ArticleCell cycle (Georgetown, Tex.)2013
Heritable one-hit events defining cancer prevention?
Article in Cell cycle (Georgetown, Tex.), 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 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
9 citing papers in PubMed, 10 citations in OpenAlex.
- Hereditary Pancreatic Cancer: Genetic Risk, Surveillance Strategies, and Therapeutic Implications.International journal of molecular sciences · 2026Review
- Review
- 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
- Patched1 haploinsufficiency severely impacts intermediary metabolism in the skin of Ptch1Scientific reports · 2019Article
- ETHE1 overexpression promotes SIRT1 and PGC1α mediated aerobic glycolysis, oxidative phosphorylation, mitochondrial biogenesis and colorectal cancer.Oncotarget · 2019Article
- Global gene expression of histologically normal primary skin cells from BCNS subjects reveals "single-hit" effects that are influenced by rapamycin.Oncotarget · 2019Article
- Haploinsufficiency in tumor predisposition syndromes: altered genomic transcription in morphologically normal cells heterozygous for VHL or TSC mutation.Oncotarget · 2017Article
- Article
- 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 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Over 100 years ago (1902-1914) Theodor Boveri suggested a role for mutations in cancer. Boveri's ideas were derived from the then "just-emerging" chromosome theory of inheritance. While demonstrating chromosomal aberrations as a cause of genetic imbalance, Boveri suggested that possible causes of malignancy may include events such as aneuploidy that are now defined as gene mutations, asserting all the while that malignancy occurs at the cellular level. Indeed, studies to date essentially uniformly show that cancer is a genetic disease.
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.