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Related Concept Videos

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...
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...
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...
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...
Treatment Resistent Cancers02:56

Treatment Resistent 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...
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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Related Experiment Video

Updated: Jun 16, 2026

Methods for Evaluating the Role of c-Fos and Dusp1 in Oncogene Dependence
10:09

Methods for Evaluating the Role of c-Fos and Dusp1 in Oncogene Dependence

Published on: January 7, 2019

Why doesn't imatinib cure chronic myeloid leukemia?

Robert L Redner1

  • 1University of Pittsburgh Cancer Institute, Pittsburgh, Pennsylvania, USA. redner@pitt.edu

The Oncologist
|February 4, 2010
PubMed
Summary

Imatinib therapy often fails to cure chronic myeloid leukemia (CML) because CML stem cells are inherently resistant. This resistance may even increase during imatinib treatment, necessitating lifelong therapy.

Area of Science:

  • Hematology
  • Oncology
  • Molecular Biology

Background:

  • Imatinib mesylate revolutionized chronic myeloid leukemia (CML) treatment, achieving high remission rates.
  • Despite its efficacy, imatinib rarely cures CML, leading to recommendations for lifelong therapy.

Purpose of the Study:

  • To analyze the biological mechanisms underlying imatinib's failure to eradicate CML.
  • To investigate the role of leukemic stem cells (LSCs) in CML treatment resistance.

Main Methods:

  • Review of existing scientific literature on imatinib efficacy and CML biology.
  • Analysis of evidence regarding LSC resistance to tyrosine kinase inhibitors.
  • Examination of studies on the impact of imatinib treatment on LSC properties.

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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

Related Experiment Videos

Last Updated: Jun 16, 2026

Methods for Evaluating the Role of c-Fos and Dusp1 in Oncogene Dependence
10:09

Methods for Evaluating the Role of c-Fos and Dusp1 in Oncogene Dependence

Published on: January 7, 2019

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

Main Results:

  • CML LSCs exhibit intrinsic resistance to imatinib.
  • Imatinib treatment may paradoxically enhance the resistance of CML stem cells.
  • This inherent and acquired resistance contributes to the persistence of CML.

Conclusions:

  • The inherent resistance of CML stem cells is a primary reason for imatinib's inability to achieve a cure.
  • Further research into overcoming LSC resistance is crucial for developing curative CML therapies.
  • Understanding these resistance mechanisms may inform future treatment strategies beyond lifelong imatinib therapy.