Uveal Melanoma Metastasis

Uveal melanoma (UM) is characterized by relatively few, highly incident molecular alterations and their association with metastatic risk is deeply understood. Nevertheless, this knowledge has so far not led to innovative therapies for the successful treatment of UM metastases or for adjuvant therapy...

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Autores principales:	Ernesto Rossi, Michela Croce, Francesco Reggiani, Giovanni Schinzari, Marianna Ambrosio, Rosaria Gangemi, Giampaolo Tortora, Ulrich Pfeffer, Adriana Amaro
Formato:	article
Lenguaje:	EN
Publicado:	MDPI AG 2021
Materias:	uveal melanoma tumorigenesis molecular classification targeted therapy immune checkpoint Neoplasms. Tumors. Oncology. Including cancer and carcinogens RC254-282
Acceso en línea:	https://doaj.org/article/2947af99c68b4c61bb8ab6fba3d0366d
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spelling	oai:doaj.org-article:2947af99c68b4c61bb8ab6fba3d0366d2021-11-25T17:02:39ZUveal Melanoma Metastasis10.3390/cancers132256842072-6694https://doaj.org/article/2947af99c68b4c61bb8ab6fba3d0366d2021-11-01T00:00:00Zhttps://www.mdpi.com/2072-6694/13/22/5684https://doaj.org/toc/2072-6694Uveal melanoma (UM) is characterized by relatively few, highly incident molecular alterations and their association with metastatic risk is deeply understood. Nevertheless, this knowledge has so far not led to innovative therapies for the successful treatment of UM metastases or for adjuvant therapy, leaving survival after diagnosis of metastatic UM almost unaltered in decades. The driver mutations of UM, mainly in the G-protein genes GNAQ and GNA11, activate the MAP-kinase pathway as well as the YAP/TAZ pathway. At present, there are no drugs that target the latter and this likely explains the failure of mitogen activated kinase kinase inhibitors. Immune checkpoint blockers, despite the game changing effect in cutaneous melanoma (CM), show only limited effects in UM probably because of the low mutational burden of 0.5 per megabase and the unavailability of antibodies targeting the main immune checkpoint active in UM. The highly pro-tumorigenic microenvironment of UM also contributes to therapy resistance. However, T-cell redirection by a soluble T-cell receptor that is fused to an anti-CD3 single-chain variable fragment, local, liver specific therapy, new immune checkpoint blockers, and YAP/TAZ specific drugs give new hope to repeating the success of innovative therapy obtained for CM.Ernesto RossiMichela CroceFrancesco ReggianiGiovanni SchinzariMarianna AmbrosioRosaria GangemiGiampaolo TortoraUlrich PfefferAdriana AmaroMDPI AGarticleuveal melanomatumorigenesismolecular classificationtargeted therapyimmune checkpointNeoplasms. Tumors. Oncology. Including cancer and carcinogensRC254-282ENCancers, Vol 13, Iss 5684, p 5684 (2021)
institution	DOAJ
collection	DOAJ
language	EN
topic	uveal melanoma tumorigenesis molecular classification targeted therapy immune checkpoint Neoplasms. Tumors. Oncology. Including cancer and carcinogens RC254-282
spellingShingle	uveal melanoma tumorigenesis molecular classification targeted therapy immune checkpoint Neoplasms. Tumors. Oncology. Including cancer and carcinogens RC254-282 Ernesto Rossi Michela Croce Francesco Reggiani Giovanni Schinzari Marianna Ambrosio Rosaria Gangemi Giampaolo Tortora Ulrich Pfeffer Adriana Amaro Uveal Melanoma Metastasis
description	Uveal melanoma (UM) is characterized by relatively few, highly incident molecular alterations and their association with metastatic risk is deeply understood. Nevertheless, this knowledge has so far not led to innovative therapies for the successful treatment of UM metastases or for adjuvant therapy, leaving survival after diagnosis of metastatic UM almost unaltered in decades. The driver mutations of UM, mainly in the G-protein genes GNAQ and GNA11, activate the MAP-kinase pathway as well as the YAP/TAZ pathway. At present, there are no drugs that target the latter and this likely explains the failure of mitogen activated kinase kinase inhibitors. Immune checkpoint blockers, despite the game changing effect in cutaneous melanoma (CM), show only limited effects in UM probably because of the low mutational burden of 0.5 per megabase and the unavailability of antibodies targeting the main immune checkpoint active in UM. The highly pro-tumorigenic microenvironment of UM also contributes to therapy resistance. However, T-cell redirection by a soluble T-cell receptor that is fused to an anti-CD3 single-chain variable fragment, local, liver specific therapy, new immune checkpoint blockers, and YAP/TAZ specific drugs give new hope to repeating the success of innovative therapy obtained for CM.
format	article
author	Ernesto Rossi Michela Croce Francesco Reggiani Giovanni Schinzari Marianna Ambrosio Rosaria Gangemi Giampaolo Tortora Ulrich Pfeffer Adriana Amaro
author_facet	Ernesto Rossi Michela Croce Francesco Reggiani Giovanni Schinzari Marianna Ambrosio Rosaria Gangemi Giampaolo Tortora Ulrich Pfeffer Adriana Amaro
author_sort	Ernesto Rossi
title	Uveal Melanoma Metastasis
title_short	Uveal Melanoma Metastasis
title_full	Uveal Melanoma Metastasis
title_fullStr	Uveal Melanoma Metastasis
title_full_unstemmed	Uveal Melanoma Metastasis
title_sort	uveal melanoma metastasis
publisher	MDPI AG
publishDate	2021
url	https://doaj.org/article/2947af99c68b4c61bb8ab6fba3d0366d
work_keys_str_mv	AT ernestorossi uvealmelanomametastasis AT michelacroce uvealmelanomametastasis AT francescoreggiani uvealmelanomametastasis AT giovannischinzari uvealmelanomametastasis AT mariannaambrosio uvealmelanomametastasis AT rosariagangemi uvealmelanomametastasis AT giampaolotortora uvealmelanomametastasis AT ulrichpfeffer uvealmelanomametastasis AT adrianaamaro uvealmelanomametastasis
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Uveal Melanoma Metastasis

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