Evidence map›Paper›PMID 33099471›Full record

ArticleCancer genomics & proteomics

Deletion of Histone Methyltransferase G9a Suppresses Mutant Kras-driven Pancreatic Carcinogenesis.

Hiroyuki Kato, Keisuke Tateishi, Hiroaki Fujiwara, Hideaki Ijichi, Keisuke Yamamoto, Takuma Nakatsuka, Miwako Kakiuchi, Makoto Sano, Yotaro Kudo, Yoku Hayakawa and 7 more

Open access · diamondAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cancer genomics & proteomics. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
0.9field-weighted citation impact, top 26% 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

9 citing papers in PubMed, 15 citations in OpenAlex.

  1. Article
  2. Review
  3. Cancer Stem Cells in Pancreatic Ductal Adenocarcinoma.International journal of molecular sciences · 2023
    Review
  4. Review
  5. Article
  6. Review
  7. Article
  8. Inactivation of the Euchromatic Histone-LysineFrontiers in cell and developmental biology · 2021
    Article
  9. Review
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

17 authors at 4 institutions in 1 country.

Hiroyuki KatoDepartment of Gastroenterology, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan.
Keisuke TateishiDepartment of Gastroenterology, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan ktate-tky@umin.ac.jp.
Hiroaki FujiwaraDepartment of Gastroenterology, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan.
Hideaki IjichiDepartment of Gastroenterology, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan.
Keisuke YamamotoDepartment of Gastroenterology, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan.
Takuma NakatsukaDepartment of Gastroenterology, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan.
Miwako KakiuchiDepartment of Gastroenterology, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan.
Makoto SanoDepartment of Gastroenterology, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan.
Yotaro KudoDepartment of Gastroenterology, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan.
Yoku HayakawaDepartment of Gastroenterology, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan.
Hayato NakagawaDepartment of Gastroenterology, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan.
Yasuo TanakaDepartment of Gastroenterology, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan.
Motoyuki OtsukaDepartment of Gastroenterology, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan.
Yoshihiro HirataDivision of Clinical Genome Research, Advanced Clinical Research Center, Institute of Medical Science, The University of Tokyo, Tokyo, Japan.
Makoto TachibanaLaboratory of Epigenome Dynamics, Graduate School of Frontier Biosciences, Osaka University, Osaka, Japan.
Yoichi ShinkaiCellular Memory Laboratory, RIKEN Advanced Science Institute, Saitama, Japan.
Kazuhiko KoikeDepartment of Gastroenterology, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan.
The University of Tokyo · JPNihon University · JPOsaka University · JPRIKEN Advanced Science Institute · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

BACKGROUND/

aimThe entire mechanisms by which epigenetic modifiers contribute to the development of pancreatic cancer remain unknown. Although the histone methyltransferase G9a is a promising target in human cancers, its role in pancreatic carcinogenesis has been under-studied. The aim of the study was to examine the role of G9a in pancreatic carcinogenesis by a gene-targeting mouse model. MATERIALS AND

methodsWe established pancreas-specific G9a

resultsG9a deficiency impaired the progression of pancreatic intraepithelial neoplasia (PanIN) and prolonged the survival of KC mice. The number of phosphorylated Erk-positive cells and Dclk1-positive cells, which are reported to be essential for the progression of PanIN, were decreased by G9a deletion. UNC0638, an inhibitor of G9a, suppressed the growth of organoids and increased global chromatin accessibility, especially around the regions including the protein phosphatase 2A genes.

conclusionThus, our study suggested the functional interaction of G9a, Dclk1 and Mapk pathway in the Kras-driven pancreatic carcinogenesis. The inhibition of G9a may suppress the initiation of oncogenic Kras-driven pancreatic carcinogenesis.

Indexed as

Gene Expression Regulation, NeoplasticMutationAnimalsCarcinogenesisHistone-Lysine N-MethyltransferaseMiceMice, Inbred C57BLMice, KnockoutPancreatic NeoplasmsProto-Oncogene Proteins p21(ras)G9a protein, mouseHistone-Lysine N-MethyltransferaseKRAS protein, humanProto-Oncogene Proteins p21(ras)Carcinogenesischromatin accessibilityepigeneticsPanINPDAC

Identifiers

PMID33099471
PMCPMC7675651
OpenAlexW3094259002

What OpenQuestion holds

Textmetadata
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.