Evidence map›Paper›PMID 42527418›Full record

ArticleScientific reports2026

SMARCA2 and SMARCA4-deficiency is associated with a distinct molecular and microenvironmental subtype of esophageal adenocarcinoma.

Matteo Montalbano, Karl Knipper, Hans A Schlößer, Bastian Grothey, Reinhard Buettner, Christiane Josephine Bruns, Thomas Zander, Su Ir Lyu, Alexander Quaas

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In one paragraph

Article in Scientific reports, 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
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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

9 authors.

Matteo Montalbano *Institute of Pathology, Medical Faculty, University Hospital Cologne, University of Cologne, Kerpener Str. 62, Cologne, 50937, Germany. matteo.montalbano01@unipa.it.
Karl Knipper *Department of General, Visceral, Thoracic and Transplantation Surgery, Medical Faculty, University Hospital Cologne, University of Cologne, Cologne, Germany.
Hans A SchlößerDepartment of General, Visceral, Thoracic and Transplantation Surgery, Medical Faculty, University Hospital Cologne, University of Cologne, Cologne, Germany.
Bastian GrotheyInstitute of Pathology, Medical Faculty, University Hospital Cologne, University of Cologne, Kerpener Str. 62, Cologne, 50937, Germany.
Reinhard BuettnerInstitute of Pathology, Medical Faculty, University Hospital Cologne, University of Cologne, Kerpener Str. 62, Cologne, 50937, Germany.
Christiane Josephine BrunsDepartment of General, Visceral, Thoracic and Transplantation Surgery, Medical Faculty, University Hospital Cologne, University of Cologne, Cologne, Germany.
Thomas ZanderDepartment of Internal Medicine I, Medical Faculty, University Hospital Cologne, University of Cologne, Cologne, Germany.
Su Ir LyuInstitute of Pathology, Medical Faculty, University Hospital Cologne, University of Cologne, Kerpener Str. 62, Cologne, 50937, Germany.
Alexander QuaasInstitute of Pathology, Medical Faculty, University Hospital Cologne, University of Cologne, Kerpener Str. 62, Cologne, 50937, Germany.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Dysregulation of chromatin remodeling is a key driver of malignant progression. The SWI/SNF ATPase subunits SMARCA2 and SMARCA4 are essential for chromatin dynamics, yet the clinicopathological and microenvironmental landscape of SMARCA2/4-deficient esophageal adenocarcinoma (EAC) remains insufficiently defined. We analyzed 722 resected EACs from a large Western cohort. SMARCA2 and SMARCA4 status were assessed by immunohistochemistry, and tumors were classified as SMARCA-intact or SMARCA-deficient (complete loss of nuclear expression in tumor cells with internal controls). Molecular co-alterations were evaluated by immunohistochemistry and fluorescence in situ hybridization, including amplifications of MET, ERBB2 (HER2), EGFR, PIK3CA, MYC, MDM2, TERT, and Y-chromosome loss (LOY). Several markers were available from prior works. Digital pathology workflows quantified CAF markers (SMA, PDGFRβ, FAP, Periostin, Tenascin) and immune infiltrates (including CD4, CD8, FOXP3, CD20, MUM1, mast cell tryptase). Overall survival was examined using Kaplan-Meier estimates and Cox regression models. SMARCA2/4-deficient tumors accounted for 11.2% of the cohort (81/722) and were enriched among patients aged ≥ 65 years. SMARCA-deficient EACs showed a significantly higher frequency of MET amplification (16.9%), particularly after neoadjuvant therapy. Within SMARCA-deficient tumors, PDGFRβ-positive CAFs, increased plasma cell (MUM1+) and mast cell infiltrates correlated with a favorable outcome, whereas loss of Y-chromosome (LOY) identified an adverse-risk subgroup with particularly poor prognosis. This largest-to-date study defines SMARCA-deficient EAC as a distinct subtype characterized by frequent MET amplification and high-risk interaction with LOY, alongside prognostically relevant stromal-immune features, supporting refined biomarker-based risk stratification and therapeutic exploration.

Indexed as

AdenocarcinomaDNA HelicasesEsophageal NeoplasmsNuclear ProteinsTranscription FactorsTumor MicroenvironmentAgedBiomarkers, TumorFemaleHumansIn Situ Hybridization, FluorescenceMaleMiddle AgedPrognosisBiomarkers, TumorDNA HelicasesNuclear ProteinsSMARCA2 protein, humanSMARCA4 protein, humanTranscription FactorsEsophageal adenocarcinomaMET amplificationSMARCA2/SMARCA4 deficiencySWI/SNF chromatin remodelingTumor microenvironment

Identifiers

PMID42527418
PMCPMC13421451

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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.