端粒酶
端粒
干细胞
增生
祖细胞
间质细胞
端粒酶逆转录酶
基础(医学)
癌症研究
前列腺
生物
细胞
细胞生长
病理
医学
细胞生物学
内分泌学
内科学
DNA
遗传学
癌症
基因
胰岛素
作者
Jayant K. Rane,Sarah Greener,Fiona M. Frame,Vincent M. Mann,Matthew Simms,Anne T. Collins,Daniel M. Berney,Norman J. Maitland
标识
DOI:10.1016/j.eururo.2015.09.039
摘要
Benign prostatic hyperplasia (BPH) treatments have changed little over many years and do not directly address the underlying cause. Because BPH is characterised by uncontrolled cell growth, the chromosomal telomeres should be eroded in the reported absence or low levels of telomerase activity, but this is not observed. We investigated the telomere biology of cell subpopulations from BPH patients undergoing transurethral resection of prostate (TURP). Measurement of TERC, TERT, and telomerase activity revealed that only the epithelial stem-like and progenitor fractions expressed high levels of telomerase activity (p<0.01) and individual enzyme components (p<0.01). Telomerase activity and TERT expression were not detected in stromal cells. Telomere length measurements reflected this activity, although the average telomere length of (telomerase-negative) luminal cells was equivalent to that of telomerase-expressing stem/progenitor cells. Immunohistochemical analysis of patient-derived BPH arrays identified distinct areas of luminal hyperproliferation, basal hyperproliferation, and basal-luminal hyperproliferation, suggesting that basal and luminal cells can proliferate independently of each other. We propose a separate lineage for the luminal and basal cell components in BPH.We unexpectedly found an enzyme called telomerase in the cells that maintain benign prostatic hyperplasia (BPH), suggesting that telomerase inhibitors could be used to alleviate BPH symptoms.
科研通智能强力驱动
Strongly Powered by AbleSci AI