Related Experiment Video
Updated: Aug 16, 2025
Generation of High-Throughput Three-Dimensional Tumor Spheroids for Drug Screening
Published on: September 5, 2018
HER3 Alterations in Cancer and Potential Clinical Implications
Mary Kate Kilroy1, SoYoung Park1,2, Wasim Feroz1
1Department of Pharmaceutical Sciences, James L. Winkle College of Pharmacy, University of Cincinnati, Cincinnati, OH 45267, USA.
Abstract:
In recent years, the third member of the HER family, kinase impaired HER3, has become a target of interest in cancer as there is accumulating evidence that HER3 plays a role in tumor growth and progression. This review focuses on HER3 activation in bladder, breast, colorectal, and lung cancer disease progression. HER3 mutations occur at a rate up to ~10% of tumors dependent on the tumor type. With patient tumors routinely sequenced for gene alterations in recent years, we have focused on HER3 mutations in bladder, breast, colon, and lung cancers particularly in response to targeted therapies and the potential to become a resistance mechanism. There are currently several HER3 targeting drugs in the pipeline, possibly improving outcomes for cancer patients with tumors containing HER3 activation and/or alterations.
Insights
The human epidermal growth factor receptor 3 (HER3) is implicated in various cancers. Understanding HER3 mutations and activation is key for developing targeted therapies and overcoming treatment resistance.
Area of Science:
- Oncology
- Molecular Biology
- Genetics
Background:
- The human epidermal growth factor receptor 3 (HER3) is increasingly recognized for its role in cancer progression.
- HER3 activation and mutations are observed across multiple cancer types, including bladder, breast, colorectal, and lung cancers.
- Tumor genetic sequencing frequently identifies HER3 alterations, highlighting its clinical relevance.
Purpose of the Study:
- To review the role of HER3 activation and mutations in the progression of bladder, breast, colorectal, and lung cancers.
- To examine HER3 alterations as potential mechanisms of resistance to targeted therapies.
- To discuss the implications of HER3 targeting drugs currently in development.
Main Methods:
- Literature review focusing on studies investigating HER3 in cancer progression and targeted therapy resistance.
- Analysis of reported frequencies of HER3 mutations across different cancer types.
- Overview of current and emerging HER3-targeting therapeutic strategies.
Main Results:
- HER3 mutations occur in up to approximately 10% of tumors, varying by cancer type.
- HER3 activation is linked to tumor growth and progression in key solid tumors.
- HER3 alterations represent a significant factor in the development of resistance to cancer therapies.
Conclusions:
- HER3 is a critical factor in the pathogenesis and progression of several major cancers.
- Targeting HER3 holds promise for overcoming therapeutic resistance and improving patient outcomes.
- Ongoing development of HER3-targeted drugs may offer new treatment avenues for patients with specific tumor alterations.
Related Concept Videos
02:38Mitogens and the Cell Cycle
02:53Adaptive Mechanisms in Cancer Cells
Some of the advantages that cancer cells have on normal cells include - enhanced ability to divide without terminally differentiating, induce new blood vessel formation,...
02:23Abnormal Proliferation
03:03mTOR Signaling and Cancer Progression
The mTOR pathway or the...
02:07Tumor Progression
Colon cancer is one of the best-documented examples of tumor progression. Early mutation in the APC gene in colon cells causes a small growth on the colon wall called a polyp. With time, this polyp grows into a benign, pre-cancerous tumor. Further...
01:05Cancer-Critical Genes II: Tumor Suppressor Genes
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...