alexa Targeted Therapies in Melanoma: Knowledge, Resistance a
ISSN: 2157-2518

Journal of Carcinogenesis & Mutagenesis
Open Access

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Review Article

Targeted Therapies in Melanoma: Knowledge, Resistance and Perspectives

Maria Colombino1*, Maria Cristina Sini1, Amelia Lissia2, Antonio Cossu2 and Giuseppe Palmieri1

1Unit of Cancer Genetics, Institute of Biomolecular Chemistry (ICB), National Research Council (CNR), Italy

2University Hospital Health Unit - Azienda Ospedaliero Universitaria (AOU), Via Matteotti, 07100 Sassari, Italy

*Corresponding Author:
Dr. Maria Colombino
Unit of Cancer Genetics, Institute of Biomolecular Chemistry (ICB)
National Research Council (CNR), Traversa La Crucca
3 - Baldinca Li Punti, 07100 Sassari, Italy
Tel: +39 079 2841239
Fax: +39 079 2841299
E-mail: [email protected]

Received date: March 18, 2014; Accepted date: May 25, 2014; Published date: May 31, 2014

Citation: Colombino M, Sini MC, Lissia A, Cossu A, Palmieri G (2014) Targeted Therapies in Melanoma: Knowledge, Resistance and Perspectives. J Carcinog Mutagen S4:004. doi: 10.4172/2157-2518.S4-004

Copyright: © 2014 Colombino M, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

 

Abstract

Several molecular mechanism appear to play a major role in melanoma genesis and progression. Current targeted therapies focus on contrasting the activation of RAS/RAF/MEK/ERK and, to a less extent, PI3K/AKT pathways. Development of inhibitors of key effectors (mainly, BRAF mutant and MEK) has significantly improved treatment of patients with advanced melanoma. However, only rarely tumours present a durable regression due to a large variety of acquired and intrinsic mechanisms that drive resistance to the main targeted inhibitors. All these evidence suggest that in melanoma, as probably in all types of cancer, use of a combinatorial treatment approach, instead of targeting a single component of melanomagenesis pathways, could delay or prevent the emergence of resistance mechanisms responsible to tumour relapse. In this sense, a crucial step is thus represented by the full knowledge of such molecular mechanisms.

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