ReviewThe Biochemical journal1996
Myc oncogenes: the enigmatic family.
Review in The Biochemical journal, 1996. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 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
44 citing papers in PubMed, 175 citations in OpenAlex.
- Review
- Isoform-Directed Control of c-Myc Functions: Understanding the Balance from Proliferation to Growth Arrest.International journal of molecular sciences · 2023Review
- G-Quadruplexes in c-MYC Promoter as Targets for Cancer Therapy.Biomedicines · 2023Review
- miR-542-5p targets c-myc and negates the cell proliferation effect of SphK1 in intestinal epithelial cells.American journal of physiology. Cell physiology · 2023Article
- Precision Anti-Cancer Medicines by Oligonucleotide Therapeutics in Clinical Research Targeting Undruggable Proteins and Non-Coding RNAs.Pharmaceutics · 2022Review
- Human Papillomaviruses and Epstein-Barr Virus Interactions in Colorectal Cancer: A Brief Review.Pathogens (Basel, Switzerland) · 2020Review
- Association Between Amplification and Expression of C-MYC Gene and Clinicopathological Characteristics of Stomach Cancer.Iranian Red Crescent medical journal · 2016Article
- Deregulation of MYC and TP53 through genetic and epigenetic alterations in gallbladder carcinomas.Clinical and experimental medicine · 2015Article
- Sphingosine kinase 1 overexpression stimulates intestinal epithelial cell proliferation through increased c-Myc translation.American journal of physiology. Cell physiology · 2013Article
- A tumor-immune mathematical model of CD4+ T helper cell dependent tumor regression by oncogene inactivation.Annual International Conference of the IEEE Engineering in Medicine and Biology Society. IEEE Engineering in Medicine and Biology Society. Annual International Conference · 2013Article
- Article
- Humanized c-Myc mouse.PloS one · 2012Article
- Human papillomavirus DNA and oncogene alterations in colorectal tumors.Pathology oncology research : POR · 2010Article
- Regulation of survival, proliferation, invasion, angiogenesis, and metastasis of tumor cells through modulation of inflammatory pathways by nutraceuticals.Cancer metastasis reviews · 2010Review
- Polyamines regulate c-Myc translation through Chk2-dependent HuR phosphorylation.Molecular biology of the cell · 2009Article
- The cell cycle and Myc intersect with mechanisms that regulate pluripotency and reprogramming.Cell stem cell · 2009Review
- Phenotypic expression of maternally inherited deafness is affected by RNA modification and cytoplasmic ribosomal proteins.Molecular genetics and metabolism · 2009Article
- Article
- Behavioral genetics of the depression/cancer correlation: a look at the Ras oncogene family and the 'cerebral diabetes paradigm'.Journal of molecular neuroscience : MN · 2008Review
- Article
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
No grant is acknowledged in the PubMed record.
Abstract
The myc family of proto-oncogenes is believed to be involved in the establishment of many types of human malignancy. The members of this family have been shown to function as transcription factors, and through a designated target sequence bring about continued cell-cycle progression, cellular immortalization and blockages to differentiation in many lineages. However, while much of the recent work focusing on the c-myc oncogene has provided some very important advances, it has also brought to light a large amount of conflicting data as to the mechanism of action of the gene product. In this regard, it has now been shown that c-myc is effective in transcriptional repression as well as transcriptional activation and, perhaps more paradoxically, that it has a role in programmed cell death (apoptosis) as well as in processes of cell-cycle progression. In addition, particular interest has surrounded the distinct roles of the two alternative translation products of the c-myc gene, c-Myc 1 and c-Myc 2. The intriguing observation that the ratio of c-Myc 1 to c-Myc 2 increases markedly upon cellular quiescence led to the discovery that the enforced expression of the two proteins individually showed that c-Myc 2 stimulates cell growth, whereas c-Myc 1 appears to be growth suppressing. Clearly, the disparities in the activities of c-Myc, together with the consistent occurrence of mutations of c-myc in human malignancies, means that, although reaching an understanding of the functions of the myc gene family might not be simple, it remains well worthy of pursuit.
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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.