Evidence map›Paper›PMID 25910225›Full record

ArticleScientific reports2015

Loss of PTPRM associates with the pathogenic development of colorectal adenoma-carcinoma sequence.

Putty-Reddy Sudhir, Shiu-Ting Lin, Chien Chia-Wen, Shung-Haur Yang, Anna Fen-Yau Li, Rai-Hua Lai, Mei-Jung Wang, Yuan-Tsong Chen, Chian-Feng Chen, Yuh-Shan Jou and 1 more

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
0.7field-weighted citation impact, top 30% 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

15 citing papers in PubMed, 24 citations in OpenAlex.

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  7. Prognostic impact of high-risk factors andAnnals of translational medicine · 2022
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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

11 authors at 3 institutions in 1 country.

Putty-Reddy SudhirInstitute of Biomedical Sciences, Academia Sinica, Taipei, Taiwan, ROC.
Shiu-Ting LinInstitute of Biomedical Sciences, Academia Sinica, Taipei, Taiwan, ROC.
Chien Chia-WenInstitute of Biomedical Sciences, Academia Sinica, Taipei, Taiwan, ROC.
Shung-Haur YangDepartment of Surgery, Taipei Veterans General Hospital, Taiwan, ROC.
Anna Fen-Yau LiDepartment of Pathology, Taipei Veterans General Hospital, Taiwan, ROC.
Rai-Hua LaiInstitute of Biomedical Sciences, Academia Sinica, Taipei, Taiwan, ROC.
Mei-Jung WangInstitute of Biomedical Sciences, Academia Sinica, Taipei, Taiwan, ROC.
Yuan-Tsong ChenInstitute of Biomedical Sciences, Academia Sinica, Taipei, Taiwan, ROC.
Chian-Feng ChenVYM Genome Research Center, Taiwan, ROC.
Yuh-Shan JouInstitute of Biomedical Sciences, Academia Sinica, Taipei, Taiwan, ROC.
Jeou-Yuan Chen1] Institute of Biomedical Sciences, Academia Sinica, Taipei, Taiwan, ROC [2] Institute of Genome Sciences, National Yang-Ming University, Taipei, Taiwan, ROC.
Institute of Biomedical Sciences, Academia Sinica · TWTaipei Veterans General Hospital · TWNational Yang Ming Chiao Tung University · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Identification and functional analysis of genes from genetically altered chromosomal regions would suggest new molecular targets for cancer diagnosis and treatment. Here we performed a genome-wide analysis of chromosomal copy number alterations (CNAs) in matching sets of colon mucosa-adenoma-carcinoma samples using high-throughput oligonucleotide microarray analysis. In silico analysis of NCBI GEO and TCGA datasets allowed us to uncover the significantly altered genes (p ≤ 0.001) associated with the identified CNAs. We performed quantitative PCR analysis of the genomic and complementary DNA derived from primary mucosa, adenoma, and carcinoma samples, and confirmed the recurrent loss and down-regulation of PTPRM in colon adenomas and carcinomas. Functional characterization demonstrated that PTPRM negatively regulates cell growth and colony formation, whereas loss of PTPRM promotes oncogenic cell growth. We further showed that, in accordance to Knudson's two-hit hypothesis, inactivation of PTPRM in colon cancer was mainly attributed to loss of heterozygosity and promoter hypermethylation. Taken together, this study demonstrates a putative tumor suppressive role for PTPRM and that genetic and epigenetic alterations of PTPRM may contribute to early step of colorectal tumorigenesis.

Indexed as

AdenomaCarcinomaCell ProliferationColorectal NeoplasmsDatabases, GeneticDNA Copy Number VariationsDNA MethylationDown-RegulationGenotypeHumansIntestinal MucosaLoss of HeterozygosityOligonucleotide Array Sequence AnalysisPolymorphism, Single NucleotidePromoter Regions, GeneticReal-Time Polymerase Chain ReactionPTPRM protein, humanReceptor-Like Protein Tyrosine Phosphatases, Class 2RNA, Small Interfering

Identifiers

PMID25910225
PMCPMC5386118
OpenAlexW2010093095

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.