Background: Physician treatment preference may influence how risks are communicated in prostate cancer consultations. We identified persuasive language used when describing cancer prognosis, life expectancy, and side effects in relation to a physician's recommendation for aggressive (surgery/radiation) or nonaggressive (active surveillance/watchful waiting) treatment.
Methods: A qualitative analysis was performed on transcribed treatment consultations of 40 men with low- and intermediate-risk prostate cancer across 10 multidisciplinary providers.
Background: Life expectancy (LE) impacts effectiveness and morbidity of prostate cancer (CaP) treatment, but its impact on cost-effectiveness is unknown. We sought to evaluate the impact of LE on the cost-effectiveness of radical prostatectomy (RP), radiation therapy (RT), and active surveillance (AS) for clinically localized disease.
Methods: We created a Markov model to calculate incremental cost-effectiveness ratios (ICERs) for RP, RT, and AS over a 20-year time horizon from a Medicare payer perspective for low- and intermediate-risk CaP.
Background: High-risk ureteral tumors represent an understudied subset of upper tract urothelial carcinoma, whose surgical management can range from a radical nephroureterectomy (NU) to segmental ureterectomy (SU).
Objectives: To evaluate contemporary trends in the management of high-risk ureteral tumors, the utilization of lymphadenectomy and peri-operative chemotherapy, and their impact on overall survival (OS).
Design, Setting, And Participants: We performed a retrospective cohort study of patients in the National Cancer Database from years 2006 to 2013 with clinically localized high-risk ureteral tumors treated with NU or SU.
Hepatocyte growth factor (HGF), through activation of the c-MET receptor, mediates biological processes critical for tissue regeneration; however, its clinical application is limited by protein instability and poor recombinant expression. We previously engineered an HGF fragment (eNK1) that possesses increased stability and expression yield and developed a c-MET agonist by coupling eNK1 through an introduced cysteine residue. Here, we further characterize this eNK1 dimer and show it elicits significantly greater c-MET activation, cell migration, and proliferation than the eNK1 monomer.
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