Chun-Te Wu

Education ● MD, Taipei Medical University, Taiwan ● PhD, Graduate Institute of Clinical Medical Science, Chang Gung University, Taoyuan, Taiwan Experiences ● Attending staff, Department of urology, Chang Gung Memorial Hospital, Taoyuan, Taiwan ● Post-doc, research fellow, Department of pathology, George H. Whipple Laboratory of Cancer, Research University of Rochester Medical, Center Rochester, NY, USA ● Chief, Division of urology, Chang Gung Memorial Hospital, Keelung, Taiwan ● Vice Chairman, Department of Surgery, Chang Gung Memorial Hospital, Keelung, Taiwan ● Chairman, Department of Surgery, Chang Gung Memorial Hospital, Keelung, Taiwan Current Appointment ● Superintendent, Chang Gung Memorial Hospital Keelung, Taiwan ● Deputy superintendent, Chang Gung Memorial Hospital Linkou, Taiwan ● Professor, School of Medicine, Chang Gung University

15th August 2025

Time Session
10:30
12:00
  • John DavisUnited States Speaker Open Surgery Training: Is It Necessary in the Era of Robotics?Open surgery training in the era of robotics may or may not be a training environment that urology has control of, given worldwide access to robotic or at least laparoscopic techniques and strong patient preference. There may be some applications where a given experienced urologist can prefer open over minimally invasive surgery (MIS), such as radical cystectomy, or indications possibly outside of MIS feasibility such as large renal tumors with caval thrombus. Specific to training and expertise, there are 3 principle features of surgical skills desired: 1) knowing ideal exposure, 2) recognition of surgical planes, and 3) knowing anatomy before it can be seen. Although some trainees may only see MIS for certain indications, open surgery may expedite the process. There are no human studies identified on the topic, but a skills lab study was instructive (Farah, J Surgical Education 2023) showing that interns with open and MIS training performed higher comparing pre-intern to post intern bootcamp skills. The benefits of a solid training pathway including open experience are to move trainees towards the faster-to-progress part of the learning curve such that the attending can offer a safe training environment while moving the case along efficiently.The Future of Surgical Skills Evaluation: What Is on Your Wish List?Surgical skills training vary significantly by region with some systems putting trainees on a timed set of years, while others apprentice trainees until meeting a threshold for skills. Early training assessments were basic timed events with qualitative scores (subject to strong attending selection for success). Trainees should experience and/or study the key pitfalls to avoid and performance goals. Surgical simulation can be highly useful, but tend to improve only certain skills and not full case needs. Updated simulation moves from digital to hands on surgical models and may move the needle towards human experience. Training can be augmented with descriptors of surgical gestures and measuring which ones are most effective. The experience for the trainee is often depicted as an "autonomy gap" whereby the training desires to have case control, possibly before they are ready. Progression can be measured by descriptors of performance from assistance through full performance without coaching. The next frontier will be artificial intelligence guided measurement where specific performances can be characterized and diagnosed for success. My ultimate wishlist would be for methods to correlate skills to outcomes, optimized curricula, and a specific pathway to correct underperformance.Tips and Tricks in Challenging Cases of Robotic Radical ProstatectomyThere are many specific challenges with robotic radical prostatectomy (RARP) that can be described and illustrated--the most 5 common are 1) difficulty access, 2) obesity, 3) pubic arch interference, 4) anatomic challenges, and 5) reconstruction challenges. In this video sample, we demonstrate 2 challenges: obesity requiring a pelvic lymph node dissection and significant pelvic de-fatting to identify the proper surgical landmarks. Next a massive sized prostate that has had a partial transurethral resection--together presenting challenges with landmarks, a difficult bladder neck to diagnose, and final reconstruction challenges.
  • Chun-Te WuTaiwan Moderator 健保各領域審查共識及討論-泌尿腫瘤
    Véronique PhéFrance Speaker New Artificial Urinary SphinterStress urinary incontinence remains a major quality-of-life concern, particularly following pelvic surgery. Despite being the gold standard, the AMS 800 artificial urinary sphincter (AUS) presents significant limitations, including mechanical failure, urethral atrophy, and challenges for elderly or disabled patients. Recent innovations in AUS design now incorporate mechatronics, remote control, adaptive pressure systems, and miniaturized components aimed at improving usability, autonomy, and continence outcomes. This presentation reviews the current landscape of next-generation AUS, focusing on ARTUS, UroActive®, and other devices under clinical evaluation. We discuss preclinical and first-in-human data, regulatory pathways, patient-reported preferences, and remaining barriers such as infection risks and training requirements. Intelligent, connected AUS devices hold promise to transform continence care after decades of technological stagnation.Choosing between Laparoscopic Sacrocolpopexy and Lateral Suspension: Weighing the Pros and ConsPelvic organ prolapse (POP) is a common condition requiring surgical intervention to restore apical support. Among minimally invasive options, laparoscopic sacrocolpopexy (LSCP) remains the gold standard, while laparoscopic lateral suspension (LLS) is gaining renewed interest for its reduced invasiveness and simplified technique. This presentation compares LSCP and LLS across multiple dimensions: anatomical restoration, functional outcomes, complication profiles, patient selection, and surgical learning curves. LSCP offers robust long-term results and better posterior compartment support but carries increased operative complexity. LLS provides effective anterior/apical