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Targeted Cancer Therapies

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...

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Related Experiment Video

Updated: Jun 8, 2026

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

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

Published on: July 25, 2020

Targeting erbB receptors.

Zheng Cai¹, Hongtao Zhang, Jing Liu

¹Department of Pathology and Laboratory Medicine, University of Pennsylvania, Philadelphia, PA 19104-6082, USA.

Seminars in Cell & Developmental Biology

|September 21, 2010

Summary

This summary is machine-generated.

Targeted cancer therapies disabling epidermal growth factor receptor (EGFR) family kinases, like HER2, are crucial. Our review details mechanisms of action for novel therapeutics to combat human tumors.

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Area of Science:

Oncology
Molecular Biology
Biochemistry

Background:

Members of the epidermal growth factor receptor (EGFR) family of tyrosine kinases, also known as erbB or HER receptors, are frequently overexpressed or activated in human tumors.
These receptors are critical targets for developing effective cancer therapies.
Targeted therapy strategies aim to disable these receptors to reverse tumor malignancy.

Purpose of the Study:

To review the mechanisms of action for various therapeutic approaches targeting erbB family receptors.
To elucidate the biochemical and biological principles underlying the disabling of HER2 homomeric or HER2-EGFR heteromeric receptors.
To inform the development of novel and more efficient therapeutics for cancers driven by erbB family signaling.

Main Methods:

Review of studies detailing mechanisms of action for monoclonal antibodies, peptide mimetics, recombinant proteins, and small molecules.
Analysis of approaches developed in-house and by other researchers.
Examination of biochemical and biological principles derived from studies on HER2 and EGFR receptor interactions.

Main Results:

Disabling HER2 receptors with monoclonal antibodies reverses the malignant phenotype through distinct mechanisms compared to blocking ligand binding to EGFR.
Various therapeutic modalities, including antibodies, peptide mimetics, recombinant proteins, and small molecules, have been developed to target erbB receptors.
Understanding the principles of disabling HER2 homomeric or HER2-EGFR heteromeric receptors is key to advancing targeted cancer therapy.

Conclusions:

Targeted therapies offer a promising strategy for cancer treatment by disabling key signaling pathways.
The mechanisms of action for therapeutics targeting erbB family receptors are diverse and depend on the specific receptor and modality used.
Further research into the biochemical and biological principles of erbB receptor inhibition will lead to improved cancer therapeutics.