ArticleScience (New York, N.Y.)2024
Lineage-specific intolerance to oncogenic drivers restricts histological transformation.
Article in Science (New York, N.Y.), 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 68 papers, 1 of them a synthesis that pooled 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.
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
68 citing papers in PubMed, 1 synthesis or guideline pooled it, 81 citations in OpenAlex.
- Histological transformation in lung cancer: a single-arm meta-analysis and systematic review.BMC cancer · 2026Pooled it
- Phase II study of olaparib plus durvalumab in EGFR-mutant NSCLC transformed to small cell lung cancer.The oncologist · 2026Trial
- Lineage identity governs oncogene dependence in mouse NSCLC models of KRAS inhibitor resistance.Nature genetics · 2026Article
- RAD51AP1-MYC-Sam68 positive transcriptional feedback loop maintains lung cancer stemness.iScience · 2026Article
- Article
- MYC in Oncogenesis and Therapeutic Implications.MedComm · 2026Review
- Nicotinic Acid Restriction Enhances the Therapeutic Benefit of NAMPT Inhibition in Small-Cell Lung Cancer Models.Cancer science · 2026Article
- Integrated stress response couples mitochondrial fitness with lineage reprogramming to drive cancer evolution.Nature cell biology · 2026Article
- The dual role of the crosstalk between autophagy and ferroptosis in lung cancer treatment: Advances in mechanisms and therapeutic strategies (Review).International journal of molecular medicine · 2026Review
- Single-cell spatial transcriptomics reveals tumor microenvironment heterogeneity in primary and lymph node-metastatic small cell lung cancer.Cell reports. Medicine · 2026Article
- RB loss modulates chromatin organization by regulating cohesin-dependent loops and enhancer-promoter interactions.Nature communications · 2026Article
- Stem cell control and cancer initiation by an autocrine, injury-activated Igf complex.bioRxiv : the preprint server for biology · 2026Article
- Longitudinal, Retrospective Use of a Circulating Tumor DNA Methylation Signature Successfully Captures Small Cell Evolution in a Patient With Metastatic EGFR-Mutant Non-Small Cell Lung Cancer.JCO precision oncology · 2026Article
- Tolerance and Resistance to Targeted Therapy in NSCLC: Emerging Concepts and Strategies.JTO clinical and research reports · 2026Review
- Single-cell profiling of tumor lineage plasticity and the immune microenvironment in transformed small cell lung cancer.Journal of translational medicine · 2026Article
- Small Cell Lung Cancer Classification: Unraveling Heterogeneity to Enable Personalized Treatments.Cancer research · 2026Review
- Lineage plasticity: a new dilemma in lung cancer treatment.Molecular biology reports · 2026Review
- Case report: ALK inhibitor-induced transformation of ALK fusion-positive lung adenocarcinoma to large cell neuroendocrine carcinoma.NPJ precision oncology · 2026Article
- Navigating the landscape of EGFR TKI resistance in EGFR-mutant NSCLC - mechanisms and evolving treatment approaches.Nature reviews. Clinical oncology · 2026Review
- Lineage plasticity and immune invisibility in primary SCLC and LUAD-to-SCLC transformation: antigen presentation loss and therapeutic redirection.Frontiers in immunology · 2026Review
8 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors at 1 institution in 1 country.
Funding
Abstract
Lung adenocarcinoma (LUAD) and small cell lung cancer (SCLC) are thought to originate from different epithelial cell types in the lung. Intriguingly, LUAD can histologically transform into SCLC after treatment with targeted therapies. In this study, we designed models to follow the conversion of LUAD to SCLC and found that the barrier to histological transformation converges on tolerance to Myc, which we implicate as a lineage-specific driver of the pulmonary neuroendocrine cell. Histological transformations are frequently accompanied by activation of the Akt pathway. Manipulating this pathway permitted tolerance to Myc as an oncogenic driver, producing rare, stem-like cells that transcriptionally resemble the pulmonary basal lineage. These findings suggest that histological transformation may require the plasticity inherent to the basal stem cell, enabling tolerance to previously incompatible oncogenic driver programs.
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.