ReviewMedical sciences (Basel, Switzerland)2017
Melanoma: Genetic Abnormalities, Tumor Progression, Clonal Evolution and Tumor Initiating Cells.
Review in Medical sciences (Basel, Switzerland), 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 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
25 citing papers in PubMed, 43 citations in OpenAlex.
- Review
- Identification and Validation of an E2F Targets-Related Gene Signature Risk Score Predicting the Prognosis of Patients with Uveal Melanoma.Ocular oncology and pathology · 2026Article
- Melanoma treatment in the era of nanotechnology and precision medicine.Journal of nanobiotechnology · 2025Review
- Review
- Braf-Mutant Melanomas: Biology and Therapy.Current oncology (Toronto, Ont.) · 2024Review
- Review
- Current understanding of epigenetics role in melanoma treatment and resistance.Cancer cell international · 2022Review
- Marine Compounds for Melanoma Treatment and Prevention.International journal of molecular sciences · 2022Review
- UV-Induced Somatic Mutations Driving Clonal Evolution in Healthy Skin, Nevus, and Cutaneous Melanoma.Life (Basel, Switzerland) · 2022Review
- Statistical Classification for Raman Spectra of Tumoral Genomic DNA.Micromachines · 2022Article
- Genomic and Transcriptomic Underpinnings of Melanoma Genesis, Progression, and Metastasis.Cancers · 2021Review
- Normal Skin Cells Increase Aggressiveness of Cutaneous Melanoma by Promoting Epithelial-to-Mesenchymal Transition via Nodal and Wnt Activity.International journal of molecular sciences · 2021Article
- Decursinol Angelate Arrest Melanoma Cell Proliferation by Initiating Cell Death and Tumor Shrinkage via Induction of Apoptosis.International journal of molecular sciences · 2021Article
- The Impact of Hyaluronan on Tumor Progression in Cutaneous Melanoma.Frontiers in oncology · 2021Review
- Targeting Extracellular Matrix Remodeling Restores BRAF Inhibitor Sensitivity in BRAFi-resistant Melanoma.Clinical cancer research : an official journal of the American Association for Cancer Research · 2020Article
- Development ofClinical & experimental metastasis · 2020Article
- Activation of STAT3 is a key event in TLR4 signaling-mediated melanoma progression.Cell death & disease · 2020Article
- Vitamin A Enhances Macrophages Activity Against B16-F10 Malignant Melanocytes: A New Player for Cancer Immunotherapy?Medicina (Kaunas, Lithuania) · 2019Article
- Review
- TNF-alpha and metalloproteases as key players in melanoma cells aggressiveness.Journal of experimental & clinical cancer research : CR · 2018Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Melanoma is an aggressive neoplasia issued from the malignant transformation of melanocytes, the pigment-generating cells of the skin. It is responsible for about 75% of deaths due to skin cancers. Melanoma is a phenotypically and molecularly heterogeneous disease: cutaneous, uveal, acral, and mucosal melanomas have different clinical courses, are associated with different mutational profiles, and possess distinct risk factors. The discovery of the molecular abnormalities underlying melanomas has led to the promising improvement of therapy, and further progress is expected in the near future. The study of melanoma precursor lesions has led to the suggestion that the pathway of tumor evolution implies the progression from benign naevi, to dysplastic naevi, to melanoma in situ and then to invasive and metastatic melanoma. The gene alterations characterizing melanomas tend to accumulate in these precursor lesions in a sequential order. Studies carried out in recent years have, in part, elucidated the great tumorigenic potential of melanoma tumor cells. These findings have led to speculation that the cancer stem cell model cannot be applied to melanoma because, in this malignancy, tumor cells possess an intrinsic plasticity, conferring the capacity to initiate and maintain the neoplastic process to phenotypically different tumor cells.
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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.