Evidence map›Paper›PMID 41824277›Full record

ArticleBreast cancer (Tokyo, Japan)2026

Expression of HER2, HER3, and TROP2 in primary tumors and brain metastases of breast cancer.

S Kusuhara, T Kogawa, M Shimokawa, C Funasaka, C Kondoh, K Harano, N Matsubara, Y Naito, A Hosono, K Satomi and 10 more

Abstract read
PubMed Publisher
In one paragraph

Article in Breast cancer (Tokyo, Japan), 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
2citing 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

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

  1. Pooled it
  2. Article
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

20 authors.

S KusuharaDepartment of Medical Oncology, National Cancer Center Hospital East, 6-5-1 Kashiwanoha, Kashiwa, Chiba, 277-8577, Japan.
T Kogawa *Department of Medical Oncology, National Cancer Center Hospital East, 6-5-1 Kashiwanoha, Kashiwa, Chiba, 277-8577, Japan. takahiro.kogawa@jfcr.or.jp.ORCID http://orcid.org/0000-0003-3730-6591
M ShimokawaDepartment of Biostatistics, Yamaguchi University Graduate School of Medicine, 1-1-1 Minamiogushi, Ube, Yamaguchi, 755-8505, Japan.
C FunasakaDepartment of Medical Oncology, National Cancer Center Hospital East, 6-5-1 Kashiwanoha, Kashiwa, Chiba, 277-8577, Japan.
C KondohDepartment of Medical Oncology, National Cancer Center Hospital East, 6-5-1 Kashiwanoha, Kashiwa, Chiba, 277-8577, Japan.
K HaranoDepartment of Medical Oncology, National Cancer Center Hospital East, 6-5-1 Kashiwanoha, Kashiwa, Chiba, 277-8577, Japan.
N MatsubaraDepartment of Medical Oncology, National Cancer Center Hospital East, 6-5-1 Kashiwanoha, Kashiwa, Chiba, 277-8577, Japan.
Y NaitoDepartment of Medical Oncology, National Cancer Center Hospital East, 6-5-1 Kashiwanoha, Kashiwa, Chiba, 277-8577, Japan.
A HosonoDepartment of Medical Oncology, National Cancer Center Hospital East, 6-5-1 Kashiwanoha, Kashiwa, Chiba, 277-8577, Japan.
K SatomiDepartment of Diagnostic Pathology, National Cancer Center Hospital, 5-1-1 Tsukiji, Chuo-ku, Tokyo, 104-0045, Japan.
M YoshidaDepartment of Diagnostic Pathology, National Cancer Center Hospital, 5-1-1 Tsukiji, Chuo-ku, Tokyo, 104-0045, Japan.
S FujiiDepartment of Molecular Pathology, Yokohama City University Hospital, 3-9 Fukuura, Kanazawa-ku, Yokohama, Kanagawa, 236-0004, Japan.
T OnishiDepartment of Breast Surgery, National Cancer Center Hospital East, 6-5-1 Kashiwanoha, Kashiwa, Chiba, 277-8577, Japan.
A SutoDepartment of Breast Surgery, National Cancer Center Hospital, 5-1-1 Tsukiji, Chuo-ku, Tokyo, 104-0045, Japan.
K YonemoriDepartment of Medical Oncology, National Cancer Center Hospital, 5-1-1 Tsukiji, Chuo-ku, Tokyo, 104-0045, Japan.
K KoyamaTranslational Research Laboratories, Daiichi Sankyo Co., Ltd., Shinagawa R&D Center, 1-2-58 Hiromachi, Shinagawa-ku, Tokyo, 140-0005, Japan.
R NakamuraTranslational Research Laboratories, Daiichi Sankyo Co., Ltd., Shinagawa R&D Center, 1-2-58 Hiromachi, Shinagawa-ku, Tokyo, 140-0005, Japan.
N MaedaTranslational Research Laboratories, Daiichi Sankyo Co., Ltd., Shinagawa R&D Center, 1-2-58 Hiromachi, Shinagawa-ku, Tokyo, 140-0005, Japan.
Y NaritaDepartment of Neurosurgery and Neuro-Oncology, National Cancer Center Hospital, 5-1-1 Tsukiji, Chuo-ku, Tokyo, 104-0045, Japan.
T Mukohara *Department of Medical Oncology, National Cancer Center Hospital East, 6-5-1 Kashiwanoha, Kashiwa, Chiba, 277-8577, Japan.

Funding

Japan Society for the Promotion of Science 20K08973
6 · The paper itself

Abstract

backgroundHuman epidermal growth factor receptor 2 (HER2)-directed antibody–drug conjugate (ADC) therapy has shown efficacy in HER2-positive breast cancer brain metastases. However, there is still an unmet medical need for further exploration of other suitable targets for ADCs in brain metastases (BMs).

methodsThe expression of HER2, HER3, and trophoblast surface antigen 2 (TROP2) was evaluated using immunohistochemistry (IHC) in pairs of primary tumors (PTs) and surgically resected BMs from 44 patients with breast cancer. Expression levels were classified as 0, 1 + , 2 + , or 3 + based on IHC intensity and the proportion of positive cells.

resultsThe analysis revealed that HER3 and TROP2 expression (IHC ≥ 1 +) was observed in all but one BM specimen. TROP2 was highly expressed (IHC ≥ 2 +) in both BMs and PTs (86% and 70%, respectively; p = 0.11). High expression of HER3 was more frequent in BMs than in PTs (91% and PTs 59%, respectively; p < 0.01), regardless of breast cancer subtype. In individual paired samples, 95.5% (42/44) exhibited equal or higher HER3 expression in BMs than in PTs. In contrast, high HER2 expression (IHC ≥ 2 +) was observed in similar proportions between BMs and PTs (43% and 41%, respectively; p = 1.00).

conclusionsThe observation of more frequent high-level expression of HER3 in BMs than in PTs, and high-level expression of TROP2 in both BMs and PTs suggests the potential of HER3- and TROP2-based ADC therapy for BMs from breast cancer. Further prospective studies are warranted to validate this hypothesis.

Indexed as

Antigens, NeoplasmBrain NeoplasmsBreast NeoplasmsCell Adhesion MoleculesErb-b2 Receptor Tyrosine KinasesReceptor, ErbB-3AdultAgedBiomarkers, TumorFemaleHumansImmunohistochemistryMiddle AgedAntigens, NeoplasmBiomarkers, TumorCell Adhesion MoleculesERBB2 protein, humanErb-b2 Receptor Tyrosine KinasesERBB3 protein, humanReceptor, ErbB-3TACSTD2 protein, humanBrain metastasisBreast cancerHER2HER3TROP2

Identifiers

PMID41824277

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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.