ArticleOncotarget2016
Growth suppression by MYC inhibition in small cell lung cancer cells with TP53 and RB1 inactivation.
Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 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
48 citing papers in PubMed, 78 citations in OpenAlex.
- Review
- Targeting RAB27A-mediated small extracellular vesicle secretion via CRISPR-Cas9 negatively affects proliferation and metastasis in both in vitro and in vivo SCLC models.Cancer gene therapy · 2026Article
- mTOR in radiotherapy of lung cancer: Mechanisms of radiation resistance and therapeutic implications (Review).International journal of oncology · 2026Review
- HIST1H4L promotes small cell lung cancer tumorigenesis by regulating the PI3K/Akt pathway and serves as a potential diagnostic biomarker.Frontiers in oncology · 2026Article
- MYC at the tumor-immune interface: mechanisms of immune escape and immunotherapy resistance.Frontiers in immunology · 2026Review
- Lineage plasticity and histological transformation: tumor histology as a spectrum.Cell research · 2025Review
- Myc family proteins: Molecular drivers of tumorigenesis and resistance in neuroendocrine tumors.Biochimica et biophysica acta. Reviews on cancer · 2025Review
- MYC in cancer: from undruggable target to clinical trials.Nature reviews. Drug discovery · 2025Review
- DNA Damage-Induced Ferroptosis: A Boolean Model Regulating p53 and Non-Coding RNAs in Drug Resistance.Proteomes · 2025Article
- Epigenetic Mechanisms, Assessment and Therapeutics of Epidermal Stem Cells in Skin Aging.Stem cells international · 2025Review
- MYC and KRAS cooperation: from historical challenges to therapeutic opportunities in cancer.Signal transduction and targeted therapy · 2024Review
- Landscape and Treatment Options of Shapeshifting Small Cell Lung Cancer.Journal of clinical medicine · 2024Review
- MYC targeting by OMO-103 in solid tumors: a phase 1 trial.Nature medicine · 2024Article
- Promises of Protein Kinase Inhibitors in Recalcitrant Small-Cell Lung Cancer: Recent Scenario and Future Possibilities.Cancers · 2024Review
- C-Myc protein expression indicates unfavorable clinical outcome in surgically resected small cell lung cancer.World journal of surgical oncology · 2024Article
- Actionable Driver Events in Small Cell Lung Cancer.International journal of molecular sciences · 2023Review
- ATR inhibition augments the efficacy of lurbinectedin in small-cell lung cancer.EMBO molecular medicine · 2023Article
- Review
- Targeting c-MYC: a potential non-hormonal therapeutic approach for endometriosis treatment.Frontiers in cell and developmental biology · 2023Article
- Novel nutritional indicator as predictors among subtypes of lung cancer in diagnosis.Frontiers in nutrition · 2023Article
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 3 institutions in 1 country.
Funding
Abstract
Small cell lung cancer (SCLC) is the most aggressive type of lung cancer with high mortality. One of the MYC family genes, MYC, MYCL or MYCN, is amplified in ~20% of the SCLCs; therefore, MYC proteins are potential therapeutic targets in SCLC patients. We investigated the therapeutic impact of Omomyc, a MYC dominant negative, in a panel of SCLC cell lines. Strikingly, Omomyc suppressed the growth of all tested cell lines by inducing cell cycle arrest and/or apoptosis. Induction of G1 arrest by Omomyc was found to be dependent on the activation of CDKN1A, in part, through the TP73 pathway. Our results strongly indicate that SCLC cells carrying amplification of MYC, MYCL or MYCN are addicted to MYC function, suggesting that MYC targeting would be an efficient therapeutic option for SCLC patients.
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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.