BAUS Section of Academic Urology Oral Abstracts

Abstract

Introduction: Stem cells accumulate non-pathogenic mitochondrial DNA (mtDNA) mutations, resulting in a measurable defect in oxidative phosphorylation (OXPHOS), which is transmitted to their progeny. This method allows the mapping of the fate of stem cells in situ. This novel method is used in this instance to study human prostate stem cells. Methods: Histologically benign specimens were studied from 30 patients. Sequential enzyme histochemistry and immunofluorescence were employed to identify respiratory chain defects and prostate histology. mtDNA mutations were confirmed by whole mitochondrial genome sequencing of areas of interest, following laser capture microdissection. Results: Respiratory chain defects due to somatic mtDNA mutations can be found within prostate epithelia and are seen to clonally expand along acini. Neighbouring acini deficient in OXPHOS are seen to share mtDNA mutations, supporting that a single stem cells clonally expands to generate entire branching networks of the gland either through branching or gland fission. A common clonal origin for basal, luminal and neuroendocrine cells was demonstrated, resolving key areas of debate in prostate stem cell biology. Formal 3D reconstruction of samples will allow the further characterisation of stem cell fate, identification of where prostate stem cells reside in the gland and identification of novel and improved markers of prostatic stem cells.

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