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Genetic polymorphisms in drug targets have emerged as critical determinants of interindividual variability in drug response and toxicity. Pharmacogenomic investigations increasingly focus on identifying these variations to personalize and optimize therapeutic interventions. A drug target may be a receptor, enzyme, or signaling protein involved in pharmacologic responses or disease-related pathways. While early pharmacogenetic studies focused primarily on drug metabolism, current research...
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Related Experiment Video

Updated: Mar 18, 2026

Colorectal Cancer Cell Surface Protein Profiling Using an Antibody Microarray and Fluorescence Multiplexing
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BRAF V600E Mutant Colorectal Cancer Subtypes Based on Gene Expression.

David Barras1, Edoardo Missiaglia2, Pratyaksha Wirapati2

  • 1Swiss Institute of Bioinformatics, Bioinformatics Core Facility, Lausanne, Switzerland. david.barras@unil.ch Mauro.delorenzi@unil.ch sabine.tejpar@uzleuven.be.

Clinical Cancer Research : an Official Journal of the American Association for Cancer Research
|June 30, 2016
PubMed
Summary
This summary is machine-generated.

BRAF V600E colorectal cancers are not a single entity. Two distinct subtypes, BM1 and BM2, show different pathway activations, suggesting tailored drug targeting strategies for this poor-prognosis cancer group.

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Area of Science:

  • Oncology
  • Molecular Biology
  • Genomics

Background:

  • BRAF V600E mutations occur in ~10% of colorectal cancers, associated with poor prognosis.
  • Current targeted therapies for BRAF V600E colorectal cancer show limited and heterogeneous responses.
  • Understanding the underlying biology of BRAF V600E colorectal cancer is crucial for developing effective treatments.

Purpose of the Study:

  • To identify and characterize distinct molecular subgroups within BRAF V600E colorectal cancers.
  • To investigate the biological pathways and molecular features associated with these subgroups.
  • To provide insights for developing targeted therapeutic strategies for specific BRAF V600E colorectal cancer subtypes.

Main Methods:

  • Utilized non-negative matrix factorization for unsupervised clustering on gene expression data from 218 BRAF V600E colorectal cancer patients.
  • Performed pathway analysis to characterize identified subgroups.
  • Validated findings using proteomics data.

Main Results:

  • Identified two distinct BRAF V600E colorectal cancer subtypes, BM1 and BM2, independent of MSI status, PI3K mutation, gender, and sidedness.
  • BM1 subtype is characterized by KRAS/AKT pathway activation, mTOR/4EBP deregulation, and epithelial-mesenchymal transition (EMT).
  • BM2 subtype displays significant cell cycle deregulation, with high CDK1 and low cyclin D1 levels.

Conclusions:

  • BRAF V600E colorectal cancer patients exhibit heterogeneous biology and should not be treated as a single group.
  • Characterization of BM1 and BM2 subtypes reveals distinct molecular motifs exploitable for targeted drug development.
  • Further research into these subtypes may lead to improved therapeutic outcomes for BRAF V600E colorectal cancer.