Evidence map›Paper›PMID 36499737›Full record

ReviewInternational journal of molecular sciences2022

Revisiting the Anti-Cancer Toxicity of Clinically Approved Platinating Derivatives.

Benjamin N Forgie, Rewati Prakash, Carlos M Telleria

Open access · goldAbstract readReview
In one paragraph

Review in International journal of molecular sciences, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.

0numbers the graph read from it
0cells of the map it votes in
43citing papers in PubMed
5.4field-weighted citation impact, top 3% 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

43 citing papers in PubMed, 66 citations in OpenAlex.

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  9. Protective effects ofVeterinary world · 2026
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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

3 authors at 2 institutions in 1 country.

Benjamin N ForgieExperimental Pathology Unit, Department of Pathology, McGill University, Montreal, QC H3A 2B4, Canada.
Rewati PrakashExperimental Pathology Unit, Department of Pathology, McGill University, Montreal, QC H3A 2B4, Canada.
Carlos M TelleriaExperimental Pathology Unit, Department of Pathology, McGill University, Montreal, QC H3A 2B4, Canada.ORCID 0000-0003-1070-3538
McGill University · CAMcGill University Health Centre · CA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cisplatin (CDDP), carboplatin (CP), and oxaliplatin (OXP) are three platinating agents clinically approved worldwide for use against a variety of cancers. They are canonically known as DNA damage inducers; however, that is only one of their mechanisms of cytotoxicity. CDDP mediates its effects through DNA damage-induced transcription inhibition and apoptotic signalling. In addition, CDDP targets the endoplasmic reticulum (ER) to induce ER stress, the mitochondria via mitochondrial DNA damage leading to ROS production, and the plasma membrane and cytoskeletal components. CP acts in a similar fashion to CDDP by inducing DNA damage, mitochondrial damage, and ER stress. Additionally, CP is also able to upregulate micro-RNA activity, enhancing intrinsic apoptosis. OXP, on the other hand, at first induces damage to all the same targets as CDDP and CP, yet it is also capable of inducing immunogenic cell death via ER stress and can decrease ribosome biogenesis through its nucleolar effects. In this comprehensive review, we provide detailed mechanisms of action for the three platinating agents, going beyond their nuclear effects to include their cytoplasmic impact within cancer cells. In addition, we cover their current clinical use and limitations, including side effects and mechanisms of resistance.

Indexed as

Antineoplastic AgentsNeoplasmsApoptosisCarboplatinCell Line, TumorCisplatinHumansOxaliplatinAntineoplastic AgentsCarboplatinCisplatinOxaliplatincarboplatincellular uptakechemoresistancecisplatinclinical usagesDNA damageER stress responseimmunogenic cell deathinflux and efflux pumpsinterstrand and intrastrand DNA crosslinksmechanisms of actionnon-nuclear targetsoxaliplatinribosome biogenesistranscription regulation

Identifiers

PMID36499737
PMCPMC9793759
OpenAlexW4311677544

What OpenQuestion 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 OpenQuestion graph.