Evidence map›Paper›PMID 41837391›Full record

ArticleThe journal of pathology. Clinical research2026

Spatial heterogeneity of antibody-drug conjugate targets in pancreatic ductal adenocarcinoma.

Deema Sabtan, Marie-Lisa Eich, Florian Loch, Julen Karl Pérez Zuschneid, Markus Möbs, Judith Böhme, Frederick Klauschen, David Horst, Mihnea P Dragomir, Gabriel Dernbach and 1 more

Abstract read
In one paragraph

Article in The journal of pathology. Clinical research, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

11 authors.

Deema SabtanInstitute of Pathology, Charite, Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin and Humboldt Universität zu Berlin, Berlin, Germany.
Marie-Lisa EichInstitute of Pathology, Charite, Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin and Humboldt Universität zu Berlin, Berlin, Germany.
Florian LochDepartment of Surgery, Charité - Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin and Humboldt-Universität zu Berlin, Berlin, Germany.
Julen Karl Pérez ZuschneidInstitute of Pathology, Charite, Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin and Humboldt Universität zu Berlin, Berlin, Germany.
Markus MöbsInstitute of Pathology, Charite, Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin and Humboldt Universität zu Berlin, Berlin, Germany.
Judith BöhmeInstitute of Pathology, Charite, Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin and Humboldt Universität zu Berlin, Berlin, Germany.
Frederick KlauschenInstitute of Pathology, Charite, Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin and Humboldt Universität zu Berlin, Berlin, Germany.
David HorstInstitute of Pathology, Charite, Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin and Humboldt Universität zu Berlin, Berlin, Germany.
Mihnea P DragomirInstitute of Pathology, Charite, Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin and Humboldt Universität zu Berlin, Berlin, Germany.ORCID https://orcid.org/0000-0002-5550-3516
Gabriel DernbachInstitute of Pathology, Charite, Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin and Humboldt Universität zu Berlin, Berlin, Germany.
Simon SchallenbergInstitute of Pathology, Charite, Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin and Humboldt Universität zu Berlin, Berlin, Germany.

Funding

Berlin Institute of Health, Clinician Scientist ProgramBundesministerium für Bildung und Forschung 16LW0239KCharite University Medicine Berlin MSTARS-2DKTK Berlin Young Investigator Grant 2022Else Kröner-Fresenius-Stiftung 2024_EKEA.77
6 · The paper itself

Abstract

Pancreatic ductal adenocarcinoma (PDAC) is a lethal disease, with limited therapeutic options, few patients showing targetable molecular changes. New therapeutic strategies are necessary. Antibody-drug conjugates (ADCs) have emerged as alternative therapeutic strategies across various cancer types. Herein, we analyze the expression and spatial heterogeneity (six cores per patients) of three ADC targets (c-MET, NECTIN4, and TROP-2) in a cohort of 62 PDAC patients (1,116 tissue cores) and associate their levels with clinicopathological and genomic parameters, and the expression of immune checkpoints. c-MET exhibited significantly higher expression at the tumor front versus tumor center, along with notable intratumoral heterogeneity. In contrast, NECTIN4 and TROP-2 displayed homogeneous expression patterns, with NECTIN4 being absent in approximately two-thirds of cases, while TROP-2 showed consistently strong positivity across tumor regions (98% 3+). By simulating sampling sufficiency for reliable scoring, we observed that, for c-MET, two tumor samples were sufficient to achieve a maximum score of 1+, while for higher scores (2+ and 3+), four samples were required. For NECTIN4, four samples were necessary to detect scores of 1+ and 2+. For TROP-2, for a 3+ score, just two samples were sufficient to reach the maximum score. c-MET or TROP-2 expression scores were not associated with any clinicopathological parameters. In contrast, NECTIN4 expression showed an association with tumor grade. Correlations with immune checkpoints revealed that high TROP-2 expression was inversely correlated with PD-L1 expression. For all three markers no significant differences in expression were found between SMAD4 wild-type and SMAD4-mutated tumors, nor between TP53 wild-type and TP53-mutated tumors. Furthermore, analysis of lymph node and distant (liver and peritoneal) metastases revealed significantly higher c-MET and NECTIN4 expression in the metastatic setting. In conclusion, TROP-2 is highly expressed in most PDACs, independent of clinicopathological and genomic parameters, and inversely correlating with PD-L1, making TROP-2 an ideal ADC target.

Indexed as

Biomarkers, TumorCarcinoma, Pancreatic DuctalCell Adhesion MoleculesImmunoconjugatesPancreatic NeoplasmsAgedAged, 80 and overAntigens, NeoplasmFemaleHumansMaleMiddle AgedNectinsProto-Oncogene Proteins c-metAntigens, NeoplasmBiomarkers, TumorCell Adhesion MoleculesImmunoconjugatesMET protein, humanNECTIN4 protein, humanNectinsProto-Oncogene Proteins c-metTACSTD2 protein, humanantibody–drug conjugatesc‐METNECTIN4pancreatic ductal adenocarcinomaspatial heterogeneitytargeted therapyTROP‐2

Identifiers

PMID41837391
PMCPMC13093404

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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.