Evidence map›Paper›PMID 32152266›Full record

ArticleCell death & disease2020

MCL1 inhibition is effective against a subset of small-cell lung cancer with high MCL1 and low BCL-X

Yuto Yasuda, Hiroaki Ozasa, Young Hak Kim, Masatoshi Yamazoe, Hitomi Ajimizu, Tomoko Yamamoto Funazo, Takashi Nomizo, Takahiro Tsuji, Hironori Yoshida, Yuichi Sakamori and 5 more

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
2.5field-weighted citation impact, top 9% 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

24 citing papers in PubMed, 51 citations in OpenAlex.

  1. Review
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  4. Observational
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  14. BCL-2 protein family: attractive targets for cancer therapy.Apoptosis : an international journal on programmed cell death · 2023
    Review
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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

15 authors at 3 institutions in 1 country.

Yuto YasudaDepartment of Respiratory Medicine, Kyoto University Graduate School of Medicine, Kyoto, Japan.ORCID http://orcid.org/0000-0002-5703-4119
Hiroaki OzasaDepartment of Respiratory Medicine, Kyoto University Graduate School of Medicine, Kyoto, Japan. ozahiro@kuhp.kyoto-u.ac.jp.
Young Hak KimDepartment of Respiratory Medicine, Kyoto University Graduate School of Medicine, Kyoto, Japan.
Masatoshi YamazoeDepartment of Respiratory Medicine, Kyoto University Graduate School of Medicine, Kyoto, Japan.
Hitomi AjimizuDepartment of Respiratory Medicine, Kyoto University Graduate School of Medicine, Kyoto, Japan.
Tomoko Yamamoto FunazoDepartment of Respiratory Medicine, Kyoto University Graduate School of Medicine, Kyoto, Japan.
Takashi NomizoDepartment of Respiratory Medicine, Takatsuki Red Cross Hospital, Takatsuki, Japan.
Takahiro TsujiDepartment of Respiratory Medicine, Kyoto University Graduate School of Medicine, Kyoto, Japan.ORCID http://orcid.org/0000-0002-5706-8300
Hironori YoshidaDepartment of Respiratory Medicine, Kyoto University Graduate School of Medicine, Kyoto, Japan.
Yuichi SakamoriDepartment of Respiratory Medicine, Kyoto University Graduate School of Medicine, Kyoto, Japan.
Naoki NakajimaDepartment of Diagnostic Pathology, Kyoto University Hospital, Kyoto, Japan.
Toshi MenjuDepartment of Thoracic Surgery, Kyoto University Graduate School of Medicine, Kyoto, Japan.
Akihiko YoshizawaDepartment of Diagnostic Pathology, Kyoto University Hospital, Kyoto, Japan.
Hiroshi DateDepartment of Thoracic Surgery, Kyoto University Graduate School of Medicine, Kyoto, Japan.
Toyohiro HiraiDepartment of Respiratory Medicine, Kyoto University Graduate School of Medicine, Kyoto, Japan.
Kyoto University · JPKyoto University Hospital · JPTakatsuki Red Cross Hospital · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

There have been few advances in the treatment of small-cell lung cancer (SCLC) because of the lack of targets. MCL1, a member of the anti-apoptotic BCL-2 family, may be a treatment target in several cancers, including SCLC. However, whether the expression profile of the anti-apoptotic BCL-2 family affects MCL1 inhibition strategy is unknown. A tissue microarray (TMA) was created from consecutive patients who were diagnosed with SCLC and had previously undergone surgery at Kyoto University Hospital (Kyoto, Japan) between 2001 and 2017. We used S63845, a MCL1 inhibitor, to assess the cytotoxic capacity in SCLC cell lines including a patient-derived cell line in vitro and in vivo. The combination of S63845 with navitoclax, a double BCL-X

Indexed as

AgedAntineoplastic AgentsApoptosisbcl-X ProteinCell Line, TumorFemaleHumansLung NeoplasmsMaleMiddle AgedMyeloid Cell Leukemia Sequence 1 ProteinProto-Oncogene Proteins c-bcl-2PyrimidinesSmall Cell Lung CarcinomaThiophenesAntineoplastic AgentsBCL2 protein, humanbcl-X ProteinMCL1 protein, humanMyeloid Cell Leukemia Sequence 1 ProteinProto-Oncogene Proteins c-bcl-2PyrimidinesS63845Thiophenes

Identifiers

PMID32152266
PMCPMC7063049
OpenAlexW3009472834

What OpenQuestion holds

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LicenceCC BY
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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.