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Related Concept Videos

Treatment Resistant Cancers02:56

Treatment Resistant Cancers

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...
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 specific...
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...
Cancer Stem Cells and Tumor Maintenance02:40

Cancer Stem Cells and Tumor Maintenance

Early diagnosis and treatment can often cure cancer. However, even with treatment, residual cells called cancer stem cells (CSC) might remain, often causing tumor recurrence. These cancer stem cells possess the potential for self-renewal and multi-lineage differentiation and are often responsible for the therapeutic resistance displayed in most cancers.
Cancer stem cells are thought to originate from tissue-specific normal stem cells or progenitor cells. The normal stem cells usually reside in...
Inhibition of Cdk Activity02:34

Inhibition of Cdk Activity

The orderly progression of the cell cycle depends on the activation of Cdk protein by binding to its cyclin partner. However, the cell cycle must be restricted when undergoing abnormal changes. Most cancers correlate to the deregulated cell cycle, and since Cdks are a central component of the cell cycle, Cdk inhibitors are extensively studied to develop anticancer agents. For instance, cyclin D associates with several Cdks, such as Cdk 4/6, to form an active complex. The cyclin D-Cdk4/6 complex...
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...

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Updated: Jul 3, 2026

A Method for Screening and Validation of Resistant Mutations Against Kinase Inhibitors
12:40

A Method for Screening and Validation of Resistant Mutations Against Kinase Inhibitors

Published on: December 7, 2014

Imatinib resistance in CML.

Gisella Volpe1, Cristina Panuzzo, Stefano Ulisciani

  • 1Division of Hematology and Internal Medicine, Department of Clinical and Biological Sciences, University of Turin, Regione Gonzole 10, San Luigi Hospital, 10043 Orbassano, Turin, Italy. gisella.volpe@unito.it

Cancer Letters
|July 26, 2008
PubMed
Summary
This summary is machine-generated.

Imatinib resistance in chronic myeloid leukaemia can occur due to mutations or gene amplification. Researchers are exploring new drugs and immune responses to overcome this resistance.

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Last Updated: Jul 3, 2026

A Method for Screening and Validation of Resistant Mutations Against Kinase Inhibitors
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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

Area of Science:

  • Oncology
  • Molecular Biology
  • Pharmacology

Background:

  • Imatinib is a primary treatment for chronic myeloid leukaemia (CML).
  • While effective, some patients develop resistance to imatinib, either primarily or after initial response.
  • Mechanisms of resistance include BCR/ABL mutations, amplification, and activation of other oncogenic pathways.

Purpose of the Study:

  • To elucidate the molecular mechanisms underlying imatinib resistance in CML.
  • To highlight the importance of molecular monitoring in managing CML.
  • To review current strategies for overcoming imatinib resistance.

Main Methods:

  • Review of molecular mechanisms of imatinib resistance.
  • Discussion of molecular monitoring techniques.
  • Overview of emerging therapeutic strategies.

Main Results:

  • BCR/ABL kinase domain mutations are a key cause of imatinib resistance.
  • BCR/ABL amplification and overexpression also contribute to resistance.
  • Clonal evolution involving additional oncogenic pathways is another mechanism.

Conclusions:

  • Understanding imatinib resistance mechanisms is crucial for effective CML treatment.
  • Molecular monitoring aids in early detection of resistance.
  • New drug development and immunotherapy show promise in overcoming resistance.