ReviewJournal of medical genetics2001
Two hits revisited again.
Review in Journal of medical genetics, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 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
16 citing papers in PubMed.
- Identification and management of genetic susceptibility to cancer: UK perspective.BMJ oncology · 2026Review
- Exome Sequencing Reveals Novel Germline Variants in Breast Cancer Patients in the Southernmost Region of Thailand.Journal of personalized medicine · 2023Article
- Single-nucleus DNA sequencing reveals hidden somatic loss-of-heterozygosity in Cerebral Cavernous Malformations.Nature communications · 2023Article
- Inherited mutations affecting the SRCAP complex are central in moderate-penetrance predisposition to uterine leiomyomas.American journal of human genetics · 2023Article
- Revisiting Brain Tuberous Sclerosis Complex in Rat and Human: Shared Molecular and Cellular Pathology Leads to Distinct Neurophysiological and Behavioral Phenotypes.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2021Review
- Inherited Variants inCancers · 2019Article
- Systematic characterization of germline variants from the DiscovEHR study endometrial carcinoma population.BMC medical genomics · 2019Article
- Mutation spectrums of TSC1 and TSC2 in Chinese women with lymphangioleiomyomatosis (LAM).PloS one · 2019Article
- There is a world beyond protein mutations: the role of non-coding RNAs in melanomagenesis.Experimental dermatology · 2013Article
- Expression Profiles in Stage II Colon Cancer According to APC Gene Status.Translational oncology · 2012Article
- Mismatch repair deficient colorectal cancer in the era of personalized treatment.Nature reviews. Clinical oncology · 2010Review
- A frame-shift mutation of PMS2 is a widespread cause of Lynch syndrome.Journal of medical genetics · 2008Article
- From gene mutations to tumours--stem cells in gastrointestinal carcinogenesis.Cell proliferation · 2005Review
- Genetic and pathologic changes associated with lymphovascular invasion of colorectal adenocarcinoma.Clinical & experimental metastasis · 2005Article
- Gastrointestinal stem cells and cancer: bridging the molecular gap.Stem cell reviews · 2005Review
- Emerging mechanism and therapeutic potential of neurofibromatosis type 1-related nerve system tumor: Advancing insights into tumor development.Neuro-oncology advancesReview
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
INTRODUCTION AND
methodsSince the concept of the "two hit hypothesis" was introduced over 20 years ago, a wealth of genetic data has accumulated on the mutations found at tumour suppressor loci. Perhaps surprisingly, these data conceal large gaps in our knowledge which genetic and functional studies are beginning to uncover. The "two hit hypothesis" must be updated to take account of this new information. RESULTS AND DISCUSSION: Here, we discuss both the results of recent studies and some of the questions that they highlight. In particular, how valid are conclusions from inherited Mendelian syndromes when applied to sporadic cancers? Why is allelic loss so common and how does it occur? Are the "two hits" random or interdependent? Is abolition of protein function always optimal for tumorigenesis? Can "third hits" occur and, if so, why? How can mismatch repair deficiency and the methylator phenotype be incorporated into the "two hit" hypothesis? We suggest that the "two hit hypothesis" is not fixed but is evolving as our knowledge expands.
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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.