ArticleNPJ precision oncology2025
Integrating bulk, single-cell, and spatial transcriptomics to identify and functionally validate novel targets to enhance immunotherapy in NSCLC.
Article in NPJ precision oncology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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
6 citing papers in PubMed.
- Multi-task spatial distillation reveals cell-type-resolved programmed cell death landscapes in the human kidney.Briefings in bioinformatics · 2026Article
- Immune checkpoint blockade in cancer: current insights and future horizons.Discover oncology · 2026Review
- Targeted Therapy-Induced Interstitial Lung Disease in NSCLC: Mechanisms, Clinical Signatures, and a Precision Medicine Roadmap.Drug design, development and therapy · 2026Review
- Applications of Spatial Transcriptomics in Veterinary Medicine: A Scoping Review of Research, Diagnostics, and Treatment Strategies.International journal of molecular sciences · 2025Article
- Immuno-Oncology at the Crossroads: Confronting Challenges in the Quest for Effective Cancer Therapies.International journal of molecular sciences · 2025Review
- Autophagy in the lung: guardian of homeostasis or driver of disease.Autophagy reports · 2025Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
14 authors.
Funding
Abstract
Programmed cell deaths (PCDs) are crucial for tumor progression. By analyzing 18 PCDs, we generated a robust multigene signature, Combined Cell Death Index (CCDI), comprising necroptosis and autophagy genes for non-small cell lung cancer (NSCLC). The CCDI accurately stratified patients by survival prognosis and predicted immunotherapy responses. We validated CCDI and prioritized CCDI genes using five single-cell RNA sequencing and two spatial transcriptomics datasets. CCDI positively correlates with tumor malignancy, invasiveness, and immunotherapy resistance. Four necroptosis genes (PTGES3, MYO6, CCT6A, and CTSH) may affect cancer cell evolution. In vitro, CTSH overexpression or PTGES3 knockdown inhibited NSCLC cell proliferation and migration while inducing necroptosis with necrosome formation. Moreover, we observed diminished CTSH, heightened PTGES3, and low necroptosis activity in 12 pairs of NSCLC tumors and normal tissues. CTSH overexpression or PTGES3 knockdown induced necroptosis and improved anti-PD1 therapy efficiency in syngeneic cancer mouse models. These findings indicate necroptosis genes as potential therapeutic targets in cancer treatments.
Identifiers
What Socratic 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 Socratic graph.