Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Concept Videos

Mismatch Repair01:20

Mismatch Repair

6.8K
Organisms are capable of detecting and fixing nucleotide mismatches that occur during DNA replication. This sophisticated process requires identifying the new strand and replacing the erroneous bases with correct nucleotides. Mismatch repair is coordinated by many proteins in both prokaryotes and eukaryotes.
The Mutator Protein Family Plays a Key Role in DNA Mismatch Repair
The human genome has more than 3 billion base pairs of DNA per cell. Prior to cell division, that vast amount of genetic...
6.8K
Mismatch Repair01:36

Mismatch Repair

44.3K
Overview
44.3K
The Retinoblastoma Gene01:20

The Retinoblastoma Gene

4.9K
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,...
4.9K
Cancer-Critical Genes I: Proto-oncogenes01:33

Cancer-Critical Genes I: Proto-oncogenes

11.7K
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.
When the function of certain critical genes, especially those involved in cell cycle regulation and cell growth signaling cascades, gets disrupted, it upsets the cell cycle progression. Such cells with unchecked cell cycles start proliferating uncontrollably and eventually develop into tumors.
Such genes that act...
11.7K
Cancer-Critical Genes II: Tumor Suppressor Genes01:05

Cancer-Critical Genes II: Tumor Suppressor Genes

10.0K
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.
When the function of certain critical genes, especially those involved in cell cycle regulation and cell growth signaling cascades, gets disrupted, it upsets the cell cycle progression. Such cells with unchecked cell cycles start proliferating uncontrollably and eventually develop into tumors.
Such genes that act...
10.0K
Mutagenicity and Carcinogenicity01:25

Mutagenicity and Carcinogenicity

2.1K
Mutagenicity and carcinogenicity refer to the ability of drugs to cause genetic defects and induce cancer, respectively. The International Agency for Research on Cancer (IARC) classifies agents into four groups based on their carcinogenic potential. Group 1 agents are known human carcinogens; group 2A agents are probably carcinogenic to humans; group 3 agents lack data to support their role in carcinogenesis; and group 4 includes agents for which data support that they are not likely to be...
2.1K

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

A cancer stem cell-directed nano-chemotherapy enhances anti-PD-L1 immunotherapy in breast cancer by inducing immunogenic cell death.

Acta biomaterialia·2026
Same author

The differential effects of psychotherapeutic and pharmacologic intervention on symptom severity and functioning in children and adolescents with internalizing problems: a systematic review protocol.

Systematic reviews·2026
Same author

A pH-sensitive nanococktail enabled cancer stem cell elimination, deep tumour penetration, and tumour shrinkage.

International journal of pharmaceutics·2026
Same author

Child maltreatment in Canada: prevalence and gender differences among youth.

Health promotion and chronic disease prevention in Canada : research, policy and practice·2026
Same author

Breast cancer specialists' experiences and attitudes towards mainstream genetic testing for patients with breast cancer.

Hereditary cancer in clinical practice·2026
Same author

Poly(ethylene furanoate) (PEF): Advances in Synthesis, Properties, Recycling, Applications, and Future Challenges.

ACS polymers Au·2026
Same journal

CDK2 Inhibition Exerts RB-Independent Antitumor Activity in CDK4/6 Inhibitor-Resistant HR+/HER2- Breast Cancer.

Cancer research·2026
Same journal

A Clinically Integrated Pediatric Patient-Derived Xenograft Program Enables Evaluation of Cohort and Patient-Specific Biology and Therapeutic Strategies.

Cancer research·2026
Same journal

Editor's Note: Heterodimerization of Insulin-like Growth Factor Receptor/Epidermal Growth Factor Receptor and Induction of Survivin Expression Counteract the Antitumor Action of Erlotinib.

Cancer research·2026
Same journal

Editor's Note: Deguelin Analogue SH-1242 Inhibits Hsp90 Activity and Exerts Potent Anticancer Efficacy with Limited Neurotoxicity.

Cancer research·2026
Same journal

Retraction: Two Functional Epitopes of Pigment Epithelial-Derived Factor Block Angiogenesis and Induce Differentiation in Prostate Cancer.

Cancer research·2026
Same journal

Editor's Note: Chronic Stress Facilitates Lung Tumorigenesis by Promoting Exocytosis of IGF2 in Lung Epithelial Cells.

Cancer research·2026
See all related articles

Related Experiment Video

Updated: Mar 8, 2026

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

12.7K

Out-RANKing BRCA1 in Mutation Carriers.

Emma Nolan1,2, Geoffrey J Lindeman1,3,4, Jane E Visvader5,2

  • 1Stem Cells and Cancer Division, The Walter and Eliza Hall Institute of Medical Research, Parkville, Victoria, Australia.

Cancer Research
|January 21, 2017
PubMed
Summary
This summary is machine-generated.

BRCA1 mutation carriers have limited breast cancer prevention options. Targeting progesterone and RANKL pathways in specific progenitor cells offers a promising new strategy to reduce cancer risk in high-risk women.

More Related Videos

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

15.1K
Functional Assessment of BRCA1 variants using CRISPR-Mediated Base Editors
09:22

Functional Assessment of BRCA1 variants using CRISPR-Mediated Base Editors

Published on: February 28, 2021

6.0K

Related Experiment Videos

Last Updated: Mar 8, 2026

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

12.7K
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

15.1K
Functional Assessment of BRCA1 variants using CRISPR-Mediated Base Editors
09:22

Functional Assessment of BRCA1 variants using CRISPR-Mediated Base Editors

Published on: February 28, 2021

6.0K

Area of Science:

  • Oncology
  • Genetics
  • Cell Biology

Background:

  • BRCA1 mutation carriers face limited options beyond mastectomy for breast cancer risk reduction.
  • Progesterone signaling and RANKL pathways are implicated in breast cancer development in BRCA1 mutation carriers.
  • Aberrant activation of RANK and NF-κB pathways is observed in precancerous BRCA1-mutant breast tissue.

Purpose of the Study:

  • To investigate the role of progesterone and RANK/NF-κB signaling in breast cancer development in BRCA1 mutation carriers.
  • To identify specific cellular targets for breast cancer prevention strategies.
  • To explore novel therapeutic targets for high-risk women.

Main Methods:

  • Analysis of aberrant signaling pathways in preneoplastic BRCA1-mutant breast tissue.
  • Investigation of luminal progenitor cell proliferation and DNA damage.
  • Targeting specific progenitor cell subsets for prevention strategies.

Main Results:

  • Progesterone signaling axis is amplified in precancerous BRCA1-mutant tissue.
  • RANK and NF-κB pathways are aberrantly activated in luminal progenitor cells.
  • Augmented proliferation and DNA damage susceptibility in these cells contribute to oncogenesis.
  • Targeting this progenitor subset presents a novel prevention strategy.

Conclusions:

  • A hyperactive progesterone and NF-κB signaling pathway in BRCA1-mutant luminal progenitor cells drives breast cancer susceptibility.
  • Targeting these specific progenitor cells offers a promising prevention strategy for BRCA1 mutation carriers and other high-risk women.