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Performing Data Mining And Integrative Analysis Of Biomarker in Breast Cancer Using Multiple Publicly Accessible Databases
07:41

Performing Data Mining And Integrative Analysis Of Biomarker in Breast Cancer Using Multiple Publicly Accessible Databases

Published on: May 17, 2019

Functional analysis-make or break for cancer predictability.

Miriam Deniz1, Karlheinz Holzmann2, Lisa Wiesmüller1

  • 1Department of Obstetrics and Gynaecology, Ulm University, Germany.

Mutation Research
|April 2, 2013
PubMed
Summary
This summary is machine-generated.

Copy number variations (CNVs) can lead to breast cancer. Defects in DNA repair pathways, particularly homologous recombination (HR) repair, promote error-prone repair, driving cancer formation and progression.

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10:27

Testing Targeted Therapies in Cancer using Structural DNA Alteration Analysis and Patient-Derived Xenografts

Published on: July 25, 2020

Area of Science:

  • Genetics
  • Cancer Biology
  • Genomic Instability

Background:

  • Copy number variations (CNVs), including deletions and amplifications, are genetic alterations often found in unstable genomic regions.
  • CNVs, particularly small ones, can initiate larger copy number aberrations (CNAs) that promote cancer development.
  • Previous research links CNVs to increased breast cancer risk and accelerated progression when affecting key genes.

Purpose of the Study:

  • To analyze DNA damage repair mechanisms in relation to copy number variations (CNVs) and breast cancer.
  • To investigate the role of homologous recombination (HR) pathway defects and alternative DNA double-strand break (DSB) repair pathways in breast carcinogenesis.
  • To explore the potential of detecting error-prone DSB repair as a biomarker for hereditary breast cancer risk.

Main Methods:

  • Utilizing high-resolution genome-wide techniques for CNV detection.
  • Analyzing DNA damage manifestations resulting from defects in various DSB repair mechanisms.
  • Investigating peripheral blood lymphocytes from individuals with familial breast cancer risk.
  • Performing sequence analysis of breakpoint regions in breast cancer specimens.

Main Results:

  • Defects in homologous recombination (HR) repair are linked to breast cancer, shifting DNA repair to error-prone pathways like microhomology-mediated non-homologous end joining (mmNHEJ).
  • Increased error-prone DSB repair activity was observed in lymphocytes of individuals with familial breast cancer risk.
  • Sequence analysis revealed that mmNHEJ is the primary mechanism forming most genome aberrations in breast cancer specimens.

Conclusions:

  • Microhomology-mediated non-homologous end joining (mmNHEJ) plays a significant role in forming genome aberrations in breast cancer.
  • Functional testing for pathway-specific error-prone DSB repair activities could serve as a biomarker for hereditary breast cancer risk and treatment response.
  • Targeting specific error-prone DSB repair mechanisms offers potential avenues for breast cancer prevention.