Evidence map›Paper›PMID 31349215›Full record

ArticleEndocrine connections2019

PTPRM, a candidate tumor suppressor gene in small intestinal neuroendocrine tumors.

Elham Barazeghi, Per Hellman, Gunnar Westin, Peter Stålberg

Open access · goldAbstract read
In one paragraph

Article in Endocrine connections, 2019. 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
0.8field-weighted citation impact, top 29% 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.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Multifaceted modeling of small intestinal neuroendocrine tumors.Endocrine oncology (Bristol, England) · 2024
    Review
  8. Article
  9. Article
  10. Article
  11. Article
  12. PTPRM Is Critical for Synapse Formation Regulated by Zinc Ion.Frontiers in molecular neuroscience · 2022
    Article
  13. Article
  14. Review
  15. 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

4 authors at 1 institution in 1 country.

Elham BarazeghiDepartment of Surgical Sciences, Uppsala University, Uppsala University Hospital, Rudbeck Laboratory, Uppsala, Sweden.
Per HellmanDepartment of Surgical Sciences, Uppsala University, Uppsala University Hospital, Rudbeck Laboratory, Uppsala, Sweden.
Gunnar WestinDepartment of Surgical Sciences, Uppsala University, Uppsala University Hospital, Rudbeck Laboratory, Uppsala, Sweden.
Peter StålbergDepartment of Surgical Sciences, Uppsala University, Uppsala University Hospital, Rudbeck Laboratory, Uppsala, Sweden.
Uppsala University Hospital · SE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Small intestinal neuroendocrine tumors (SI-NETs) are small, slow growing neoplasms with loss of one copy of chromosome 18 as a common event. Frequently mutated genes on chromosome 18 or elsewhere have not been found so far. The aim of this study was to investigate a possible tumor suppressor role of the transmembrane receptor type tyrosine phosphatase PTPµ (PTPRM at 18p11) in SI-NETs. Immunohistochemistry, quantitative RT-PCR, colony formation assay and quantitative CpG methylation analysis by pyrosequencing were performed. Undetectable/very low levels of PTPRM or aberrant pattern of immunostaining, with both negative and positive areas, were detected in the majority of tumors (33/40), and a significantly reduced mRNA expression in metastases compared to primary tumors was observed. Both the DNA methylation inhibitor 5-aza-2'-deoxycytidine and the S-adenosylhomocysteine hydrolase inhibitor 3-deazaneplanocin A (DZNep) induced PTPRM expression in CNDT2.5 and KRJ-I SI-NET cells. CpG methylation of upstream regulatory regions, the promoter region and the exon 1/intron 1 boundary was detected by pyrosequencing analysis of the two cell lines and not in the analyzed SI-NETs. Overexpression of PTPRM in the SI-NET cell lines reduced cell growth and cell proliferation and induced apoptosis. The tyrosine phosphatase activity of PTPRM was not involved in cell growth inhibition. The results support a role for PTPRM as a dysregulated candidate tumor suppressor gene in SI-NETs and further analyses of the involved mechanisms are warranted.

Indexed as

DNA methylationepigeneticneuroendocrine tumorsPTPRMSI-NETs

Identifiers

PMID31349215
PMCPMC6687034
OpenAlexW2957398407

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.