Autophagy, or “self eating,” is an adaptive process that helps cells cope with metabolic, toxic, and even infectious stressors. While the adaptive capability of autophagy is generally beneficial, autophagy can also facilitate enhanced nutrient utilization and improved growth characteristics in cancer cells. Moreover, autophagy can promote greater cellular robustness in the context of therapeutic intervention. This has proven to be the case in advanced prostate cancer, where preclinical data largely supports that autophagy facilitates both disease progression and therapeutic resistance. Notably, androgen deprivation therapy, taxane-based chemotherapy, targeted kinase inhibition, and nutrient restriction all induce significant cellular distress. Autophagy is subsequently up-regulated through core metabolic regulatory signaling cascades (i.e. AMPK, PI3K, and mTOR), and more favorable growth and nutrient conditions are established. Current research also demonstrates that when the autophagic machinery is inhibited, greater cell killing and tumor responsiveness can be obtained. In this review, we will cover current prostate cancer treatments associated with alterations in autophagy; data supporting autophagic modulation with added emphasis on alterations occurring within prostate cancer models; and finally, research supporting adjuvant autophagic modulation with current prostate cancer treatment paradigms.
In the absence of local invasion, the outcomes of laparoscopic adrenalectomy for patients with tumours >/=6 cm were comparable to those with tumours <6 cm. This has helped confirm a policy of initial laparoscopic resection for all noninvasive adrenal tumours can be applied safely.
Purpose: We sought to evaluate outcomes of lymph node dissection (LND) in patients with upper tract urothelial carcinoma. Materials and Methods: We performed a multicenter retrospective analysis utilizing the ROBUUST (for RObotic surgery for Upper Tract Urothelial Cancer Study) registry for patients who did not undergo LND (pNx), LND with negative lymph nodes (pN0) and LND with positive nodes (pND). Primary and secondary outcomes were overall survival (OS) and recurrence-free survival (RFS). Multivariable analyses evaluated predictors of outcomes and pathological node positivity. Kaplan-Meier analyses (KMAs) compared survival outcomes. Results: A total of 877 patients were analyzed (LND performed in 358 [40.8%]/pND in 73 [8.3%]). Median nodes obtained were 10.2 for pND and 9.8 for pN0. Multivariable analyses noted increasing age (OR 1.1, p <0.001), pND (OR 3.1, p <0.001) and pathological stage pTis/3/4 (OR 3.4, p <0.001) as predictors for all-cause mortality. Clinical high-grade tumors (OR 11.74, p[0.015) and increasing tumor size
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