ArticleCells2021
PARP1 as a Marker of an Aggressive Clinical Phenotype in Cutaneous Melanoma-A Clinical and an In Vitro Study.
Article in Cells, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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.
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
14 citing papers in PubMed, 20 citations in OpenAlex.
- PARP1 as a biomarker for differentiating melanoma from benign melanocytic lesions.The Journal of investigative dermatology · 2026Article
- Mendelian Randomization Unveils Poly(ADP-ribose) Polymerase 1 as Causal Plasma Protein Target in Melanoma, Integrated Multi-omics.Plastic and reconstructive surgery. Global open · 2026Article
- PARP-1 in tumor complicated with depression-possible role and therapeutic perspective: a narrative review.Translational cancer research · 2025Review
- The examination of in vitro photosensitizing efficacy of aloe-emodin loaded liposome following photodynamic therapy on melanoma cell lines.Scientific reports · 2025Article
- Association of DNA damage response pathway genes with rheumatoid arthritis risks: a case-control study.Scientific reports · 2025Article
- Systematic analysis of the transcriptional landscape of melanoma reveals drug-target expression plasticity.Briefings in functional genomics · 2025Article
- Poly(ADP-Ribose) Polymerase (PARP) Inhibitors for Cancer Therapy: Advances, Challenges, and Future Directions.Biomolecules · 2024Review
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- Expression of cannabinoid (CB1 and CB2) and cannabinoid-related receptors (TRPV1, GPR55, and PPARα) in the synovial membrane of the horse metacarpophalangeal joint.Frontiers in veterinary science · 2023Article
- BMN673 Is a PARP Inhibitor with Unique Radiosensitizing Properties: Mechanisms and Potential in Radiation Therapy.Cancers · 2022Review
- Emerging Roles of Post-Translational Modifications in Skin Diseases: Current Knowledge, Challenges and Future Perspectives.Journal of inflammation research · 2022Review
- DNA damage repair-related gene signature predicts prognosis and indicates immune cell infiltration landscape in skin cutaneous melanoma.Frontiers in endocrinology · 2022Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
14 authors at 7 institutions in 3 countries.
Funding
Abstract
(1) Background: Poly(ADP-ribose) polymerase 1) (PARP1) is a pleiotropic enzyme involved in several cellular processes, e.g., DNA damage repair, regulation of mitosis, and immune response. Little is known about the role of PARP1 in melanoma development and progression. We aimed to investigate the prognostic significance of PARP1 expression in cutaneous melanoma through evaluation of mRNA and protein levels of PARP1 in normal melanocytes and melanoma cell lines, as well as in patients' tissue material from surgical resections. (2) Methods: An in vitro model was based on two types of normal human melanocytes (HEMn-DP and HEMn-LP) and four melanoma cell lines (A375, WM1341D, Hs294T, and WM9).
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What OpenQuestion holds
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.