Evidence map›Paper›PMID 26516076›Full record

ReviewCancer metastasis reviews2015

Tumor cell survival pathways activated by photodynamic therapy: a molecular basis for pharmacological inhibition strategies.

Mans Broekgaarden, Ruud Weijer, Thomas M van Gulik, Michael R Hamblin, Michal Heger

Open access · hybridAbstract readReview
In one paragraph

Review in Cancer metastasis reviews, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 114 papers.

0numbers the graph read from it
0cells of the map it votes in
114citing papers in PubMed
11.5field-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

114 citing papers in PubMed, 251 citations in OpenAlex.

  1. Shedding light on the cancer cell death mechanism in photodynamic therapy.Apoptosis : an international journal on programmed cell death · 2026
    Review
  2. Article
  3. Article
  4. Review
  5. Review
  6. Review
  7. Special Issue "Molecular Advances in Oncological Photodynamic Therapy".International journal of molecular sciences · 2026
    Article
  8. Review
  9. Light as a Weapon: Redefining Cancer Care with Photodynamic Therapy.International journal of biological sciences · 2026
    Review
  10. Article
  11. Enhanced photodynamic disruption of multidrug-resistantBiochemistry and biophysics reports · 2025
    Article
  12. Article
  13. Article
  14. Article
  15. Review
  16. Review
  17. Article
  18. Article
  19. Article
  20. Review

54 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

5 authors at 3 institutions in 2 countries.

Mans BroekgaardenDepartment of Experimental Surgery, Academic Medical Center, University of Amsterdam, Meibergdreef 9, 1105 AZ, Amsterdam, The Netherlands.
Ruud WeijerDepartment of Experimental Surgery, Academic Medical Center, University of Amsterdam, Meibergdreef 9, 1105 AZ, Amsterdam, The Netherlands.
Thomas M van GulikDepartment of Experimental Surgery, Academic Medical Center, University of Amsterdam, Meibergdreef 9, 1105 AZ, Amsterdam, The Netherlands.
Michael R HamblinWellman Center for Photomedicine, Massachusetts General Hospital, Boston, MA, USA.
Michal HegerDepartment of Experimental Surgery, Academic Medical Center, University of Amsterdam, Meibergdreef 9, 1105 AZ, Amsterdam, The Netherlands. m.heger@amc.uva.nl.
Academic Medical Center · NLUniversity of Amsterdam · NLHarvard University · US

Funding

Photodynamic Therapy of Localized InfectionsR01AI050875 · NIAID · MASSACHUSETTS GENERAL HOSPITAL · PI HAMBLIN, MICHAEL R · 2003 to 2017
$4.8M
NIAID NIH HHS R01 AI050875
6 · The paper itself

Abstract

Photodynamic therapy (PDT) has emerged as a promising alternative to conventional cancer therapies such as surgery, chemotherapy, and radiotherapy. PDT comprises the administration of a photosensitizer, its accumulation in tumor tissue, and subsequent irradiation of the photosensitizer-loaded tumor, leading to the localized photoproduction of reactive oxygen species (ROS). The resulting oxidative damage ultimately culminates in tumor cell death, vascular shutdown, induction of an antitumor immune response, and the consequent destruction of the tumor. However, the ROS produced by PDT also triggers a stress response that, as part of a cell survival mechanism, helps cancer cells to cope with the PDT-induced oxidative stress and cell damage. These survival pathways are mediated by the transcription factors activator protein 1 (AP-1), nuclear factor E2-related factor 2 (NRF2), hypoxia-inducible factor 1 (HIF-1), nuclear factor κB (NF-κB), and those that mediate the proteotoxic stress response. The survival pathways are believed to render some types of cancer recalcitrant to PDT and alter the tumor microenvironment in favor of tumor survival. In this review, the molecular mechanisms are elucidated that occur post-PDT to mediate cancer cell survival, on the basis of which pharmacological interventions are proposed. Specifically, pharmaceutical inhibitors of the molecular regulators of each survival pathway are addressed. The ultimate aim is to facilitate the development of adjuvant intervention strategies to improve PDT efficacy in recalcitrant solid tumors.

Indexed as

ApoptosisCell SurvivalEndoplasmic Reticulum StressHumansMAP Kinase Signaling SystemNeoplasmsNF-E2-Related Factor 2NF-kappa BOxidative StressPhotochemotherapyPhotosensitizing AgentsReactive Oxygen SpeciesNFE2L2 protein, humanNF-E2-Related Factor 2NF-kappa BPhotosensitizing AgentsReactive Oxygen SpeciesAntioxidant responseApoptosis signaling kinase 1ER stressHeat shock factor 1Inflammatory responseProteotoxic stress

Identifiers

PMID26516076
PMCPMC4661210
OpenAlexW1833716810

What OpenQuestion holds

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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.