Evidence map›Paper›PMID 41826692›Full record

ArticleCommunications medicine2026

Machine learning-based proteogenomic data modeling identifies circulating plasma biomarkers for early detection of lung cancer.

Marcela A Johnson, Shirley Nieves-Rodriguez, Liping Hou, Bevan Emma Huang, Assieh Saadatpour, Abolfazl Doostparast Torshizi

Abstract read
In one paragraph

Article in Communications medicine, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

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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

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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. 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

6 authors.

Marcela A JohnsonPopulation Analytics & Insights, DPDS, Data Sciences & Digital Health, Johnson & Johnson, Spring House, PA, USA.ORCID http://orcid.org/0000-0002-8446-2493
Shirley Nieves-RodriguezPopulation Analytics & Insights, DPDS, Data Sciences & Digital Health, Johnson & Johnson, Spring House, PA, USA.ORCID http://orcid.org/0000-0002-2329-4879
Liping HouPopulation Analytics & Insights, DPDS, Data Sciences & Digital Health, Johnson & Johnson, Spring House, PA, USA.
Bevan Emma HuangInterventional Oncology, Johnson & Johnson, New Brunswick, NJ, USA.
Assieh SaadatpourInterventional Oncology, Johnson & Johnson, New Brunswick, NJ, USA. asaadatp@its.jnj.com.
Abolfazl Doostparast TorshiziPopulation Analytics & Insights, DPDS, Data Sciences & Digital Health, Johnson & Johnson, Spring House, PA, USA. adoostpa@its.jnj.com.ORCID http://orcid.org/0000-0002-3327-699X

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundGenetic aberrations are among the critical driving factors of lung cancer. Importantly, the impact of genetic variations on proteomic dysregulations with the goal of characterizing potential diagnostic biomarkers at the population-level requires additional investigation. Modeling such proteogenomic interactions is crucial in understanding early-stage biological disruptions to inform biomarker discovery, successful clinical trials, and developing effective therapeutics.

methodsWe investigated two complementary aspects of lung cancer risk. First, we performed a genome-wide association study of lung cancer using population-scale datasets, then examined whether lung cancer risk-associated variants influence plasma protein levels using the UK Biobank Pharma Proteomics Project data. Second, we identified plasma proteomic dysregulations in presymptomatic and symptomatic patients with the objective of pinpointing diagnostic biomarkers through leveraging machine learning methods.

resultsUsing the identified proteins, machine learning models achieved median cross-validated AUCs of 0.85-0.88 (0-4 years before diagnosis [YBD]), 0.81-0.84 (5-9 YBD), and 0.80-0.86 (0-9 YBD). Performing survival analyses within the 5-9 YBD group, elevated levels of eight proteins, such as CALCB, PLAUR, and CD74, were found to significantly associate with lower survival. We identified 22 disease-associated proteins, of which 14 have been previously implicated in lung cancer, including CEACAM5, CXCL17, GDF15, WFDC2 along with 8 novel proteins. These proteins were enriched in pathways related to cytokine signaling, interleukin regulation, neutrophil degranulation, and lung fibrosis.

conclusionsWhile these findings do not establish mechanistic causality, they highlight proteomic alterations reflecting systemic changes preceding the diagnosis. Our study contributes to understanding genome-proteome relationships in lung cancer and identifies circulating proteins warranting further investigation as potential early biomarkers for screening and risk stratification.

Identifiers

PMID41826692
PMCPMC13125223

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