ArticleOncogene2022
Lineage-restricted neoplasia driven by Myc defaults to small cell lung cancer when combined with loss of p53 and Rb in the airway epithelium.
Article in Oncogene, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 31 citations in OpenAlex.
- Lineage plasticity: a new dilemma in lung cancer treatment.Molecular biology reports · 2026Review
- Unmasking biomarkers in small cell lung cancer: implication for precision oncology.Frontiers in oncology · 2026Review
- Advancing small cell lung cancer metastasis research: innovations in preclinical mouse models.Cancer metastasis reviews · 2025Review
- Article
- Challenges of small cell lung cancer heterogeneity and phenotypic plasticity.Nature reviews. Cancer · 2025Review
- Current and future therapies for small cell lung carcinoma.Journal of hematology & oncology · 2025Review
- Lethal co-expression intolerance underlies the mutually exclusive expression of ASCL1 and NEUROD1 in SCLC cells.NPJ precision oncology · 2025Article
- Concurrent RB1 and P53 pathway disruption predisposes to the development of a primitive neuronal component in high-grade gliomas depending on MYC-driven EBF3 transcription.Acta neuropathologica · 2025Article
- A STAT3-STING-IFN axis controls the metastatic spread of small cell lung cancer.Nature immunology · 2024Article
- Small cell lung cancer: emerging subtypes, signaling pathways, and therapeutic vulnerabilities.Experimental hematology & oncology · 2024Review
- Olfactory neuroblastoma mimics molecular heterogeneity and lineage trajectories of small-cell lung cancer.Cancer cell · 2024Article
- Genomic and transcriptomic profiling of combined small-cell lung cancer through microdissection: unveiling the transformational pathway of mixed subtype.Journal of translational medicine · 2024Article
- Review
- Novel Therapeutic Options for Small Cell Lung Cancer.Current oncology reports · 2023Review
- Data-driven structural analysis of small cell lung cancer transcription factor network suggests potential subtype regulators and transition pathways.NPJ systems biology and applications · 2023Article
- Understanding SCLC heterogeneity and plasticity in cancer metastasis and chemotherapy resistance.Acta biochimica et biophysica Sinica · 2023Review
- MYC drives platinum resistant SCLC that is overcome by the dual PI3K-HDAC inhibitor fimepinostat.Journal of experimental & clinical cancer research : CR · 2023Article
- Extrachromosomal DNA Amplification Contributes to Small Cell Lung Cancer Heterogeneity and Is Associated with Worse Outcomes.Cancer discovery · 2023Article
- Predicting specific mortality from laryngeal cancer based on competing risk model: a retrospective analysis based on the SEER database.Annals of translational medicine · 2023Article
- Review
Corrections and comments
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Authors and funding
13 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Small cell lung cancer (SCLC) is an aggressive neuroendocrine cancer characterized by loss of function TP53 and RB1 mutations in addition to mutations in other oncogenes including MYC. Overexpression of MYC together with Trp53 and Rb1 loss in pulmonary neuroendocrine cells of the mouse lung drives an aggressive neuroendocrine low variant subtype of SCLC. However, the transforming potential of MYC amplification alone on airway epithelium is unclear. Therefore, we selectively and conditionally overexpressed MYC stochastically throughout the airway or specifically in neuroendocrine, club, or alveolar type II cells in the adult mouse lung. We observed that MYC overexpression induced carcinoma in situ which did not progress to invasive disease. The formation of adenoma or SCLC carcinoma in situ was dependent on the cell of origin. In contrast, MYC overexpression combined with conditional deletion of both Trp53 and Rb1 exclusively gave rise to SCLC, irrespective of the cell lineage of origin. However, cell of origin influenced disease latency, metastatic potential, and the transcriptional profile of the SCLC phenotype. Together this reveals that MYC overexpression alone provides a proliferative advantage but when combined with deletion of Trp53 and Rb1 it facilitates the formation of aggressive SCLC from multiple cell lineages.
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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.