Evidence map›Paper›PMID 27108383›Full record

ArticleNeoplasia (New York, N.Y.)2016

A Potent Derivative of Indolizino[6,7-b]Indole for Treatment of Human Non-Small Cell Lung Cancer Cells.

Chi-Wei Chen, Ming-Hsi Wu, Yi-Fan Chen, Tsai-Yi Yen, Yi-Wen Lin, Shu-Hsin Chao, Satishkumar Tala, Tung-Hu Tsai, Tsann-Long Su, Te-Chang Lee

Erratum issuedOpen access · goldAbstract read
In one paragraph

Article in Neoplasia (New York, N.Y.), 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
1.6field-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

6 citing papers in PubMed, 20 citations in OpenAlex.

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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

10 authors at 3 institutions in 1 country.

Chi-Wei ChenInstitute of Biopharmaceutical Sciences, National Yang-Ming University, Taipei 11221, Taiwan; Institute of Biomedical Sciences, Academia Sinica, Taipei 11529, Taiwan.
Ming-Hsi WuInstitute of Biomedical Sciences, Academia Sinica, Taipei 11529, Taiwan.
Yi-Fan ChenInstitute of Biopharmaceutical Sciences, National Yang-Ming University, Taipei 11221, Taiwan; Institute of Biomedical Sciences, Academia Sinica, Taipei 11529, Taiwan.
Tsai-Yi YenInstitute of Traditional Medicine, National Yang-Ming University, Taipei 11221, Taiwan.
Yi-Wen LinInstitute of Biomedical Sciences, Academia Sinica, Taipei 11529, Taiwan.
Shu-Hsin ChaoInstitute of Biomedical Sciences, Academia Sinica, Taipei 11529, Taiwan.
Satishkumar TalaInstitute of Biomedical Sciences, Academia Sinica, Taipei 11529, Taiwan.
Tung-Hu TsaiInstitute of Traditional Medicine, National Yang-Ming University, Taipei 11221, Taiwan.
Tsann-Long SuInstitute of Biomedical Sciences, Academia Sinica, Taipei 11529, Taiwan.
Te-Chang LeeInstitute of Biopharmaceutical Sciences, National Yang-Ming University, Taipei 11221, Taiwan; Institute of Biomedical Sciences, Academia Sinica, Taipei 11529, Taiwan; Institute of Pharmacology, National Yang-Ming University, Taipei 11221, Taiwan. Electronic address: bmtcl@ibms.sinica.edu.tw.
Institute of Biomedical Sciences, Academia Sinica · TWNational Yang Ming Chiao Tung University · TWNational Yang Ming Chiao Tung University · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The therapeutic effect in non-small cell lung cancer (NSCLC) patients is limited because of intrinsic and acquired resistance. Thus, an unmet need exists for the development of new drugs to improve the therapeutic efficacy in NSCLC patients. In this study, the novel small molecule indolizino[6,7-b]indole derivative BO-1978 was selected to evaluate its therapeutic effects on NSCLC and its preclinical toxicity in animal models. An in vitro cytotoxicity assay revealed that BO-1978 significantly suppressed the growth of various NSCLC cell lines with or without mutations in epidermal growth factor receptor (EGFR). Mechanistically, we demonstrated that BO-1978 exhibited multiple modes of action, including inhibition of topoisomerase I/II and induction of DNA cross-linking. Treatment of NSCLC cells with BO-1978 caused DNA damage, disturbed cell cycle progression, and triggered apoptotic cell death. Furthermore, BO-1978 significantly suppressed the growth of EGFR wild-type and mutant NSCLC tumors in xenograft tumor and orthotopic lung tumor models with negligible body weight loss. The combination of BO-1978 with gefitinib further suppressed EGFR mutant NSCLC cell growth in xenograft tumor and orthotopic lung tumor models. Preclinical toxicity studies showed that BO-1978 administration did not cause apparent toxicity in mice. Based on its significant therapeutic efficacy and low drug toxicity, BO-1978 is a potential therapeutic agent for treatment of NSCLC.

Identifiers

PMID27108383
PMCPMC4840272
OpenAlexW2306694709

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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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.