Evidence map›Paper›PMID 36157542›Full record

ReviewWorld journal of gastroenterology2022

Mechanistic and functional extrapolation of SET and MYND domain-containing protein 2 to pancreatic cancer.

Eid Alshammari, Ying-Xue Zhang, Zhe Yang

Abstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in World journal of gastroenterology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
–field-weighted citation impact
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

3 citing papers in PubMed.

  1. Review
  2. Article
  3. 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

3 authors.

Eid AlshammariDepartment of Biochemistry, Microbiology, and Immunology, Wayne State University, Detroit, MI 48201, United States.
Ying-Xue ZhangDepartment of Biochemistry, Microbiology, and Immunology, Wayne State University, Detroit, MI 48201, United States.
Zhe YangDepartment of Biochemistry, Microbiology, and Immunology, Wayne State University School of Medicine, Detroit, MI 48201, United States. zyang@med.wayne.edu.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Pancreatic ductal adenocarcinoma (PDAC) is one of the most lethal neoplasms worldwide and represents the vast majority of pancreatic cancer cases. Understanding the molecular pathogenesis and the underlying mechanisms involved in the initiation, maintenance, and progression of PDAC is an urgent need, which may lead to the development of novel therapeutic strategies against this deadly cancer. Here, we review the role of SET and MYND domain-containing protein 2 (SMYD2) in initiating and maintaining PDAC development through methylating multiple tumor suppressors and oncogenic proteins. Given the broad substrate specificity of SMYD2 and its involvement in diverse oncogenic signaling pathways in many other cancers, the mechanistic extrapolation of SMYD2 from these cancers to PDAC may allow for developing new hypotheses about the mechanisms driving PDAC tumor growth and metastasis, supporting a proposition that targeting SMYD2 could be a powerful strategy for the prevention and treatment of PDAC.

Indexed as

Carcinoma, Pancreatic DuctalPancreatic NeoplasmsCell Line, TumorHistone-Lysine N-MethyltransferaseHumansMYND DomainsHistone-Lysine N-MethyltransferaseSMYD2 protein, humanHistone/non-histone methylationMethyltransferase inhibitorsOncogenic signaling pathwaysPancreatic ductal adenocarcinomaProtein lysine methyltransferase

Identifiers

PMID36157542
PMCPMC9367238

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.