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

4.2K
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,...
4.2K
Cancers Originate from Somatic Mutations in a Single Cell02:21

Cancers Originate from Somatic Mutations in a Single Cell

13.2K
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...
13.2K
Mismatch Repair01:20

Mismatch Repair

5.3K
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...
5.3K
Cancer-Critical Genes I: Proto-oncogenes01:33

Cancer-Critical Genes I: Proto-oncogenes

9.2K
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...
9.2K
Cancer Prevention02:59

Cancer Prevention

6.3K
Several factors can increase the risk of cancer in an individual. About 50% of cancer cases can be prevented by adopting a healthy lifestyle, regular exercise, eating healthy, and following a modest cancer prevention diet. Epidemiological studies have consistently shown that populations with vegetable and fruit-rich diets have reduced the incidence of cancer. On the other hand, populations who have a diet rich in animal fat, red meat, junk food, or high calories are predisposed to cancer.
Some...
6.3K
The Ras Gene02:38

The Ras Gene

6.5K
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...
6.5K

You might also read

Related Articles

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

Sort by
Same author

Tucatinib in patients with HER2-positive advanced/metastatic breast cancer: A systematic literature review of real-world evidence.

Breast (Edinburgh, Scotland)·2026
Same author

Can DNA Methylation in Peritumoral and Contralateral Breast Tissue Predict Recurrence or Second Breast Cancers?

Current issues in molecular biology·2026
Same author

Effect of a Single-Session Therapeutic Patient Education Intervention on Physical Activity in Patients Initiating Cancer Therapy: A Randomized Controlled Trial.

JCO oncology practice·2026
Same author

Ductus Venosus Agenesis: A Case Report and Review of the Literature.

Cureus·2026
Same author

The role of external quality assessment in detecting immunohistochemical analyses with inferior performance: focus on the anti-ER SP1 clone.

Virchows Archiv : an international journal of pathology·2026
Same author

Current and emerging pharmacotherapies for treating vascular malformations.

Expert review of clinical pharmacology·2026

Related Experiment Video

Updated: Sep 26, 2025

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

14.8K

BRCA1 Mutation: An Insidious Enemy with Multiple Facets….

Pierrick Godin1, Francois P Duhoux1, Filomena Mazzeo1

  • 1King Albert II Cancer Institute, (Department) Cliniques Universitaires Saint- Luc, Catholic University of Louvain, Brussels, Belgium.

Case Reports in Oncology
|April 18, 2022
PubMed
Summary
This summary is machine-generated.

Hereditary breast cancer, often linked to BRCA1/BRCA2 mutations, can present with rare secondary cancers like angiosarcoma and ovarian cancer. This case highlights the complex management and links between these conditions.

Keywords:
AngiosarcomaHereditary breast and ovarian cancerPARP inhibitors

More Related Videos

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

12.4K
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

5.6K

Related Experiment Videos

Last Updated: Sep 26, 2025

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

14.8K
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

12.4K
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

5.6K

Area of Science:

  • Oncology
  • Genetics
  • Pathology

Background:

  • Hereditary predisposition accounts for approximately 10% of breast cancers, with BRCA1 and BRCA2 mutations significantly increasing cancer risk.
  • BRCA1 carriers face a 72% cumulative breast cancer risk by age 80, while BRCA2 carriers have a 69% risk. Ovarian cancer risks are 44% for BRCA1 and 17% for BRCA2 carriers.
  • The association between BRCA mutations and rare secondary malignancies, such as angiosarcoma and extra-ovarian ovarian-type cancers, requires further investigation.

Observation:

  • A 59-year-old woman with a diagnosed BRCA1 mutation developed breast cancer, followed by angiosarcoma in the same breast, and later an ovarian-origin gastric tumor.
  • The patient underwent multiple treatments including surgery, radiotherapy, chemotherapy (carboplatin, paclitaxel), and targeted therapy (olaparib).
  • A recurrence of high-grade angiosarcoma in the chest was treated with further resection.

Findings:

  • This case illustrates a complex clinical presentation of multiple rare cancers in a BRCA1 mutation carrier.
  • The study discusses the potential link between BRCA mutations and the development of angiosarcomas.
  • It also addresses therapeutic strategies for extragonadal ovarian cancer and angiosarcoma.

Implications:

  • The findings underscore the importance of vigilant surveillance and multidisciplinary management for individuals with hereditary cancer syndromes.
  • Understanding the association between BRCA mutations and rare malignancies like angiosarcoma is crucial for risk assessment and treatment planning.
  • This case contributes to the literature on managing complex oncological challenges in BRCA-positive patients.