Abstract
Long term-side effects from cancer therapies are a growing health care concern as life expectancy among cancer survivors increases. Damage to the bladder is common in patients treated with radiation therapy for pelvic cancers and can result in radiation (hemorrhagic) cystitis (RC). The disease progression of RC consists of an acute and chronic phase, separated by a symptom-free period. Gaining insight in tissue changes associated with these phases is necessary to develop appropriate interventions. Using a mouse preclinical model, we have previously shown that fibrosis and vascular damage are the predominant pathological features of chronic RC. The goal of this study was to determine the pathological changes during acute RC. We identified that radiation treatment results in a temporary increase in micturition frequency and decrease in void volume 4–8 weeks after irradiation. Histologically, the micturition defect is associated with thinning of the urothelium, loss of urothelial cell–cell adhesion and tight junction proteins and decrease in uroplakin III expression. By 12 weeks, the urothelium had regenerated and micturition patterns were similar to littermate controls. No inflammation or fibrosis were detected in bladder tissues after irradiation. We conclude that functional bladder defects during acute RC are driven primarily by a urothelial defect.
Highlights
Decades of extensive cancer research and subsequent improved cancer screenings and treatments have resulted in an increasing number of patients overcoming their cancer diagnosis
We have shown that, during the chronic phase of radiation (hemorrhagic) cystitis (RC), radiation exposure results in long-term micturition defects, including frequency and decreased bladder capacity
To fully understand the bladder changes that characterize the different phases of RC, the goal of this study was to determine the mechanism that induces the symptoms during the acute phase of RC
Summary
Decades of extensive cancer research and subsequent improved cancer screenings and treatments have resulted in an increasing number of patients overcoming their cancer diagnosis. The patient enters the chronic phase, during which the patient has evident symptoms of bladder disease including frequency, urgency, nocturia, incontinence, dysuria, pelvic pain, and h ematuria[2,3,4,5] While each of these symptoms severely impacts the quality-of-life of a cancer survivor, the presence of hematuria can make RC a life-threatening condition arresting the bleeding becomes the focus of treatment[7]. We have previously developed a preclinical RC model that closely mimics the human c ondition[10] In this model, we have shown that, during the chronic phase of RC, radiation exposure results in long-term micturition defects, including frequency and decreased bladder capacity. To fully understand the bladder changes that characterize the different phases of RC, the goal of this study was to determine the mechanism that induces the symptoms during the acute phase of RC
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