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Related Concept Videos

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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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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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Related Experiment Video

Updated: Jun 13, 2025

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Biomarker-directed therapy in multiple myeloma.

Adam Bryant1, Hang Quach2

  • 1Liverpool Hospital, University of New South Wales, Sydney.

Current Opinion in Oncology
|September 9, 2024
PubMed
Summary

Personalized medicine for multiple myeloma is advancing. Biomarkers like t(11;14) translocation predict response to targeted therapies, such as BCL-2 inhibitors, moving beyond one-size-fits-all treatments.

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Area of Science:

  • Hematology
  • Oncology
  • Molecular Biology

Background:

  • Multiple myeloma exhibits significant heterogeneity in patient outcomes and molecular profiles.
  • Current treatments often employ a one-size-fits-all approach, failing to address individual patient or disease characteristics.

Purpose of the Study:

  • To review the shift towards personalized medicine in multiple myeloma treatment.
  • To highlight the role of predictive biomarkers in tailoring therapy.
  • To discuss emerging targeted therapies and their predictive markers.

Main Methods:

  • Evaluation of established prognostic biomarkers (cytogenetic risk, frailty) as predictive tools.
  • Investigation of targeted therapies based on identified molecular vulnerabilities.
  • Focus on biomarkers predicting response to specific drugs, like BCL-2 inhibitors.

Main Results:

  • Cytogenetic risk and frailty status are being assessed for predictive potential.
  • Targeted therapies can exploit specific molecular pathways in myeloma cells.
  • The t(11;14) translocation is a key biomarker for venetoclax response in 15-20% of cases.

Conclusions:

  • Research is actively exploring venetoclax combination therapies and new BCL-2 inhibitors.
  • Beyond BCL-2, other cellular pathways are being investigated as predictive biomarkers for novel targeted therapies in multiple myeloma.