Evidence map›Paper›PMID 26721253›Full record

ArticleJournal of cancer research and clinical oncology2016

Expression of the apoptosis repressor with caspase recruitment domain (ARC) in liver metastasis of colorectal cancer and its correlation with DNA mismatch repair proteins and p53.

Csaba Tóth, Jeannine Meinrath, Esther Herpel, Jutta Derix, Jochen Fries, Reinhard Buettner, Peter Schirmacher, Sebastian Heikaus

Open access · greenAbstract readComparative Study
In one paragraph

Article in Journal of cancer research and clinical oncology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
0.9field-weighted citation impact, top 25% 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

11 citing papers in PubMed, 17 citations in OpenAlex.

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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

8 authors at 3 institutions in 1 country.

Csaba TóthInstitute of Pathology, University Hospital Cologne, Cologne, Germany. csaba.toth@med.uni-heidelberg.de.
Jeannine MeinrathInstitute of Pathology, University Hospital Cologne, Cologne, Germany.
Esther HerpelInstitute of Pathology, University Hospital Heidelberg, Im Neuenheimer Feld 224, Heidelberg, Germany.
Jutta DerixUniversity Hospital Düsseldorf, Düsseldorf, Germany.
Jochen FriesInstitute of Pathology, University Hospital Cologne, Cologne, Germany.
Reinhard BuettnerInstitute of Pathology, University Hospital Cologne, Cologne, Germany.
Peter SchirmacherInstitute of Pathology, University Hospital Heidelberg, Im Neuenheimer Feld 224, Heidelberg, Germany.
Sebastian HeikausUniversity Hospital Düsseldorf, Düsseldorf, Germany.
University Hospital Cologne · DEDüsseldorf University Hospital · DEHeidelberg University · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

introductionApoptotic signaling is one of the most important processes in the measurement of chemotherapeutic effectiveness. In apoptotic machinery, various pathways and proteins are involved (i.e., mismatch repair proteins, p53). One of the regulatory proteins is ARC, which can inhibit not only the extrinsic but also the intrinsic apoptotic signaling. MATERIALS AND

methodsIn this study, we investigated the expression levels of ARC in colorectal liver metastasis and compared them with the expression of mismatch repair proteins and p53. Furthermore, we investigated ARC expression level depending on sex, age, tumor grade, mucin production, tumor size and number of liver metastasis.

resultsARC expression level in colorectal cancer liver metastasis was independent from clinical data (i.e., age, gender, tumor size, tumor number or mucin production) but strongly correlated with MSH2 and MSH6 expression, which further supported the evidence for the regulatory role of MSH2 and MSH6 in apoptosis; i.e., in case of sufficient MSH2 and MSH6 expression, significantly higher ARC level is required to suppress the apoptosis. A regulatory interaction between ARC and p53 has been described, but we found no correlation between p53 expression levels and ARC levels.

conclusionFurther studies are needed to define the exact role of ARC in apoptotic signaling and thus its role in chemoresistance and survival of tumor cells.

Indexed as

Adaptor Proteins, Signal TransducingAdenosine TriphosphatasesAdultAgedAged, 80 and overApoptosis Regulatory ProteinsBiomarkers, TumorCase-Control StudiesColonColorectal NeoplasmsDNA-Binding ProteinsDNA Repair EnzymesFemaleFollow-Up StudiesHumansImmunoenzyme TechniquesAdaptor Proteins, Signal TransducingAdenosine TriphosphatasesApoptosis Regulatory ProteinsBiomarkers, TumorDNA-Binding ProteinsDNA Repair EnzymesG-T mismatch-binding proteinMismatch Repair Endonuclease PMS2MLH1 protein, humanMSH2 protein, humanMuscle ProteinsMutL Protein Homolog 1MutS Homolog 2 ProteinNOL3 protein, humanNuclear ProteinsPMS2 protein, humanTP53 protein, humanTumor Suppressor Protein p53ApoptosisARCColorectal cancerLiver metastasisMMR proteinsp53

Identifiers

PMID26721253
PMCPMC11819034
OpenAlexW2219651669

What OpenQuestion holds

Textmetadata
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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.