MicroRNAs and next generation sequencing for the prognosis of the metastatic melanoma

Rosamaria Pinto,Gabriella Guida,Sabino Strippoli,Simona De Summa,Stefania Tommasi,Ondina Popescu,Michele Guida,Amalia Azzariti

doi:10.1186/1479-5876-13-s1-p4

Abstract

Background Melanoma is the most serious form of skin cancer because of its increasing incidence. Recent studies demonstrated the involvement of specific microRNAs in the melanoma initiation, progression, diagnosis and prognosis. Currently the treatment for metastatic melanoma with the mutation of BRAF V600E expects the Vemurafenib that blocks mutated BRAF protein leading to cell-cycle arrest. Unfortunately, the reactivation of MAPK signalling or activation of an alternative signalling pathway, as PI3K/AKT/mTOR, deriving from different mechanisms of acquired tumor drug resistance (as secondary mutations in NRAS or MEK1) causes disease progression within 6–8 months after the therapy beginning. The aim of this work was to evaluate a possible MAPK reactivation due to microRNAs involvement or to unclassified gene variants not yet associated to metastatic melanoma therapy response.

Highlights

Melanoma is the most serious form of skin cancer because of its increasing incidence
Open Access microRNAs and generation sequencing for the prognosis of the metastatic melanoma Rosamaria Pinto1*, Simona De Summa1, Sabino Strippoli2, Gabriella Guida3, Ondina Popescu4, Amalia Azzariti5, Michele Guida2, Stefania Tommasi1
Materials and methods A set of 43 patients, treatment naïve and with confirmed histological stage IV of metastatic melanoma was enrolled through the Oncology Unit of the IRCCS “Giovanni Paolo II” in Bari, Italy

Summary

Introduction

Melanoma is the most serious form of skin cancer because of its increasing incidence. Recent studies demonstrated the involvement of specific microRNAs in the melanoma initiation, progression, diagnosis and prognosis. The treatment for metastatic melanoma with the mutation of BRAF V600E expects the Vemurafenib that blocks mutated BRAF protein leading to cell-cycle arrest. The reactivation of MAPK signalling or activation of an alternative signalling pathway, as PI3K/AKT/mTOR, deriving from different mechanisms of acquired tumor drug resistance (as secondary mutations in NRAS or MEK1) causes disease progression within 6–8 months after the therapy beginning. The aim of this work was to evaluate a possible MAPK reactivation due to microRNAs involvement or to unclassified gene variants not yet associated to metastatic melanoma therapy response

Objectives

Methods

Results

Conclusion