METABOLIC SYNDROME AS A FACTOR OF PROSTATE CANCER PROGRESSION
DOI:
https://doi.org/10.32471/oncology.2663-7928.t-23-3-2021-g.9577Keywords:
biochemical relapse, bone metastases, metabolic syndrome, prostate cancerAbstract
Aim: to assess the metabolic syndrome (MS) effect on progression of local prostate cancer (PC) with intermediate and high progression risk after radical prostatectomy (RP). Object and methods: The study included 106 patients with benign and malignant neoplasms of the prostate with the average age of 61.3 ± 5.4 years, who underwent inpatient treatment and follow-up at the National Cancer Institute. Eighty-one patients were diagnosed with local prostate cancer stage II-III, Grade group (GG) 2–5; 25 patients had benign prostatic hyperplasia (BPH). The patients were divided into 3 groups: 1 group — patients with intermediate progression risk, GG 2–3; group 2 — patients with high progression risk, GG 4-5; patients with BPH were in the control group. The patients underwent radical prostatectomy with standard pelvic lymph dissection or Stakhovsky adenomectomy/transurethral resection of the prostate based on medical indications. Before the surgery and every 3 months after it, patients were examined using general clinical, biochemical and instrumental methods. Statistical analysis of the results was performed based on the approaches of variation statistics using Statistica 6.0 software. Differences at p<0.05 were considered as statistically significant. Results: according to the international criteria for determining the MS, examined patients were divided into two groups: MS+ (n = 52; 49.0%) and MS– (n = 54; 51.0%). In the patients with MS, disease prolongation with the development of bone metastases was registered in 26.3% patients in the group I (PC, GG 2–3) and in 61.9% patients in the group II (PC, GG 4–5) versus 14.2% (group I) and 45% (group II) patients without MS. In the group I, the time to bone metastasis appearance was 39.1 months in MS+ versus 44.3 months in MS– patients. In the group II (patients with high progression risk), the development of bone metastases in MS+ and MS– patients was registered after, respectively, 11.6 and 14.5 months post-operatively. Conclusions: the obtained results point to the impact of MS on the development of PC bone metastases. Meanwhile, MS does not affect the development of biochemical relapse in these patients.
References
Cancer in Ukraine, 2019-2020. Incidence, mortality, activities of oncological service. Bull Nat Cancer Registry Ukr, № 22, Kyiv, 2020.
International Agency for Research on Cancer -The Global Cancer Observatory – Prostate Cancer 2019. https://gco.iarc.fr/today/data/factsheets/cancers/27-Prostate-fact-sheet.pdf.
Simmons MN, Stephenson AJ, Klein EA. Natural history of biochemical recurrence after radical prostatectomy: risk assessment for secondary therapy. Eur Urol 2007, 51 (5): 1175–84.
Han M, Partin AW, Zahurak M, et al. Biochemical (prostate specific antigen) recurrence probability following radical prostatectomy for clinically localized prostate cancer. J Urol 2003; 169 (2): 517–23.
NCCN Guidelines Insights: Prostate Cancer, Version 1. 2021.
Keum N, Greenwood DC, Lee DH, et al. Adult weight gain and adiposity-related cancers: a dose-response meta-analysis of prospective observational studies. J Natl Cancer Institute 2015; 107 (2): 284–91.
Ma J, Li H, Giovannucci E. Prediagnostic body-mass index, plasma C-peptide concentration, and prostate cancer-specific mortality in men with prostate cancer: a long-term survival analysis. Lancet Oncol 2008; 9 (11): 1039–47.
Belfiore A, Frasca F, Pandini G, et al. Insulin receptor isoforms and insulin receptor/insulin-like growth factor receptor hybrids in physiology and disease. Endocr Rev 2009; 30 (6): 586–623.
Mounier C, Posner BI. Transcriptional regulation by insulin: from the receptor to the gene. Can J Physiol Pharmacol 2006; 84 (7): 713–24.
Lubik AA, Gunter JH, Hendy SC, et al. Insulin increases de novo steroidogenesis in prostate cancer cells. Cancer Res 2011; 71 (17): 5754–64.
Lubik AA, Gunter JH, Hollier BG, et al. IGF2 increases de novo steroidogenesis in prostate cancer cells. Endocr Relat Cancer 2013; 20 (2): 173–86.
Huang CY, Yu HS, Lai TY, et al. Leptin increases motility and integrin up-regulation in human prostate cancer cells. J Cell Physiol 2011; 226 (5): 1274–82.
Collins CC, Volik SV, Lapuk AV, et al. Next generation sequencing of prostate cancer from a patient identifies a deficiency of methylthioadenosine phosphorylase, an exploitable tumor target. Mol Cancer Ther 2012; 11 (3): 775–83.
Iyer A, Fairlie DP, Prins JB, et al. Inflammatory lipid mediators in adipocyte function and obesity. Nat Rev Endocrinol 2010; 6 (2): 71–82.
Calder PC, Ahluwalia N, Browns F, et al. Dietary factors and low-grade inflammation in relation to overweight and obesity. Br J Nutr 2011; 106: S1–S78.
Khosla S. Minireview. The OPG/RANKL/RANK system. Endocrinol 2001; 142: 5050–5.
Campos RM, de Piano A, da Silva PL, et al. The role of pro/anti-inflammatory adipokines on bone metabolism in NAFLD obese adolescents: Effects of long-term interdisciplinary therapy. Endocrine 2012; 42: 146–56.
Sierra-Honigmann MR, Nath AK, Murakami C, et al. Biological action of leptin as an angiogenic factor. Science 1998; 281: 1683–6.
Cao JJ. Effects of obesity on bone metabolism. J. Orthop. Surg. Res. 2011, 6, 30.
Epstein JI, Egevad L, Amin MB, et al. The 2014 International society of urological pathology (ISUP) consensus conference on Gleason grading of prostatic carcinoma: definition of grading patterns and proposal for a new grading system, Am J Surg Pathol 2016; 40 (2): 244–52.
