ArticleBMC research notes2015
Ingenol mebutate treatment in keloids.
Article in BMC research notes, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. 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, 9 citations in OpenAlex.
- Molecular Targets in Modern Cosmetic Science.Molecules (Basel, Switzerland) · 2026Review
- miR-34 modulates apoptotic gene expression in Ingenol mebutate treated keloid fibroblasts.Molecular medicine reports · 2018Article
- Ingenol Mebutate Topical Gel A Status Report On Clinical Use Beyond Actinic Keratosis.The Journal of clinical and aesthetic dermatology · 2016Article
- Hyperbaric oxygen therapy improves the effect of keloid surgery and radiotherapy by reducing the recurrence rate.Journal of Zhejiang University. Science. BArticle
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundIngenol-mebutate has been used for the treatment of actinic keratosis. It has been shown that ingenol-mebutate inhibits the growth of cancer cells or induces tumor cell death through pro-apoptotic effects. Keloids are benign skin tumours and are the effect of a deregulated wound-healing process in genetically predisposed patients. Increased cell proliferation, which accounts for the progressive and hypertrophic nature of keloids, correlates with the failure of apoptosis and plays a role in the process of pathological scarring. Keloid cells show a mutated p53 gene resulting in functionally inactive p53 protein which cannot control genomic integrity. They tend to escape from apoptosis which leads to keloid development by means of accumulation of continuously proliferating cells. Currently, the treatment of keloids remains a challenge for high recurrence rates. However, the design and the development of pro-apoptotic therapeutic strategies would be beneficial to keloids treatment. CASE PRESENTATION: A 55-year-old caucasian woman presented recurrent keloids on a presternal scar. Standard surgical intervention was used to treat the scar. However, this was unsuccessful and a year later the patient sought treatment again, but only by alternative means as the patient refused further surgical intervention. Consequently, based on past research and experience, the authors attempted to treat these lesions with ingenol mebutate gel, due to the pro-apoptotic effects.
conclusionAfter 1 month, there was a clinical resolution of lesions, with a slightly squamous, post-inflammatory erythema. A cutaneous biopsy proved the absence of residual keloids and deregulated expression of molecular markers. The last follow-up of the patient, 1 year after treatment, showed that the patient was still free of keloids recurrence.
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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.