Evidence map›Paper›PMID 24481648›Full record

ArticleOncology reports2014

Ponatinib enhances anticancer drug sensitivity in MRP7-overexpressing cells.

Yue-Li Sun, Priyank Kumar, Kamlesh Sodani, Atish Patel, Yihang Pan, Maria R Baer, Zhe-Sheng Chen, Wen-Qi Jiang

Open access · bronzeAbstract read
In one paragraph

Article in Oncology reports, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
1.5field-weighted citation impact, top 18% 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

12 citing papers in PubMed, 26 citations in OpenAlex.

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  8. BCR-ABL Tyrosine Kinase Inhibitors: Which Mechanism(s) May Explain the Risk of Thrombosis?TH open : companion journal to thrombosis and haemostasis · 2018
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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

8 authors at 5 institutions in 2 countries.

Yue-Li SunState Key Laboratory of Oncology in South China, Guangzhou, Guangdong, P.R. China.
Priyank KumarDepartment of Pharmaceutical Sciences, College of Pharmacy and Allied Health Professionals, St. John's University, Queens, New York, NY 11439, USA.
Kamlesh SodaniDepartment of Pharmaceutical Sciences, College of Pharmacy and Allied Health Professionals, St. John's University, Queens, New York, NY 11439, USA.
Atish PatelDepartment of Pharmaceutical Sciences, College of Pharmacy and Allied Health Professionals, St. John's University, Queens, New York, NY 11439, USA.
Yihang PanCytogenetics Laboratory, Department of Pathology and Laboratory Medicine, Weill Cornell Medical College, New York, NY, USA.
Maria R BaerUniversity of Maryland Greenebaum Cancer Center and Department of Medicine, University of Maryland School of Medicine, Baltimore, MD, USA.
Zhe-Sheng ChenDepartment of Pharmaceutical Sciences, College of Pharmacy and Allied Health Professionals, St. John's University, Queens, New York, NY 11439, USA.
Wen-Qi JiangDepartment of Medical Oncology, Sun Yat-sen University Cancer Center, Guangzhou, Guangdong 510060, P.R. China.
St. John's University · USCornell University · USState Key Laboratory of Oncology in South ChinaSun Yat-sen University Cancer Center · CNUniversity of Maryland, Baltimore · US

Funding

Targeting MRP7 to Overcome Drug Resistance for Ovarian Cancer Therapy by TaxanesR15CA143701 · NCI · ST. JOHN'S UNIVERSITY · PI CHEN, ZHE-SHENG · 2010 to 2010
$245k
NCI NIH HHS 1R15CA143701NCI NIH HHS R15 CA143701
6 · The paper itself

Abstract

The presence of acquired multidrug resistance (MDR) is one of the primary impediments to the success of chemotherapy. MDR is often a result of overexpression of ATP-binding cassette (ABC) transporters, which are involved in the extrusion of therapeutic drugs. Recently, it was shown that several ABC transporters could be modulated by specific tyrosine-kinase inhibitors (TKIs). Ponatinib, a multi-targeted TKI, inhibits the activity of BCR-ABL with very high potency and broad specificity, including the T315I mutation which confers resistance to other TKIs. It was reported that ponatinib was capable of reversing breast cancer resistance protein (BCRP)- and P-glycoprotein (P-gp)-mediated MDR. In the present study, we report for the first time that ponatinib also potentiates the cytotoxicity of widely used therapeutic substrates of MRP7, such as paclitaxel, docetaxel, vincristine and vinblastine. Ponatinib significantly enhances the accumulation of [3H]-paclitaxel in cells expressing MRP7. Furthermore, accumulation of [3H]-paclitaxel was achieved by inhibition of MRP7-mediated transport. Ponatinb limited drug export via MRP7 by multiple mechanisms. In addition to inhibition of pump function, ponatinib also downregulated MRP7 protein expression in a time- and concentration-dependent manner. Thus, ponatinib may represent a potential reversal agent for the treatment of MDR and may be useful for combination therapy in MDR cancer patients in clinical practice.

Indexed as

Antineoplastic AgentsATP-Binding Cassette, Sub-Family C ProteinsBlotting, WesternCell Line, TumorDrug Resistance, MultipleDrug Resistance, NeoplasmHumansImidazolesPyridazinesReverse Transcriptase Polymerase Chain ReactionABCC10 protein, humanAntineoplastic AgentsATP-Binding Cassette, Sub-Family C ProteinsImidazolesponatinibPyridazines

Identifiers

PMID24481648
PMCPMC3975990
OpenAlexW1983600229

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.