Evidence map›Paper›PMID 41840222›Full record

ArticleEuropean journal of human genetics : EJHG2026

Evaluation of BoostDM, a somatic variant prediction tool, for the interpretation of germline variants in hereditary cancer genes.

Elisabet Munté, Ferran Muiños, Raúl Marín, Lidia Feliubadaló, Federica Brando, Núria López-Bigas, Conxi Lázaro, Abel González-Pérez, Laura Valle

Abstract readEvaluation Study
In one paragraph

Article in European journal of human genetics : EJHG, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

  1. Coding or non-coding? The question behind sequencing.European journal of human genetics : EJHG · 2026
    Article
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.

Elisabet Munté *Hereditary Cancer Program, Catalan Institute of Oncology; Oncobell Program, IDIBELL, Hospitalet de Llobregat, Barcelona, Spain.ORCID http://orcid.org/0000-0001-8396-8284
Ferran Muiños *Centro de Investigación Biomédica en Red en Cáncer (CIBERONC), Instituto de Salud Carlos III, Madrid, Spain.
Raúl Marín *Hereditary Cancer Program, Catalan Institute of Oncology; Oncobell Program, IDIBELL, Hospitalet de Llobregat, Barcelona, Spain.ORCID http://orcid.org/0000-0003-4877-4032
Lidia FeliubadalóHereditary Cancer Program, Catalan Institute of Oncology; Oncobell Program, IDIBELL, Hospitalet de Llobregat, Barcelona, Spain.ORCID http://orcid.org/0000-0002-1736-0112
Federica BrandoInstitute for Research in Biomedicine (IRB Barcelona), The Barcelona Institute of Science and Technology, Barcelona, Spain.ORCID http://orcid.org/0000-0003-0537-0281
Núria López-BigasCentro de Investigación Biomédica en Red en Cáncer (CIBERONC), Instituto de Salud Carlos III, Madrid, Spain.
Conxi LázaroHereditary Cancer Program, Catalan Institute of Oncology; Oncobell Program, IDIBELL, Hospitalet de Llobregat, Barcelona, Spain. clazaro@iconcologia.net.ORCID http://orcid.org/0000-0002-7198-5906
Abel González-PérezCentro de Investigación Biomédica en Red en Cáncer (CIBERONC), Instituto de Salud Carlos III, Madrid, Spain. abel.gonzalez@irbbarcelona.org.ORCID http://orcid.org/0000-0002-8582-4660
Laura ValleHereditary Cancer Program, Catalan Institute of Oncology; Oncobell Program, IDIBELL, Hospitalet de Llobregat, Barcelona, Spain. lvalle@idibell.cat.ORCID http://orcid.org/0000-0003-0371-0844

Funding

Generalitat de Catalunya (Government of Catalonia) AGAUR 2021SGR01112; CERCA ProgramGeneralitat de Catalunya (Government of Catalonia) CERCA ProgramMinistry of Economy and Competitiveness | Agencia Estatal de Investigación (Spanish Agencia Estatal de Investigación) PID2024-162582OB-I00; PID2020-112595RB-I00Ministry of Economy and Competitiveness | Instituto de Salud Carlos III (Institute of Health Carlos III) CIBERONC CB16/12/00234; PMP22/00064Ministry of Economy and Competitiveness | Instituto de Salud Carlos III (Institute of Health Carlos III) CIBERONC CB21/12/00013Ministry of Economy and Competitiveness | Instituto de Salud Carlos III (Institute of Health Carlos III) PI23/00017; CIBERONC CB16/12/00234; PMP22/00064
6 · The paper itself

Abstract

Classifying germline variants in hereditary cancer genes remains challenging and requires integrating diverse lines of evidence. BoostDM is a computational method originally developed to identify somatic cancer driver mutations by detecting signals of positive selection. Given the functional overlap between somatic and germline pathogenic variants in cancer genes, we evaluated the utility of BoostDM for interpreting germline variants in hereditary cancer genes. We assessed BoostDM's performance across six genes with dual roles in sporadic and hereditary cancer (ATM, BRCA1, BRCA2, CDH1, PTEN, TP53), using gene-specific BoostDM models. A total of 1275 germline single nucleotide variants with expert-reviewed pathogenic and benign classifications were included. BoostDM scores were compared to those from AlphaMissense and REVEL, two leading pathogenicity predictors for missense variants. BoostDM correctly classified 74.5% of pathogenic/likely pathogenic and 98.6% of non-synonymous benign/likely benign variants overall. It performed particularly well for non-synonymous, non-missense variants (92.3% sensitivity). For missense variants, BoostDM correctly identified 46% of pathogenic and 95.5% of benign variants. While BoostDM did not outperform AlphaMissense or REVEL, it demonstrated high specificity (99.5%) and positive predictive value (PPV = 98%) for missense variants with high scores ( > 0.5). Gene-specific performance varied, with TP53 showing the most robust results. In conclusion, BoostDM predictions are not a replacement for ACMG/AMP-guided germline variant classification, especially for missense changes. However, its high specificity and PPV suggest that high BoostDM scores can provide supportive evidence of pathogenicity, prompting further clinical and functional investigation.

Indexed as

Computational BiologyGenetic TestingGerm-Line MutationNeoplasmsSoftwareGenetic Predisposition to DiseaseHumansMutation, MissensePTEN PhosphohydrolasePTEN Phosphohydrolase

Identifiers

PMID41840222
PMCPMC13550587

What OpenQuestion holds

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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.