Evidence map›Paper›PMID 30257595›Full record

ReviewCell cycle (Georgetown, Tex.)2018

A mitochondrial based oncology platform for targeting cancer stem cells (CSCs): MITO-ONC-RX.

Federica Sotgia, Bela Ozsvari, Marco Fiorillo, Ernestina Marianna De Francesco, Gloria Bonuccelli, Michael P Lisanti

Abstract readReview
In one paragraph

Review in Cell cycle (Georgetown, Tex.), 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.

0numbers the graph read from it
0cells of the map it votes in
37citing 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

37 citing papers in PubMed.

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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.

Federica Sotgiaa Translational Medicine, School of Environment and Life Sciences, Biomedical Research Centre (BRC) , University of Salford , Greater Manchester , UK.
Bela Ozsvaria Translational Medicine, School of Environment and Life Sciences, Biomedical Research Centre (BRC) , University of Salford , Greater Manchester , UK.
Marco Fiorilloa Translational Medicine, School of Environment and Life Sciences, Biomedical Research Centre (BRC) , University of Salford , Greater Manchester , UK.ORCID 0000-0002-8055-3259
Ernestina Marianna De Francescoa Translational Medicine, School of Environment and Life Sciences, Biomedical Research Centre (BRC) , University of Salford , Greater Manchester , UK.ORCID 0000-0002-2810-6128
Gloria Bonuccellia Translational Medicine, School of Environment and Life Sciences, Biomedical Research Centre (BRC) , University of Salford , Greater Manchester , UK.
Michael P Lisantia Translational Medicine, School of Environment and Life Sciences, Biomedical Research Centre (BRC) , University of Salford , Greater Manchester , UK.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Here, we wish to propose a new systematic approach to cancer therapy, based on the targeting of mitochondrial metabolism, especially in cancer stem cells (CSCs). In the future, we envision that anti-mitochondrial therapy would ultimately be practiced as an add-on to more conventional therapy, largely for the prevention of tumor recurrence and cancer metastasis. This mitochondrial based oncology platform would require a panel of FDA-approved therapeutics (e.g. Doxycycline) that can safely be used to inhibit mitochondrial OXPHOS and/or biogenesis in CSCs. In addition, new therapeutics that target mitochondria could also be developed, to optimize their ability to eradicate CSCs. Finally, in this context, mitochondrial-based biomarkers (i.e. "Mito-signatures") could be utilized as companion diagnostics, to identify high-risk cancer patients at diagnosis, facilitating the early detection of tumor recurrence and the prevention of treatment failure. In summary, we suggest that new clinical trials are warranted to test and possibly implement this emerging treatment strategy, in a variety of human cancer types. This general approach, using FDA-approved antibiotics to target mitochondria, was effective in killing CSCs originating from many different cancer types, including DCIS, breast (ER(+) and ER(-)), prostate, ovarian, lung and pancreatic cancers, as well as melanoma and glioblastoma, among others. Thus, we propose the term MITO-ONC-RX, to describe this anti-mitochondrial platform for targeting CSCs. The use of re-purposed FDA-approved drugs will undoubtedly help to accelerate the clinical evaluation of this approach, as these drugs can move directly into Phase II clinical trials, saving considerable amounts of time (10-15 y) and billions in financial resources.

Indexed as

AnimalsBreast NeoplasmsCell ProliferationHumansMitochondriaMitomycinNeoplasm Recurrence, LocalNeoplastic Stem CellsMitomycindrug discoverymito-biomarkersMitochondriaMitoflavoscinsMitoketoscinsMitoriboscinsMito-signaturesMito-therapeuticsoncology platform

Identifiers

PMID30257595
PMCPMC6226227

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.