Evidence map›Paper›PMID 21892204›Full record

ReviewOncogene2012

Molecular mechanisms of cisplatin resistance.

L Galluzzi, L Senovilla, I Vitale, J Michels, I Martins, O Kepp, M Castedo, G Kroemer

Abstract readReview
PubMed Publisher
In one paragraph

Review in Oncogene, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1,355 papers.

0numbers the graph read from it
0cells of the map it votes in
1,355citing papers in PubMed
37.1field-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

1,355 citing papers in PubMed, 2,727 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Observation of glutathione intra- and extracellular membrane with large Stokes shift probe modified by long alkyl chains.Photochemical & photobiological sciences : Official journal of the European Photochemistry Association and the European Society for Photobiology · 2026
    Article
  5. Article
  6. Exploring the chemical and biological interplay in phenanthroline-containing copper complexes.Biometals : an international journal on the role of metal ions in biology, biochemistry, and medicine · 2026
    Article
  7. Article
  8. Article
  9. Article
  10. Review
  11. Therapy resistance-related ncRNAs in cervical cancer: biomarkers and therapeutic targets.Daru : journal of Faculty of Pharmacy, Tehran University of Medical Sciences · 2026
    Review
  12. Article
  13. Article
  14. Article
  15. Review
  16. Article
  17. Article
  18. Article
  19. Article
  20. Article

1,295 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

8 authors at 4 institutions in 1 country.

L GalluzziINSERM, U848 Apoptosis, Cancer and Immunity, Villejuif, France.
L Senovilla
I Vitale
J Michels
I Martins
O Kepp
M Castedo
G Kroemer
Institut Gustave Roussy · FRImmunité et Cancer · FRInserm · FRCentre de Recherche des Cordeliers · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Platinum-based drugs, and in particular cis-diamminedichloroplatinum(II) (best known as cisplatin), are employed for the treatment of a wide array of solid malignancies, including testicular, ovarian, head and neck, colorectal, bladder and lung cancers. Cisplatin exerts anticancer effects via multiple mechanisms, yet its most prominent (and best understood) mode of action involves the generation of DNA lesions followed by the activation of the DNA damage response and the induction of mitochondrial apoptosis. Despite a consistent rate of initial responses, cisplatin treatment often results in the development of chemoresistance, leading to therapeutic failure. An intense research has been conducted during the past 30 years and several mechanisms that account for the cisplatin-resistant phenotype of tumor cells have been described. Here, we provide a systematic discussion of these mechanism by classifying them in alterations (1) that involve steps preceding the binding of cisplatin to DNA (pre-target resistance), (2) that directly relate to DNA-cisplatin adducts (on-target resistance), (3) concerning the lethal signaling pathway(s) elicited by cisplatin-mediated DNA damage (post-target resistance) and (4) affecting molecular circuitries that do not present obvious links with cisplatin-elicited signals (off-target resistance). As in some clinical settings cisplatin constitutes the major therapeutic option, the development of chemosensitization strategies constitute a goal with important clinical implications.

Indexed as

CisplatinDNA AdductsDNA DamageDNA RepairDrug Resistance, NeoplasmHumansSignal TransductionCisplatincisplatin-DNA adductDNA Adducts

Identifiers

PMID21892204
OpenAlexW2141037581

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.