Inflammatory Pathways from Benign Prostatic Hyperplasia to Prostate Cancer - in Search of New Therapeutic Options

Janiczek-Polewska M, Szylberg L, Antosik P, Kasperska A, Malicki J and Marszałek A

Department of Clinical Oncology, Greater Poland Cancer Center, Poland
Department of Tumor Pathology and Pathomorphology, Franciszek Łukaszczyk Memorial Hospital, Poland
Department of Obstetrics, Gynecology and Oncology, Nicolaus Copernicus University in Torun, Poland
Department of Clinical Pathomorphology, Nicolaus Copernicus University in Torun, Poland
Department of Electroradiology, Poznan University of Medical Sciences, Poland
Department of Clinical Pathology, Poznan University of Medical Sciences and Greater Poland Cancer Center, Poland
These authors contributed equally to this work

^*Correspondance to: Marlena Janiczek-Polewska 

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Abstract:

Introduction: The inflammatory process has impact on tumor cells development or anti-tumor responses. Inadequate innate or acquired stimulation of the immune system can cause chronic inflammation that can lead to oncogenesis. Benign Prostatic Hyperplasia (BPH) and Prostate Cancer (PCa) can be combined at the cellular and molecular level on hormonal, genetic and inflammatory platforms, suggesting that these prostate diseases share common pathophysiological factors. Aim: The aim of the study is to retrospectively assess the histological material of BPH and PCa with divided into few groups using the Gleason score and correlation with inflammatory factors. The evaluation of the expression of pro-inflammatory factors such as IL-17A, IL-17F, IL-17RA, IL-17RC, AKT1, C/EBPbeta, TRAF-6 and NF-kB made it possible to assess the influence of the inflammatory process on the development of BPH with regards to their PCa risk. Material and Method: Studies were carried out on archival tissue material in the form of paraffin blocks of 40 men with PCa after radical prostatectomy. The control group was 10 men with Benign Prostatic Hyperplasia (BPH). The material was obtained by the Transurethral Resection of the Prostate (TURP). The immunohistochemistry was performed on the material using specific primary antibodies against IL-17A, IL-17F, IL-17RA, IL-17RC, ACT1, TRAF-6, C/EBPbeta and NF- kB. The expression of the antibody was examined using the light microscopy and the Remmele Stegner score (IRS). Statistical analysis was performed using the non-parametric Kruskal-Walli’s test. Results: In statistical analysis, it was shown that the inflammatory pathway IL17A/IL-17RC/TRAF6/ NF-kB and IL17A/IL-17RC/AKT1/NF-kB occurs in both BPH and PCa. IL-17RA did not show expression in any group of patients and in the control group. In addition, along with the increase in the grading of Gleason score, a decrease in the expression of the tested inflammatory parameters was demonstrated. Summary and Conclusion: The inflammatory process has an impact on the BPH and PCa. The presence of the inflammatory pathways IL17A/IL-17RC/TRAF6/NF-kB and IL17A/IL-17RC/ AKT1/NF-kB in BPH with increased risk to development of PCa. The inflammatory process correlated with increased risk to development of PCa with a lower histological grade according to Gleason score.

Keywords:

Prostate cancer; Benign prostatic hyperplasia; Cytokines; Pathogenesis; Cancer immunology

Cite the Article:

Janiczek-Polewska M, Szylberg L, Antosik P, Kasperska A, Malicki J, Marszałek A. Inflammatory Pathways from Benign Prostatic Hyperplasia to Prostate Cancer - in Search of New Therapeutic Options. Clin Oncol. 2023;8:2024..