correction with fewer vascular risks and a shorter learning curve. Both techniques have comparable mesh exposure rates and subjective success. Individualized decision-making based on patient anatomy, comorbidities, and surgeon expertise remains key. Emerging technologies and robotic assistance may further refine these approaches in the future.Robotic Novel Artificial Urinary Sphincter ImplantationThis video shows a step by step robotic artificial urinary sphincter implantation in women using AMS800 and Artus devices.First robot-assisted implantation of ARTUS (Affluent Medical) electromechanical artificial urinary sphincter in a female cadaverIntroduction Artificial urinary sphincters (AUS) are effective tools for the treatment of female stress urinary incontinence. Nonetheless, hydraulic sphincters present with some limitations: complex and time-consuming preparation, need for preserved manual dexterity and constant pressure exertion on the bladder neck. The ARTUS® Artificial Urinary Sphincter is a novel electro-mechanical device designed to overcome these limitations thanks to its rapid and straight-forward implantation, intuitive remotely controlled manipulation and continuously adjustable cuff pressure. Materials and methods The ARTUS® system is currently under pre-market investigation in men, in an interventional, prospective, single arm, multicentric, international study. A cadaver lab session was carried out in Decembre 2024 to test the technical feasibility of ARTUS® implantation in female patients. The procedure was performed by an expert surgeon with extensive experience in AUS implantation and robotic surgery. Results One female patient was successfully implanted during the session. The technique has been developed following the principles of the traditional robot-assisted AUS implantation: the patient is placed in gynecological 23° Trendelenburg position. The robot has a 4-arms configuration. The procedure starts with the dissection of the vesicovaginal plane, to approach the bladder neck posteriorly. The lateral surfaces of the bladder neck are developed on both sides. The anterior peritoneum is opened to gain access to the antero-lateral surfaces of the bladder. The separation of the bladder neck from the vagina is performed through dissection of the pre-vaginal fascia bilaterally. The cuff is introduced and it is passed through the antero-lateral peri-vesical spaces, sliding behind the bladder neck from the right side to the left side. The anterior peritoneum is opened to gain access to the anterior surface of the bladder neck. The cuff is closed anteriorly, passing the transmission line inside the hole at the distal part of the cuff. The tightening around the bladder neck is achieved by pulling the transmission cable through. An optimal adjustment of the cuff around the bladder neck is provided tightening the ARTUS cuff clamping notch. Then, a supra-pubic 4 cm skin incision is made to implant the control unit. The tip of the cuff is passed outside through the incision. A lodge is prepared incising along the external oblique muscle aponeurosis. The cuff is connected to the control unit and a test with the remote control is performed to verify the functioning of the system. Finally, the control unit is placed into the lodge, anchored with non-absorbable sutures to the aponeurosis. Conclusions Robot-assisted ARTUS® implantation is technically feasible in female patients. This straight-forward technique may reduce operative time. The device has the potential to reduce the pressure and facilitate manipulation in patients with impaired dexterity.
  • David WinkleAustralia Moderator Meatal and Fossa Navicularis Stricture Due to Lichen Sclerosus
    Howard GoldmanUnited States Speaker Anti-Cholinergics: Does Treating the Bladder Put the Brain at Risk?Recent evidence suggests an association between Overactive Bladder Anticholinergic medication and dementia. Do these medications really increase one's risk of dementia. We will examine the evidence.Surgical Treatments for Recurrent SUI/POPEven the best of surgeon's will have patients who have recurrence after a stress incontinence or pelvic organ prolapse procedure. If the recurrent is bothersome the patient may need repeat surgery. How to decide on the ideal surgery for recurrent symptoms will be examined
  • Tai-Lung ChaTaiwan Speaker Novel Target for GU Cancer Metastasis and TherapeuticsCancer progression is shaped by both cell-intrinsic adaptations and complex extrinsic interactions within the tumor microenvironment (TME). Here, we identify a transmembrane protein, Meta1, as a shared therapeutic target that exhibits a Janus-like role: promoting malignant phenotypes in cancer cells while restraining tumor-supportive functions in non-cancerous stromal and immune cells. Meta1 is expressed in both compartments of the TME, orchestrating a dual program that supports metastasis and immune evasion. Mechanistically, we uncovered a malignancy-promoting factor (MPF) that acts as a functional ligand for Meta1, selectively enhancing pro-invasive signaling in cancer cells. We further identify Meta1 as an unconventional G protein–coupled receptor (GPCR) that plays as an accelerator in cancer cells of the TME. Meta1 interacts with Rho-GDI and Gαq to activate RhoA-mediated cytoskeletal remodeling and amoeboid migration, facilitating metastatic dissemination. We further identify MPF binding to Meta1 initiates Gβγ signaling, elevating intracellular cAMP and activating Rap1, thereby amplifying cell motility and metastatic potential. Leveraging the Meta1–MPF interaction, we designed MPF-derived peptides that specifically bind Meta1 and serve as the basis for a novel peptide-based PROTAC, which efficiently induces degradation of Meta1 and abrogates its pro-metastatic functions. Our study unveils Meta1 as an atypical GPCR with canonical signaling capacity and topological divergence, representing a shared and targetable vulnerability that bridges cancer cell-intrinsic adaptation with extrinsic TME communication. These findings establish the Meta1–MPF axis as a compelling therapeutic target for suppressing metastasis and reprogramming the TME.
