Evidence map›Paper›PMID 26928578›Full record

ArticleBMC research notes2016

BMS-754807 is cytotoxic to non-small cell lung cancer cells and enhances the effects of platinum chemotherapeutics in the human lung cancer cell line A549.

S Elizabeth Franks, Robert A Jones, Ritesh Briah, Payton Murray, Roger A Moorehead

Open access · goldAbstract read
In one paragraph

Article in BMC research notes, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
1.3field-weighted citation impact, top 19% 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

22 citing papers in PubMed, 30 citations in OpenAlex.

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  20. In vivo evaluation of IGF1R/IR PET ligand [Bioorganic & medicinal chemistry letters · 2017
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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

5 authors at 1 institution in 1 country.

S Elizabeth FranksDepartment of Biomedical Science, Ontario Veterinary College, University of Guelph, 50 Stone Road East, Guelph, ON, N1G2W1, Canada. sfranks@uoguelph.ca.
Robert A JonesDepartment of Biomedical Science, Ontario Veterinary College, University of Guelph, 50 Stone Road East, Guelph, ON, N1G2W1, Canada. rjones12@uoguelph.ca.
Ritesh BriahDepartment of Biomedical Science, Ontario Veterinary College, University of Guelph, 50 Stone Road East, Guelph, ON, N1G2W1, Canada. rbriah@uoguelph.ca.
Payton MurrayDepartment of Biomedical Science, Ontario Veterinary College, University of Guelph, 50 Stone Road East, Guelph, ON, N1G2W1, Canada. paytonmu@uoguelph.ca.
Roger A MooreheadDepartment of Biomedical Science, Ontario Veterinary College, University of Guelph, 50 Stone Road East, Guelph, ON, N1G2W1, Canada. rmoorehe@uoguelph.ca.
University of Guelph · CA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundDespite advances in targeted therapy for lung cancer, survival for patients remains poor and lung cancer remains the leading cause of cancer-related deaths worldwide. The type I insulin-like growth factor receptor (IGF-IR) has emerged as a potential target for lung cancer treatment, however, clinical trials to date have provided disappointing results. Further research is needed to identify if certain patients would benefit from IGF-IR targeted therapies and the ideal approach to incorporate IGF-IR targeted agents with current therapies.

methodsThe dual IGF-IR/insulin receptor inhibitor, BMS-754807, was evaluated alone and in combination with platinum-based chemotherapeutics in two human non-small cell lung cancer (NSCLC) cell lines. Cell survival was determined using WST-1 assays and drug interaction was evaluated using Calcusyn software. Proliferation and apoptosis were determined using immunofluorescence for phospho-histone H3 and cleaved caspase 3, respectively.

resultsTreatment with BMS-754807 alone reduced cell survival and wound closure while enhancing apoptosis in both human lung cancer cell lines. These effects appear to be mediated through IGF-IR/IR signaling and, at least in part, through the PI3K/AKT pathway as administration of BMS-754807 to A549 or NCI-H358 cells significantly suppressed IGF-IR/IR and AKT phosphorylation. In addition of BMS-754807 enhanced the cytotoxic effects of carboplatin or cisplatin in a synergistic manner when given simultaneously to A549 cells.

conclusionsBMS-754807 may be an effective therapeutic agent for the treatment of NSCLC, particularly in lung cancer cells expressing high levels of IGF-IR.

Indexed as

Gene Expression Regulation, NeoplasticAntineoplastic AgentsApoptosisCarboplatinCaspase 3Cell Line, TumorCell ProliferationCell SurvivalCisplatinDrug CombinationsDrug SynergismEpithelial CellsHistonesHumansInhibitory Concentration 50Insulin-Like Growth Factor IAntineoplastic AgentsBMS 754807CarboplatinCASP3 protein, humanCaspase 3CisplatinDrug CombinationsHistonesIGF1 protein, humanInsulin-Like Growth Factor IPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktPyrazolesReceptor, InsulinTriazines

Identifiers

PMID26928578
PMCPMC4772483
OpenAlexW2289682633

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.