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Re: CMTM3 Inhibits Human Testicular Cancer Cell Growth through Inducing Cell-Cycle Arrest and Apoptosis
706
MALE AND FEMALE SEXUAL FUNCTION AND DYSFUNCTION; ANDROLOGY
Male and Female Sexual Function and Dysfunction; Andrology Re: Urinary Incontinence and Erectile Dysfunction after Robotic versus Open Radical Prostatectomy: A Prospective, Controlled, Nonrandomised Trial €ng, T. Thorsteinsdottir, E. Haglind, S. Carlsson, J. Stranne, A. Wallerstedt, U. Wildera M. Lagerkvist, J. E. Damber, A. Bjartell, J. Hugosson, P. Wiklund and G. Steineck; LAPPRO Steering Committee Department of Surgery and Division of Clinical Cancer Epidemiology, Department of Oncology, Institute of Clinical Sciences, Sahlgrenska Academy, University of Gothenburg and Sahlgrenska University Hospital, Go¨teborg, Department of Molecular Medicine and Surgery, Section of Urology, and Department of Oncology and Pathology, Division of Clinical Cancer Epidemiology, Karolinska Institutet and UroClinic, Stockholm and Department of Urology, Ska˚ne University Hospital, Lund University, Malmo¨, Sweden, and Faculty of Nursing, School of Health Sciences, University of Iceland, Reykjavı´k, Iceland Eur Urol 2015; Epub ahead of print.
Abstract for this article http://dx.doi.org/10.1016/j.juro.2015.06.061 available at http://jurology.com/ Editorial Comment: Robot-assisted laparoscopic radical prostatectomy (RALP) has become widely used without high grade evidence of superiority regarding long-term clinical outcomes compared to open retropubic radical prostatectomy (RRP), the gold standard. These authors describe patient reported urinary incontinence and erectile dysfunction (ED) 12 months after RALP or RRP. This was a prospective, controlled, nonrandomized trial of patients undergoing prostatectomy at 14 centers using RALP or RRP. Clinical record forms and validated patient questionnaires at baseline and 12 months postoperatively were collected. Of 2,625 eligible men 2,431 (93%) could be evaluated for the primary end point. At 12 months after RALP 366 men (21.3%) were incontinent, as were 144 (20.2%) after RRP (adjusted OR 1.08, 95% CI 0.87e1.34). ED was observed in 1,200 men (70.4%) 12 months after RALP and in 531 (74.7%) after RRP (adjusted OR 0.81, 95% CI 0.66e0.98). The frequency of positive surgical margins did not differ significantly between the groups, at 21.8% in the RALP group and 20.9% in the RRP group (adjusted OR 1.09, 95% CI 0.87e1.35). In a Swedish setting RALP for prostate cancer was modestly beneficial in preserving erectile function compared to RRP, without a statistically significant difference regarding urinary incontinence or surgical margins. These data highlight important outcomes of RALP vs RPP concerning urinary incontinence and ED. There seem to be minimal differences based on these data. Allen D. Seftel, MD
Suggested Reading Hartz A, He T, Strope S et al: Surgeon variation in patient quality of life after radical prostatectomy. J Urol 2013; 189: 1295.
Urological Oncology: Testis Cancer and Advances in Oncologic Therapy Re: CMTM3 Inhibits Human Testicular Cancer Cell Growth through Inducing Cell-Cycle Arrest and Apoptosis Z. Li, J. Xie, J. Wu, W. Li, L. Nie, X. Sun, A. Tang, X. Li, R. Liu, H. Mei, F. Wang, Z. Wang, Y. Gui and Z. Cai Shenzhen Key Laboratory of Genitourinary Tumor, Shenzhen Second People’s Hospital, First Affiliated Hospital of Shenzhen University, and Department of Clinical Laboratory and Guandong Key Laboratory of Male Reproductive Medicine and Genetics, Peking University Shenzhen Hospital, Shenzhen PKU-HKUST Medical Center, Shenzhen, Department of Urology, Suzhou Municipal Hospital, Suzhou, Anhui and Department of Urology, Second Hospital of Lanzhou University, Lanzhou, China PLoS One 2014; 9: e88965.
