ReviewNucleic acids research2006
Molecular models for the tissue specificity of DNA mismatch repair-deficient carcinogenesis.
Review in Nucleic acids research, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers, 1 of them a synthesis that pooled it.
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
46 citing papers in PubMed, 1 synthesis or guideline pooled it, 103 citations in OpenAlex.
- Association between MutL homolog 1 polymorphisms and the risk of colorectal cancer: a meta-analysis.Journal of cancer research and clinical oncology · 2015Pooled it
- Why are Some Tissues More Vulnerable? Revisiting Tissue Specificity in Hereditary Cancer Syndromes.Molecular diagnosis & therapy · 2026Review
- A maternal germline mutator phenotype in a family affected by heritable colorectal cancer.Genetics · 2024Article
- A maternal germline mutator phenotype in a family affected by heritable colorectal cancer.medRxiv : the preprint server for health sciences · 2024Article
- Repetitive Sequence Stability in Embryonic Stem Cells.International journal of molecular sciences · 2024Review
- DNA damage remodels the MITF interactome to increase melanoma genomic instability.Genes & development · 2024Article
- Article
- DNA damage in preimplantation embryos and gametes: specification, clinical relevance and repair strategies.Human reproduction update · 2022Review
- Do non-pathogenic variants of DNA mismatch repair genes modify neurofibroma load in neurofibromatosis type 1?Child's nervous system : ChNS : official journal of the International Society for Pediatric Neurosurgery · 2022Review
- Mismatch repair deficiency in early-onset duodenal, ampullary, and pancreatic carcinomas is a strong indicator for a hereditary defect.The journal of pathology. Clinical research · 2022Article
- Review
- The multilayer community structure of medulloblastoma.iScience · 2021Article
- Breast-Specific Epigenetic Regulation of DeltaNp73 and Its Role in DNA-Damage-Response ofCancers · 2020Article
- Loss of mismatch repair signaling impairs the WNT-bone morphogenetic protein crosstalk and the colonic homeostasis.Journal of molecular cell biology · 2020Article
- Molecular mutation characteristics of mismatch and homologous recombination repair genes in gastrointestinal cancer.Oncology letters · 2019Article
- Tissue specificity of DNA damage response and tumorigenesis.Cancer biology & medicine · 2019Article
- Progression inference for somatic mutations in cancer.Heliyon · 2017Article
- Novel Implications in Molecular Diagnosis of Lynch Syndrome.Gastroenterology research and practice · 2017Review
- Association between Mismatch-repair Genetic variation and the Risk of Multiple Primary Cancers: A Meta-Analysis.Journal of Cancer · 2017Article
- Data sources for in vivo molecular profiling of human phenotypes.Wiley interdisciplinary reviews. Systems biology and medicine · 2016Review
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
Abstract
A common feature of all the known cancer genetic syndromes is that they predispose only to selective types of malignancy. However, many of the genes mutated in these syndromes are ubiquitously expressed, and influence seemingly universal processes such as DNA repair or cell cycle control. The tissue specificity of cancers that arise from malfunction of these apparently universal traits remains a key puzzle in cancer genetics. Mutations in DNA mismatch repair (MMR) genes cause the most common known cancer genetic syndrome, hereditary non-polyposis colorectal cancer, and the fundamental biology of MMR is one of the most intensively studied processes in laboratories all around the world. This review uses MMR as a model system to understand mechanisms that may explain the selective development of tumors in particular cell types despite the universal nature of this process. We evaluate recent data giving insights into the specific tumor types that are attributable to defective MMR in humans and mice under different modes of inheritance, and propose models that may explain the spectrum of cancer types observed.
Indexed as
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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.