  • En MengTaiwan Moderator
    Chun-Hou LiaoTaiwan Speaker Regeneration Medicine in Urology - A Promising Future or Hoax?Regenerative medicine comprises therapeutic strategies aimed at restoring tissue structure and function, rather than merely alleviating symptoms. By deploying cells, biomaterials, bioactive molecules, or combinations thereof, these interventions stimulate the body’s intrinsic repair mechanisms. This paradigm extends beyond traditional symptomatic treatment, offering the potential for true self-healing and organ reconstruction—ultimately prioritizing cure over chronic disease management. Cell-based therapy has emerged as a promising intervention for various urogenital disorders, including erectile dysfunction (ED), bladder dysfunction, and male infertility. Current clinical research primarily focuses on mesenchymal stem cells (MSCs), investigating their safety, tolerability, and preliminary efficacy. Although early-phase studies suggest functional benefits—such as improved hemodynamics and tissue regeneration—most programs remain in preclinical or early clinical stages. A critical limitation remains the lack of standardization in MSC source, dose, and delivery route. Among alternative sources, human amniotic fluid-derived stem cells (hAFSCs) have shown particular promise. In preclinical models of cavernous nerve injury, hAFSCs demonstrated prolonged retention in penile tissue and in-situ differentiation into α-smooth muscle actin-positive corporal smooth muscle cells, effectively replacing damaged tissue and restoring function. These findings represent an encouraging step toward curative therapy. However, the mechanisms governing their in vivo behavior—such as engraftment, differentiation, and immunogenicity—will ultimately determine their clinical translatability and therapeutic stability. Whether cell-based approaches can evolve from experimental platforms into routine clinical care remains a central question. Platelet-Rich Plasma (PRP) Platelet-rich plasma (PRP) is an autologous biologic product enriched with supraphysiologic levels of platelets, growth factors, chemokines, and extracellular vesicles. Upon activation, PRP releases a bioactive cocktail that promotes angiogenesis, neuroregeneration, and antifibrotic remodeling—key processes in the restoration of urogenital tissues. In rodent models of cavernous nerve injury, PRP has been shown to preserve corporal sinusoidal endothelial cells and axonal scaffolds, while restoring erectile hemodynamics. Clinical studies further support PRP's safety in humans and report variable but promising improvements in IIEF scores following intracavernous injection. Nevertheless, the therapeutic response appears heterogeneous, likely influenced by patient factors, PRP preparation techniques, and injection protocols. Beyond ED, PRP has shown potential in other urologic indications such as stress urinary incontinence (SUI), interstitial cystitis/bladder pain syndrome (IC/BPS), and chronic pelvic pain, where it may contribute to tissue regeneration and symptom relief. However, broader adoption will require the establishment of individualized blood-quality metrics, standardized preparation methods, and randomized controlled trials demonstrating durable benefit. Emerging Regenerative Strategies Beyond cell-based and autologous biologics, a suite of innovative regenerative technologies is progressing from bench to bedside. These include: Energy-based devices such as low-intensity extracorporeal shock wave therapy (Li-ESWT), which promotes neovascularization and tissue regeneration via mechanotransduction pathways. Gene therapies, targeting dysfunctional or absent proteins in disorders like overactive bladder. Smart biomaterials, capable of delivering cells or bioactive molecules in a controlled, responsive manner. Extracellular vesicle (EV)-based therapeutics, which leverage cell-free vesicles derived from MSCs or urine-derived stem cells. These EVs carry signaling molecules (e.g., microRNAs, cytokines, growth factors) that mimic the paracrine effects of stem cells, offering a potentially safer and more scalable alternative to cell transplantation. In preclinical models of ED and bladder dysfunction, EVs have demonstrated the capacity to promote smooth muscle regeneration, nerve sprouting, and fibrosis reduction, with functional improvements comparable to stem cell therapy. Regenerative medicine has propelled the field of urologic tissue repair from theoretical promise to an early clinical reality. While substantial challenges remain—including the need for deeper mechanistic insight, protocol standardization, and regulatory clarity—the field is advancing rapidly. The convergence of cell therapy, PRP, EVs, and device-based modalities is creating a multifaceted toolkit for urologic regeneration. With continued scientific rigor, large-scale clinical trials, and interdisciplinary collaboration, regenerative medicine holds the potential to shift urologic care from chronic symptomatic management to durable, tissue-level cure.Stem Cell Therapy: Advancements and Clinical Insights for Erectile Dysfunction Treatment Erectile dysfunction (ED)—defined as the persistent inability to achieve or maintain an erection sufficient for satisfactory sexual activity—affects over 150 million men worldwide. While phosphodiesterase-5 inhibitors (PDE5is) remain the first-line treatment, many patients, particularly those with diabetes, age-related vascular decline, or neuropathy following radical prostatectomy, show suboptimal responses. Consequently, regenerative medicine—particularly stem-cell therapy—has gained interest for its potential to address the root causes of ED rather than merely managing symptoms. Stem-cell therapy offers a multifaceted approach to treating ED through neuroregeneration, angiogenesis, anti-apoptotic signaling, and fibrosis inhibition. Once introduced into the target tissue, stem cells can differentiate into specific cell types or exert paracrine effects via secretion of growth factors and extracellular vesicles. Among the various sources studied, bone marrow-derived mesenchymal stem cells (BM-MSCs), adipose-derived stem cells (ADSCs), and umbilical cord-derived MSCs (UC-MSCs) have been most extensively explored. Preclinical studies consistently demonstrate that MSC-based therapies enhance cavernous nerve regeneration, suppress fibrosis, and preserve endothelial integrity. In rat models of diabetes- or nerve-injury-induced ED, intracavernosal injections of ADSCs or BM-MSCs significantly restore intracavernosal pressure (ICP) and improve corpus cavernosum histology. Phase I/II clinical trials also support the safety and preliminary efficacy of stem-cell approaches. For example, in men with diabetic ED treated with autologous BM-MSCs, significant improvements in International Index of Erectile Function-5 (IIEF-5) scores and penile arterial flow have been reported without major adverse events. Similarly, ADSC therapy in post-prostatectomy ED has shown encouraging short-term results. However, large-scale trials are needed to clarify long-term efficacy, immune responses, and safety profiles. Human amniotic fluid stem cells (hAFSCs) represent a promising alternative, offering characteristics that bridge embryonic and adult stem-cell profiles. These include broad multipotency, high proliferation, and low immunogenicity—traits ideal for allogeneic use and neuroregenerative purposes. Notably, hAFSCs secrete potent regenerative mediators such as brain-derived neurotrophic factor (BDNF), vascular endothelial growth factor (VEGF), and insulin-like growth factor-1 (IGF-1), all of which support neurovascular repair and smooth muscle integrity. Our recent studies demonstrate, for the first time, that hAFSCs persist long-term in penile tissue and can differentiate into cavernous smooth-muscle cells, effectively replacing damaged tissue and improving erectile function even in chronic neurogenic ED models. Despite these advantages, our findings did not reveal in-vivo homing of hAFSCs to nerve injury sites or differentiation into neural tissue. This suggests a need for future studies to identify the specific microenvironmental cues required to induce such responses. Additionally, combining hAFSCs with platelet-rich plasma (PRP) may provide synergistic benefits—enhancing stem-cell homing, paracrine signaling, and in-vivo differentiation—thereby advancing a more effective, scalable, and safe therapeutic strategy.
