BRAF/NRAS Wild-Type Melanomas Have a High Mutation Load Correlating with Histological and Molecular Signatures of UV Damage

“The mutation load in melanoma is generally high compared to other tumor types due to extensive UV damage. Translation of exome sequencing data into clinically relevant information is therefore challenging. This study sought to characterize mutations identified in primary cutaneous melanomas and correlate these with clinico-pathologic features.”


Multidisciplinary Team Tackles Personalized Medicine for Melanoma Patients with Normal BRAF Gene


A group of melanoma researchers and clinicians have received funding to address an important question in melanoma treatment: are there molecular targets for melanomas that do not harbor a mutation in the BRAF gene? And can we identify drug candidates for these new molecular targets? The Stand Up to Cancer (SUC2) philanthropic program and the Melanoma Research Alliance are jointly funding the 3-year, eight-institution endeavor. Continue reading…


P21-Activated Kinase 1 (PAK1) as a Therapeutic Target in BRAF Wild-Type Melanoma

Background: Although remarkable clinical response rates in melanoma have been observed using vemurafenib or dabrafenib in patients with tumors carrying oncogenic mutations in BRAF, a substantial unmet medical need remains for the subset of patients with wild-type BRAF tumors. Methods: To investigate the role of p21-activated kinases (PAKs) in melanoma, we determined PAK1 genomic copy number and protein expression for a panel of human melanoma tissues…”