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

Targeted Cancer Therapies02:57

Targeted Cancer Therapies

The targeted cancer therapies, also known as “molecular targeted therapies,” take advantage of the molecular and genetic differences between the cancer cells and the normal cells. It needs a thorough understanding of the cancer cells to develop drugs that can target specific molecular aspects that drive the growth, progression, and spread of cancer cells without affecting the growth and survival of other normal cells in the body.
There are several types of targeted therapies against specific...
Targeted Cancer Therapies02:57

Targeted Cancer Therapies

The targeted cancer therapies, also known as “molecular targeted therapies,” take advantage of the molecular and genetic differences between the cancer cells and the normal cells. It needs a thorough understanding of the cancer cells to develop drugs that can target specific molecular aspects that drive the growth, progression, and spread of cancer cells without affecting the growth and survival of other normal cells in the body.
There are several types of targeted therapies against specific...
Pharmacogenetics of Drug Targets: β₂-Adrenergic Receptors, Apo E, Thymidylate Synthase01:11

Pharmacogenetics of Drug Targets: β₂-Adrenergic Receptors, Apo E, Thymidylate Synthase

Genetic polymorphisms in drug targets have emerged as critical determinants of interindividual variability in drug response and toxicity. Pharmacogenomic investigations increasingly focus on identifying these variations to personalize and optimize therapeutic interventions. A drug target may be a receptor, enzyme, or signaling protein involved in pharmacologic responses or disease-related pathways. While early pharmacogenetic studies focused primarily on drug metabolism, current research...
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...
Cancer-Critical Genes II: Tumor Suppressor Genes01:05

Cancer-Critical Genes II: Tumor Suppressor Genes

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 II: Tumor Suppressor Genes01:05

Cancer-Critical Genes II: Tumor Suppressor Genes

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...

You might also read

Related Articles

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

Sort by
Same author

Quantitative Pharmacology Justifying Ribociclib Dose in Early Breast Cancer.

Clinical pharmacokinetics·2026
Same author

Midkine and pleiotrophin in glioma: From mechanistic insights to therapeutic potential.

Neoplasia (New York, N.Y.)·2026
Same author

Correction to: GPX4 is a key ferroptosis regulator orchestrating T cells and CAR-T-cells sensitivity to ferroptosis.

Cancer immunology, immunotherapy : CII·2026
Same author

Physiologically-Based Pharmacokinetics of Ribociclib Drug-Drug Interactions and Organ Impairment Pharmacokinetics in Early Breast Cancer.

Pharmaceuticals (Basel, Switzerland)·2026
Same author

Sex Hormones-Mediated Modulation of Immune Checkpoints in Pregnancy and Recurrent Pregnancy Loss.

International journal of molecular sciences·2026
Same author

3D Bioprinting Strategies in Autoimmune Disease Models.

International journal of molecular sciences·2026

Related Experiment Video

Updated: May 31, 2026

Looking for Driver Pathways of Acquired Resistance to Targeted Therapy: Drug Resistant Subclone Generation and Sensitivity Restoring by Gene Knock-down
08:59

Looking for Driver Pathways of Acquired Resistance to Targeted Therapy: Drug Resistant Subclone Generation and Sensitivity Restoring by Gene Knock-down

Published on: December 11, 2017

Truncated HER2: implications for HER2-targeted therapeutics.

Radoslaw Zagozdzon1, William M Gallagher, John Crown

  • 1Cancer Biology and Therapeutics Group, UCD Conway Institute, UCD School of Biomolecular and Biomedical Science, University College Dublin, Belfield, Dublin 4, Ireland. radoslaw.zagozdzon@ucd.ie

Drug Discovery Today
|June 28, 2011
PubMed
Summary

Trastuzumab is a key treatment for HER2-positive breast cancer, but resistance occurs. Truncated HER2 forms may cause this resistance, necessitating new therapeutic strategies for better patient outcomes.

More Related Videos

Polymalic Acid-based Nano Biopolymers for Targeting of Multiple Tumor Markers: An Opportunity for Personalized Medicine?
14:20

Polymalic Acid-based Nano Biopolymers for Targeting of Multiple Tumor Markers: An Opportunity for Personalized Medicine?

Published on: June 13, 2014

Building Up a High-throughput Screening Platform to Assess the Heterogeneity of HER2 Gene Amplification in Breast Cancers
11:34

Building Up a High-throughput Screening Platform to Assess the Heterogeneity of HER2 Gene Amplification in Breast Cancers

Published on: December 5, 2017

Related Experiment Videos

Last Updated: May 31, 2026

Looking for Driver Pathways of Acquired Resistance to Targeted Therapy: Drug Resistant Subclone Generation and Sensitivity Restoring by Gene Knock-down
08:59

Looking for Driver Pathways of Acquired Resistance to Targeted Therapy: Drug Resistant Subclone Generation and Sensitivity Restoring by Gene Knock-down

Published on: December 11, 2017

Polymalic Acid-based Nano Biopolymers for Targeting of Multiple Tumor Markers: An Opportunity for Personalized Medicine?
14:20

Polymalic Acid-based Nano Biopolymers for Targeting of Multiple Tumor Markers: An Opportunity for Personalized Medicine?

Published on: June 13, 2014

Building Up a High-throughput Screening Platform to Assess the Heterogeneity of HER2 Gene Amplification in Breast Cancers
11:34

Building Up a High-throughput Screening Platform to Assess the Heterogeneity of HER2 Gene Amplification in Breast Cancers

Published on: December 5, 2017

Area of Science:

  • Oncology
  • Molecular Biology
  • Immunotherapy

Background:

  • The Human Epidermal growth factor Receptor 2 (HER2) is a critical target in cancer therapy.
  • Trastuzumab, an anti-HER2 antibody, is a cornerstone treatment for HER2-positive breast cancer.
  • A significant challenge in HER2-targeted therapy is the development of treatment resistance.

Purpose of the Study:

  • To investigate the role of truncated HER2 forms in trastuzumab resistance.
  • To highlight the need for modified therapeutic approaches in cases of HER2-positive cancer with truncated HER2.
  • To discuss emerging therapeutic strategies for HER2-positive cancers.

Main Methods:

  • Review of existing studies on HER2 receptor variants.
  • Analysis of clinical data on trastuzumab response rates.
  • Exploration of novel therapeutic compounds targeting HER2.

Main Results:

  • Truncated forms of HER2 are implicated as a potential mechanism of trastuzumab resistance.
  • Detection of truncated HER2 suggests a need to alter standard treatment protocols.
  • Several new therapeutic agents are under development for HER2-positive cancers.

Conclusions:

  • Truncated HER2 represents a significant factor contributing to trastuzumab resistance in breast cancer.
  • Personalized therapeutic strategies incorporating detection of HER2 variants are crucial.
  • Advancements in novel compounds offer future promise for overcoming resistance in HER2-driven malignancies.