TESTIS CANCER AND ADVANCES IN ONCOLOGIC THERAPY
707
Abstract for this article http://dx.doi.org/10.1016/j.juro.2015.06.010 available at http://jurology.com/ Editorial Comment: Molecular mechanisms operating in testicular germ cell tumors are not fully understood. CMTM3, a transmembrane domain belonging to the chemokine-like factor gene superfamily, is one of several chemokine-like factor genes located in a cluster on chromosome 16q22. CMTM3 is highly expressed in the male reproductive system, with the greatest expression level in the testis. Studies have indicated that several members of the CMTM superfamily have an important role in tumorigenesis, especially in the male reproductive system. The authors used a human seminoma cell line as well as matched pairs of testicular cancer tissue and noncancerous testicular tumor from patients undergoing primary surgery. CMTM3 was frequently down-regulated in testicular cancer cell lines but highly expressed in normal testis tissue. Reexpression of CMTM3 suppressed colony formation, proliferation and migration capacity by inducing G2 cycle arrest and apoptosis. Downregulation of CMTM3 in clinical tumor tissues was associated with the methylation of a single CpG site in the core promoter. These results indicate that CMTM3 can function as a tumor suppressor through induction of cell cycle arrest and apoptosis. This finding may have implications in the development of additional treatments for patients with testicular cancer. Jerome P. Richie, MD
MALE AND FEMALE SEXUAL FUNCTION AND DYSFUNCTION; ANDROLOGY
Male and Female Sexual Function and Dysfunction; Andrology Re: Urinary Incontinence and Erectile Dysfunction after Robotic versus Open Radical Prostatectomy: A Prospective, Controlled, Nonrandomised Trial €ng, T. Thorsteinsdottir, E. Haglind, S. Carlsson, J. Stranne, A. Wallerstedt, U. Wildera M. Lagerkvist, J. E. Damber, A. Bjartell, J. Hugosson, P. Wiklund and G. Steineck; LAPPRO Steering Committee Department of Surgery and Division of Clinical Cancer Epidemiology, Department of Oncology, Institute of Clinical Sciences, Sahlgrenska Academy, University of Gothenburg and Sahlgrenska University Hospital, Go¨teborg, Department of Molecular Medicine and Surgery, Section of Urology, and Department of Oncology and Pathology, Division of Clinical Cancer Epidemiology, Karolinska Institutet and UroClinic, Stockholm and Department of Urology, Ska˚ne University Hospital, Lund University, Malmo¨, Sweden, and Faculty of Nursing, School of Health Sciences, University of Iceland, Reykjavı´k, Iceland Eur Urol 2015; Epub ahead of print.
Abstract for this article http://dx.doi.org/10.1016/j.juro.2015.06.061 available at http://jurology.com/ Editorial Comment: Robot-assisted laparoscopic radical prostatectomy (RALP) has become widely used without high grade evidence of superiority regarding long-term clinical outcomes compared to open retropubic radical prostatectomy (RRP), the gold standard. These authors describe patient reported urinary incontinence and erectile dysfunction (ED) 12 months after RALP or RRP. This was a prospective, controlled, nonrandomized trial of patients undergoing prostatectomy at 14 centers using RALP or RRP. Clinical record forms and validated patient questionnaires at baseline and 12 months postoperatively were collected. Of 2,625 eligible men 2,431 (93%) could be evaluated for the primary end point. At 12 months after RALP 366 men (21.3%) were incontinent, as were 144 (20.2%) after RRP (adjusted OR 1.08, 95% CI 0.87e1.34). ED was observed in 1,200 men (70.4%) 12 months after RALP and in 531 (74.7%) after RRP (adjusted OR 0.81, 95% CI 0.66e0.98). The frequency of positive surgical margins did not differ significantly between the groups, at 21.8% in the RALP group and 20.9% in the RRP group (adjusted OR 1.09, 95% CI 0.87e1.35). In a Swedish setting RALP for prostate cancer was modestly beneficial in preserving erectile function compared to RRP, without a statistically significant difference regarding urinary incontinence or surgical margins. These data highlight important outcomes of RALP vs RPP concerning urinary incontinence and ED. There seem to be minimal differences based on these data. Allen D. Seftel, MD
Suggested Reading Hartz A, He T, Strope S et al: Surgeon variation in patient quality of life after radical prostatectomy. J Urol 2013; 189: 1295.
Urological Oncology: Testis Cancer and Advances in Oncologic Therapy Re: CMTM3 Inhibits Human Testicular Cancer Cell Growth through Inducing Cell-Cycle Arrest and Apoptosis Z. Li, J. Xie, J. Wu, W. Li, L. Nie, X. Sun, A. Tang, X. Li, R. Liu, H. Mei, F. Wang, Z. Wang, Y. Gui and Z. Cai Shenzhen Key Laboratory of Genitourinary Tumor, Shenzhen Second People’s Hospital, First Affiliated Hospital of Shenzhen University, and Department of Clinical Laboratory and Guandong Key Laboratory of Male Reproductive Medicine and Genetics, Peking University Shenzhen Hospital, Shenzhen PKU-HKUST Medical Center, Shenzhen, Department of Urology, Suzhou Municipal Hospital, Suzhou, Anhui and Department of Urology, Second Hospital of Lanzhou University, Lanzhou, China PLoS One 2014; 9: e88965.
TESTIS CANCER AND ADVANCES IN ONCOLOGIC THERAPY
707
Abstract for this article http://dx.doi.org/10.1016/j.juro.2015.06.010 available at http://jurology.com/ Editorial Comment: Molecular mechanisms operating in testicular germ cell tumors are not fully understood. CMTM3, a transmembrane domain belonging to the chemokine-like factor gene superfamily, is one of several chemokine-like factor genes located in a cluster on chromosome 16q22. CMTM3 is highly expressed in the male reproductive system, with the greatest expression level in the testis. Studies have indicated that several members of the CMTM superfamily have an important role in tumorigenesis, especially in the male reproductive system. The authors used a human seminoma cell line as well as matched pairs of testicular cancer tissue and noncancerous testicular tumor from patients undergoing primary surgery. CMTM3 was frequently down-regulated in testicular cancer cell lines but highly expressed in normal testis tissue. Reexpression of CMTM3 suppressed colony formation, proliferation and migration capacity by inducing G2 cycle arrest and apoptosis. Downregulation of CMTM3 in clinical tumor tissues was associated with the methylation of a single CpG site in the core promoter. These results indicate that CMTM3 can function as a tumor suppressor through induction of cell cycle arrest and apoptosis. This finding may have implications in the development of additional treatments for patients with testicular cancer. Jerome P. Richie, MD