Evidence map›Paper›PMID 21568910›Full record

ReviewCurrent medicinal chemistry2011

Mechanisms of resistance to photodynamic therapy.

A Casas, G Di Venosa, T Hasan, Al Batlle

Abstract readReview
In one paragraph

Review in Current medicinal chemistry, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 111 papers.

0numbers the graph read from it
0cells of the map it votes in
111citing papers in PubMed
8.2field-weighted citation impact, top 2% 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

111 citing papers in PubMed, 314 citations in OpenAlex.

  1. Trial
  2. Review
  3. Photodynamic treatment of glioblastoma plus endothelial cell spheroid models: increased proliferative and migratory aggressiveness of surviving tumor cells due to iNOS/NO upregulation.Photochemical & photobiological sciences : Official journal of the European Photochemistry Association and the European Society for Photobiology · 2026
    Article
  4. Special Issue "Molecular Advances in Oncological Photodynamic Therapy".International journal of molecular sciences · 2026
    Article
  5. Article
  6. Review
  7. Article
  8. Article
  9. Review
  10. Review
  11. Article
  12. Review
  13. Review
  14. Review
  15. Article
  16. Article
  17. Review
  18. Article
  19. Determinants of Photodynamic Therapy Resistance in Cancer Cells.International journal of molecular sciences · 2024
    Review
  20. Article

51 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 1 institution in 1 country.

A CasasCentro de Invesigaciones sobre Porfirinas y Porfirias (CIPYP), CONICET and Hospital de Clinicas José de San Martin, University of Buenos Aires Córdoba 2351 ler subsuelo, Argentina. adriana@qb.fcen.uba.ar
G Di Venosa
T Hasan
Al Batlle
Consejo Nacional de Investigaciones Científicas y Técnicas · AR

Funding

Small Molecule Enhancers of Photodynamic Therapy for Skin CancerP01CA084203 · NCI · MASSACHUSETTS GENERAL HOSPITAL · PI Bryan Quilty Spring · 2001 to 2026
$27.9M
Targeted Photoactivatable Nanocells to Image and Treat Metastic Ovarian CancerRC1CA146337 · NCI · MASSACHUSETTS GENERAL HOSPITAL · PI HASAN, TAYYABA · 2009 to 2010
$971k
NCI NIH HHS P01 CA084203NCI NIH HHS RC1 CA146337NCI NIH HHS RC1CA146337
6 · The paper itself

Abstract

Photodynamic therapy (PDT) involves the administration of a photosensitizer (PS) followed by illumination with visible light, leading to generation of reactive oxygen species. The mechanisms of resistance to PDT ascribed to the PS may be shared with the general mechanisms of drug resistance, and are related to altered drug uptake and efflux rates or altered intracellular trafficking. As a second step, an increased inactivation of oxygen reactive species is also associated to PDT resistance via antioxidant detoxifying enzymes and activation of heat shock proteins. Induction of stress response genes also occurs after PDT, resulting in modulation of proliferation, cell detachment and inducing survival pathways among other multiple extracellular signalling events. In addition, an increased repair of induced damage to proteins, membranes and occasionally to DNA may happen. PDT-induced tissue hypoxia as a result of vascular damage and photochemical oxygen consumption may also contribute to the appearance of resistant cells. The structure of the PS is believed to be a key point in the development of resistance, being probably related to its particular subcellular localization. Although most of the features have already been described for chemoresistance, in many cases, no cross-resistance between PDT and chemotherapy has been reported. These findings are in line with the enhancement of PDT efficacy by combination with chemotherapy. The study of cross resistance in cells with developed resistance against a particular PS challenged against other PS is also highly complex and comprises different mechanisms. In this review we will classify the different features observed in PDT resistance, leading to a comparison with the mechanisms most commonly found in chemo resistant cells.

Indexed as

Drug ResistancePhotochemotherapyAnimalsCell ProliferationCell SurvivalHumansPhotosensitizing AgentsReactive Oxygen SpeciesPhotosensitizing AgentsReactive Oxygen Species

Identifiers

PMID21568910
PMCPMC3780570
OpenAlexW2078225696

What OpenQuestion holds

Textmetadata
LicenceTDM
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.