Evidence map›Paper›PMID 41708901›Full record

ArticleNPJ precision oncology2026

Charting cell-type-specific positive genetic interaction at single-cell resolution for lung adenocarcinoma.

Bo Chen, Mingyue Liu, Qi Dong, Chen Lv, Kaidong Liu, Huiming Han, Linzhu Wang, Nan Zhang, Wenyuan Zhao, Junjie Lv and 1 more

Abstract read
In one paragraph

Article in NPJ precision oncology, 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

11 authors.

Bo Chen *Department of Systems Biology, College of Bioinformatics Science and Technology, Harbin Medical University, Harbin, 150081, China.
Mingyue Liu *Department of Systems Biology, College of Bioinformatics Science and Technology, Harbin Medical University, Harbin, 150081, China.
Qi Dong *Department of Systems Biology, College of Bioinformatics Science and Technology, Harbin Medical University, Harbin, 150081, China.
Chen LvDepartment of Systems Biology, College of Bioinformatics Science and Technology, Harbin Medical University, Harbin, 150081, China.
Kaidong LiuDepartment of Systems Biology, College of Bioinformatics Science and Technology, Harbin Medical University, Harbin, 150081, China.
Huiming HanDepartment of Systems Biology, College of Bioinformatics Science and Technology, Harbin Medical University, Harbin, 150081, China.
Linzhu WangDepartment of Systems Biology, College of Bioinformatics Science and Technology, Harbin Medical University, Harbin, 150081, China.
Nan ZhangDepartment of Systems Biology, College of Bioinformatics Science and Technology, Harbin Medical University, Harbin, 150081, China.
Wenyuan ZhaoDepartment of Systems Biology, College of Bioinformatics Science and Technology, Harbin Medical University, Harbin, 150081, China.
Junjie LvDepartment of Biological Physics, College of Bioinformatics Science and Technology, Harbin Medical University, Harbin, 150081, China. lvjunjie525@126.com.
Yunyan GuDepartment of Systems Biology, College of Bioinformatics Science and Technology, Harbin Medical University, Harbin, 150081, China. guyunyan@ems.hrbmu.edu.cn.

Funding

Chunyan Team Program of Heilongjiang Province CYQN24043National Multidisciplinary Innovation Team Project in Traditional Chinese Medicine ZYYCXTD-D-202407National Natural Science Foundation of China 32470702Scientific Research Project of Provincial Scientific Research Institutes of Heilongjiang Province CZKYF2024-1-A010the National Key Research and Development Program of China 2023YFF1204600
6 · The paper itself

Abstract

Genetic interactions (GIs) drive carcinogenesis and treatment resistance via non-additive phenotypic effects between genes. Traditional bulk-based methods fail to capture cell-type-specific interactions in heterogeneous tumors like lung adenocarcinoma (LUAD), limiting precision oncology. Resolving cell-type-specific GIs at single-cell resolution persists as a major hurdle, hindered by limited analytical methodologies. Here, we develop scPGI-finder, a computational framework that identifies gene pairs whose coordinated high expression is associated with higher proliferation-related fitness at single-cell resolution, which we refer to operationally as single-cell positive genetic interactions (scPGIs). Using scPGI-finder, we identify 49,808 and 15,896 scPGIs spanning epithelial cells and T cells in LUAD, respectively. The predicted scPGIs display tighter junctions in the protein interaction network compared to non-scPGIs. Furthermore, we demonstrate the predictive power of scPGIs for malignancy and immunotherapy response through multi-omics validation across diverse cohorts. Notably, with a mean area under the ROC curve (AUROC) of 0.974 in bulk tissue validation, the epithelial-derived scPGI classifier enables concordant malignancy identification across scales ranging from epithelial single cells and lung cancer cell lines, through spatial transcriptomic maps, to bulk LUAD tissue profiles. Additionally, a six-scPGI T cell signature reliably forecasts immunotherapy efficacy, with AUROC values exceeding 0.80 across multiple datasets. Together, our research advances the understanding of underlying cancer-positive GIs at the single-cell level. scPGIs of epithelial and T cells serve as robust biomarkers for malignancy evaluation and treatment response, offering a translational framework for precision oncology.

Identifiers

PMID41708901
PMCPMC13031792

What Socratic holds

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LicenceCC BY-NC-ND
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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 Socratic graph.