Evidence map›Paper›PMID 42127888›Full record

ArticleESMO open2026

Clinicopathologic characteristics and genomic profiling of HER2-low advanced gastric or gastroesophageal junction cancer.

C K Lee, D H Seo, S Park, T Yuh, Y Kim, H Park, J S Shim, H Kim, H S Kim, M Jung and 2 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in ESMO open, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed, 1 pooled it
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

6 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Guideline
  2. Review
  3. Article
  4. Article
  5. Review
  6. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

12 authors.

C K LeeDivision of Medical Oncology, Department of Internal Medicine, Yonsei Cancer Center, Yonsei University College of Medicine, Seoul, South Korea; Song-Dang Institute for Cancer Research, Yonsei University College of Medicine, Seoul, South Korea.
D H SeoSong-Dang Institute for Cancer Research, Yonsei University College of Medicine, Seoul, South Korea; Department of Internal Medicine, Yonsei University College of Medicine, Seoul, South Korea.
S ParkSong-Dang Institute for Cancer Research, Yonsei University College of Medicine, Seoul, South Korea.
T YuhDepartment of Internal Medicine, Yonsei University College of Medicine, Seoul, South Korea.
Y KimDepartment of Internal Medicine, Yonsei University College of Medicine, Seoul, South Korea.
H ParkDepartment of Internal Medicine, Yonsei University College of Medicine, Seoul, South Korea.
J S ShimDepartment of Internal Medicine, Yonsei University College of Medicine, Seoul, South Korea.
H KimDepartment of Pathology, Yonsei University College of Medicine, Seoul, South Korea.
H S KimDivision of Medical Oncology, Department of Internal Medicine, Yonsei Cancer Center, Yonsei University College of Medicine, Seoul, South Korea; Song-Dang Institute for Cancer Research, Yonsei University College of Medicine, Seoul, South Korea.
M JungDivision of Medical Oncology, Department of Internal Medicine, Yonsei Cancer Center, Yonsei University College of Medicine, Seoul, South Korea; Song-Dang Institute for Cancer Research, Yonsei University College of Medicine, Seoul, South Korea.
H C ChungDivision of Medical Oncology, Department of Internal Medicine, Yonsei Cancer Center, Yonsei University College of Medicine, Seoul, South Korea; Song-Dang Institute for Cancer Research, Yonsei University College of Medicine, Seoul, South Korea.
S Y RhaDivision of Medical Oncology, Department of Internal Medicine, Yonsei Cancer Center, Yonsei University College of Medicine, Seoul, South Korea; Song-Dang Institute for Cancer Research, Yonsei University College of Medicine, Seoul, South Korea; Department of Brain Korea 21 PLUS Project for Medical Science, Yonsei University College of Medicine, Seoul, South Korea. Electronic address: RHA7655@yuhs.ac.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundHuman epidermal growth factor 2 (HER2)-low expression has recently emerged as a potential therapeutic target with the advent of HER2-directed antibody-drug conjugates. However, the clinicopathologic and molecular features of HER2-low advanced gastric or gastroesophageal junction (G/GEJ) cancer remain inadequately characterized. PATIENTS AND

methodsWe retrospectively analyzed 2007 patients with stage IV G/GEJ cancer treated between 2015 and 2022 at Yonsei Cancer Center, Korea. HER2 status was classified as HER2-high (immunohistochemistry [IHC] 3+ or IHC 2+/in situ hybridization [ISH]+), HER2-low (IHC 2+/ISH- or IHC 1+) and HER2-null (IHC 0). Clinicopathologic features and survival outcomes were assessed in patients receiving first-line doublet chemotherapy with or without immune checkpoint inhibitors (ICIs). For molecular analyses, pretreatment tumors from 777 patients underwent in-house next-generation sequencing (NGS), excluding Epstein-Barr virus (EBV)-positive and microsatellite instability (MSI)-high cases.

resultsAmong 2007 patients, 372 (18.5%) were HER2-high, 523 (26.1%) were HER2-low, and 1112 (55.4%) were HER2-null. HER2-low tumors closely resembled HER2-null tumors in histopathology, EBV status, MSI, and programmed death-ligand 1 status. In the survival analysis cohort (n = 1417), first-line progression-free survival was 8.0 months (HER2-high), 6.0 months (HER2-low), and 6.1 months (HER2-null), while overall survival was 17.2, 13.4, and 14.5 months, respectively. Combination with ICIs conferred greater survival benefit in HER2-low tumors compared with HER2-null tumors. In the NGS cohort (n = 777), HER2-low tumors were significantly enriched for angiogenesis pathway alterations, which were associated with worse survival, a pattern not observed in other subgroups.

conclusionsHER2-low G/GEJ cancer represents a distinct biological subtype with intermediate survival outcomes and specific angiogenesis-related molecular features. These findings support the need for dedicated therapeutic strategies and further clinical research in HER2-low G/GEJ cancer.

Indexed as

Erb-b2 Receptor Tyrosine KinasesEsophageal NeoplasmsEsophagogastric JunctionStomach NeoplasmsAgedBiomarkers, TumorFemaleHumansMaleMiddle AgedRetrospective StudiesBiomarkers, TumorERBB2 protein, humanErb-b2 Receptor Tyrosine Kinasesgastric cancergastroesophageal junction cancerHER2-lowimmunotherapymolecular profiling

Identifiers

PMID42127888
PMCPMC13196360

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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.