Evidence map›Paper›PMID 42092301›Full record

ArticleThe Journal of pathology2026

Genetic analysis of primary lung interdigitating dendritic cell sarcomas.

Mikhail S Ermakov, Juliana Faria Filipe, Sylvia Eidenhammer, German Ott, Iris Halbwedl, Karl Kashofer, Helmut Popper

Abstract read
In one paragraph

Article in The Journal of pathology, 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

7 authors.

Mikhail S ErmakovDiagnostic & Research Institute of Pathology, Medical University Graz, Graz, Austria.ORCID https://orcid.org/0000-0001-7107-4187
Juliana Faria FilipePathology Centre of Champalimaud Centre for the Unknown and Botton-Champalimaud Pancreatic Cancer Centre, Lisbon, Portugal.ORCID https://orcid.org/0000-0001-9978-5642
Sylvia EidenhammerDiagnostic & Research Institute of Pathology, Medical University Graz, Graz, Austria.
German OttDepartment of Clinical Pathology, Robert-Bosch-Krankenhaus, Robert-Bosch Clinics, Stuttgart, Germany.
Iris HalbwedlDiagnostic & Research Institute of Pathology, Medical University Graz, Graz, Austria.
Karl Kashofer *Diagnostic & Research Institute of Pathology, Medical University Graz, Graz, Austria.ORCID https://orcid.org/0000-0002-5803-4014
Helmut Popper *Diagnostic & Research Institute of Pathology, Medical University Graz, Graz, Austria.ORCID https://orcid.org/0000-0003-4970-1265

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Interdigitating dendritic cell sarcomas (IDCSs) are rare tumors that commonly arise in the hematopoietic system and rarely outside. The genetic drivers of IDCS carcinogenesis are unknown; therefore, therapeutic options are limited. We investigated somatic gene mutations and copy-number alterations (CNAs) in nine IDCSs arising in the lung by whole-exome sequencing (WES) paired with shallow whole-genome sequencing (sWGS). Using a panel of immunohistochemical markers, follicular dendritic sarcomas and Langerhans cell sarcomas were excluded, and inflammatory myofibroblastic tumors were excluded based on morphology. The Ki-67 score was used to stratify the tumors into low-grade (≤ 20%) and high-grade (> 20%) tumors. The main question addressed by the study was whether genetic aberrations can be identified in IDCSs and whether these are druggable. High-grade IDCSs showed a higher fraction of genome altered by CNA (48.42%) than low-grade IDCSs (18.15%) and tended to have greater tumor mutation burden (7.56 versus 0.88 mut/Mb; not significant). Heterogeneous gains on chromosome 17 were characteristic of almost all IDCS cases (eight of nine cases, 89%), independent of grade. CNA in cancer-actionable genes was independent of clinicopathological characteristics and included amplifications in EGFR, MYC, MDM4, ERBB2, CCNE1, and BRAF and losses in MTAP, CDKN2A, CDKN2B, MLH1, and VHL, as well as homozygous losses in SMAD2/4, ATM, and TP53. Somatic gene mutations in cancer-related genes were identified in seven of nine IDCSs. No common driver mutations were identified. The heterogeneous genetic landscape suggests a mixed etiology of IDCS carcinogenesis and genomic instability in high-grade tumors. Distinct druggable biomarkers have been identified in almost all tumors, providing novel therapeutic options. © 2026 The Author(s). The Journal of Pathology published by John Wiley & Sons Ltd on behalf of The Pathological Society of Great Britain and Ireland.

Indexed as

Biomarkers, TumorDendritic Cell Sarcoma, InterdigitatingLung NeoplasmsAdultAgedDNA Copy Number VariationsExome SequencingFemaleGenetic Predisposition to DiseaseHumansMaleMiddle AgedMutationBiomarkers, Tumorcopy‐number alterationsdendritic cell sarcomadruggable driversgenetic aberrationslow and high‐gradelung tumorsnext‐generation sequencing

Identifiers

PMID42092301
PMCPMC13341275

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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.