Evidence map›Paper›PMID 24853187›Full record

ArticleBritish journal of cancer2014

Prevention of multidrug resistance (MDR) in osteosarcoma by NSC23925.

X Yang, P Yang, J Shen, E Osaka, E Choy, G Cote, D Harmon, Z Zhang, H Mankin, F J Hornicek and 1 more

Open access · hybridAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in British journal of cancer, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed, 1 pooled it
2.2field-weighted citation impact, top 11% 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

26 citing papers in PubMed, 1 synthesis or guideline pooled it, 49 citations in OpenAlex.

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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

11 authors at 4 institutions in 2 countries.

X Yang1] Sarcoma Biology Laboratory, Center for Sarcoma and Connective Tissue Oncology, Massachusetts General Hospital and Harvard Medical School, 100 Blossom Street, Jackson 1115, Boston, MA 02114, USA [2] Department of Gynaecology and Obstetrics, The Third Affiliated Hospital of Zhengzhou University, Zhengzhou 450052, Henan Province, China.
P YangSarcoma Biology Laboratory, Center for Sarcoma and Connective Tissue Oncology, Massachusetts General Hospital and Harvard Medical School, 100 Blossom Street, Jackson 1115, Boston, MA 02114, USA.
J ShenSarcoma Biology Laboratory, Center for Sarcoma and Connective Tissue Oncology, Massachusetts General Hospital and Harvard Medical School, 100 Blossom Street, Jackson 1115, Boston, MA 02114, USA.
E OsakaSarcoma Biology Laboratory, Center for Sarcoma and Connective Tissue Oncology, Massachusetts General Hospital and Harvard Medical School, 100 Blossom Street, Jackson 1115, Boston, MA 02114, USA.
E ChoySarcoma Biology Laboratory, Center for Sarcoma and Connective Tissue Oncology, Massachusetts General Hospital and Harvard Medical School, 100 Blossom Street, Jackson 1115, Boston, MA 02114, USA.
G CoteSarcoma Biology Laboratory, Center for Sarcoma and Connective Tissue Oncology, Massachusetts General Hospital and Harvard Medical School, 100 Blossom Street, Jackson 1115, Boston, MA 02114, USA.
D HarmonSarcoma Biology Laboratory, Center for Sarcoma and Connective Tissue Oncology, Massachusetts General Hospital and Harvard Medical School, 100 Blossom Street, Jackson 1115, Boston, MA 02114, USA.
Z ZhangDepartment of Gynaecology and Obstetrics, The Third Affiliated Hospital of Zhengzhou University, Zhengzhou 450052, Henan Province, China.
H MankinSarcoma Biology Laboratory, Center for Sarcoma and Connective Tissue Oncology, Massachusetts General Hospital and Harvard Medical School, 100 Blossom Street, Jackson 1115, Boston, MA 02114, USA.
F J HornicekSarcoma Biology Laboratory, Center for Sarcoma and Connective Tissue Oncology, Massachusetts General Hospital and Harvard Medical School, 100 Blossom Street, Jackson 1115, Boston, MA 02114, USA.
Z DuanSarcoma Biology Laboratory, Center for Sarcoma and Connective Tissue Oncology, Massachusetts General Hospital and Harvard Medical School, 100 Blossom Street, Jackson 1115, Boston, MA 02114, USA.
Harvard University · USSarcoma Oncology Center · USMassachusetts General Hospital · USZhengzhou University · CN

Funding

COMBINATORIAL-DESIGNED NANO-PLATFORMS TO OVERCOME TUMOR DRUG RESISTANCEU01CA151452 · NCI · NORTHEASTERN UNIVERSITY · PI AMIJI, MANSOOR M., DUAN, ZHENFENG · 2010 to 2014
$2.1M
NCI NIH HHS U01 CA 151452NCI NIH HHS U01 CA151452
6 · The paper itself

Abstract

backgroundThe major limitation to the success of chemotherapy in osteosarcoma is the development of multidrug resistance (MDR). Preventing the emergence of MDR during chemotherapy treatment has been a high priority of clinical and investigational oncology, but it remains an elusive goal. The NSC23925 has recently been identified as a novel and potent MDR reversal agent. However, whether NSC23925 can prevent the development of MDR in cancer is unknown. Therefore, this study aims to evaluate the effects of NSC23925 on prevention of the development of MDR in osteosarcoma.

methodsHuman osteosarcoma cell lines U-2OS and Saos were exposed to increasing concentrations of paclitaxel alone or in combination with NSC23925 for 6 months. Cell sublines selected at different time points were evaluated for their drug sensitivity, drug transporter P-glycoprotein (Pgp) expression and activity.

resultsWe observed that tumour cells selected with increasing concentrations of paclitaxel alone developed MDR with resistance to paclitaxel and other Pgp substrates, whereas cells cultured with paclitaxel-NSC23925 did not develop MDR and cells remained sensitive to chemotherapeutic agents. Paclitaxel-resistant cells showed high expression and activity of the Pgp, whereas paclitaxel-NSC23925-treated cells did not express Pgp. No changes in IC50 and Pgp expression and activity were observed in cells grown with the NSC23925 alone.

conclusionsOur findings suggest that NSC23925 may prevent the development of MDR by specifically preventing the overexpression of Pgp. Given the significant incidence of MDR in osteosarcoma and the lack of effective agents for prevention of MDR, NSC23925 and derivatives hold the potential to improve the outcome of cancer patients with poor prognosis due to drug resistance.

Indexed as

Antineoplastic Agents, PhytogenicAntineoplastic Combined Chemotherapy ProtocolsATP Binding Cassette Transporter, Subfamily B, Member 1Bone NeoplasmsCell Line, TumorDrug Resistance, MultipleDrug Resistance, NeoplasmDrug SynergismHumansOsteosarcomaPaclitaxelPiperidinesQuinolines(2-(4-methoxyphenyl)-4-quinolinyl)(2-piperidinyl)methanolAntineoplastic Agents, PhytogenicATP Binding Cassette Transporter, Subfamily B, Member 1PaclitaxelPiperidinesQuinolines

Identifiers

PMID24853187
PMCPMC4056062
OpenAlexW2131909571

What OpenQuestion holds

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LicenceCC BY-NC-SA
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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.