Evidence map›Paper›PMID 31844142›Full record

ArticleScientific reports2019

A genome-scale CRISPR/Cas9 knockout screening reveals SH3D21 as a sensitizer for gemcitabine.

Mohammad Masoudi, Motoaki Seki, Razieh Yazdanparast, Nozomu Yachie, Hiroyuki Aburatani

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
0.3field-weighted citation impact, top 42% 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

11 citing papers in PubMed, 12 citations in OpenAlex.

  1. Article
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  3. Molecular biology research communications · 2026
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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

5 authors at 3 institutions in 3 countries.

Mohammad MasoudiMolecular Biology Department, Graduate School of Medicine, The University of Tokyo, Tokyo, 153-8904, Japan.ORCID http://orcid.org/0000-0001-9434-1524
Motoaki SekiSynthetic Biology Division, Research Center for Advance Science and Technology, The University of Tokyo, Tokyo, 153-8904, Japan.
Razieh YazdanparastMolecular Biology Laboratory, Institute of Biochemistry and Biophysics, University of Tehran, Tehran, 13145-1384, Iran. ryazdan@ut.ac.ir.
Nozomu YachieSynthetic Biology Division, Research Center for Advance Science and Technology, The University of Tokyo, Tokyo, 153-8904, Japan.
Hiroyuki AburataniMolecular Biology Department, Graduate School of Medicine, The University of Tokyo, Tokyo, 153-8904, Japan. haburata-tky@umin.ac.jp.ORCID http://orcid.org/0000-0003-0438-1544
The University of Tokyo · JPUniversity of Tehran · IRTokyo University of Science · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Gemcitabine, 2',2'-difluoro-2'-deoxycytidine, is used as a pro-drug in treatment of variety of solid tumour cancers including pancreatic cancer. After intake, gemcitabine is transferred to the cells by the membrane nucleoside transporter proteins. Once inside the cells, it is converted to gemcitabine triphosphate followed by incorporation into DNA chains where it causes inhibition of DNA replication and thereby cell cycle arrest and apoptosis. Currently gemcitabine is the standard drug for treatment of pancreatic cancer and despite its widespread use its effect is moderate. In this study, we performed a genome-scale CRISPR/Cas9 knockout screening on pancreatic cancer cell line Panc1 to explore the genes that are important for gemcitabine efficacy. We found SH3D21 as a novel gemcitabine sensitizer implying it may act as a therapeutic target for improvement of gemcitabine efficacy in treatment of pancreatic cancer.

Indexed as

Antimetabolites, AntineoplasticApoptosisCell Cycle CheckpointsCell LineCell Line, TumorCRISPR-Cas SystemsDeoxycytidineDNA ReplicationDrug Resistance, NeoplasmGemcitabineHEK293 CellsHumansPancreatic NeoplasmsAntimetabolites, AntineoplasticDeoxycytidineGemcitabine

Identifiers

PMID31844142
PMCPMC6915784
OpenAlexW2996600540

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.