ArticleESMO gastrointestinal oncology2026
Impact of claudin 18.2 expression on the efficacy of trastuzumab deruxtecan in patients with HER2-positive gastric or gastroesophageal junction cancer.
Article in ESMO gastrointestinal oncology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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Who cites it
2 citing papers in PubMed.
- Dynamic HER2 reassessment and precision sequencing after trastuzumab in HER2-positive advanced gastric cancer.ESMO gastrointestinal oncology · 2026Review
- Exploratory analysis of HER2-positive/CLDN18.2-positive metastatic gastric and gastroesophageal junction cancer toward future therapeutic development.ESMO gastrointestinal oncology · 2026Article
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Authors and funding
25 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Human epidermal growth factor receptor 2 (HER2) and claudin 18.2 (CLDN18.2) are key therapeutic targets in metastatic gastric and gastroesophageal junction cancer (mGC/GEJC). Trastuzumab deruxtecan (T-DXd) is standard care for previously treated HER2-positive mGC/GEJC, but the prognostic impact of CLDN18.2 remains unclear. Patients and methods: We retrospectively reviewed patients with HER2-positive mGC/GEJC treated with T-DXd at National Cancer Center Hospital East until February 2025. T-DXd outcomes were compared between CLDN18.2-positive (≥2+ in ≥75% of tumor cells) and -negative patients in two cohorts: those with HER2 positivity before first-line therapy (overall cohort) and those maintaining HER2 positivity immediately before T-DXd (remaining HER2 cohort). CLDN18.2 expression was evaluated at any time before T-DXd administration. Results: Eighty-seven patients were included in the overall cohort and 30 in the remaining HER2 cohort. In the overall cohort, progression-free survival (PFS) was shorter in CLDN18.2-positive patients [3.9 versus 5.3 months; hazard ratio (HR) 1.87, 95% confidence interval (CI) 1.04-3.34, Conclusions: CLDN18.2 positivity may attenuate the efficacy of T-DXd in HER2-positive mGC/GEJC, supporting the rationale for dual blockade of CLDN18.2 and HER2.
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