  • Yao-Chi ChuangTaiwan Moderator Road to Excellent ResearchYao Chi Chuang, Professor of Urology, Kaohsiung Chang Gung Memorial Hospital, and National Sun Yat-sen University Taiwan. Medical research is what allows doctors to explore unmet medical need and decide how to best treat patients. It is what makes the development of new diagnostic tools, new biomarkers, new medicines, and new procedures. Without medical research, we would not be able to creative new knowledge and decide if new treatments are better than our current treatments. There are some Tips on what to do about what research is and how to get into it: 1. Ask a good question from your daily practice, what is unmet medical need? 2. Search the old literature of your research interests- what is known? What is unknown? 3. Find a new method to solve your question or an old method but applying to a new field. 4. Start from jointing a pre-planned research project, and join a research collaborative. 5. Try to be an independent researcher from a small project without funding support, retrospective study. 6. Try to get funding support from your institute, national grant, or industry. As a young doctor, it’s important to look after yourself and maintain a healthy balance between daily practice and research work. There is a range of options for doctors interested in research, from smaller time commitments as a co-investigator to longer-term projects and experience as chief investigator. Research works are all optional activities, so do what you can but don’t overwhelm yourself. Road to Excellent Research
    Chawnshang ChangUnited States Speaker The Roles of Androgen Receptor in Bladder and Kidney Cancers1- Study why prostate cancer (PCa) may develop to the castration-resistant PCa, and develop new therapy to overcome the CRPC. 2- Study the roles of androgen receptor in the bladder cancer early development and later metastasis stage. 3- Cloning the 2nd androgen receptor in the bladder cancer
TICC - 3F Banquet Hall
15:30
17:00
Novel Advances (B): Bladder
Chun-Te WuTaiwan Moderator 健保各領域審查共識及討論-泌尿腫瘤
Jian-Ri LiTaiwan Moderator Applying Vision Augmentation in Robotic Surgery: Reality or FictionApplying Vision Augmentation in Robotic Surgery: Reality or Fiction
Seong Il SeoKorea (Republic of) Moderator Comparison of Remal Function between Radiofrequency Ablation versus Robot Assisted Laparoscopic Patial Nephrectomy for Small Renal Mass in Elderly PatientsComparison of renal function between radiofrequency ablation versus robot assisted laparoscopic partial nephrectomy for small renal mass in elderly patients Jiwoong Yu, Seongil Seo Sungkyunkwan University, Samsung Medical Center The incidence of small renal masses (SRMs) in patients ≥75 years has increased up to 30-fold [J Urol 2014]. In this age group, treatment should balance cancer control and renal function preservation. Robot-assisted partial nephrectomy (RAPN) and radiofrequency ablation (RFA) are two main options. RAPN offers excellent cancer control but requires general anesthesia and ischemia, which may pose risks in older patients. RFA is less invasive, avoids vascular clamping, and is often preferred for high-risk patients, as supported by EAU and AUA guidelines. RFA generally preserves renal function better [Front Oncol 2022], though outcomes vary by technique. At our center, RFA under general anesthesia with wide safety margins may compromise parenchymal preservation. While both approaches show favorable cancer control, RFA has a slightly higher recurrence rate. Pantelidou et al. reported 6 recurrences in 63 RFA cases vs. 1 in 63 RAPN cases [Cardiovasc Intervent Radiol 2016], and Park et al. reported 2-year recurrence-free survival (RFS) of 95.2% in RFA vs. 100% in RAPN [Eur Radiol 2018]. NCCN guidelines note that RFA may require repeat treatment to match surgical outcomes. Our institutional matched analysis (63 RAPN vs. 63 RFA) showed RFS of 100% vs. 95.2% (p = 0.029), and immediate eGFR preservation of 91.7% vs. 86.8% [Eur Radiol 2018;28:2979–2985]. A subsequent analysis of older patients presented at AUA 2024 included 137 patients aged ≥75, the rate of ≥25% eGFR decline at one year was 28.6% for RFA vs. 2.0% for RAPN (HR 11.3, p = 0.002), with 4 recurrences in RFA and none in RAPN. In conclusion, both RFA and RAPN are viable options for elderly patients with small renal masses. RFA is less invasive but may carry a slightly higher risk of recurrence and, depending on institutional technique, some degree of renal function loss. Treatment should be individualized based on tumor anatomy, patient condition, and institutional expertise.
TWTC - 1F Exhibition Hall

16th August 2025

Time Session
12:00
13:00
Redefining the Trajectory of Prostate Cancer
  • Tai-Lung ChaTaiwan Speaker Novel Target for GU Cancer Metastasis and TherapeuticsCancer progression is shaped by both cell-intrinsic adaptations and complex extrinsic interactions within the tumor microenvironment (TME). Here, we identify a transmembrane protein, Meta1, as a shared therapeutic target that exhibits a Janus-like role: promoting malignant phenotypes in cancer cells while restraining tumor-supportive functions in non-cancerous stromal and immune cells. Meta1 is expressed in both compartments of the TME, orchestrating a dual program that supports metastasis and immune evasion. Mechanistically, we uncovered a malignancy-promoting factor (MPF) that acts as a functional ligand for Meta1, selectively enhancing pro-invasive signaling in cancer cells. We further identify Meta1 as an unconventional G protein–coupled receptor (GPCR) that plays as an accelerator in cancer cells of the TME. Meta1 interacts with Rho-GDI and Gαq to activate RhoA-mediated cytoskeletal remodeling and amoeboid migration, facilitating metastatic dissemination. We further identify MPF binding to Meta1 initiates Gβγ signaling, elevating intracellular cAMP and activating Rap1, thereby amplifying cell motility and metastatic potential. Leveraging the Meta1–MPF interaction, we designed MPF-derived peptides that specifically bind Meta1 and serve as the basis for a novel peptide-based PROTAC, which efficiently induces degradation of Meta1 and abrogates its pro-metastatic functions. Our study unveils Meta1 as an atypical GPCR with canonical signaling capacity and topological divergence, representing a shared and targetable vulnerability that bridges cancer cell-intrinsic adaptation with extrinsic TME communication. These findings establish the Meta1–MPF axis as a compelling therapeutic target for suppressing metastasis and reprogramming the TME.
