Evidence map›Paper›PMID 30514247›Full record

ArticleBMC cancer2018

MEF2 plays a significant role in the tumor inhibitory mechanism of encapsulated RENCA cells via EGF receptor signaling in target tumor cells.

Prithy C Martis, Atira T Dudley, Melissa A Bemrose, Hunter L Gazda, Barry H Smith, Lawrence S Gazda

Registry-linked trialOpen access · goldAbstract read
In one paragraph

Article in BMC cancer, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT01053013 (An Open-Label Phase 2 Efficacy Trial of the Implantation of Mouse Renal Adenocarcinoma Cell-Containing Agarose-Agarose Macrobeads in the Treatment of Patients With Treatment-Resistant, Metastatic Pancreatic or Colorectal Cancer), which is not on this map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
0.3field-weighted citation impact, top 39% 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.

NCT01053013 phase2completednot on this map

An Open-Label Phase 2 Efficacy Trial of the Implantation of Mouse Renal Adenocarcinoma Cell-Containing Agarose-Agarose Macrobeads in the Treatment of Patients With Treatment-Resistant, Metastatic Pancreatic or Colorectal Cancer

TypeinterventionalSponsorThe Rogosin InstituteRan2010 to 2016Enrolled58ConditionsPancreatic Adenocarcinoma Non-resectable, Pancreatic Adenocarcinoma Metastatic, Colorectal Cancer MetastaticArmsRENCA macrobeads
3 · Its place in the literature

Who cites it

4 citing papers in PubMed, 13 citations in OpenAlex.

  1. Oral streptococciInfection and immunity · 2024
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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 2 institutions in 1 country.

Prithy C MartisThe Rogosin Institute-Xenia Division, 740 Birch Road, Xenia, OH, 45385, USA. pmartis@rixd.org.ORCID http://orcid.org/0000-0002-4743-0521
Atira T DudleyThe Rogosin Institute-Xenia Division, 740 Birch Road, Xenia, OH, 45385, USA.
Melissa A BemroseThe Rogosin Institute-Xenia Division, 740 Birch Road, Xenia, OH, 45385, USA.
Hunter L GazdaThe Rogosin Institute-Xenia Division, 740 Birch Road, Xenia, OH, 45385, USA.
Barry H SmithThe Rogosin Institute, New York, NY, 10021, USA.
Lawrence S GazdaThe Rogosin Institute-Xenia Division, 740 Birch Road, Xenia, OH, 45385, USA.
The Rogosin Institute · USCornell University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundAgarose encapsulated murine renal adenocarcinoma cells (RENCA macrobeads) are currently being investigated in clinical trials as a treatment for therapy-resistant metastatic colorectal cancer. We have previously demonstrated the capacity of RENCA macrobeads to produce diffusible substances that markedly inhibit the proliferation of epithelial-derived tumor cells outside the macrobead environment. This study examined the molecular mechanisms underlying the observed inhibition in targeted tumor cells exposed to RENCA macrobeads.

methodsWe evaluated changes in transcription factor responses, participating intracellular signaling pathways and the involvement of specific cellular receptors in targeted tumor cells exposed to RENCA macrobeads.

resultsFactors secreted by RENCA macrobeads significantly up-regulated the activity of the MEF2 transcription factor as well as altered the transcription of MEF2b and MEF2d isoforms in targeted tumor cells. Suppression of individual or multiple MEF2 isoforms in target tumor cells markedly reduced the growth inhibitory effects of RENCA macrobeads. Furthermore, these effects were linked to the activation of the EGF receptor as attenuation of EGFR resulted in a substantial reduction of the cancer cell growth-inhibitory effect.

conclusionsSince interruption of the EGFR signaling cascade did not eliminate RENCA macrobead-induced growth control, our data suggests that RENCA macrobeads exert their full growth inhibitory effects through the simultaneous activation of multiple signaling pathways. In contrast to a precision medicine approach targeting single molecular abnormalities, the RENCA macrobead functions as a biological-systems therapy to re-establish regulation in a highly dysfunctional and dysregulated cancer system.

Indexed as

MicrospheresAnimalsAntineoplastic AgentsCarcinoma, Renal CellCell Line, TumorDose-Response Relationship, DrugErbB ReceptorsGefitinibHumansKidney NeoplasmsMEF2 Transcription FactorsMiceMice, Inbred BALB CSignal TransductionAntineoplastic AgentsEGFR protein, humanErbB ReceptorsGefitinibMEF2B protein, humanMEF2 Transcription FactorsCell therapyEGFRMEF2Tumor inhibition

Identifiers

PMID30514247
PMCPMC6280513
OpenAlexW2903437959

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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.