ArticleAnimal models and experimental medicine2026
Systematic pathway-level analysis defines conserved transcriptional divergence between primary lung tumors and cell line models.
Article in Animal models and experimental medicine, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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.
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.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundCancer cell lines are widely used in preclinical oncology, yet their fidelity in modeling primary tumors remains uncertain.
methodsWe performed a systematic pathway-level transcriptomic comparison of lung adenocarcinoma (LUAD) primary tumors from The Cancer Genome Atlas (TCGA; n = 513) and LUAD cell lines from the Cancer Cell Line Encyclopedia (CCLE; n = 45). Single-sample gene set enrichment analysis (ssGSEA) combined with L1-penalized logistic regression was applied to identify a discriminatory pathway signature.
resultsFive Hallmark pathways (E2F targets, interferon-gamma response, epithelial-mesenchymal transition, coagulation, and G2M checkpoint) distinguished primary lung tumors from cell line models. Cell lines exhibited significant enrichment of proliferation-associated pathways, whereas primary tumors retained immune- and microenvironment-related programs. Tumor-normal comparisons revealed significant pathway alterations in TCGA samples that were not fully recapitulated in CCLE models. Gene-level analyses confirmed depletion of stromal and vascular markers in cell lines. CCLE samples also demonstrated significantly higher tumor mutational burden and increased frequencies of TP53 and STK11 mutations. These pathway-level distinctions were conserved in lung squamous cell carcinoma, indicating generalizability across major NSCLC subtypes.
conclusionThese findings define a pathway-based framework for evaluating transcriptional fidelity between cell lines and primary tumors, highlighting fundamental transcriptional divergence with implications for rational model selection in lung cancer research.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.