Evidence map›Paper›PMID 28445002›Full record

ArticleCancer science2017

Glucose metabolism-targeted therapy and withaferin A are effective for epidermal growth factor receptor tyrosine kinase inhibitor-induced drug-tolerant persisters.

Kei Kunimasa, Tatsuya Nagano, Yohei Shimono, Ryota Dokuni, Tatsunori Kiriu, Shuntaro Tokunaga, Daisuke Tamura, Masatsugu Yamamoto, Motoko Tachihara, Kazuyuki Kobayashi and 2 more

Open access · goldAbstract read
In one paragraph

Article in Cancer science, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
0.6field-weighted citation impact, top 31% 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

27 citing papers in PubMed, 36 citations in OpenAlex.

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  16. Pharmaceutics · 2022
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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

12 authors at 2 institutions in 1 country.

Kei KunimasaDivision of Respiratory Medicine, Kobe University Graduate School of Medicine, Kobe, Japan.
Tatsuya NaganoDivision of Respiratory Medicine, Kobe University Graduate School of Medicine, Kobe, Japan.ORCID http://orcid.org/0000-0003-0790-5139
Yohei ShimonoDivision of Medical Oncology/Hematology Department of Internal Medicine, Kobe University Graduate School of Medicine, Kobe, Japan.
Ryota DokuniDivision of Respiratory Medicine, Kobe University Graduate School of Medicine, Kobe, Japan.
Tatsunori KiriuDivision of Respiratory Medicine, Kobe University Graduate School of Medicine, Kobe, Japan.
Shuntaro TokunagaDivision of Respiratory Medicine, Kobe University Graduate School of Medicine, Kobe, Japan.
Daisuke TamuraDivision of Respiratory Medicine, Kobe University Graduate School of Medicine, Kobe, Japan.
Masatsugu YamamotoDivision of Respiratory Medicine, Kobe University Graduate School of Medicine, Kobe, Japan.
Motoko TachiharaDivision of Respiratory Medicine, Kobe University Graduate School of Medicine, Kobe, Japan.
Kazuyuki KobayashiDivision of Respiratory Medicine, Kobe University Graduate School of Medicine, Kobe, Japan.
Miyako SatouchiDepartment of Thoracic Oncology, Hyogo Cancer Center, Akashi, Japan.
Yoshihiro NishimuraDivision of Respiratory Medicine, Kobe University Graduate School of Medicine, Kobe, Japan.
Kobe University · JPHyogo Prefectural Cancer Center · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

In pathway-targeted cancer drug therapies, the relatively rapid emergence of drug-tolerant persisters (DTPs) substantially limits the overall therapeutic benefit. However, little is known about the roles of DTPs in drug resistance. In this study, we investigated the features of epidermal growth factor receptor-tyrosine kinase inhibitor-induced DTPs and explored a new treatment strategy to overcome the emergence of these DTPs. We used two EGFR-mutated lung adenocarcinoma cell lines, PC9 and II-18. They were treated with 2 μM gefitinib for 6, 12, or 24 days or 6 months. We analyzed the mRNA expression of the stem cell-related markers by quantitative RT-PCR and the expression of the cellular senescence-associated proteins. Then we sorted DTPs according to the expression pattern of CD133 and analyzed the features of sorted cells. Finally, we tried to ablate DTPs by glucose metabolism targeting therapies and a stem-like cell targeting drug, withaferin A. Drug-tolerant persisters were composed of at least two types of cells, one with the properties of cancer stem-like cells (CSCs) and the other with the properties of therapy-induced senescent (TIS) cells. The CD133

Indexed as

AdenocarcinomaAdenocarcinoma of LungAnimalsBlotting, WesternCarcinoma, Non-Small-Cell LungCell Line, TumorCellular SenescenceDrug Resistance, NeoplasmErbB ReceptorsFlow CytometryGefitinibGlucoseHumansLung NeoplasmsMiceMice, Inbred BALB CEGFR protein, humanErbB ReceptorsGefitinibGlucosePhloretinProtein Kinase InhibitorsQuinazolineswithaferin AWithanolidesCell interactiondrug resistanceEGFR-TKIsenescent cellsstem-like cells

Identifiers

PMID28445002
PMCPMC5497794
OpenAlexW2609872963

What Socratic holds

Textmetadata
LicenceCC BY-NC
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 Socratic graph.