ArticleMolecular carcinogenesis2016
A murine model for the development of melanocytic nevi and their progression to melanoma.
Article in Molecular carcinogenesis, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 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
13 citing papers in PubMed, 20 citations in OpenAlex.
- Novel CRISPR-Cas9 BAP1 knockout pre-clinical tumor model recapitulates human melanoma tumorigenesis and immune evolution.Communications biology · 2026Article
- Antagonistic stem cell fates under stress govern decisions between hair greying and melanoma.Nature cell biology · 2025Article
- The Original Mouse Models of Glioblastoma: Analysis of Pathophysiological Characteristics of Transplanted Tumor Tissue.Sovremennye tekhnologii v meditsine · 2025Article
- The Challenge of Melanoma Chemoprevention.Cancer prevention research (Philadelphia, Pa.) · 2022Article
- Review
- Review
- Regulatory T Cells Play an Important Role in the Prevention of Murine Melanocytic Nevi and Melanomas.Cancer prevention research (Philadelphia, Pa.) · 2021Article
- Melanoma Metabolism: Cell Survival and Resistance to Therapy.Advances in experimental medicine and biology · 2020Review
- Systemic Platelet-Activating Factor-Receptor Agonism Enhances Non-Melanoma Skin Cancer Growth.International journal of molecular sciences · 2018Article
- Oncogenic BRAF mutations and p16 expression in melanocytic nevi and melanoma in the Polish population.Postepy dermatologii i alergologii · 2017Article
- IL-23 Inhibits Melanoma Development by Augmenting DNA Repair and Modulating T Cell Subpopulations.Journal of immunology (Baltimore, Md. : 1950) · 2017Article
- Genetics of melanocytic nevi.Pigment cell & melanoma research · 2015Review
- Murine Skin Carcinogenesis and the Role of Immune System Dysregulation in the Tumorigenicity of 2-Ethylhexyl Acrylate.Biomedicine hubReview
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 1 institution in 1 country.
Funding
Abstract
Acquired melanocytic nevi are commonly found in sun exposed and unexposed human skin, but the potential for their transformation into invasive melanoma is not clear. Therefore, a mouse model of nevus initiation and progression was developed in C3H/HeN mice using a modified chemical carcinogenesis protocol. Nevi develop due to DNA damage initiated by dimethylbenz(a) anthracene (DMBA) followed by chronic promotion with 12-O-tetradecanoyl-phorbol-13-acetate (TPA). Dysplastic pigmented skin lesions appeared in 7-9 wk with 100% penetrance. Nests of melanocytic cells appeared in a subset of skin draining lymph nodes (dLN) by 25 wk, but not in age matched controls. Immunohistochemistry, real-time PCR, and flow cytometric analyses confirmed their melanocytic origin. Transformed cells were present in a subset of nevi and dLNs, which exhibited anchorage-independent growth, tumor development, and metastasis in nude mice. Approximately 50% of the cell lines contained H-Ras mutations and lost tumor suppressor p16(Ink4a) expression. While most studies of melanoma focus on tumor progression in transgenic mouse models where the mutations are present from birth, our model permits investigation of acquired mutations at the earliest stages of nevus initiation and promotion of nevus cell transformation. This robust nevus/melanoma model may prove useful for identifying genetic loci associated with nevus formation, novel oncogenic pathways, tumor targets for immune-prevention, screening therapeutics, and elucidating mechanisms of immune surveillance and immune evasion.
Indexed as
Identifiers
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.