Evidence map›Paper›PMID 42882853›Full record

ReviewCancers2026

AI-Driven Multi-Omics Approaches for Deciphering Small-Cell Lung Cancer Heterogeneity Using Nucleic-Acid-Based Features.

Saman Zeeshan, Caila McVey, Shafaq Majeed, Zeeshan Ahmed, Mark Nichols

Abstract readReview
In one paragraph

Review in Cancers, 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

5 authors.

Saman ZeeshanDepartment of Biomedical and Health Informatics, School of Medicine, The University of Missouri-Kansas City, Kansas City, MO 64110, USA.ORCID 0000-0001-9278-6204
Caila McVeyDepartment of Biomedical and Health Informatics, School of Medicine, The University of Missouri-Kansas City, Kansas City, MO 64110, USA.ORCID 0009-0007-6583-526X
Shafaq MajeedDepartment of Bio Sciences, COMSATS University, Islamabad 45550, Pakistan.
Zeeshan AhmedRutgers Institute for Health, Health Care Policy and Aging Research, Rutgers, The State University of New Jersey, New Brunswick, NJ 08901, USA.ORCID 0000-0002-7065-1699
Mark NicholsDepartment of Biomedical and Health Informatics, School of Medicine, The University of Missouri-Kansas City, Kansas City, MO 64110, USA.ORCID 0009-0003-5887-1685

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundSmall-cell lung cancer (SCLC) is a rare but highly aggressive malignancy defined by rapid progression, early metastasis, and profound therapeutic resistance. Its extensive heterogeneity across genomic, transcriptomic, epigenetic, proteomic, and microenvironmental levels continues to undermine precision medicine. Emerging evidence highlights the complex role of epidermal growth factor receptor (

methodsThis review synthesizes current literature encompassing nucleic-acid-based determinants of resistance, SCLC molecular architecture, transformation biology, and subtype evolution, integrating findings from genomic, transcriptomic, epigenetic, proteomic, imaging, and clinical studies. We additionally evaluated artificial intelligence (AI) and machine learning (ML) methodologies with potential to unify multi-omics, radiomics, and clinical variables to model subtype plasticity, clonal evolution, and therapy-induced rewiring.

resultsThe evidence demonstrates that traditional single-layer analyses are insufficient to capture the multiscale architecture of SCLC biology or the nonlinear interactions driving resistance, whereas AI-enabled multi-omics approaches offer advantages in enhancing subtype classification, supporting early detection, and improving prediction of therapeutic response. Key barriers such as tissue scarcity, limited biomarker availability, and extreme intratumoral heterogeneity remain significant challenges, though increasingly addressable through integrative computational frameworks.

conclusionAI-driven systems-level integration reframes SCLC as a dynamically evolving, multilayered disease process, where nucleic-acid alterations are central to subtype evolution and treatment resistance, providing a conceptual model to guide biomarker discovery and therapeutic development. By leveraging AI-enabled multi-omics and radiomics, this framework has the potential to advance personalized clinical management and overcome longstanding diagnostic and therapeutic challenges in SCLC.

Indexed as

AImachine learningmulti-omicsnucleic acid profilingresistance mechanismssmall-cell lung cancertumor heterogeneity

Identifiers

PMID42882853
PMCPMC13664549

What OpenQuestion holds

Textmetadata
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Registered trials

None linked

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.