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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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The Retinoblastoma Gene

Tumor suppressor genes are normal genes that can slow down cell division, repair DNA mistakes, or program the cells for apoptosis in case of irreparable damage. Hence, they play an essential role in preventing the proliferation of damaged cells.
The first-ever tumor suppressor gene called Rb was identified in retinoblastoma - a rare eye tumor in children. In inherited forms of the disease, a child inherits one defective copy of the Rb gene, which predisposes them to retinoblastoma. However,...
Targeted Cancer Therapies02:57

Targeted Cancer Therapies

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.
There are several types of targeted therapies against specific...
Targeted Cancer Therapies02:57

Targeted Cancer Therapies

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.
There are several types of targeted therapies against specific...
Treatment Resistent Cancers02:56

Treatment Resistent 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...
Combination Therapies and Personalized Medicine02:50

Combination Therapies and Personalized Medicine

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.
The combination of the drug acetazolamide and sulforaphane is a good example of combination therapy to treat cancer. The cells in the interior of a large tumor often die due to the hypoxic and...

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Updated: Jun 12, 2026

Identifying the Effects of BRCA1 Mutations on Homologous Recombination using Cells that Express Endogenous Wild-type BRCA1
08:53

Identifying the Effects of BRCA1 Mutations on Homologous Recombination using Cells that Express Endogenous Wild-type BRCA1

Published on: February 17, 2011

BRCA1/2 Reversion Mutations and Cancer Therapy Resistance.

Wenjing Qi1, Gege Yang1, Yingyi Zhang1

  • 1Department of Bioscience, Changchun Normal University, Changchun 130032, China.

Biology
|June 11, 2026
PubMed
Summary
This summary is machine-generated.

Germline mutations in BRCA1 and BRCA2 genes increase cancer risk. Understanding these gene variants is crucial for developing targeted therapies and overcoming treatment resistance in homologous recombination-deficient cancers.

Keywords:
BRCA1/2chemoresistancehomologous recombination deficient tumorsreversion mutation

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Last Updated: Jun 12, 2026

Identifying the Effects of BRCA1 Mutations on Homologous Recombination using Cells that Express Endogenous Wild-type BRCA1
08:53

Identifying the Effects of BRCA1 Mutations on Homologous Recombination using Cells that Express Endogenous Wild-type BRCA1

Published on: February 17, 2011

Functional Assessment of BRCA1 variants using CRISPR-Mediated Base Editors
09:22

Functional Assessment of BRCA1 variants using CRISPR-Mediated Base Editors

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gDNA Enrichment by a Transposase-based Technology for NGS Analysis of the Whole Sequence of BRCA1, BRCA2, and 9 Genes Involved in DNA Damage Repair
08:15

gDNA Enrichment by a Transposase-based Technology for NGS Analysis of the Whole Sequence of BRCA1, BRCA2, and 9 Genes Involved in DNA Damage Repair

Published on: October 6, 2014

Area of Science:

  • Genetics and Genomics
  • Cancer Biology
  • Molecular Oncology

Background:

  • Germline loss-of-function mutations in BRCA1 and BRCA2 significantly elevate susceptibility to breast, ovarian, and other cancers.
  • BRCA2 is essential for RAD51 recruitment to DNA damage sites, while BRCA1 regulates homologous recombination repair (HRR) and DNA damage response signaling.
  • Poly (ADP-ribose) polymerase inhibitors (PARPis) exploit synthetic lethality in homologous recombination-deficient tumors, showing clinical benefit in BRCA1/2-mutated cancers.

Purpose of the Study:

  • To review the structural and functional domains of BRCA1/2.
  • To analyze pathogenic mutation profiles of BRCA1/2.
  • To discuss therapeutic strategies for BRCA1/2-deficient cancers and identify knowledge gaps.

Main Methods:

  • Literature review of BRCA1/2 function, mutations, and therapeutic strategies.
  • Analysis of existing data on PARPi efficacy and resistance mechanisms.
  • Synthesis of information on the role of specific BRCA1/2 domains and residual protein activities.

Main Results:

  • PARPi therapy is effective in BRCA1/2-mutated cancers, but resistance, often due to secondary mutations restoring protein function, is a significant challenge.
  • Critical gaps remain in understanding how specific BRCA1/2 domains and residual protein activities influence tumorigenesis and treatment response.
  • Pathogenic mutation profiles highlight the importance of precise genetic alterations in disease susceptibility and therapeutic outcomes.

Conclusions:

  • Further functional studies of BRCA1/2 variants are essential for refining cancer risk prediction.
  • Developing mutation-tailored therapies is necessary to improve treatment efficacy for BRCA1/2-deficient cancers.
  • Addressing resistance mechanisms and understanding the impact of specific BRCA1/2 domains will advance precision oncology.