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

The Retinoblastoma Gene01:20

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,...
Abnormal Proliferation02:23

Abnormal Proliferation

Under normal conditions, most adult cells remain in a non-proliferative state unless stimulated by internal or external factors to replace lost cells. Abnormal cell proliferation is a condition in which the cell's growth exceeds and is uncoordinated with normal cells. In such situations, cell division persists in the same excessive manner even after cessation of the stimuli, leading to persistent tumors. The tumor arises from the damaged cells that replicate to pass the damage to the daughter...
Cancers Originate from Somatic Mutations in a Single Cell02:21

Cancers Originate from Somatic Mutations in a Single Cell

Cancer arises from mutations in the critical genes that allow healthy cells to escape cell cycle regulation and acquire the ability to proliferate indefinitely. Though originating from a single mutation event in one of the originator cells, cancer progresses when the mutant cell lines continue to gain more and more mutations, and finally, become malignant. For example, chronic myelogenous leukemia (CML) develops initially as a non-lethal increase in white blood cells, which progressively...
Loss of Tumor Suppressor Gene Functions01:12

Loss of Tumor Suppressor Gene Functions

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.
When the tumor suppressor genes develop mutations or are lost, cells start growing out of control, leading to cancer. However, a single functional copy of the tumor suppressor gene is enough for the cells to maintain their normal functions and cell...
Loss of Tumor Suppressor Gene Functions01:12

Loss of Tumor Suppressor Gene Functions

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.
When the tumor suppressor genes develop mutations or are lost, cells start growing out of control, leading to cancer. However, a single functional copy of the tumor suppressor gene is enough for the cells to maintain their normal functions and cell...
The Ras Gene02:38

The Ras Gene

The Ras-gene-encoded proteins are regulators of signaling pathways controlling cell proliferation, differentiation, or cell survival. The Ras-gene family in humans constitutes three primary members—the HRas, NRas, and KRas. These genes code for four functionally distinct yet closely related proteins—the HRas, NRas, KRas4A, and KRas4B. The involvement of mutant Ras genes in human cancer was first discovered in 1982 and is among the most common causes of human tumorigenesis.
Ras is a superfamily...

You might also read

Related Articles

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

Sort by
Same author

Computational design of highly signalling-active membrane receptors through solvent-mediated allosteric networks.

Nature chemistry·2025
Same author

The inclusion of adults with intellectual disabilities in health research - challenges, barriers and opportunities: a mixed-method study among stakeholders in England.

Journal of intellectual disability research : JIDR·2023
Same author

'Vancowax' for haemostasis and topical antibiotic post sternotomy.

Annals of the Royal College of Surgeons of England·2022
Same author

Incidence of candidaemia in prolonged venovenous extracorporeal membrane oxygenation.

The Journal of hospital infection·2021
Same author

What place does nurse-led research have in the COVID-19 pandemic?

International nursing review·2021
Same author

Correction: A chemical inhibitor of PPM1D that selectively kills cells overexpressing PPM1D.

Oncogene·2020

Related Experiment Video

Updated: Jul 19, 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 dysfunction in sporadic basal-like breast cancer.

N C Turner1, J S Reis-Filho, A M Russell

  • 1Chester Beatty Laboratories, The Breakthrough Breast Cancer Research Centre, Institute of Cancer Research, London, UK.

Oncogene
|October 4, 2006
PubMed
Summary

BRCA1 dysfunction is common in basal-like breast cancers, with reduced BRCA1 expression and increased ID4 levels. This dysfunction, particularly prevalent in metaplastic breast cancers, offers potential therapeutic targets.

More Related Videos

Silencing of BRCA2 to Identify Novel BRCA2-regulated Biological Functions in Cultured Human Cells
09:24

Silencing of BRCA2 to Identify Novel BRCA2-regulated Biological Functions in Cultured Human Cells

Published on: August 12, 2015

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

Related Experiment Videos

Last Updated: Jul 19, 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

Silencing of BRCA2 to Identify Novel BRCA2-regulated Biological Functions in Cultured Human Cells
09:24

Silencing of BRCA2 to Identify Novel BRCA2-regulated Biological Functions in Cultured Human Cells

Published on: August 12, 2015

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:

  • Oncology
  • Molecular Biology
  • Genetics

Background:

  • Basal-like breast cancer is a distinct subtype characterized by basal/myoepithelial cell markers.
  • Germline BRCA1 mutations are frequently observed in basal-like breast cancers, suggesting BRCA1's role in sporadic cases.
  • Understanding BRCA1 dysfunction in basal-like breast cancer is crucial for targeted therapies.

Purpose of the Study:

  • To investigate the prevalence and mechanisms of BRCA1 downregulation in sporadic basal-like breast cancers.
  • To explore the correlation between BRCA1 downregulation and basal markers.
  • To assess BRCA1 methylation in metaplastic breast cancers.

Main Methods:

  • Analysis of 37 sporadic basal-like breast cancers and matched controls for BRCA1 downregulation.
  • Assessment of BRCA1 promoter methylation and BRCA1 messenger RNA (mRNA) expression.
  • Quantification of ID4 expression as a potential regulator of BRCA1.
  • Evaluation of BRCA1 methylation in metaplastic breast cancers.

Main Results:

  • BRCA1 mRNA expression was twofold lower in basal-like breast cancers compared to controls (P=0.008).
  • ID4, a negative regulator of BRCA1, was significantly upregulated (9.1-fold) in basal-like breast cancer (P<0.0001).
  • BRCA1 downregulation correlated with multiple basal markers, indicating phenotypic heterogeneity.
  • 63% of metaplastic breast cancers exhibited BRCA1 methylation, significantly higher than controls (P<0.0001).

Conclusions:

  • BRCA1 dysfunction is prevalent in sporadic basal-like breast cancers, mediated by reduced mRNA expression and potentially regulated by ID4.
  • The high frequency of BRCA1 dysfunction, especially in metaplastic subtypes, presents a potential therapeutic vulnerability.
  • Targeted treatment strategies exploiting BRCA1 dysfunction could benefit patients with basal-like breast cancer.