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Patients with benign prostatic hyperplasia show shorter leukocyte telomere length but no association with telomerase gene polymorphisms in Han Chinese males

  • Cheng, Guanghui1
  • Dai, Mingkai1
  • Xin, Qian1
  • Wang, Lina1
  • Kong, Feng2
  • Xu, Dawei3
  • 1 Central Research Laboratory, The Second Hospital, Cheeloo College of Medicine, Shandong University, Jinan 250033, PR China
  • 2 Engineering Laboratory of Urinary Organ and Functional Reconstruction of Shandong Province, 250013, PR China
  • 3 Department of Medicine, Division of Hematology, Center for Molecular Medicine and Bioclinicum, Karolinsk Institutet and Karolinska University Hospital Solna, Stockholm, SE-17176, Sweden
Published Article
International journal of clinical and experimental pathology
Publication Date
Aug 01, 2020
PMID: 32922609
PMCID: PMC7476938
PubMed Central


Objective: Benign prostatic hyperplasia (BPH) is an age-related disease, occurring in >70% of men of age >60. Because telomeres and telomerase play a key role in aging and age-related diseases, and certain telomerase gene single nucleotide polymorphisms (SNPs) are shown to be associated with the susceptibility to age-related diseases, we wanted to determine the relationship between BPH and leukocyte telomere length (LTL) and telomere length-related single nucleotide polymorphisms (SNPs) of the telomerase holoenzyme genes. Methods: Peripheral blood was collected from both BPH patients and age-matched healthy male controls and genomic DNA was extracted. rs2736100 and rs2736098 at the TERT and rs12696304 at the TERC locus were analysed using pre-designed TaqMan SNP genotyping assay kits. LTL was determined using qPCR. Results: Patients with BPH had significantly shorter LTL (1.231 ± 0.532 vs 0.899 ± 0.322, P < 0.001). The genotyping results show similar frequencies in rs2736100, rs2736098 and rs12696304 between healthy and BPH individuals. Conclusions: Shorter telomeres but not telomerase SNPs at the TERT and TERC loci, are associated with BPH. Short telomeres may promote senescence of a fraction of prostatic epithelial cells, while senescent cells in turn facilitate epithelial and stromal cell proliferation by the senescence-associated secretory phenotype mechanism, thereby eventually leading to BPH development.

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