Evidence map›Paper›PMID 22552371›Full record

ArticleClinical & experimental metastasis2012

hMLH1 promoter hypermethylation and MSI status in human endometrial carcinomas with and without metastases.

J Bischoff, A Ignatov, A Semczuk, C Schwarzenau, T Ignatov, T Krebs, D Küster, D Przadka-Rabaniuk, A Roessner, S D Costa and 1 more

Abstract read
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Article in Clinical & experimental metastasis, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
1.0field-weighted citation impact, top 24% 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

14 citing papers in PubMed, 24 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Review
  5. Review
  6. Article
  7. Journal of Cancer · 2018
    Article
  8. Article
  9. Article
  10. Biomarkers of genome instability and cancer epigenetics.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2016
    Review
  11. Article
  12. DNA methylation and cancer diagnosis.International journal of molecular sciences · 2013
    Review
  13. Emerging therapeutic biomarkers in endometrial cancer.BioMed research international · 2013
    Review
  14. 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

11 authors at 3 institutions in 2 countries.

J BischoffDepartment of Gynecology, Otto-von-Guericke University, Magdeburg, Germany.
A Ignatov
A Semczuk
C Schwarzenau
T Ignatov
T Krebs
D Küster
D Przadka-Rabaniuk
A Roessner
S D Costa
R Schneider-Stock
Otto-von-Guericke University Magdeburg · DEMedical University of Lublin · PLFriedrich-Alexander-Universität Erlangen-Nürnberg · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

We investigated the methylation status of mismatch repair gene hMLH1 in 80 primary human endometrial carcinomas (ECs) and in 30 metastatic lesions. It was correlated to the expression of hMLH1 protein, microsatellite instability (MSI) of ECs and to the well-known clinico-pathological variables of cancer. The hMLH1 promoter methylation was detected in 24 out of 64 (37.5 %) primary ECs but only in one out of 18 (5.6 %) metastatic lesions investigated. Promoter hMLH1 hypermethylation was found more often in early stage ECs and was associated with a decrease of hMLH1 protein expression immunohistochemically. An inverse relationship between hMLH1 expression and clinical stage of the disease was found (p = 0.048). Interestingly, there was a significant correlation between MSI and hMLH1 protein expression level (p = 0.042). MSI phenotype was found more often in EC metastases compared to the primary tumors (66.7 % vs 29.3 %; p = 0.039). However, neither hMLH1 promoter hypermethylation nor MSI was independent predictive factors for patient's outcome. Using an in vitro model we showed that hMLH1 methylation is reversible. These data showed that hMLH1 methylation with a consequent protein decrease occurred early during EC tumorigenesis and may cause a MSI phenotype, which occurs relatively late. MSI may be an important mechanism supporting further the tumor progression. These findings may have importance for the specific chemosensitization of the primary tumors/metastases and can improve our understanding of endometrial carcinogenesis in humans.

Indexed as

DNA MethylationMicrosatellite InstabilityAdaptor Proteins, Signal TransducingAdultAgedAged, 80 and overAzacitidineCell Line, TumorDNA, NeoplasmDNA RepairDNA Repair EnzymesEndometrial NeoplasmsFemaleHumansMicrosatellite RepeatsMiddle AgedAdaptor Proteins, Signal TransducingAzacitidineDNA, NeoplasmDNA Repair EnzymesMLH1 protein, humanMutL Protein Homolog 1Neoplasm ProteinsNuclear Proteins

Identifiers

PMID22552371
OpenAlexW1982692195

What OpenQuestion holds

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Read underepoch 390

Registered trials

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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.