Evidence map›Paper›PMID 22659329›Full record

ReviewPharmacological reviews2012

Cisplatin resistance: a cellular self-defense mechanism resulting from multiple epigenetic and genetic changes.

Ding-Wu Shen, Lynn M Pouliot, Matthew D Hall, Michael M Gottesman

Open access · bronzeAbstract readReview
In one paragraph

Review in Pharmacological reviews, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 447 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
447citing papers in PubMed, 1 pooled it
31.2field-weighted citation impact, top 1% 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

447 citing papers in PubMed, 1 synthesis or guideline pooled it, 961 citations in OpenAlex.

  1. Pooled it
  2. Current clinical applications and future developments of platinum-based anticancer drugs.Journal of biological inorganic chemistry : JBIC : a publication of the Society of Biological Inorganic Chemistry · 2026
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387 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

4 authors at 3 institutions in 1 country.

Ding-Wu ShenLaboratory of Cell Biology, National Cancer Institute, National Institutes of Health, 37 Convent Dr., Rm. 2108, Bethesda, MD 20892, USA.
Lynn M Pouliot
Matthew D Hall
Michael M Gottesman
National Cancer Institute · USCenter for Cancer Research · USNational Institutes of Health · US

Funding

Mechanisms of non-classical multidrug resistance in cancerZIABC010830 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI GOTTESMAN, MICHAEL · 2009 to 2025
$19.6M
Intramural NIH HHS
6 · The paper itself

Abstract

Cisplatin is one of the most effective broad-spectrum anticancer drugs. Its effectiveness seems to be due to the unique properties of cisplatin, which enters cells via multiple pathways and forms multiple different DNA-platinum adducts while initiating a cellular self-defense system by activating or silencing a variety of different genes, resulting in dramatic epigenetic and/or genetic alternations. As a result, the development of cisplatin resistance in human cancer cells in vivo and in vitro by necessity stems from bewilderingly complex genetic and epigenetic changes in gene expression and alterations in protein localization. Extensive published evidence has demonstrated that pleiotropic alterations are frequently detected during development of resistance to this toxic metal compound. Changes occur in almost every mechanism supporting cell survival, including cell growth-promoting pathways, apoptosis, developmental pathways, DNA damage repair, and endocytosis. In general, dozens of genes are affected in cisplatin-resistant cells, including pathways involved in copper metabolism as well as transcription pathways that alter the cytoskeleton, change cell surface presentation of proteins, and regulate epithelial-to-mesenchymal transition. Decreased accumulation is one of the most common features resulting in cisplatin resistance. This seems to be a consequence of numerous epigenetic and genetic changes leading to the loss of cell-surface binding sites and/or transporters for cisplatin, and decreased fluid phase endocytosis.

Indexed as

Epigenesis, GeneticAnimalsAntineoplastic AgentsBinding SitesCisplatinDrug Resistance, NeoplasmEndocytosisGene Expression Regulation, NeoplasticHumansNeoplasmsAntineoplastic AgentsCisplatin

Identifiers

PMID22659329
PMCPMC3400836
OpenAlexW2159515687

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.