Evidence map›Paper›PMID 18543306›Full record

ReviewCancer2008

A review of the clinical relevance of mismatch-repair deficiency in ovarian cancer.

Tuya Pal, Jenny Permuth-Wey, Thomas A Sellers

Abstract readReview
In one paragraph

Review in Cancer, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
49citing papers in PubMed, 1 pooled it
2.6field-weighted citation impact, top 11% 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

49 citing papers in PubMed, 1 synthesis or guideline pooled it, 105 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Article
  4. Review
  5. Article
  6. Review
  7. Review
  8. Article
  9. Article
  10. Article
  11. Review
  12. Article
  13. Epithelial Ovarian Cancer: Providing Evidence of Predisposition Genes.International journal of environmental research and public health · 2022
    Review
  14. Review
  15. Review
  16. Article
  17. Review
  18. Article
  19. Article
  20. mBMC bioinformatics · 2021
    Article
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.

Tuya PalDepartment of Cancer Epidemiology and Genetics, H. Lee Moffitt Cancer Center and Research Institute, Tampa, Florida 33612, USA. tuya.pal@moffitt.org
Jenny Permuth-Wey
Thomas A Sellers
Moffitt Cancer Center · US

Funding

Ovarian Cancer and Mismatch Repair DeficiencyR01CA111914 · NCI · H. LEE MOFFITT CANCER CTR &RES INST · PI PAL, TUYA · 2005 to 2009
$2.2M
Clinical Relevance of Mismatch Repair in Ovarian CancerK07CA108987 · NCI · H. LEE MOFFITT CANCER CTR & RES INST · PI PAL, TUYA · 2006 to 2010
$664k
NCI NIH HHS K07 CA108987NCI NIH HHS R01 CA111914NCI NIH HHS R01CA111914
6 · The paper itself

Abstract

Ovarian cancer ranks fifth in both cancer incidence and mortality among women in the United States. Defects in the mismatch-repair (MMR) pathway that arise through genetic and/or epigenetic mechanisms may be important etiologically in a reasonable proportion of ovarian cancers. Genetic mechanisms of MMR dysfunction include germline and somatic mutations in the MMR proteins. Germline mutations cause hereditary nonpolyposis colorectal cancer (HNPCC), which is the third most common cause of inherited ovarian cancer after BRCA1 and BRCA2 mutations. An epigenetic mechanism known to cause inactivation of the MMR system is promoter hypermethylation of 1 of the MMR genes, mutL homolog 1 (MLH1). Various laboratory methods, in addition to clinical and histopathologic criteria, can be used to identify MMR-deficient ovarian cancers. Such methods include microsatellite instability analysis, immunohistochemistry, MLH1 promoter hypermethylation testing, and germline mutation analysis. In this review, the authors describe the existing literature regarding the molecular, clinical, and histologic characteristics of MMR-deficient ovarian cancers along with the possible effect on survival and treatment response. By further defining the profile of MMR-deficient ovarian cancers and their associated etiologic mechanisms, there may be a greater potential to distinguish between those of hereditary and sporadic etiology. The ability to make such distinctions may be of diagnostic, prognostic, and therapeutic utility.

Indexed as

DNA Mismatch RepairColorectal Neoplasms, Hereditary NonpolyposisDNA Repair-Deficiency DisordersDNA Repair EnzymesFemaleHumansMutS Homolog 2 ProteinOvarian NeoplasmsDNA Repair EnzymesMutS Homolog 2 Protein

Identifiers

PMID18543306
PMCPMC2644411
OpenAlexW2012331065

What OpenQuestion holds

Textmetadata
LicenceTDM
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.