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Quantification of mtDNA copy number and telomere length in benign prostatic hyperplasia patients

  • Baumanis E.,
  • Zole E.,
  • Dale R.,
  • Leise A.,
  • Lietuvietis V.

PII: S1569-9056(16)15065-1

DOI: 10.1016/S1569-9056(16)15065-1

Introduction & Objectives: The pathogenesis of benign prostatic hyperplasia (BPH) is not completely understood. There are still issues about the mechanisms of progression and searches for better marker to predict clinically significant disease. In the medical treatment era it is actual issue when operative therapy is needed. BPH characterizes by proliferation of the prostatic stromal and epithelial cells. Thereby the BPH nodules increases in size hence the resulting difficulty in urinating. There are controversial results in other studies about telomere length (TL) in BPH patients. The length of TL could be different. Unlike prostate cancer patients to whom shorter TL were observed, in BPH patients TL length were shorter and longer in comparison to normal tissues. MtDNA copy number (CN) is not previously studied in BPH patients. It has been shown that increment of mtDNA CN in blood cells is associated with a high prostate cancer risk and high tumour burden in prostate cancer patients (Zhou et al. 2014). Quantification of mtDNA CN and TL in BPH patients could be helpful for prognosis of BPH development and cancer risk. The aim is to explore if patients with clinically severe BPH have longer telomeres or more mtDNA CN in blood cells than in control blood cells samples, and to see if there is difference between the two cell components in prostate tissue and blood cells from BPH patients.

Material & Methods: 10 blood and prostate tissue samples from operated BPH patients and 15 control samples without BPH were used in this pilot project study. Relative mtDNA CN was detected using qPCR, TaqMan assay. Relative TL – qPCR, SYBR Green assay. Statistical analyses – GraphPad Prism 5 Software.

Results: In this study an average TL in BPH patients’ blood cells are 39.7% longer than in control blood cells but the difference is not statistically significant, P=0.1025 due to large varieties among values in BPH blood cell samples. TL in BPH prostate tissue are 72.2% longer than in BPH blood cells, P=0.0079. In this small sample cohort TL does not show enough large difference between BPH patents and control samples in blood cells. An average mtDNA CN in BPH patients’ blood cells are 26.2% higher than in control blood cells, P=0.0097. mtDNA CN in BPH prostate tissue are 99.90% higher than in BPH blood cells, P<0.0001. As mtDNA CN difference is statistically significant between BPH blood samples and control samples it might be used as a marker for BPH characterization in blood cells.

Conclusions: The pilot project explored potential importance of mtDNA CN in the development of clinical significant BPH. Need for further research in specific conclusions. In our study TL from the BPH patient’s blood cells nenozimigsbe does not show enough large difference between BPH patents and control samples in blood cells.