The DOI matches its Crossref record; 35 of the 35 references it cites were found in a registry or an index.
Molecular Markers and Targets in Melanoma
Open accessAbstract
Melanoma develops as a result of several genetic alterations, with UV radiation often acting as a mutagenic risk factor. Deep knowledge of the molecular signaling pathways of different types of melanoma allows better characterization and provides tools for the development of therapies based on the intervention of signals promoted by these cascades. The latest World Health Organization classification acknowledged the specific genetic drivers leading to melanoma and classifies melanocytic lesions into nine distinct categories according to the associate cumulative sun damage (CSD), which correlates with the molecular alterations of tumors. The largest groups are melanomas associated with low-CSD or superficial spreading melanomas, characterized by frequent presentation of the BRAFV600 mutation. High-CSD melanomas include lentigo maligna type and desmoplastic melanomas, which often have a high mutation burden and can harbor NRAS, BRAFnon-V600E, or NF1 mutations. Non-CSD-associated melanomas encompass acral and mucosal melanomas that usually do not show BRAF, NRAS, or NF1 mutations (triple wild-type), but in a subset may have KIT or SF3B1 mutations. To improve survival, these driver alterations can be treated with targeted therapy achieving significant antitumor activity. In recent years, relevant improvement in the prognosis and survival of patients with melanoma has been achieved, since the introduction of BRAF/MEK tyrosine kinase inhibitors and immune checkpoint inhibitors. In this review, we describe the current knowledge of molecular pathways and discuss current and potential therapeutic targets in melanoma, focusing on their clinical relevance of development.
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Cites
Improved Survival with Ipilimumab in Patients with Metastatic Melanoma
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“ipilimumab in 2011, the first immune checkpoint inhibitor (ICI) to improve survival in the advanced setting [7,8], and vemurafenib, a v-raf murine sarcoma viral oncogene homolog B1 (BRAF) tyrosine kinase inhibitor, first in class [9,10].”
BackgroundPembrolizumab versus Ipilimumab in Advanced Melanoma
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Self-citationNivolumab in Previously Untreated Melanoma without BRAF Mutation
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Self-citationOverall Survival with Combined Nivolumab and Ipilimumab in Advanced Melanoma
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IFN-γ–related mRNA profile predicts clinical response to PD-1 blockade
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Cited by
European consensus-based interdisciplinary guideline for melanoma. Part 2: Treatment - Update 2022
Garbe, C., Amaral, T., Peris, K., Hauschild, A., Arenberger, P., Basset-Seguin, N., Bastholt, L., Bataille, V., del Marmol, V., Dréno, B., et al. (2022) · European Journal of Cancer · doi:10.1016/j.ejca.2022.04.018 · Cited by 283
Liu, Z., Dang, B., Wang, X., Liu, Y., Wang, C., & Lin, C. (2025) · Medical Oncology · doi:10.1007/s12032-025-03205-2
Metadata
- Authors
- Teixido, C., Castillo, P., Martinez-Vila, C., Arance, A., & Alos, L.
- Venue
- Cells
- Publisher
- MDPI AG
- Published
- 2021-09-05
- Volume
- 10
- Issue
- 9
- Pages
- 2320
- ISSN
- 2073-4409 (ISSN-L)
- OpenAlex
- W3196918127
- Cited by
- 219
- References
- 35
- FWCI
- 8.92
- Type
- journal article
- Language
- en
- Open access
- gold
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