing of NSCLC is critical for identifying patients eligible for targeted treatments.
  • Further research is needed to define crizotinib's role in c-Met altered malignancies.