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

Cancer-Critical Genes I: Proto-oncogenes

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

Cancer-Critical Genes I: Proto-oncogenes

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...
Mitogens and the Cell Cycle02:38

Mitogens and the Cell Cycle

Mitogens and their receptors play a crucial role in controlling the progression of the cell cycle. However, the loss of mitogenic control over cell division leads to tumor formation. Therefore, mitogens and mitogen receptors play an important role in cancer research. For instance, the epidermal growth factor (EGF) - a type of mitogen and its transmembrane receptor (EGFR), decides the fate of the cell's proliferation. When EGF binds to EGFR, a member of the ErbB family of tyrosine kinase...
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

Matching-Adjusted Indirect Comparison of Sotorasib Plus Panitumumab Versus Trifluridine/Tipiracil Plus Bevacizumab in Chemorefractory Metastatic Colorectal Cancer.

Clinical colorectal cancer·2026
Same author

Community Safety Needs and Resources and Their Alignment: A Case Study.

Journal of urban health : bulletin of the New York Academy of Medicine·2026
Same author

Podium Abstracts Presented at the 2025 Annual Meeting of the Arthroscopy Association of North America.

Arthroscopy : the journal of arthroscopic & related surgery : official publication of the Arthroscopy Association of North America and the International Arthroscopy Association·2026
Same author

A little longer, a lot better: simulation-guided exploration of extended-length single-end barcoded reads for structural variant detection.

bioRxiv : the preprint server for biology·2026
Same author

Renal tumors harboring FLCN mutations: Case series from clinical practice.

Human pathology·2026
Same author

Survey Study of Canadian Orthopedic Surgeons on the Surgical Management of Anterior Cruciate Ligament Injury.

Clinical journal of sport medicine : official journal of the Canadian Academy of Sport Medicine·2026
Same journal

Circadian Homeostasis of Liver Metabolism Suppresses Hepatocarcinogenesis.

Cancer cell·2026
Same journal

Vascular RhoJ Is an Effective and Selective Target for Tumor Angiogenesis and Vascular Disruption.

Cancer cell·2026
Same journal

Intratumoral B cells under stress.

Cancer cell·2026
Same journal

Chronic stress unleashes an intratumor phage-fibroblast-B cell circuit to promote tumor growth.

Cancer cell·2026
Same journal

Molecular phenotypes and spatial archetypes: A new framework for cancer-associated fibroblasts.

Cancer cell·2026
Same journal

OpenIO: An open framework for AI-native immunotherapy.

Cancer cell·2026
See all related articles

Related Experiment Video

Updated: May 11, 2026

Deciphering the Structural Effects of Activating EGFR Somatic Mutations with Molecular Dynamics Simulation
15:05

Deciphering the Structural Effects of Activating EGFR Somatic Mutations with Molecular Dynamics Simulation

Published on: May 20, 2020

Oncogenic ERBB3 mutations in human cancers.

Bijay S Jaiswal1, Noelyn M Kljavin, Eric W Stawiski

  • 1Department of Molecular Biology, Genentech, Inc., 1 DNA Way, South San Francisco, CA 94080, USA.

Cancer Cell
|May 18, 2013
PubMed
Summary
This summary is machine-generated.

New research identifies ERBB3 mutations in colon and gastric cancers, driving oncogenic signaling. Therapies targeting ERBB2 effectively blocked mutant ERBB3 activity and disease progression.

More Related Videos

Testing Targeted Therapies in Cancer using Structural DNA Alteration Analysis and Patient-Derived Xenografts
10:27

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

Published on: July 25, 2020

Related Experiment Videos

Last Updated: May 11, 2026

Deciphering the Structural Effects of Activating EGFR Somatic Mutations with Molecular Dynamics Simulation
15:05

Deciphering the Structural Effects of Activating EGFR Somatic Mutations with Molecular Dynamics Simulation

Published on: May 20, 2020

Testing Targeted Therapies in Cancer using Structural DNA Alteration Analysis and Patient-Derived Xenografts
10:27

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

Published on: July 25, 2020

Area of Science:

  • Oncology
  • Molecular Biology
  • Cancer Genetics

Background:

  • The human epidermal growth factor receptor (HER) family is crucial in cancer, with deregulation observed via amplification, overexpression, or mutation.
  • ERBB3/HER3, a HER family member with an impaired kinase domain, is frequently amplified or overexpressed but lacks reported oncogenic mutations.

Purpose of the Study:

  • To investigate the role of ERBB3 in cancer development by identifying and characterizing its somatic mutations.
  • To determine the oncogenic potential and therapeutic vulnerabilities of mutated ERBB3.

Main Methods:

  • Somatic mutation analysis in colon and gastric cancer cohorts.
  • In vitro transformation assays using colonic and breast epithelial cells.
  • Assessment of mutant ERBB3 activity dependence on ERBB2.
  • In vivo efficacy studies of anti-ERBB antibodies and small molecule inhibitors.

Main Results:

  • ERBB3 somatic mutations were identified in approximately 11% of colon and gastric cancers.
  • Mutant ERBB3 transformed epithelial cells independently of ligand binding.
  • Oncogenic activity of mutant ERBB3 was contingent upon kinase-active ERBB2.
  • Anti-ERBB therapies demonstrated efficacy in blocking mutant ERBB3 signaling and inhibiting disease progression in vivo.

Conclusions:

  • ERBB3 can acquire oncogenic mutations in specific cancers, contributing to malignant transformation.
  • Mutant ERBB3's oncogenic function is reliant on ERBB2, presenting a potential therapeutic target.
  • Targeted therapies against ERBB family members show promise for treating ERBB3-mutated cancers.