Evidence map›Paper›PMID 29198441›Full record

ReviewTrends in cancer2017

Mitochondria, Bioenergetics and Apoptosis in Cancer.

Peter J Burke

Abstract readReview
In one paragraph

Review in Trends in cancer, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 213 papers.

0numbers the graph read from it
0cells of the map it votes in
213citing 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

213 citing papers in PubMed.

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153 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

1 author.

Peter J BurkeDepartment of Electrical Engineering and Computer Science, University of California, Irvine, Irvine, CA, USA; Department of Chemical Engineering and Materials Science, University of California, Irvine, Irvine, CA, USA; Department of Biomedical Engineering, University of California, Irvine, Irvine, CA, USA. Electronic address: pburke@uci.edu.

Funding

High-throughput on-chip platform for interrogation of mitochondrial membrane potential and apoptosisR33CA182384 · NCI · UNIVERSITY OF CALIFORNIA-IRVINE · PI BURKE, PETER J. · 2015 to 2017
$1.2M
Nanoelectrode arrays for study of the molecular mechanisms, triggers, and inhibitR21CA143351 · NCI · UNIVERSITY OF CALIFORNIA-IRVINE · PI BURKE, PETER J. · 2010 to 2012
$631k
NCI NIH HHS R21 CA143351NCI NIH HHS R33 CA182384
6 · The paper itself

Abstract

Until recently, the dual roles of mitochondria in ATP production (bioenergetics) and apoptosis (cell life/death decision) were thought to be separate. New evidence points to a more intimate link between these two functions, mediated by the remodeling of the mitochondrial ultrastructure during apoptosis. While most of the key molecular players that regulate this process have been identified (primarily membrane proteins), the exact mechanisms by which they function are not yet understood. Because resistance to apoptosis is a hallmark of cancer, and because ultimately all chemotherapies are believed to result directly or indirectly in induction of apoptosis, a better understanding of the biophysical processes involved may lead to new avenues for therapy.

Indexed as

Adenosine TriphosphateApoptosisEnergy MetabolismHumansMitochondriaMitochondrial MembranesNeoplasmsAdenosine Triphosphateapoptosiscristaecytochrome Cmitochondria

Identifiers

PMID29198441
PMCPMC5957506

What OpenQuestion holds

Textmetadata
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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.