Evidence map›Paper›PMID 42024473›Full record

ArticleJCI insight2026

Pan-cancer polygenic risk score associates with cancer susceptibility following kidney transplantation.

Jarmo Ritari, Kati Hyvärinen, Kirsi Jahnukainen, FinnGen Consortium, Jukka Partanen, Ilkka Helanterä, Timo Jahnukainen

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Article in JCI insight, 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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1 · What the graph read from it

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2 · The registry

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3 · Its place in the literature

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4 · The record

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5 · Who and what money

Authors and funding

7 authors.

Jarmo RitariFinnish Red Cross Blood Service, Helsinki, Finland.
Kati HyvärinenFinnish Red Cross Blood Service, Helsinki, Finland.
Kirsi JahnukainenDivision of Hematology-Oncology and Stem Cell Transplantation, New Children's Hospital, Helsinki University Hospital and University of Helsinki, Helsinki, Finland.
FinnGen Consortium
Jukka PartanenFinnish Red Cross Blood Service, Helsinki, Finland.
Ilkka HelanteräTransplantation and Liver Surgery, Helsinki University Hospital and University of Helsinki, Helsinki, Finland.
Timo JahnukainenDepartment of Pediatric Nephrology and Transplantation, New Children's Hospital, Helsinki University Hospital and University of Helsinki, Helsinki, Finland.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

BACKGROUNDCancer accounts for over 20% of late posttransplant mortality, yet the contribution of genetic susceptibility to posttransplant cancer risk remains unclear. This study investigates germline genetic risk factors for posttransplant cancer in the Finnish population using data from the FinnGen cohort.METHODSA pan-cancer polygenic risk score (PRS) was constructed using genetic variants identified in UK and US populations to assess the influence of common germline variants on time to first cancer diagnosis in 1,802 Finnish kidney transplant recipients (KTRs), of whom 317 developed posttransplant cancer. The PRS was first validated in the FinnGen non-transplantation cohort and subsequently applied to KTRs, with replication in lung and liver transplant recipients (n = 476). Functional relevance was explored by assessing associations between the PRS and expression levels of 2,923 plasma proteins in the UK Biobank (n = 53,013).RESULTSCompared with a matched non-transplantation cohort (n = 68,294), KTRs exhibited earlier cancer onset. The PRS was significantly associated with time to first cancer diagnosis in the non-transplantation population (HR 1.04, 95% CI 1.038-1.056, P = 3.75 × 10-25). Among KTRs younger than 40 years, higher PRS was associated with earlier cancer onset (HR 1.08, 95% CI 1.01-1.17, P = 0.036), indicating a stronger genetic effect at younger ages. The PRS significantly (Bonferroni < 0.05) altered the regulation of 87 plasma proteins, several of which were known cancer-related markers.CONCLUSIONInherited genetic predisposition, captured by pan-cancer PRS, may contribute to individual susceptibility to cancer after solid organ transplantation, particularly at younger ages.FUNDINGState research funding (Helsinki and Uusimaa Health District), the Foundation for Pediatric Research, and the Sigrid Jusèlius Foundation.

Indexed as

Genetic Risk ScoreKidney TransplantationNeoplasmsAdultAgedCohort StudiesFemaleFinlandHumansMaleMiddle AgedRisk FactorsCancerGenetic risk factorsNephrologyOncologyTransplantation

Identifiers

PMID42024473
PMCPMC13313503

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