  • Declan MurphyAustralia Speaker PSMA PET Scan in Diagnosing Early/Advanced Localized Prostate Cancer Especially Comparing Various Radioactive Tracers
  • Ask The Experts Q&A
    Chun-Te WuTaiwan Moderator 健保各領域審查共識及討論-泌尿腫瘤
    Tai-Lung ChaTaiwan Moderator Novel Target for GU Cancer Metastasis and TherapeuticsCancer progression is shaped by both cell-intrinsic adaptations and complex extrinsic interactions within the tumor microenvironment (TME). Here, we identify a transmembrane protein, Meta1, as a shared therapeutic target that exhibits a Janus-like role: promoting malignant phenotypes in cancer cells while restraining tumor-supportive functions in non-cancerous stromal and immune cells. Meta1 is expressed in both compartments of the TME, orchestrating a dual program that supports metastasis and immune evasion. Mechanistically, we uncovered a malignancy-promoting factor (MPF) that acts as a functional ligand for Meta1, selectively enhancing pro-invasive signaling in cancer cells. We further identify Meta1 as an unconventional G protein–coupled receptor (GPCR) that plays as an accelerator in cancer cells of the TME. Meta1 interacts with Rho-GDI and Gαq to activate RhoA-mediated cytoskeletal remodeling and amoeboid migration, facilitating metastatic dissemination. We further identify MPF binding to Meta1 initiates Gβγ signaling, elevating intracellular cAMP and activating Rap1, thereby amplifying cell motility and metastatic potential. Leveraging the Meta1–MPF interaction, we designed MPF-derived peptides that specifically bind Meta1 and serve as the basis for a novel peptide-based PROTAC, which efficiently induces degradation of Meta1 and abrogates its pro-metastatic functions. Our study unveils Meta1 as an atypical GPCR with canonical signaling capacity and topological divergence, representing a shared and targetable vulnerability that bridges cancer cell-intrinsic adaptation with extrinsic TME communication. These findings establish the Meta1–MPF axis as a compelling therapeutic target for suppressing metastasis and reprogramming the TME.
  • Key Practice Points and Conclusions
    Tai-Lung ChaTaiwan Speaker Novel Target for GU Cancer Metastasis and TherapeuticsCancer progression is shaped by both cell-intrinsic adaptations and complex extrinsic interactions within the tumor microenvironment (TME). Here, we identify a transmembrane protein, Meta1, as a shared therapeutic target that exhibits a Janus-like role: promoting malignant phenotypes in cancer cells while restraining tumor-supportive functions in non-cancerous stromal and immune cells. Meta1 is expressed in both compartments of the TME, orchestrating a dual program that supports metastasis and immune evasion. Mechanistically, we uncovered a malignancy-promoting factor (MPF) that acts as a functional ligand for Meta1, selectively enhancing pro-invasive signaling in cancer cells. We further identify Meta1 as an unconventional G protein–coupled receptor (GPCR) that plays as an accelerator in cancer cells of the TME. Meta1 interacts with Rho-GDI and Gαq to activate RhoA-mediated cytoskeletal remodeling and amoeboid migration, facilitating metastatic dissemination. We further identify MPF binding to Meta1 initiates Gβγ signaling, elevating intracellular cAMP and activating Rap1, thereby amplifying cell motility and metastatic potential. Leveraging the Meta1–MPF interaction, we designed MPF-derived peptides that specifically bind Meta1 and serve as the basis for a novel peptide-based PROTAC, which efficiently induces degradation of Meta1 and abrogates its pro-metastatic functions. Our study unveils Meta1 as an atypical GPCR with canonical signaling capacity and topological divergence, representing a shared and targetable vulnerability that bridges cancer cell-intrinsic adaptation with extrinsic TME communication. These findings establish the Meta1–MPF axis as a compelling therapeutic target for suppressing metastasis and reprogramming the TME.
TICC - 2F 201DE
12:00
13:00
Redefining the Trajectory of Prostate Cancer
  • Tai-Lung ChaTaiwan Moderator Novel Target for GU Cancer Metastasis and TherapeuticsCancer progression is shaped by both cell-intrinsic adaptations and complex extrinsic interactions within the tumor microenvironment (TME). Here, we identify a transmembrane protein, Meta1, as a shared therapeutic target that exhibits a Janus-like role: promoting malignant phenotypes in cancer cells while restraining tumor-supportive functions in non-cancerous stromal and immune cells. Meta1 is expressed in both compartments of the TME, orchestrating a dual program that supports metastasis and immune evasion. Mechanistically, we uncovered a malignancy-promoting factor (MPF) that acts as a functional ligand for Meta1, selectively enhancing pro-invasive signaling in cancer cells. We further identify Meta1 as an unconventional G protein–coupled receptor (GPCR) that plays as an accelerator in cancer cells of the TME. Meta1 interacts with Rho-GDI and Gαq to activate RhoA-mediated cytoskeletal remodeling and amoeboid migration, facilitating metastatic dissemination. We further identify MPF binding to Meta1 initiates Gβγ signaling, elevating intracellular cAMP and activating Rap1, thereby amplifying cell motility and metastatic potential. Leveraging the Meta1–MPF interaction, we designed MPF-derived peptides that specifically bind Meta1 and serve as the basis for a novel peptide-based PROTAC, which efficiently induces degradation of Meta1 and abrogates its pro-metastatic functions. Our study unveils Meta1 as an atypical GPCR with canonical signaling capacity and topological divergence, representing a shared and targetable vulnerability that bridges cancer cell-intrinsic adaptation with extrinsic TME communication. These findings establish the Meta1–MPF axis as a compelling therapeutic target for suppressing metastasis and reprogramming the TME.
