Evidence map›Paper›PMID 26983831›Full record

ReviewCellular and molecular neurobiology2016

Exosomes as Tools to Suppress Primary Brain Tumor.

Mark Katakowski, Michael Chopp

Abstract readReview
In one paragraph

Review in Cellular and molecular neurobiology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.

0numbers the graph read from it
0cells of the map it votes in
45citing papers in PubMed
–field-weighted citation impact
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

45 citing papers in PubMed.

  1. Review
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  13. Exosomes as Novel Diagnostic Biomarkers and Therapeutic Tools in Gliomas.International journal of molecular sciences · 2023
    Review
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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.

Mark KatakowskiDepartment of Neurology, Henry Ford Hospital, Detroit, MI, USA.
Michael ChoppDepartment of Neurology, Henry Ford Hospital, Detroit, MI, USA. chopp@neuro.hfh.edu.

Funding

miR-17-92 exosome treatment of strokeR01NS088656 · NINDS · HENRY FORD HEALTH SYSTEM · PI CHOPP, MICHAEL · 2015 to 2019
$1.6M
NINDS NIH HHS R01 NS088656
6 · The paper itself

Abstract

Exosomes are small microvesicles released by cells that efficiently transfer their molecular cargo to other cells, including tumor. Exosomes may pass the blood-brain barrier and have been demonstrated to deliver RNAs contained within to brain. As they are non-viable, the risk profile of exosomes is thought to be less than that of cellular therapies. Exosomes can be manufactured at scale in culture, and exosomes can be engineered to incorporate therapeutic miRNAs, siRNAs, or chemotherapeutic molecules. As natural biological delivery vehicles, interest in the use of exosomes as therapeutic delivery agents is growing. We previously demonstrated a novel treatment whereby mesenchymal stromal cells were employed to package tumor-suppressing miR-146b into exosomes, which were then used to reduce malignant glioma growth in rat. The use of exosomes to raise the immune system against tumor is also drawing interest. Exosomes from dendritic cells which are antigen-presenting, and have been used for treatment of brain tumor may be divided into three categories: (1) exosomes for immunomodulation-based therapy, (2) exosomes as delivery vehicles for anti-tumor nucleotides, and (3) exosomes as drug delivery vehicles. Here, we will provide an overview of these three applications of exosomes to treat brain tumor, and examine their prospects on the long road to clinical use.

Indexed as

AnimalsAntineoplastic AgentsBrain NeoplasmsDrug CarriersDrug Delivery SystemsExosomesHumansImmunotherapyAntineoplastic AgentsDrug CarriersBrain tumorExosomesExosome therapyGlioblastomaGliomamiRNA

Identifiers

PMID26983831
PMCPMC11482504

What OpenQuestion holds

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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.