Evidence map›Paper›PMID 38151292›Full record

ArticleCancer genomics & proteomics

Depletion of

Masato Yoshizawa, Atsushi Shiozaki, Eishi Ashihara

Open access · diamondAbstract read
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 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
1.2field-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

4 citing papers in PubMed, 5 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. 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 at 2 institutions in 1 country.

Masato YoshizawaLaboratory of Clinical and Translational Physiology, Kyoto Pharmaceutical University, Kyoto, Japan; kd20011@ms.kyoto-phu.ac.jp.
Atsushi ShiozakiDivision of Digestive Surgery, Department of Surgery, Kyoto Prefectural University of Medicine, Kyoto, Japan.
Eishi AshiharaLaboratory of Clinical and Translational Physiology, Kyoto Pharmaceutical University, Kyoto, Japan; ash@mb.kyoto-phu.ac.jp.
Kyoto Pharmaceutical University · JPKyoto Prefectural University of Medicine · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

BACKGROUND/

aimPancreatic cancer is one of the most lethal malignant cancers worldwide and the seventh most common cause of cancer-related death in both sexes. Herein, we analyzed open access data and discovered that expression of a gene called deoxynucleotidyltransferase terminal-interacting protein 2 (DNTTIP2) is linked to prognosis of pancreatic ductal adenocarcinoma (PDAC). We then elucidated the role of DNTTIP2 in the proliferation of pancreatic cancer cells in vitro. MATERIALS AND

methodsA WST-8 assay, cell cycle analysis, Annexin-V staining, quantitative reverse transcription-PCR, and western blot analysis were conducted to assess cell proliferation, cell cycle, apoptosis, and expression of DNTTIP2 mRNA and protein, respectively, in DNTTIP2-depleteted MIA-PaCa-2 and PK-1 cells.

resultsDepletion of DNTTIP2 induced G

conclusionDNTTIP2 is involved in proliferation of pancreatic cancer cells. Thus, DNTTIP2 is a potential target for inhibiting progression of pancreatic cancers.

Indexed as

Matrix Attachment Region Binding ProteinsPancreatic NeoplasmsApoptosisCell CycleCell Cycle CheckpointsCell Line, TumorCell ProliferationFemaleHumansMaleRNA-Binding ProteinsTranscription FactorsDNTTIP2 protein, humanMatrix Attachment Region Binding ProteinsRNA-Binding ProteinsSATB1 protein, humanTranscription FactorsCDK1CDK6cellsDNTTIP2Pancreatic cancerSATB1

Identifiers

PMID38151292
PMCPMC10756344
OpenAlexW4390267682

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.