  • Declan MurphyAustralia Speaker PSMA PET Scan in Diagnosing Early/Advanced Localized Prostate Cancer Especially Comparing Various Radioactive Tracers
  • Ask The Experts Q&A
    Chun-Te WuTaiwan Moderator 健保各領域審查共識及討論-泌尿腫瘤
    Tai-Lung ChaTaiwan Moderator Novel Target for GU Cancer Metastasis and TherapeuticsCancer progression is shaped by both cell-intrinsic adaptations and complex extrinsic interactions within the tumor microenvironment (TME). Here, we identify a transmembrane protein, Meta1, as a shared therapeutic target that exhibits a Janus-like role: promoting malignant phenotypes in cancer cells while restraining tumor-supportive functions in non-cancerous stromal and immune cells. Meta1 is expressed in both compartments of the TME, orchestrating a dual program that supports metastasis and immune evasion. Mechanistically, we uncovered a malignancy-promoting factor (MPF) that acts as a functional ligand for Meta1, selectively enhancing pro-invasive signaling in cancer cells. We further identify Meta1 as an unconventional G protein–coupled receptor (GPCR) that plays as an accelerator in cancer cells of the TME. Meta1 interacts with Rho-GDI and Gαq to activate RhoA-mediated cytoskeletal remodeling and amoeboid migration, facilitating metastatic dissemination. We further identify MPF binding to Meta1 initiates Gβγ signaling, elevating intracellular cAMP and activating Rap1, thereby amplifying cell motility and metastatic potential. Leveraging the Meta1–MPF interaction, we designed MPF-derived peptides that specifically bind Meta1 and serve as the basis for a novel peptide-based PROTAC, which efficiently induces degradation of Meta1 and abrogates its pro-metastatic functions. Our study unveils Meta1 as an atypical GPCR with canonical signaling capacity and topological divergence, representing a shared and targetable vulnerability that bridges cancer cell-intrinsic adaptation with extrinsic TME communication. These findings establish the Meta1–MPF axis as a compelling therapeutic target for suppressing metastasis and reprogramming the TME.
  • Key Practice Points and Conclusions
    Tai-Lung ChaTaiwan Speaker Novel Target for GU Cancer Metastasis and TherapeuticsCancer progression is shaped by both cell-intrinsic adaptations and complex extrinsic interactions within the tumor microenvironment (TME). Here, we identify a transmembrane protein, Meta1, as a shared therapeutic target that exhibits a Janus-like role: promoting malignant phenotypes in cancer cells while restraining tumor-supportive functions in non-cancerous stromal and immune cells. Meta1 is expressed in both compartments of the TME, orchestrating a dual program that supports metastasis and immune evasion. Mechanistically, we uncovered a malignancy-promoting factor (MPF) that acts as a functional ligand for Meta1, selectively enhancing pro-invasive signaling in cancer cells. We further identify Meta1 as an unconventional G protein–coupled receptor (GPCR) that plays as an accelerator in cancer cells of the TME. Meta1 interacts with Rho-GDI and Gαq to activate RhoA-mediated cytoskeletal remodeling and amoeboid migration, facilitating metastatic dissemination. We further identify MPF binding to Meta1 initiates Gβγ signaling, elevating intracellular cAMP and activating Rap1, thereby amplifying cell motility and metastatic potential. Leveraging the Meta1–MPF interaction, we designed MPF-derived peptides that specifically bind Meta1 and serve as the basis for a novel peptide-based PROTAC, which efficiently induces degradation of Meta1 and abrogates its pro-metastatic functions. Our study unveils Meta1 as an atypical GPCR with canonical signaling capacity and topological divergence, representing a shared and targetable vulnerability that bridges cancer cell-intrinsic adaptation with extrinsic TME communication. These findings establish the Meta1–MPF axis as a compelling therapeutic target for suppressing metastasis and reprogramming the TME.
TICC - 1F 101C
Redefining the Trajectory of Prostate Cancer
  • Tai-Lung ChaTaiwan Speaker Novel Target for GU Cancer Metastasis and TherapeuticsCancer progression is shaped by both cell-intrinsic adaptations and complex extrinsic interactions within the tumor microenvironment (TME). Here, we identify a transmembrane protein, Meta1, as a shared therapeutic target that exhibits a Janus-like role: promoting malignant phenotypes in cancer cells while restraining tumor-supportive functions in non-cancerous stromal and immune cells. Meta1 is expressed in both compartments of the TME, orchestrating a dual program that supports metastasis and immune evasion. Mechanistically, we uncovered a malignancy-promoting factor (MPF) that acts as a functional ligand for Meta1, selectively enhancing pro-invasive signaling in cancer cells. We further identify Meta1 as an unconventional G protein–coupled receptor (GPCR) that plays as an accelerator in cancer cells of the TME. Meta1 interacts with Rho-GDI and Gαq to activate RhoA-mediated cytoskeletal remodeling and amoeboid migration, facilitating metastatic dissemination. We further identify MPF binding to Meta1 initiates Gβγ signaling, elevating intracellular cAMP and activating Rap1, thereby amplifying cell motility and metastatic potential. Leveraging the Meta1–MPF interaction, we designed MPF-derived peptides that specifically bind Meta1 and serve as the basis for a novel peptide-based PROTAC, which efficiently induces degradation of Meta1 and abrogates its pro-metastatic functions. Our study unveils Meta1 as an atypical GPCR with canonical signaling capacity and topological divergence, representing a shared and targetable vulnerability that bridges cancer cell-intrinsic adaptation with extrinsic TME communication. These findings establish the Meta1–MPF axis as a compelling therapeutic target for suppressing metastasis and reprogramming the TME.
  • Declan MurphyAustralia Speaker PSMA PET Scan in Diagnosing Early/Advanced Localized Prostate Cancer Especially Comparing Various Radioactive Tracers
  • Ask The Experts Q&A
    Chun-Te WuTaiwan Moderator 健保各領域審查共識及討論-泌尿腫瘤
    Tai-Lung ChaTaiwan Moderator Novel Target for GU Cancer Metastasis and TherapeuticsCancer progression is shaped by both cell-intrinsic adaptations and complex extrinsic interactions within the tumor microenvironment (TME). Here, we identify a transmembrane protein, Meta1, as a shared therapeutic target that exhibits a Janus-like role: promoting malignant phenotypes in cancer cells while restraining tumor-supportive functions in non-cancerous stromal and immune cells. Meta1 is expressed in both compartments of the TME, orchestrating a dual program that supports metastasis and immune evasion. Mechanistically, we uncovered a malignancy-promoting factor (MPF) that acts as a functional ligand for Meta1, selectively enhancing pro-invasive signaling in cancer cells. We further identify Meta1 as an unconventional G protein–coupled receptor (GPCR) that plays as an accelerator in cancer cells of the TME. Meta1 interacts with Rho-GDI and Gαq to activate RhoA-mediated cytoskeletal remodeling and amoeboid migration, facilitating metastatic dissemination. We further identify MPF binding to Meta1 initiates Gβγ signaling, elevating intracellular cAMP and activating Rap1, thereby amplifying cell motility and metastatic potential. Leveraging the Meta1–MPF interaction, we designed MPF-derived peptides that specifically bind Meta1 and serve as the basis for a novel peptide-based PROTAC, which efficiently induces degradation of Meta1 and abrogates its pro-metastatic functions. Our study unveils Meta1 as an atypical GPCR with canonical signaling capacity and topological divergence, representing a shared and targetable vulnerability that bridges cancer cell-intrinsic adaptation with extrinsic TME communication. These findings establish the Meta1–MPF axis as a compelling therapeutic target for suppressing metastasis and reprogramming the TME.
