Evidence map›Paper›PMID 29967475›Full record

ArticleScientific reports2018

T315I mutation of BCR-ABL1 into human Philadelphia chromosome-positive leukemia cell lines by homologous recombination using the CRISPR/Cas9 system.

Minori Tamai, Takeshi Inukai, Satoru Kojika, Masako Abe, Keiko Kagami, Daisuke Harama, Tamao Shinohara, Atsushi Watanabe, Hiroko Oshiro, Koshi Akahane and 4 more

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
1.3field-weighted citation impact, top 19% 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

19 citing papers in PubMed, 26 citations in OpenAlex.

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  14. Anticancer drug resistance: An update and perspective.Drug resistance updates : reviews and commentaries in antimicrobial and anticancer chemotherapy · 2021
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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

14 authors at 3 institutions in 1 country.

Minori TamaiDepartment of Pediatrics, School of Medicine, University of Yamanashi, Chuo, Japan.
Takeshi InukaiDepartment of Pediatrics, School of Medicine, University of Yamanashi, Chuo, Japan. tinukai@yamanashi.ac.jp.
Satoru KojikaDepartment of Pediatrics, School of Medicine, University of Yamanashi, Chuo, Japan.
Masako AbeDepartment of Pediatrics, School of Medicine, University of Yamanashi, Chuo, Japan.
Keiko KagamiDepartment of Pediatrics, School of Medicine, University of Yamanashi, Chuo, Japan.
Daisuke HaramaDepartment of Pediatrics, School of Medicine, University of Yamanashi, Chuo, Japan.
Tamao ShinoharaDepartment of Pediatrics, School of Medicine, University of Yamanashi, Chuo, Japan.
Atsushi WatanabeDepartment of Pediatrics, School of Medicine, University of Yamanashi, Chuo, Japan.
Hiroko OshiroDepartment of Pediatrics, School of Medicine, University of Yamanashi, Chuo, Japan.
Koshi AkahaneDepartment of Pediatrics, School of Medicine, University of Yamanashi, Chuo, Japan.
Kumiko GoiDepartment of Pediatrics, School of Medicine, University of Yamanashi, Chuo, Japan.
Eiji SugiharaInnovation Medical Research Institute, Research and Development Center for Precision Medicine, University of Tsukuba, Ibaraki, Japan.
Shinichiro NakadaDepartment of Bioregulation and Cellular Response, Graduate School of Medicine, Osaka University, Osaka, Japan.
Kanji SugitaDepartment of Pediatrics, School of Medicine, University of Yamanashi, Chuo, Japan.
University of Yamanashi · JPOsaka University · JPUniversity of Tsukuba · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

In many cancers, somatic mutations confer tumorigenesis and drug-resistance. The recently established clustered regularly interspaced short palindromic repeats (CRISPR)/Cas9 system is a potentially elegant approach to functionally evaluate mutations in cancers. To reproduce mutations by homologous recombination (HR), the HR pathway must be functional, but DNA damage repair is frequently impaired in cancers. Imatinib is a tyrosine kinase inhibitor for BCR-ABL1 in Philadelphia chromosome-positive (Ph+) leukemia, and development of resistance due to kinase domain mutation is an important issue. We attempted to introduce the T315I gatekeeper mutation into three Ph+ myeloid leukemia cell lines with a seemingly functional HR pathway due to resistance to the inhibitor for poly (ADP) ribose polymerase1. Imatinib-resistant sublines were efficiently developed by the CRISPR/Cas9 system after short-term selection with imatinib; resulting sublines acquired the T315I mutation after HR. Thus, the usefulness of CRISPR/Cas9 system for functional analysis of somatic mutations in cancers was demonstrated.

Indexed as

CRISPR-Cas SystemsHomologous RecombinationMutationCell Line, TumorDrug Resistance, NeoplasmFusion Proteins, bcr-ablHumansImatinib MesylateK562 CellsLeukemia, Myelogenous, Chronic, BCR-ABL PositivePhthalazinesPiperazinesPoly(ADP-ribose) Polymerase InhibitorsProtein Kinase InhibitorsPyrimidinesSchiff Bases5,6-bis(benzylideneamino)-2-mercaptopyrimidin-4-olBCR-ABL1 fusion protein, humanFusion Proteins, bcr-ablImatinib MesylateolaparibPhthalazinesPiperazinesPoly(ADP-ribose) Polymerase InhibitorsProtein Kinase InhibitorsPyrimidinesSchiff Bases

Identifiers

PMID29967475
PMCPMC6028382
OpenAlexW2810106557

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

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.