Evidence map›Paper›PMID 26961349›Full record

ArticleJournal of the American Society of Nephrology : JASN2016

Dichloroacetate Prevents Cisplatin-Induced Nephrotoxicity without Compromising Cisplatin Anticancer Properties.

Ramindhu Galgamuwa, Kristine Hardy, Jane E Dahlstrom, Anneke C Blackburn, Elize Wium, Melissa Rooke, Jean Y Cappello, Padmaja Tummala, Hardip R Patel, Aaron Chuah and 4 more

Open access · greenAbstract read
In one paragraph

Article in Journal of the American Society of Nephrology : JASN, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
4.2field-weighted citation impact, top 6% 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

28 citing papers in PubMed, 57 citations in OpenAlex.

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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

14 authors at 5 institutions in 3 countries.

Ramindhu GalgamuwaDepartments of Cancer Biology and Therapeutics and.
Kristine HardyFaculty of Education, Science, Technology and Mathematics, University of Canberra, Australian Capital Territory, Australia.
Jane E DahlstromACT Pathology and ANU Medical School, The Canberra Hospital, Australian Capital Territory, Australia.
Anneke C BlackburnDepartments of Cancer Biology and Therapeutics and.
Elize WiumDepartments of Cancer Biology and Therapeutics and.
Melissa RookeDepartments of Cancer Biology and Therapeutics and.
Jean Y CappelloDepartments of Cancer Biology and Therapeutics and.
Padmaja TummalaDepartments of Cancer Biology and Therapeutics and.
Hardip R PatelGenome Sciences, and.
Aaron ChuahGenome Discovery Unit, John Curtin School of Medical Research, Australian National University, Australian Capital Territory, Australia.
Luyang TianInstitute of Biophysics, Chinese Academy of Sciences, Beijing, China; and.
Linda McMorrowArchaeogeochemistry and Marine Biogeochemistry Groups, Research School of Earth Sciences, Australian National University, Australian Capital Territory, Australia.
Philip G BoardDepartments of Cancer Biology and Therapeutics and.
Angelo TheodoratosDepartments of Cancer Biology and Therapeutics and angelo.theodoratos@anu.edu.au.
Australian National University · AUACT GovernmentCanberra Hospital · AUChinese Academy of Sciences · CNHuman Genome Sciences (United States) · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cisplatin is an effective anticancer drug; however, cisplatin use often leads to nephrotoxicity, which limits its clinical effectiveness. In this study, we determined the effect of dichloroacetate, a novel anticancer agent, in a mouse model of cisplatin-induced AKI. Pretreatment with dichloroacetate significantly attenuated the cisplatin-induced increase in BUN and serum creatinine levels, renal tubular apoptosis, and oxidative stress. Additionally, pretreatment with dichloroacetate accelerated tubular regeneration after cisplatin-induced renal damage. Whole transcriptome sequencing revealed that dichloroacetate prevented mitochondrial dysfunction and preserved the energy-generating capacity of the kidneys by preventing the cisplatin-induced downregulation of fatty acid and glucose oxidation, and of genes involved in the Krebs cycle and oxidative phosphorylation. Notably, dichloroacetate did not interfere with the anticancer activity of cisplatin in vivo. These data provide strong evidence that dichloroacetate preserves renal function when used in conjunction with cisplatin.

Indexed as

AnimalsAntineoplastic AgentsCisplatinDichloroacetic AcidFemaleKidney DiseasesMaleMiceMice, Inbred BALB CAntineoplastic AgentsCisplatinDichloroacetic Acidacute renal failurecisplatin nephrotoxicityrenal protection

Identifiers

PMID26961349
PMCPMC5084882
OpenAlexW2299986792

What OpenQuestion holds

Textmetadata
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.