Evidence map›Paper›PMID 40068557›Full record

ReviewDNA repair2025

Advances in diagnostic and therapeutic applications of mismatch repair loss in cancer.

J T DeWitt, D Jimenez-Tovar, A Mazumder, S Haricharan

Abstract readReview
In one paragraph

Review in DNA repair, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
–field-weighted citation impact
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

5 citing papers in PubMed.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Review
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

4 authors.

J T DeWittDept of Biology, San Diego State University, San Diego, CA, USA; Cancer Biology and Signaling Program, UCSD Moores Cancer Center, San Diego, CA, USA.
D Jimenez-TovarDept of Biology, San Diego State University, San Diego, CA, USA.
A MazumderDept of Biology, San Diego State University, San Diego, CA, USA.
S HaricharanDept of Biology, San Diego State University, San Diego, CA, USA; Cancer Biology and Signaling Program, UCSD Moores Cancer Center, San Diego, CA, USA. Electronic address: sharicharan@sdsu.edu.

Funding

Regulation of the tumor microenvironment by DNA damage repair proteinsR37CA270362 · NCI · SANFORD BURNHAM PREBYS MEDICAL DISCOVERY INSTITUTE · PI Svasti Haricharan · 2023 to 2026
$1.8M
Cancer Targets and Drug DiscoveryT32CA211036 · NCI · SANFORD BURNHAM PREBYS MEDICAL DISCOVERY INSTITUTE · PI COSFORD, NICHOLAS DAVID · 2018 to 2022
$1.2M
NCI NIH HHS R37 CA270362NCI NIH HHS T32 CA211036
6 · The paper itself

Abstract

Mismatch repair (MMR) is a highly conserved, fundamental DNA damage repair pathway that maintains genomic fidelity during cell replication. MMR dysregulation contributes to tumor formation by promoting genomic instability thereby increasing the frequency of potentially oncogenic mutational events. Therefore, MMR dysregulation, in its tumor suppressor role, is largely studied in the context of genomic instability and associated response to immune checkpoint blockade therapies. However, a growing body of literature suggests that the impact of MMR dysregulation on tumor phenotypes is more nuanced than a concerted impact on genomic stability. Rather, loss of individual MMR genes promotes distinct cancer-relevant biological phenotypes, and these phenotypes are further modulated by the tissue of tumor origin. Here, we explore relevant literature and review the prognostic and predictive significance of these non-canonical discoveries.

Indexed as

DNA Mismatch RepairNeoplasmsAnimalsGenomic InstabilityHumansCancerCancer diagnosticsCancer therapyMismatch repairSomatic loss

Identifiers

PMID40068557
PMCPMC12817362

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
Read underepoch 390

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.