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 Experiment Videos

The neu (c-erbB-2) oncogene.

H C Maguire1, M I Greene

  • 1Department of Pathology, School of Medicine, University of Pennsylvania, Philadelphia 19104-6082.

Seminars in Oncology
|April 1, 1989
PubMed
Summary
This summary is machine-generated.

Related Concept Videos

You might also read

Related Articles

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

Sort by
Same author

FoxP3 in T<sub>reg</sub> cell biology: a molecular and structural perspective.

Clinical and experimental immunology·2019
Same author

Genetic and molecular aspects of demyelination.

Immunology today·2014
Same author

The I-J subregion and surveillance.

Immunology today·2014
Same author

Survivin as a therapeutic target in Sonic hedgehog-driven medulloblastoma.

Oncogene·2014
Same author

In vivo molecular imaging of HER2 expression in a rat model of Barrett's esophagus adenocarcinoma.

Diseases of the esophagus : official journal of the International Society for Diseases of the Esophagus·2014
Same author

YAP modifies cancer cell sensitivity to EGFR and survivin inhibitors and is negatively regulated by the non-receptor type protein tyrosine phosphatase 14.

Oncogene·2012
Same journal

A systematic scoping review of cancer-related anemia treatment: Comparative trial outcomes, current guidelines, and future perspectives.

Seminars in oncology·2026
Same journal

Steroid-induced tumor lysis syndrome in solid tumors: A case report and review of the literature.

Seminars in oncology·2026
Same journal

PSMA PET/CT staging in intermediate-risk prostate cancer: Toward risk-adapted implementation.

Seminars in oncology·2026
Same journal

Angiogenesis and the corresponding antiangiogenic therapy in gastroenteropancreatic neuroendocrine neoplasms.

Seminars in oncology·2026
Same journal

Post-translational regulation of steroidogenesis and its clinical relevance in hormone responsive cancers.

Seminars in oncology·2026
Same journal

Physics-informed machine learning for tumor microenvironment-responsive nanomedicine: Recent updates.

Seminars in oncology·2026
See all related articles

The neu gene, or c-erbB-2, is a receptor in humans linked to various adenocarcinomas. Overexpression of this gene is common in breast, colon, and pancreatic cancers, but its specific role remains unclear.

Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Background:

  • The neu gene was initially discovered in rat tumors induced by ethyl nitrosourea.
  • Its human counterpart, c-erbB-2, is located on chromosome 17q21.
  • c-erbB-2 encodes a transmembrane receptor similar to the Epidermal Growth Factor Receptor (EGFr/c-erbB-1).

Purpose of the Study:

  • To investigate the role of c-erbB-2 in human cancers.
  • To understand the implications of c-erbB-2 amplification and overexpression.

Main Methods:

  • Gene mapping to identify the location of the human c-erbB-2 gene.
  • Analysis of tumor samples for gene amplification and protein overexpression.

Main Results:

Related Experiment Videos

  • c-erbB-2 is amplified and/or overexpressed in a significant percentage of adenocarcinomas, particularly those of the breast, colon, and pancreas.
  • The specific ligand for c-erbB-2 has not yet been identified.
  • The distinct characteristics of tumors overexpressing c-erbB-2 are not yet fully understood.

    • Conclusions:

    • c-erbB-2 is a significant factor in certain adenocarcinomas.
    • Further research is needed to identify the c-erbB-2 ligand and elucidate the functional consequences of its overexpression in cancer.