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

Cancer-Critical Genes II: Tumor Suppressor Genes01:05

Cancer-Critical Genes II: Tumor Suppressor Genes

7.3K
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...
7.3K
Metastasis02:30

Metastasis

5.5K
Metastasis is the spread of cancer cells from the original site to distant locations in the body. Cancer cells can spread via blood vessels (hematogenous) as well as lymph vessels in the body.
Epithelial-to-Mesenchymal Transition
The epithelial-to-mesenchymal transition or EMT is a developmental process commonly observed in wound healing, embryogenesis, and cancer metastasis. EMT is induced by transforming growth factor-beta (TGF-β) or receptor tyrosine kinase (RTK) ligands, which further...
5.5K
Mitogens and the Cell Cycle02:38

Mitogens and the Cell Cycle

6.4K
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...
6.4K

You might also read

Related Articles

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

Sort by
Same author

NaHS inhibits cell proliferation by enhancing oxidative stress and apoptosis in HCT116 cells.

Molecular biology reports·2026
Same author

Intra-articular VEGF inhibition attenuates cartilage degeneration in a rat model of post-traumatic osteoarthritis: a pilot histopathological study.

Rheumatology international·2026
Same author

Therapeutic Effect of Parthenolide on Paclitaxel-Induced Cardiotoxicity in Rats.

Journal of cellular biochemistry·2026
Same author

Pycnogenol attenuates thioacetamide-induced neurobehavioral impairment and hepatotoxicity via multi-target molecular modulation.

BMC pharmacology & toxicology·2026
Same author

Local Energy Decomposition of Intramolecular Interactions: The CovaLED Approach and Its Application to Molecular Recognition in Biomolecular Assemblies.

ACS central science·2026
Same author

Targeting Oxidative Stress and Inflammation in Pembrolizumab-Induced Renal Injury: A Comparative Evaluation of the Protective Effects of Flunarizine and Carvacrol in Rats.

Biomolecules·2026

Related Experiment Video

Updated: Jun 4, 2025

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

12.6K

HER-2 SMASH.

Celal Alandağ1, Ayşegül Öztürk2, Fatih Yulak3

  • 1Department of Medical Oncology, Sivas Medicana Hospital, Sivas, Türkiye. dralandag@hotmail.com.

Cancer Chemotherapy and Pharmacology
|December 23, 2024
PubMed
Summary

Lapatinib treatment upregulates human epidermal growth factor-2 (HER-2) receptors in cancer cells, enhancing the effectiveness of HER-2 targeted therapies like trastuzumab and T-DM1. This novel "smash method" broadens treatment applicability for HER-2 low or negative tumors.

Keywords:
Her-2 overexpressionLapatinibSmash methodTrastuzumab

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

7.2K
Optimization of a Multiplex RNA-based Expression Assay Using Breast Cancer Archival Material
11:12

Optimization of a Multiplex RNA-based Expression Assay Using Breast Cancer Archival Material

Published on: August 1, 2018

8.0K

Related Experiment Videos

Last Updated: Jun 4, 2025

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

12.6K
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

7.2K
Optimization of a Multiplex RNA-based Expression Assay Using Breast Cancer Archival Material
11:12

Optimization of a Multiplex RNA-based Expression Assay Using Breast Cancer Archival Material

Published on: August 1, 2018

8.0K

Area of Science:

  • Oncology
  • Molecular Biology
  • Pharmacology

Background:

  • HER-2 targeted therapies are effective only in a subset of cancers with HER-2 overexpression.
  • Many cancer types, including breast and colon cancers, naturally exhibit low or absent HER-2 expression, limiting treatment options.

Purpose of the Study:

  • To investigate the upregulation of human epidermal growth factor-2 (HER-2) receptors in HER-2 negative/low cancer cell lines (MCF-7 and HT-29).
  • To evaluate the impact of lapatinib-induced HER-2 upregulation on the efficacy of HER-2 targeted therapies (trastuzumab, T-DM1).

Main Methods:

  • Non-cytotoxic lapatinib doses were administered for 10 days to MCF-7 and HT-29 cell lines to induce HER-2 overexpression.
  • HER-2 levels were quantified using ELISA and immunofluorescence assays before and after lapatinib treatment.
  • The impact of trastuzumab and T-DM1 on cell viability was assessed, alongside analysis of HER-2 pathway proteins to elucidate mechanisms.

Main Results:

  • Lapatinib administration for 10 days successfully induced significant HER-2 receptor overexpression in both MCF-7 and HT-29 cells.
  • A notable increase in the anti-cancer activity and cytotoxicity of trastuzumab and T-DM1 was observed following lapatinib-induced HER-2 upregulation.

Conclusions:

  • The developed 'smash method' effectively converts HER-2 negative or low tumors into HER-2 overexpressing ones, iatrogenically.
  • This approach holds potential for expanding the patient population eligible for HER-2 targeted therapies, improving treatment outcomes across diverse cancer types.