Reporting HER2 IHC in 2026: CAP-Aligned Reporting Across Tumor Types and the Impact of Intratumoral Heterogeneity

REFINING HER2 IHC ASSESSMENT GUIDED BY CAP REPORTING TEMPLATE: ENABLING ACCURATE CLASSIFICATION ACROSS SOLID TUMORS AND ADDRESSING INTRATUMORAL HETEROGENEITY

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The use of IHC staining of tissue samples to guide targeted treatment is widely used in clinical practice, and is recommended by expert groups for many tumor types and biomarkers. [11,12] The classical approach to IHC scoring for biomarkers, such as human epidermal growth factor receptor-2 (HER2), classifies specimens as either ‘positive’ or ‘negative’, scoring samples as IHC0, 1+, 2+ or 3+ per pathologists’ visual interpretation. [11,12]

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HER2 Unraveled—The Vital Distinction Between Overexpression and Gene Amplification in Cancer

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Human epidermal growth factor receptor 2 (HER2) is a crucial biomarker in contemporary cancer management. Alterations in the HER2 protein or in the protein-coding gene, erythroblastic leukemia viral oncogene homolog 2 (ERBB2; hereafter referred to as HER2 in line with common practice), have significant clinical implications. Overexpression of the HER2 protein, gene amplification or activating mutations can overactivate or enhance downstream HER2 signaling pathways. Increased HER2 signaling drives key processes in tumorigenesis, including cellular transformation, survival, proliferation, and invasion.

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Navigating HER2 Testing: Unveiling the Strengths and Limitations to Optimize Biomarker Assessment

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Due to the availability of human epidermal growth factor receptor 2 (HER2)-directed therapies, testing for HER2 alterations, including overexpression, gene amplification or mutations is recommended in treatment guidelines for various tumor types, including breast cancer, gastric cancer, biliary tract cancer, cervical cancer, colorectal cancer, non-small cell lung cancer (NSCLC), and others.1-10

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Prevalence and role of HER2 driver mutations in cancers

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Apart from Human Epidermal Growth Factor Receptor 2 (HER2) gene amplification or receptor protein overexpression (discussed in Article 1 and Article 3), dysregulation of HER2 activity may also be caused by HER2 gene mutations.1 Approximately 90% of the mutations are clustered in the extracellular dimerization domain and intracellular kinase domain, with the remainder occurring within the juxtamembrane or transmembrane domains.

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Decoding HER2 IHC Scoring Guidelines: Understanding Immunohistochemistry Scoring in Different Cancers

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Human Epidermal Growth Factor Receptor 2 (HER2) aberrations, such as overexpression, HER2 gene amplification, and HER2 mutations, have been extensively researched and are associated with tumor proliferation in various solid tumor types including breast cancer, gastric cancer, gastroesophageal junction (GEJ) cancer, biliary tract cancer, colorectal cancer (CRC), non-small cell lung cancer (NSCLC), and bladder cancer.1 The presence of HER2 aberrations is linked to reduced survival, increased chance of brain metastasis, and treatment resistance.2

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Redefining-HERness-HER2-low-and-ultralow-breast-cancers

Redefining HERness: HER2-low and ultralow breast cancers

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The 2018 guidelines from the American Society of Clinical Oncology (ASCO) and the College of American Pathology (CAP) classify human epidermal growth factor receptor-2 (HER2) status in breast cancer (BC) according to immunohistochemistry (IHC) staining results of biopsy specimens, ranging from IHC 0 to IHC 3+, plus in situ hybridization (ISH) test results.1

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HER2 as a biomarker in cancers_0824

HER2 as a biomarker in cancers

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Human epidermal growth factor receptor-2 (HER2) is a member of the erythroblastic oncogene B (ERBB) family of transmembrane tyrosine kinase receptors that also includes epidermal growth factor receptor (EGFR, also known as HER1), and human epidermal growth factor receptors -3 and -4 (HER3, HER4).1,2 Despite being a receptor, HER2 has no known ligand, but its conformation is similar to the ligand-activated form of other ERBB family members, favoring heterodimerization with them.1,3

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