RESEARCH ARTICLE s g

Every year 223,000 men will be diagnosed with prostate cancer in the United States with most patients having androgen dependent disease at the initial stages [1]. Although there have been recent advances in treating castration resistant prostate cancer, prognoses are still poor once the disease progresses to the castration resistant, metastatic state [2,3]. There have been numerous mech-anisms reported which can enable castration resistant growth including intracrine synthesis of androgen, upreg-ulation of the androgen receptor (AR), co-activation of the AR by other pathways, or complete bypass of androgen signaling through the activation of other pathways [4-6]. These mechanisms can include activation of oncogenes, mutation of tumor suppressors, epigenetic alterations, or activation of a pathway through extracellular matrix or * Correspondence: david.kaplan@tufts.eduKeywords: Prostate cancer, Phosphoproteome, CastrationAbstrac