  • Key Practice Points and Conclusions
    Tai-Lung ChaTaiwan Speaker Novel Target for GU Cancer Metastasis and TherapeuticsCancer progression is shaped by both cell-intrinsic adaptations and complex extrinsic interactions within the tumor microenvironment (TME). Here, we identify a transmembrane protein, Meta1, as a shared therapeutic target that exhibits a Janus-like role: promoting malignant phenotypes in cancer cells while restraining tumor-supportive functions in non-cancerous stromal and immune cells. Meta1 is expressed in both compartments of the TME, orchestrating a dual program that supports metastasis and immune evasion. Mechanistically, we uncovered a malignancy-promoting factor (MPF) that acts as a functional ligand for Meta1, selectively enhancing pro-invasive signaling in cancer cells. We further identify Meta1 as an unconventional G protein–coupled receptor (GPCR) that plays as an accelerator in cancer cells of the TME. Meta1 interacts with Rho-GDI and Gαq to activate RhoA-mediated cytoskeletal remodeling and amoeboid migration, facilitating metastatic dissemination. We further identify MPF binding to Meta1 initiates Gβγ signaling, elevating intracellular cAMP and activating Rap1, thereby amplifying cell motility and metastatic potential. Leveraging the Meta1–MPF interaction, we designed MPF-derived peptides that specifically bind Meta1 and serve as the basis for a novel peptide-based PROTAC, which efficiently induces degradation of Meta1 and abrogates its pro-metastatic functions. Our study unveils Meta1 as an atypical GPCR with canonical signaling capacity and topological divergence, representing a shared and targetable vulnerability that bridges cancer cell-intrinsic adaptation with extrinsic TME communication. These findings establish the Meta1–MPF axis as a compelling therapeutic target for suppressing metastasis and reprogramming the TME.
TICC - 1F 101D
13:30
15:00
Advancing Urologic Care Through Technology and Minimally Invasive Innovation
  • Hann-Chorng KuoTaiwan Moderator ACU Lecture: Videourodynamic Study for Precision Diagnosis and Management of Lower Urinary Tract DysfunctionVideourodynamic Study in the Precision Diagnosis and Management of Lower Urinary Tract Dysfunctions Hann-Chorng Kuo, M.D. Department of Urology, Hualien Tzu Chi Hospital, Buddhist Tzu Chi Medical Foundation, Tzu Chi University, Hualien, Taiwan As a urologist, we are dealing with patients with lower urinary tract symptoms everyday. We did transurethral resection of the prostate (TURP) for elderly men with bothersome lower urinary tract symptoms (LUTS). We put a suburethral sling for women with stress urinary incontinence (SUI). We prescribed alpha-blocker for those who had difficulty in urination. We add antimuscarinics for patients with urgency urinary incontinence. Our seniors always told us these treatments are effective in treating patients with LUTS. However, patients still had LUTS after TURP, women still complained of urgency and dysuria after anti-incontinence surgery. Medication based on storage or emptying LUTS do not work all the time. Why? Because symptoms are not reliable, a large prostate does not indicate bladder outlet obstruction (BOO), and SUI is not solely a result of urethral incompetence. Therefore, in diagnosis and management of LUTS, we need precision medicine to direct an accurate pathophysiology of LUTS, and to guide an appropriate management based on the bladder and bladder outlet dysfunction. When we encounter patients who have LUTS refractory to the treatment based on our initial diagnosis, when we are treating patients who have complicated storage and emptying LUTS, when we are not sure patients could benefit from the invasive procedures for their LUTS, or patients who had both lower and upper urinary tract dysfunctions, videourodynamic study (VUDS) is an essential investigation for diagnosis and management of LUTS. In additional to benign prostate hyperplasia (BPH) and BOO, male patients with emptying LUTS might result from detrusor underactivity (DU), bladder neck dysfunction (BND), urethral sphincter dysfunction, or a hypersensitive bladder, which is not related with the prostate. Patients with BPH and LUTS might have latent neurogenic lesion, such as minor stroke, Parkinson's disease, or early dementia, causing LUTS. TURP without known the neurological disease might exacerbate LUTS after surgery. Mixed SUI comprises intrinsic sphincter deficiency (ISD) and detrusor overactivity (DO). The overactive bladder (OAB) symptoms may also result from an incompetent bladder outlet. Without comprehensive VUDS, we might cure the SUI, but OAB remains after placing a mid-urethral sling. Bladder pain is the cardinal symptoms of interstitial cystitis. However, bladder pain perceived by the patient might also originate from BOO or pelvic floor fascitis. VUDS can help in discrimination. DU and low compliant bladder and ISD could result in complicated storage and emptying LUTS. Large post-void residual (PVR) should alert us to investigate whether it is originated from low compliance or ISD. Dysfunctional voiding (DV) and BND in women with emptying LUTS. OAB symptoms are not always coming from the DO. BOO such as BND, DV, or urethral stricture might exist in men and women without voiding symptoms. Urinary difficulty in women is usually a result from low detrusor contractility, due to DU, or through inhibitory effect from a poorly relaxed pelvic floor or urethral sphincter. A simple bladder neck incision can effectively restore spontaneous voiding in men or women with dysuria due to DU or BND. However, a tight BN is necessary to predict a successful treatment outcome. Patients with central nervous system (CNS) disorders or spinal cord injury usually have complicated LUTD, including DO, BND, DV, detrusor sphincter dyssynergia (DSD), and vesicoureteral reflux (VUR). Management of LUTS in CNS disorders or SCI patients should know the current bladder and bladder outlet dysfunctions. Pediatric incontinence, children with myelomeningocele, DV, or recurrent urinary tract infection are complicated and need precision diagnosis before treatment. Especially when surgery is planned. Lower urinary tract dysfunctions is a dynamic condition. The bladder and bladder outlet dysfunction might change with time. Although VUDS is considered as an invasive investigation with radiation exposure, the advantages in accurate diagnosis and guiding management outweigh these disadvantages.
