Evidence map›Paper›PMID 30626133›Full record

ReviewInternational journal of molecular sciences2019

Targeting Mitochondria for Treatment of Chemoresistant Ovarian Cancer.

Edith Emmings, Sally Mullany, Zenas Chang, Charles N Landen, Stig Linder, Martina Bazzaro

Open access · goldAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in International journal of molecular sciences, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 72 papers.

0numbers the graph read from it
0cells of the map it votes in
72citing papers in PubMed
6.0field-weighted citation impact, top 2% 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

72 citing papers in PubMed, 124 citations in OpenAlex.

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12 more citing papers are in PubMed but not listed here.

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 3 institutions in 2 countries.

Edith EmmingsMasonic Cancer Center and Department of Obstetrics, Gynecology and Women's Heath, University of Minnesota, Minneapolis, MN 55455, USA. edieb.543@gmail.com.
Sally MullanyMasonic Cancer Center and Department of Obstetrics, Gynecology and Women's Heath, University of Minnesota, Minneapolis, MN 55455, USA. smullany@umn.edu.
Zenas ChangMasonic Cancer Center and Department of Obstetrics, Gynecology and Women's Heath, University of Minnesota, Minneapolis, MN 55455, USA. zechang@umn.edu.
Charles N LandenDepartment of Obstetrics and Gynecology, University of Virginia, Charlottesville, VA 22908, USA. CL3NJ@hscmail.mcc.virginia.edu.
Stig LinderCancer Center Karolinska, Department of Oncology and Pathology, Karolinska Institute, S-171 76 Stockholm, Sweden. Stig.Linder@liu.se.ORCID 0000-0002-4952-445X
Martina BazzaroMasonic Cancer Center and Department of Obstetrics, Gynecology and Women's Heath, University of Minnesota, Minneapolis, MN 55455, USA. mbazzaro@umn.edu.
University of Minnesota · USLinköping University · SEUniversity of Virginia · US

Funding

Women's Oncology Program - WONP30CA044579 · NCI · UNIVERSITY OF VIRGINIA CHARLOTTESVILLE · PI Dina Gould Halme · 1987 to 2026
$72.1M
Defense Ovarian Cancer Research Program OC160377NCI NIH HHS P30 CA044579
6 · The paper itself

Abstract

Ovarian cancer is the leading cause of death from gynecologic malignancy in the Western world. This is due, in part, to the fact that despite standard treatment of surgery and platinum/paclitaxel most patients recur with ultimately chemoresistant disease. Ovarian cancer is a unique form of solid tumor that develops, metastasizes and recurs in the same space, the abdominal cavity, which becomes a unique microenvironment characterized by ascites, hypoxia and low glucose levels. It is under these conditions that cancer cells adapt and switch to mitochondrial respiration, which becomes crucial to their survival, and therefore an ideal metabolic target for chemoresistant ovarian cancer. Importantly, independent of microenvironmental factors, mitochondria spatial redistribution has been associated to both tumor metastasis and chemoresistance in ovarian cancer while specific sets of genetic mutations have been shown to cause aberrant dependence on mitochondrial pathways in the most aggressive ovarian cancer subtypes. In this review we summarize on targeting mitochondria for treatment of chemoresistant ovarian cancer and current state of understanding of the role of mitochondria respiration in ovarian cancer. We feel this is an important and timely topic given that ovarian cancer remains the deadliest of the gynecological diseases, and that the mitochondrial pathway has recently emerged as critical in sustaining solid tumor progression.

Indexed as

Drug Resistance, NeoplasmDrug Evaluation, PreclinicalFemaleHumansMitochondriaOvarian NeoplasmsSpheroids, CellularTumor Microenvironmentasciteschemoresistant ovarian cancermitochondrial inhibitorOXPHOSSWI/SNF complex

Identifiers

PMID30626133
PMCPMC6337358
OpenAlexW2910760721

What Socratic 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 Socratic graph.