Evidence map›Paper›PMID 26708047›Full record

ReviewDNA repair2016

Mouse models of DNA mismatch repair in cancer research.

Kyeryoung Lee, Elena Tosti, Winfried Edelmann

Abstract readReview
In one paragraph

Review in DNA repair, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
3.1field-weighted citation impact, top 9% of its field
1 · What the graph read from 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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

26 citing papers in PubMed, 38 citations in OpenAlex.

  1. Article
  2. Review
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  13. Antitumor Drugs and Their Targets.Molecules (Basel, Switzerland) · 2020
    Review
  14. Article
  15. Frontiers in cellular and infection microbiology · 2020
    Article
  16. Review
  17. Article
  18. Article
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

3 authors at 1 institution in 1 country.

Kyeryoung LeeDepartment of Cell Biology, Albert Einstein College of Medicine, 1301 Morris Park Ave, Bronx, NY 10461, United States.
Elena TostiDepartment of Cell Biology, Albert Einstein College of Medicine, 1301 Morris Park Ave, Bronx, NY 10461, United States.
Winfried EdelmannDepartment of Cell Biology, Albert Einstein College of Medicine, 1301 Morris Park Ave, Bronx, NY 10461, United States. Electronic address: winfried.edelmann@einstein.yu.edu.
Albert Einstein College of Medicine · US

Funding

WORD PROCESSORP30CA013330 · NCI · YESHIVA UNIVERSITY · PI THOMAS E ROHAN · 1985 to 2026
$111.2M
DNA MISMATCH REPAIR AND CANCER IN MURINE MODELSR01CA076329 · NCI · YESHIVA UNIVERSITY · PI EDELMANN, WINFRIED · 1998 to 2017
$6.9M
Mismatch repair in V region mutation and isotype switchingR01CA102705 · NCI · YESHIVA UNIVERSITY · PI SCHARFF, MATTHEW D · 2003 to 2013
$3.2M
Mismatch repair in V region mutation and isotype switchingR01AI112335 · NIAID · ALBERT EINSTEIN COLLEGE OF MEDICINE, INC · PI SCHARFF, MATTHEW D · 2014 to 2017
$1.5M
NCI NIH HHS CA102705NCI NIH HHS CA13330NCI NIH HHS CA76329NCI NIH HHS P30 CA013330NCI NIH HHS R01 CA076329NCI NIH HHS R01 CA102705NIAID NIH HHS R01 AI112335
6 · The paper itself

Abstract

Germline mutations in DNA mismatch repair (MMR) genes are the cause of hereditary non-polyposis colorectal cancer/Lynch syndrome (HNPCC/LS) one of the most common cancer predisposition syndromes, and defects in MMR are also prevalent in sporadic colorectal cancers. In the past, the generation and analysis of mouse lines with knockout mutations in all of the known MMR genes has provided insight into how loss of individual MMR genes affects genome stability and contributes to cancer susceptibility. These studies also revealed essential functions for some of the MMR genes in B cell maturation and fertility. In this review, we will provide a brief overview of the cancer predisposition phenotypes of recently developed mouse models with targeted mutations in MutS and MutL homologs (Msh and Mlh, respectively) and their utility as preclinical models. The focus will be on mouse lines with conditional MMR mutations that have allowed more accurate modeling of human cancer syndromes in mice and that together with new technologies in gene targeting, hold great promise for the analysis of MMR-deficient intestinal tumors and other cancers which will drive the development of preventive and therapeutic treatment strategies.

Indexed as

Biomedical ResearchDisease Models, AnimalAnimalsDNA Mismatch RepairGenes, Tumor SuppressorHumansMiceMutationNeoplasmsDNA mismatch repairHereditary non-polyposis colon cancerLynch syndromeMlh1Mouse modelsMsh2

Identifiers

PMID26708047
PMCPMC4754788
OpenAlexW2186419937

What OpenQuestion holds

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Registered trials

None linked

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.