ArticleCell proliferation2016
Photodynamic therapy with 5-aminolaevulinic acid and DNA damage: unravelling roles of p53 and ABCG2.
Article in Cell proliferation, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It carries an expression of concern. Cited by 4 papers.
What it found
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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.
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.
Who cites it
4 citing papers in PubMed, 12 citations in OpenAlex.
- EXPRESSION OF CONCERN: Photodynamic Therapy with 5-Aminolaevulinic Acid and DNA Damage: Unravelling Roles of p53 and ABCG2.Cell proliferation · 2026Article
- CRISPR editing to mimic porphyria combined with light: A new preclinical approach for prostate cancer.Molecular therapy. Oncology · 2024Article
- Sulphur-doped carbon dots as a highly efficient nano-photodynamic agent against oral squamous cell carcinoma.Cell proliferation · 2020Article
- Augmentation of 5-Aminolevulinic Acid Treatment of Glioblastoma by Adding Ciprofloxacin, Deferiprone, 5-Fluorouracil and Febuxostat: The CAALA Regimen.Brain sciences · 2018Article
Corrections and comments
- Expression of concern
Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectivesIn spite of high sensitivity of A549 cells (p53(+/+) ) to lethal effects of photodynamic therapy with 5-aminolaevulinic acid (5-ALA/PDT), DNA damage was observed only in H1299 cells (p53(-/-) ), suggesting that p53 may exert a protective effect. Studies on human colon adenocarcinoma cell lines HCT-116, and their cognate knockouts for p53, were not entirely consistent with the assumption above. Exploring alternative explanations for such conflicting behaviour, we observed that expression of the ATP-binding cassette G2 (ABCG2), a regulator of cell component efflux, had important effects on PDT-generated DNA injury in PC3 cells (prostate) which are p53(-/-) and positive for ABCG2. Addition of an ABCG2 inhibitor in ABCG2 positive A549 (p53(+/+) ) and PC3 (p53(-/-) ) cells eliminated resistance to DNA damage. MATERIALS AND
methodsAll cell lines investigated were incubated with 5-ALA and irradiated. Effects of PDT were evaluated assessing residual cell viability, cell-cycle profiles, PpIX localization, comet assay and Western blotting. Identical measurements were made in the presence of ABCG2 inhibitor, in cells expressing the transporter.
resultsOur data show that cell aptitude to defend its DNA from PDT-induced injury was mainly ruled by ABCG2 expression. These findings, while providing helpful information in predicting effectiveness of 5-ALA/PDT, may indicate a way to shift PDT from a palliative to a more effective approach in anti-cancer therapy.
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Registered trials
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.