ArticleChinese medical journal pulmonary and critical care medicine2023
Role of c-Myc in lung cancer: Progress, challenges, and prospects.
Article in Chinese medical journal pulmonary and critical care medicine, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 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
28 citing papers in PubMed, 24 citations in OpenAlex.
- Divergent c-MYC Expression Patterns in NET and NEC: Insights from a Multicentre Cohort of 1380 Neuroendocrine Neoplasms.Endocrine pathology · 2026Article
- ERCC6 at the Transcription-Replication Interface: Integration of Transcription-Coupled Repair with Replication Stress Responses.International journal of molecular sciences · 2026Review
- Crotonylation impedes c-Myc oncogenic activity.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Targeting glutamine metabolism to modulate macrophage functions in the tumor microenvironment.Discover oncology · 2026Review
- Interpretable Machine Learning to Understand Wildfire Toxicity: Bridging Chemicals, Omics, and Toxicological Outcomes via Symbolic Regression with Novel Feature Scoring.Chemical research in toxicology · 2026Article
- Dissecting origin factors of lymph node metastasis in non-small cell lung cancer via multimodal omics.Nature communications · 2026Article
- Prognostic impact of c-MYC and EZH2 expression in small cell and non-small cell lung carcinoma: a single-center retrospective study.Discover oncology · 2026Article
- Review
- NPC2 suppresses osteolytic metastasis in lung adenocarcinoma via the AKT/mTOR pathway and tumor-osteoclast crosstalk.iScience · 2026Article
- The oncogenome of the domestic cat.Science (New York, N.Y.) · 2026Article
- Decoding thebioRxiv : the preprint server for biology · 2026Article
- Article
- Advances in Metabolic Reprogramming and Immune Regulatory Mechanisms in Lung Cancer.Oncology research · 2026Review
- Activating NRF2Cancer gene therapy · 2025Article
- Targeting MKK3/c-Myc interaction to overcome osimertinib acquired resistance in EGFR mutant lung cancer.Cancer letters · 2025Article
- Precise modulation of BRG1 levels reveals features of mSWI/SNF dosage sensitivity.Nature genetics · 2025Article
- The Interplay Between Oxidant/Antioxidant System, Transcription Factors, and Non-Coding RNA in Lung Cancer.International journal of molecular sciences · 2025Review
- Double trouble: cytosolic and nuclear IKKα in cancer.Open biology · 2025Review
- Lactate dehydrogenase A: a potential new target for tumor drug resistance intervention.Journal of translational medicine · 2025Review
- DCAF13 influences breast cancer chemotherapy resistance through metabolic reprogramming by regulating c-Myc expression.Medical oncology (Northwood, London, England) · 2025Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Lung cancer remains the leading cause of cancer-related deaths worldwide. Despite the recent advances in cancer therapies, the 5-year survival of non-small cell lung cancer (NSCLC) patients hovers around 20%. Inherent and acquired resistance to therapies (including radiation, chemotherapies, targeted drugs, and combination therapies) has become a significant obstacle in the successful treatment of NSCLC. c-Myc, one of the critical oncoproteins, has been shown to be heavily associated with the malignant cancer phenotype, including rapid proliferation, metastasis, and chemoresistance across multiple cancer types. The c-Myc proto-oncogene is amplified in small cell lung cancers (SCLCs) and overexpressed in over 50% of NSCLCs. c-Myc is known to actively regulate the transcription of cancer stemness genes that are recognized as major contributors to tumor progression and therapeutic resistance; thus, targeting c-Myc either directly or indirectly in mitigation of the cancer stemness phenotype becomes a promising approach for development of a new strategy against drug resistant lung cancers. This review will summarize what is currently known about the mechanisms underlying c-Myc regulation of cancer stemness and its involvement in drug resistance and offer an overview on the current progress and future prospects in therapeutically targeting c-Myc in both SCLC and NSCLC.
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.