RESUMEN
[This corrects the article DOI: 10.1155/2015/432479.].
RESUMEN
Mucosal melanoma is a rare disease, which differs from its cutaneous counterpart genetically and for its clinical behaviour. Moreover this is a heterogeneous disease based on the tissue of origin. As CT7 and CT10 are highly expressed in cutaneous melanoma and are immunogenic in this disease, we analysed their expression throughout the different subtypes of mucosal melanoma and tumor development. We detected a frequent expression of CT7 in primaries and corresponding metastases (55%) as well as for CT10 (30%). This expression resulted to be heterogeneous in the same tumor specimen and moreover influenced by the tissue of origin. Our results support the role of these antigens in immunotherapy for mucosal melanoma.
Asunto(s)
Antígenos de Neoplasias/metabolismo , Heterogeneidad Genética , Melanoma/patología , Membrana Mucosa/metabolismo , Membrana Mucosa/patología , Proteínas de Neoplasias/metabolismo , Neoplasias Cutáneas/patología , Humanos , Melanoma/metabolismo , Recurrencia Local de Neoplasia/metabolismo , Recurrencia Local de Neoplasia/patología , Neoplasias Cutáneas/metabolismoRESUMEN
A comparison of in vitro and in vivo characteristics of tumour cells derived from patients with mucosal melanoma treated with imatinib was performed with respect to KIT mutations. Three patients with mucosal melanoma were treated with imatinib. Patient-derived tumour material was used to establish melanoma cell cultures ex vivo. We evaluated tumour material and cell cultures for KIT protein expression and KIT mutation status. In addition, proliferation assays with melanoma cell cultures were performed with imatinib. Expression of KIT protein and KIT mutation was shown in two patients who responded to imatinib in vivo. Cells derived from a third patient who did not respond to imatinib did not express KIT and lacked a KIT mutation. Patient-derived melanoma cells did not show any KIT mutations, nor did they respond to imatinib in vitro. Our study underlines that melanoma consists of a heterogeneous cell population, making it imperative to use the mapping of involved activating tumour growth-driving pathways in order to improve response to therapy with kinase inhibitors.