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HER2 CRC — SCE Medical Oncology MCQ

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HardGI CancersHER2 CRCSCE Medical Oncology

A 60-year-old man with colorectal cancer has a liver metastasis biopsied. Pathology confirms adenocarcinoma consistent with CRC origin. Molecular profiling reveals KRAS wild-type, NRAS wild-type, BRAF wild-type, MSS, but HER2 amplification on IHC (3+). What is the potential therapeutic relevance?

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Correct answer: A — HER2 amplification occurs in ~3-5% of RAS/BRAF wild-type CRC and confers anti-EGFR resistance; anti-HER2 therapy (trastuzumab + pertuzumab or trastuzumab + lapatinib) has shown activity in this subgroup

HER2 amplification in CRC (approximately 3-5% of RAS/BRAF wild-type mCRC) is a mechanism of primary anti-EGFR resistance and an emerging actionable target. The HERACLES and MyPathway trials demonstrated activity of dual anti-HER2 therapy (trastuzumab + lapatinib or trastuzumab + pertuzumab) in HER2-amplified mCRC. T-DXd has also shown promising activity (DESTINY-CRC01). Comprehensive molecular profiling should include HER2 assessment in RAS/BRAF WT CRC to identify this subset.

Reference: ESMO 2024 mCRC Guidelines; HERACLES Sartore-Bianchi et al Lancet Oncol 2016; DESTINY-CRC01