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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...
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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.
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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.
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Updated: Jun 8, 2026

A Method for Screening and Validation of Resistant Mutations Against Kinase Inhibitors
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Published on: December 7, 2014

Resistance to imatinib: mutations and beyond.

Paul La Rosée1, Michael W Deininger

  • 1Klinik für Innere Medizin II, Hämatologie/Onkologie, Universitätsklinikum Jena, Jena, Germany.

Seminars in Hematology
|September 30, 2010
PubMed
Summary

Mechanisms of tyrosine kinase inhibitor (TKI) resistance in chronic myeloid leukemia (CML) are complex. Beyond BCR-ABL mutations, other factors like clonal evolution and leukemic stem cells contribute to TKI resistance, necessitating further research.

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Implementation of In Vitro Drug Resistance Assays: Maximizing the Potential for Uncovering Clinically Relevant Resistance Mechanisms
08:46

Implementation of In Vitro Drug Resistance Assays: Maximizing the Potential for Uncovering Clinically Relevant Resistance Mechanisms

Published on: December 9, 2015

Area of Science:

  • Oncology
  • Hematology
  • Pharmacology

Background:

  • Imatinib resistance in chronic myeloid leukemia (CML) is a significant clinical challenge.
  • BCR-ABL mutations were identified as a primary mechanism driving imatinib resistance.
  • Second-generation tyrosine kinase inhibitors (TKIs) were developed to overcome imatinib resistance.

Purpose of the Study:

  • To review the multifaceted mechanisms of TKI resistance in CML.
  • To discuss the biological and clinical implications of these resistance mechanisms.
  • To highlight ongoing research areas, including leukemic stem cell resistance.

Main Methods:

  • Literature review of in vitro and clinical studies on TKI resistance in CML.
  • Analysis of data on BCR-ABL mutations, clonal evolution, and other resistance factors.
  • Synthesis of current understanding of resistance biology and clinical impact.

Main Results:

  • BCR-ABL kinase domain mutations are a key resistance mechanism, guiding second-line TKI selection.
  • Additional resistance mechanisms, including clonal chromosomal evolution and BCR-ABL amplification, are implicated.
  • Leukemic stem cell (LSC) primary resistance is a critical area for understanding minimal residual disease.

Conclusions:

  • TKI resistance in CML involves multiple biological pathways beyond BCR-ABL mutations.
  • Understanding diverse resistance mechanisms is crucial for optimizing CML treatment strategies.
  • Further research is needed to fully elucidate and target these resistance mechanisms, particularly in LSCs.