Evidence map›Paper›PMID 42665817›Full record

ArticleBMC medicine2026

Systemic immune activation in hereditary cancer predisposition syndromes: a cross-sectional study.

István Kelemen, Klaudia Horti-Oravecz, Anikó Bozsik, Tímea Pócza, János Papp, István Likó, Patrícia Neuperger, Fanni Balogh, Ágnes Kemény, Petra Nagy and 8 more

Abstract read
In one paragraph

Article in BMC medicine, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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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

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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

18 authors.

István Kelemen *Department of Molecular Genetics and the National Tumorbiology Laboratory, National Institute of Oncology, Budapest, Hungary.
Klaudia Horti-Oravecz *Department of Molecular Genetics and the National Tumorbiology Laboratory, National Institute of Oncology, Budapest, Hungary.
Anikó BozsikDepartment of Molecular Genetics and the National Tumorbiology Laboratory, National Institute of Oncology, Budapest, Hungary.
Tímea PóczaDepartment of Molecular Genetics and the National Tumorbiology Laboratory, National Institute of Oncology, Budapest, Hungary.
János PappDepartment of Molecular Genetics and the National Tumorbiology Laboratory, National Institute of Oncology, Budapest, Hungary.
István LikóDepartment of Molecular Genetics and the National Tumorbiology Laboratory, National Institute of Oncology, Budapest, Hungary.
Patrícia NeupergerLaboratory of Functional Genomics, HUN-REN Biological Research Centre, Core Facility, Szeged, Hungary.
Fanni BaloghLaboratory of Functional Genomics, HUN-REN Biological Research Centre, Core Facility, Szeged, Hungary.
Ágnes KeményDepartment of Physiology and Biochemistry, University of Veterinary Medicine, Budapest, Hungary.
Petra NagyDepartment of Molecular Genetics and the National Tumorbiology Laboratory, National Institute of Oncology, Budapest, Hungary.
Viktória VereczkiDepartment of Molecular Genetics and the National Tumorbiology Laboratory, National Institute of Oncology, Budapest, Hungary.
Szonja Polett PósaDepartment of Molecular Genetics and the National Tumorbiology Laboratory, National Institute of Oncology, Budapest, Hungary.
Lőrinc Sándor PongorHUN-REN-NIO-TTK-HCEMM Oncogenomics Research Group, Budapest, Hungary.
Dorottya KövesdiDepartment of Immunology, Eötvös Loránd University, Budapest, Hungary.
Henriett ButzDepartment of Molecular Genetics and the National Tumorbiology Laboratory, National Institute of Oncology, Budapest, Hungary.
Attila PatócsDepartment of Molecular Genetics and the National Tumorbiology Laboratory, National Institute of Oncology, Budapest, Hungary.
Gábor János SzebeniLaboratory of Functional Genomics, HUN-REN Biological Research Centre, Core Facility, Szeged, Hungary.
Vince Kornél GrolmuszDepartment of Molecular Genetics and the National Tumorbiology Laboratory, National Institute of Oncology, Budapest, Hungary. grolmusz.vince@oncol.hu.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundImmune surveillance mechanisms contribute to the elimination of precancerous lesions in hereditary cancer predisposition syndromes (HCPSs).

methodsBy combining single-cell transcriptomics, multiparametric mass cytometry and cytokine profiling of the systemic immune environment in 391 individuals among whom 227 are living with HCPSs we investigated phenotypic alterations in cancer-free individuals with HCPS.

resultsA decrease in peripheral B cell abundance and their more differentiated phenotype have been confirmed both in breast cancer patients with germline pathogenic variants in BRCA1 (gpath(BRCA1)) and in patients living with Lynch syndrome (LS). Pre-cancer women with gpath(BRCA1) exhibited an activated phenotype of multiple immune cell lineages, similar to those with manifest disease. In LS, B cell phenotypes exhibited the largest changes in response to cancer eradication, while increased peripheral IL-6 levels was detected even in presymptomatic individuals with LS.

conclusionsHCPS-specific differences in the phenotype of the systemic immune system might be leveraged in future risk-reducing strategies.

Indexed as

Neoplastic Syndromes, HereditaryAdultB-LymphocytesBRCA1 ProteinCross-Sectional StudiesCytokinesFemaleGenetic Predisposition to DiseaseHumansMiddle AgedBRCA1 ProteinCytokinesBRCA1Cancer immunosurveillanceHereditary breast and ovarian cancer syndromeImmune-checkpoint inhibitorsLynch syndromeMass cytometryMultiparamteric cytokine profilingPeripheral immune phenotypePre-cancer immunitySingle-cell transcriptomics

Identifiers

PMID42665817
PMCPMC13523197

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