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Related Concept Videos

Targeted Cancer Therapies02:57

Targeted Cancer Therapies

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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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Cancer-Critical Genes II: Tumor Suppressor Genes01:05

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Genes usually encode proteins necessary for the proper functioning of a healthy cell. Mutations can often cause changes to the gene expression pattern, thereby altering the phenotype.
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Genetic Screens02:46

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Updated: Nov 19, 2025

Functional Assessment of BRCA1 variants using CRISPR-Mediated Base Editors
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3D Functional Genomics Screens Identify CREBBP as a Targetable Driver in Aggressive Triple-Negative Breast Cancer.

Barrie Peck1,2, Philip Bland1,2, Ioanna Mavrommati1,2

  • 1The Breast Cancer Now Toby Robins Research Centre, The Institute of Cancer Research, London, England, United Kingdom.

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|January 29, 2021
PubMed
Summary
This summary is machine-generated.

Researchers identified CREBBP as a tumor suppressor in triple-negative breast cancer (TNBC). Loss of CREBBP drives aggressive tumors, suggesting CDK4/6 inhibitors as a potential treatment for patients with CREBBP alterations.

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Area of Science:

  • Oncology
  • Genomics
  • Cancer Biology

Background:

  • Triple-negative breast cancer (TNBC) lacks targeted therapies due to chemoresistance and unknown drivers.
  • Accurate models are needed to identify functional driver genes in TNBC.

Purpose of the Study:

  • Identify novel tumor suppressors and therapeutic targets in TNBC.
  • Investigate the role of CREBBP in TNBC development and progression.

Main Methods:

  • Unbiased functional genomics screening using spheroid cultures.
  • Analysis of CREBBP protein expression in patient tumor samples.
  • Assessment of CDK4/6 inhibitors in preclinical models with CREBBP alterations.

Main Results:

  • CREBBP identified as a novel tumor suppressor in TNBC.
  • CREBBP loss associated with genomic heterogeneity, poorer survival, and FOXM1 program dependency.
  • CDK4/6 inhibitors selectively impaired growth in models with CREBBP alterations.

Conclusions:

  • CREBBP alterations drive aggressive TNBC, lung cancer, and lymphomas.
  • Targeting FOXM1-driven proliferation with CDK4/6 inhibitors shows therapeutic potential.
  • CREBBP alterations may serve as a biomarker for CDK4/6 inhibitor response.