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Functional interplay between secreted ligands and receptors in melanoma
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Título : Functional interplay between secreted ligands and receptors in melanoma |
Autor : Herraiz, Celia Jiménez-Cervantes, Celia Sanchez-Laorden, Berta García-Borrón, José C. |
Editor : Elsevier |
Fecha de publicación: 2017-07-01 |
URI : https://hdl.handle.net/11000/30786 |
Resumen :
Melanoma, the most aggressive form of skin cancer, results from the malignant transformation of
melanocytes located in the basement membrane separating the epidermal and dermal skin compartments.
Cutaneous melanoma is often initiated by solar ultraviolet radiation (UVR)-induced mutations.
Melanocytes intimately interact with keratinocytes, which provide growth factors and melanocortin
peptides acting as paracrine regulators of proliferation and differentiation. Keratinocyte-derived
melanocortins activate melanocortin-1 receptor (MC1R) to protect melanocytes from the carcinogenic
effect of UVR. Accordingly, MC1R is a major determinant of susceptibility to melanoma. Despite extensive
phenotypic heterogeneity and high mutation loads, the molecular basis of melanomagenesis and the
molecules mediating the crosstalk between melanoma and stromal cells are relatively well understood.
Mutations of intracellular effectors of receptor tyrosine kinase (RTK) signalling, notably NRAS and BRAF,
are major driver events more frequent than mutations in RTKs. Nevertheless, melanomas often display
aberrant signalling from RTKs such as KIT, ERRB1-4, FGFR, MET and PDGFR, which contribute to disease
progression and resistance to targeted therapies. Progress has also been made to unravel the role of the
tumour secretome in preparing the metastatic niche. However, key aspects of the melanoma-stroma
interplay, such as the molecular determinants of dormancy, remain poorly understood.
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Palabras clave/Materias: Melanoma Melanocortin-1 receptor Receptor tyrosine kinase signalling Melanoma progression Resistance to targeted therapies Therapy-induced secretome |
Tipo documento : application/pdf |
Derechos de acceso: info:eu-repo/semantics/closedAccess Attribution-NonCommercial-NoDerivatives 4.0 Internacional |
DOI : https://doi.org/10.1016/j.semcdb.2017.06.021 |
Aparece en las colecciones: Instituto de Neurociencias
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La licencia se describe como: Atribución-NonComercial-NoDerivada 4.0 Internacional.