Evidence map›Paper›PMID 27240991›Full record

ReviewJournal of biosciences2016

ABCG2 inhibition as a therapeutic approach for overcoming multidrug resistance in cancer.

Maryam Hosseini Hasanabady, Fatemeh Kalalinia

Abstract readReview
PubMed Publisher
In one paragraph

Review in Journal of biosciences, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
3.6field-weighted citation impact, top 6% 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

29 citing papers in PubMed, 53 citations in OpenAlex.

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  9. [Effects of Extracellular Vesicles on the Drug Resistance of Lung Adenocarcinoma Cells by Modulating the ATP Binding Cassette Transporter G2].Sichuan da xue xue bao. Yi xue ban = Journal of Sichuan University. Medical science edition · 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

2 authors at 2 institutions in 1 country.

Maryam Hosseini HasanabadyDepartment of Biology, Science and Research Branch, Islamic Azad University, Mashhad, Iran.
Fatemeh Kalalinia
Biotechnology Research Center · IRIslamic Azad University, Mashhad · IR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Breast cancer resistance protein (BCRP, ABCP or MXR)/ATP-binding cassette subfamily G member 2 (ABCG2) was characterized as a multidrug resistance efflux transporter in 1998. ABCG2 physiologically acts as a part of a selfdefence mechanism for the organism; it enhances eliminating of toxic xenobiotic substances and harmful agents in the intestine, as well as through the blood-brain barrier and placenta. ABCG2 recognizes and transports numerous anticancer drugs including conventional chemotherapeutic and new targeted small therapeutic molecules in clinical usage. Development of ABCG2 inhibitors for clinical usage may allow increased penetration of therapeutic agents into sanctuary sites and increases their intestinal absorption. Here we review the mechanisms that modulate MDR mediated by the ABC transporter ABCG2 in normal and cancer cells by different levels including, epigenetic modifications, transcriptional, post-transcriptional, translation and post-translational regulation. Some clinical applications of ABCG2 inhibitors are also explained.

Indexed as

Antineoplastic AgentsATP Binding Cassette Transporter, Subfamily G, Member 2Biological TransportBlood-Brain BarrierDrug Resistance, MultipleDrug Resistance, NeoplasmEpigenesis, GeneticHumansNeoplasm ProteinsNeoplasmsProtein BiosynthesisABCG2 protein, humanAntineoplastic AgentsATP Binding Cassette Transporter, Subfamily G, Member 2Neoplasm Proteins

Identifiers

PMID27240991
OpenAlexW2316699115

What OpenQuestion holds

Textmetadata
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.