ReviewCancer biology & therapy2011
c-Myc induction of programmed cell death may contribute to carcinogenesis: a perspective inspired by several concepts of chemical carcinogenesis.
Review in Cancer biology & therapy, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 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
34 citing papers in PubMed, 51 citations in OpenAlex.
- Roles of Histone Acetyltransferases and Deacetylases in the Retinal Development and Diseases.Molecular neurobiology · 2023Review
- IGFBP-1 in cancer: expression, molecular mechanisms, and potential clinical implications.American journal of translational research · 2021Review
- Rose (Molecules (Basel, Switzerland) · 2020Article
- Evidence for immortality and autonomy in animal cancer models is often not provided, which causes confusion on key issues of cancer biology.Journal of Cancer · 2020Review
- Histone deacetylase inhibitors differentially regulate c-Myc expression in retinoblastoma cells.Oncology letters · 2020Article
- The role of circadian clock genes in tumors.OncoTargets and therapy · 2019Review
- Endorsing cellular competitiveness in aberrant epithelium of oral submucous fibrosis progression: neighbourhood analysis of immunohistochemical attributes.Histochemistry and cell biology · 2018Article
- Glycolysis promotes caspase-3 activation in lipid rafts in T cells.Cell death & disease · 2018Article
- Overexpression of CLEC3A promotes tumor progression and poor prognosis in breast invasive ductal cancer.OncoTargets and therapy · 2018Article
- Evaluating the Remote Control of Programmed Cell Death, with or without a Compensatory Cell Proliferation.International journal of biological sciences · 2018Review
- There are only four basic modes of cell death, although there are many ad-hoc variants adapted to different situations.Cell & bioscience · 2018Review
- Lymphoma: current status of clinical and preclinical imaging with radiolabeled antibodies.European journal of nuclear medicine and molecular imaging · 2017Review
- C-myc overexpression drives melanoma metastasis by promoting vasculogenic mimicry via c-myc/snail/Bax signaling.Journal of molecular medicine (Berlin, Germany) · 2017Article
- Different N-terminal isoforms of Oct-1 control expression of distinct sets of genes and their high levels in Namalwa Burkitt's lymphoma cells affect a wide range of cellular processes.Nucleic acids research · 2016Article
- Article
- The well-accepted notion that gene amplification contributes to increased expression still remains, after all these years, a reasonable but unproven assumption.Journal of carcinogenesis · 2016Review
- Article
- Weaknesses and Pitfalls of Using Mice and Rats in Cancer Chemoprevention Studies.Journal of Cancer · 2015Review
- Expression and function of a novel isoform of Sox5 in malignant B cells.Leukemia research · 2014Article
- Polycomb group proteins and MYC: the cancer connection.Cellular and molecular life sciences : CMLS · 2014Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
The c-Myc protein, encoded by c-myc gene, in its wild-type form can induce tumors with a high frequency and can induce massive programmed cell death (PCD) in most transgenic mouse models, with greater efficiency than other oncogenes. Evidence also indicates that c-Myc can cause proliferative inhibition, i.e. mitoinhibition. The c-Myc-induced PCD and mitoinhibition, which may be attributable to its inhibition of cyclin D1 and induction of p53, may impose a pressure of compensatory proliferation, i.e. regeneration, onto the initiated cells (cancer progenitor cells) that occur sporadically and are resistant to the mitoinhibition. The initiated cells can thus proliferate robustly and progress to a malignancy. This hypothetical thinking, i.e. the concurrent PCD and mitoinhibition induced by c-Myc can promote carcinogenesis, predicts that an optimal balance is achieved between cell death and ensuing regeneration during oncogenic transformation by c-Myc, which can better promote carcinogenesis. In this perspective, we summarize accumulating evidence and challenge the current model that oncoprotein induces carcinogenesis by promoting cellular proliferation and/or inhibiting PCD. Inspired by c-myc oncogene, we surmise that many tumor-suppressive or growth-inhibitory genes may also be able to promote carcinogenesis in a similar way, i.e. by inducing PCD and/or mitoinhibition of normal cells to create a need for compensatory proliferation that drives a robust replication of initiating cells.
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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.