Evidence map›Paper›PMID 27047543›Full record

ArticleGastroenterology research and practice2016

The Role of Chromosomal Instability and Epigenetics in Colorectal Cancers Lacking β-Catenin/TCF Regulated Transcription.

Wael M Abdel-Rahman, Johanna E Lotsari-Salomaa, Sippy Kaur, Anni Niskakoski, Sakari Knuutila, Heikki Järvinen, Jukka-Pekka Mecklin, Päivi Peltomäki

Open access · goldAbstract read
In one paragraph

Article in Gastroenterology research and practice, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
1.7field-weighted citation impact, top 17% 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

13 citing papers in PubMed, 17 citations in OpenAlex.

  1. CAP superfamily proteins in human: a new target for cancer therapy.Medical oncology (Northwood, London, England) · 2024
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  5. [Luteolin reverses OPCML methylation to inhibit proliferation of breast cancer MDA-MB-231 cells].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2020
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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 2 countries.

Wael M Abdel-RahmanDepartment of Medical Laboratory Sciences, College of Health Sciences and Sharjah Institute for Medical Research (SIMR), University of Sharjah, P.O. Box 27272, Sharjah, UAE; Department of Medical and Clinical Genetics, University of Helsinki, 00290 Helsinki, Finland.ORCID 0000-0002-2149-1043
Johanna E Lotsari-SalomaaDepartment of Medical and Clinical Genetics, University of Helsinki, 00290 Helsinki, Finland.
Sippy KaurDepartment of Medical and Clinical Genetics, University of Helsinki, 00290 Helsinki, Finland.
Anni NiskakoskiDepartment of Medical and Clinical Genetics, University of Helsinki, 00290 Helsinki, Finland.
Sakari KnuutilaDepartment of Pathology, Haartman Institute and HUSLAB, University of Helsinki and Helsinki University Central Hospital, Helsinki, 00029 HUS, Finland.ORCID 0000-0001-5592-3839
Heikki JärvinenSecond Department of Surgery, Helsinki University Central Hospital, Helsinki, 00029 HUS, Finland.ORCID 0000-0002-5318-4507
Jukka-Pekka MecklinDepartment of Surgery, Jyväskylä Central Hospital, 40620 Jyväskylä, Finland; Institute of Clinical Medicine, University of Eastern Finland, Kuopio, Finland.
Päivi PeltomäkiDepartment of Medical and Clinical Genetics, University of Helsinki, 00290 Helsinki, Finland.ORCID 0000-0001-8819-2980
University of Helsinki · FIHelsinki University Hospital · FIUniversity of Eastern Finland · FI

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

All colorectal cancer cell lines except RKO displayed active β-catenin/TCF regulated transcription. This feature of RKO was noted in familial colon cancers; hence our aim was to dissect its carcinogenic mechanism. MFISH and CGH revealed distinct instability of chromosome structure in RKO. Gene expression microarray of RKO versus 7 colon cancer lines (with active Wnt signaling) and 3 normal specimens revealed 611 differentially expressed genes. The majority of the tested gene loci were susceptible to LOH in primary tumors with various β-catenin localizations as a surrogate marker for β-catenin activation. The immunohistochemistry of selected genes (IFI16, RGS4, MCTP1, DGKI, OBCAM/OPCML, and GLIPR1) confirmed that they were differentially expressed in clinical specimens. Since epigenetic mechanisms can contribute to expression changes, selected target genes were evaluated for promoter methylation in patient specimens from sporadic and hereditary colorectal cancers. CMTM3, DGKI, and OPCML were frequently hypermethylated in both groups, whereas KLK10, EPCAM, and DLC1 displayed subgroup specificity. The overall fraction of hypermethylated genes was higher in tumors with membranous β-catenin. We identified novel genes in colorectal carcinogenesis that might be useful in personalized tumor profiling. Tumors with inactive Wnt signaling are a heterogeneous group displaying interaction of chromosomal instability, Wnt signaling, and epigenetics.

Identifiers

PMID27047543
PMCPMC4800109
OpenAlexW2297406549

What OpenQuestion holds

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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.