Cutaneous melanoma is a common cancer and cases have steadily increased since the mid 70s. For some patients

early diagnosis and surgical removal of melanomas is lifesaving

while other patients typically turn to molecular targeted therapies and immunotherapies as treatment options. Easy sampling of melanomas allows the scientific community to identify the most prevalent mutations that initiate melanoma such as the BRAF

NRAS

and TERT genes

some of which can be therapeutically targeted. Though initially effective

many tumors acquire resistance to the targeted therapies demonstrating the need to investigate compensatory pathways. Immunotherapies represent an alternative to molecular targeted therapies. However

inter-tumoral immune cell populations dictate initial therapeutic response and even tumors that responded to treatment develop resistance in the long term. As the protocol for combination therapies develop

so will our scientific understanding of the many pathways at play in the progression of melanoma. The future direction of the field may be to find a molecule that connects all of the pathways. Meanwhile

noncoding RNAs have been shown to play important roles in melanoma development and progression. Studying noncoding RNAs may help us to understand how resistance – both primary and acquired – develops; ultimately allow us to harness the true potential of current therapies. This review will cover the basic structure of the skin

the mutations and pathways responsible for transforming melanocytes into melanomas

the process by which melanomas metastasize

targeted therapeutics

and the potential that noncoding RNAs have as a prognostic and treatment tool.