Evidence map›Paper›PMID 26110620›Full record

ArticlePloS one2015

BMI1 is expressed in canine osteosarcoma and contributes to cell growth and chemotherapy resistance.

Mehdi Hayat Shahi, Daniel York, Regina Gandour-Edwards, Sita S Withers, Roseline Holt, Robert B Rebhun

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
1.7field-weighted citation impact, top 16% 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

13 citing papers in PubMed, 19 citations in OpenAlex.

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  13. Potential role of Shh-Gli1-BMI1 signaling pathway nexus in glioma chemoresistance.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2016
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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

6 authors at 1 institution in 1 country.

Mehdi Hayat ShahiThe Comparative Oncology Laboratory and Center for Companion Animal Health, School of Veterinary Medicine, University of California Davis, Davis, CA, 95616, United States of America.
Daniel YorkThe Comparative Oncology Laboratory and Center for Companion Animal Health, School of Veterinary Medicine, University of California Davis, Davis, CA, 95616, United States of America.
Regina Gandour-EdwardsThe Department of Pathology, Comprehensive Cancer Center, University of California Davis, Davis, California, United States of America.
Sita S WithersThe Comparative Oncology Laboratory and Center for Companion Animal Health, School of Veterinary Medicine, University of California Davis, Davis, CA, 95616, United States of America.
Roseline HoltThe Comparative Oncology Laboratory and Center for Companion Animal Health, School of Veterinary Medicine, University of California Davis, Davis, CA, 95616, United States of America.
Robert B RebhunThe Comparative Oncology Laboratory and Center for Companion Animal Health, School of Veterinary Medicine, University of California Davis, Davis, CA, 95616, United States of America.
University of California, Davis · US

Funding

Staff InvestigatorsP30CA093373 · NCI · UNIVERSITY OF CALIFORNIA DAVIS · PI Laura Marcu · 2002 to 2026
$84.9M
The relationship between epidermal growth factor receptor and hedgehog signalingK01OD011111 · OD · UNIVERSITY OF CALIFORNIA AT DAVIS · PI REBHUN, ROBERT B · 2012 to 2015
$517k
The relationship between epidermal growth factor receptor and hedgehog signalingK01RR031272 · NCRR · UNIVERSITY OF CALIFORNIA AT DAVIS · PI REBHUN, ROBERT B · 2011 to 2011
$131k
NCI NIH HHS P30 CA093373NCRR NIH HHS K01 RR031272NIH HHS 8K01OD011111-02NIH HHS K01 OD011111
6 · The paper itself

Abstract

BMI1, a stem cell factor and member of the polycomb group of genes, has been shown to contribute to growth and chemoresistance of several human malignancies including primary osteosarcoma (OSA). Naturally occurring OSA in the dog represents a large animal model of human OSA, however the potential role of BMI1 in canine primary and metastatic OSA has not been examined. Immunohistochemical staining of canine primary and metastatic OSA tumors revealed strong nuclear expression of BMI1. An identical staining pattern was found in both primary and metastatic human OSA tissues. Canine OSA cell lines (Abrams, Moresco, and D17) expressed high levels of BMI1 compared with canine osteoblasts and knockdown or inhibition of BMI1 by siRNA or by small molecule BMI1-inhibitor PTC-209 demonstrated a role for BMI1 in canine OSA cell growth and resistance to carboplatin and doxorubicin chemotherapy. These findings suggest that inhibition of BMI1 in primary or metastatic OSA may improve response to chemotherapy and that the dog may serve as a large animal model to evaluate such therapy.

Indexed as

AdolescentAnimalsAntineoplastic AgentsBone NeoplasmsCarboplatinCell Line, TumorCell ProliferationDisease Models, AnimalDogsDoxorubicinDrug Resistance, NeoplasmFemaleGene Expression Regulation, NeoplasticHeterocyclic Compounds, 2-RingHumansMaleAntineoplastic AgentsCarboplatinDoxorubicinHeterocyclic Compounds, 2-RingPolycomb Repressive Complex 1PTC-209Thiazoles

Identifiers

PMID26110620
PMCPMC4482432
OpenAlexW1419112127

What OpenQuestion holds

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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.