    Marshall StollerUnited States Speaker Normothermic Ex Vivo Kidney Perfusion for Urologic Discovery
  • Chun-Te WuTaiwan Moderator 健保各領域審查共識及討論-泌尿腫瘤
    Simone CrivellaroUnited States Speaker Single-Port vs. Multi-Port Robotic Prostatectomy: Balancing Innovation, Precision, and OutcomesThe Application & Limitation of Urological SP SurgerySingle Port Retroperitoneal Partial NephrectomySingle Port Prostate Surgery
TICC - 1F 101B
15:30
17:00
PSMA – Revolutionizing Prostate Cancer Care
TICC - 1F 101B

17th August 2025

Time Session
10:30
12:00
健保與基層: 健保審查與爭議共識 & 診所開業講座之開源節稅大作戰! (中文)
  • Chun-Hou LiaoTaiwan Moderator Regeneration Medicine in Urology - A Promising Future or Hoax?Regenerative medicine comprises therapeutic strategies aimed at restoring tissue structure and function, rather than merely alleviating symptoms. By deploying cells, biomaterials, bioactive molecules, or combinations thereof, these interventions stimulate the body’s intrinsic repair mechanisms. This paradigm extends beyond traditional symptomatic treatment, offering the potential for true self-healing and organ reconstruction—ultimately prioritizing cure over chronic disease management. Cell-based therapy has emerged as a promising intervention for various urogenital disorders, including erectile dysfunction (ED), bladder dysfunction, and male infertility. Current clinical research primarily focuses on mesenchymal stem cells (MSCs), investigating their safety, tolerability, and preliminary efficacy. Although early-phase studies suggest functional benefits—such as improved hemodynamics and tissue regeneration—most programs remain in preclinical or early clinical stages. A critical limitation remains the lack of standardization in MSC source, dose, and delivery route. Among alternative sources, human amniotic fluid-derived stem cells (hAFSCs) have shown particular promise. In preclinical models of cavernous nerve injury, hAFSCs demonstrated prolonged retention in penile tissue and in-situ differentiation into α-smooth muscle actin-positive corporal smooth muscle cells, effectively replacing damaged tissue and restoring function. These findings represent an encouraging step toward curative therapy. However, the mechanisms governing their in vivo behavior—such as engraftment, differentiation, and immunogenicity—will ultimately determine their clinical translatability and therapeutic stability. Whether cell-based approaches can evolve from experimental platforms into routine clinical care remains a central question. Platelet-Rich Plasma (PRP) Platelet-rich plasma (PRP) is an autologous biologic product enriched with supraphysiologic levels of platelets, growth factors, chemokines, and extracellular vesicles. Upon activation, PRP releases a bioactive cocktail that promotes angiogenesis, neuroregeneration, and antifibrotic remodeling—key processes in the restoration of urogenital tissues. In rodent models of cavernous nerve injury, PRP has been shown to preserve corporal sinusoidal endothelial cells and axonal scaffolds, while restoring erectile hemodynamics. Clinical studies further support PRP's safety in humans and report variable but promising improvements in IIEF scores following intracavernous injection. Nevertheless, the therapeutic response appears heterogeneous, likely influenced by patient factors, PRP preparation techniques, and injection protocols. Beyond ED, PRP has shown potential in other urologic indications such as stress urinary incontinence (SUI), interstitial cystitis/bladder pain syndrome (IC/BPS), and chronic pelvic pain, where it may contribute to tissue regeneration and symptom relief. However, broader adoption will require the establishment of individualized blood-quality metrics, standardized preparation methods, and randomized controlled trials demonstrating durable benefit. Emerging Regenerative Strategies Beyond cell-based and autologous biologics, a suite of innovative regenerative technologies is progressing from bench to bedside. These include: Energy-based devices such as low-intensity extracorporeal shock wave therapy (Li-ESWT), which promotes neovascularization and tissue regeneration via mechanotransduction pathways. Gene therapies, targeting dysfunctional or absent proteins in disorders like overactive bladder. Smart biomaterials, capable of delivering cells or bioactive molecules in a controlled, responsive manner. Extracellular vesicle (EV)-based therapeutics, which leverage cell-free vesicles derived from MSCs or urine-derived stem cells. These EVs carry signaling molecules (e.g., microRNAs, cytokines, growth factors) that mimic the paracrine effects of stem cells, offering a potentially safer and more scalable alternative to cell transplantation. In preclinical models of ED and bladder dysfunction, EVs have demonstrated the capacity to promote smooth muscle regeneration, nerve sprouting, and fibrosis reduction, with functional improvements comparable to stem cell therapy. Regenerative medicine has propelled the field of urologic tissue repair from theoretical promise to an early clinical reality. While substantial challenges remain—including the need for deeper mechanistic insight, protocol standardization, and regulatory clarity—the field is advancing rapidly. The convergence of cell therapy, PRP, EVs, and device-based modalities is creating a multifaceted toolkit for urologic regeneration. With continued scientific rigor, large-scale clinical trials, and interdisciplinary collaboration, regenerative medicine holds the potential to shift urologic care from chronic symptomatic management to durable, tissue-level cure.Stem Cell Therapy: Advancements and Clinical Insights for Erectile Dysfunction Treatment Erectile dysfunction (ED)—defined as the persistent inability to achieve or maintain an erection sufficient for satisfactory sexual activity—affects over 150 million men worldwide. While phosphodiesterase-5 inhibitors (PDE5is) remain the first-line treatment, many patients, particularly those with diabetes, age-related vascular decline, or neuropathy following radical prostatectomy, show suboptimal responses. Consequently, regenerative medicine—particularly stem-cell therapy—has gained interest for its potential to address the root causes of ED rather than merely managing symptoms. Stem-cell therapy offers a multifaceted approach to treating ED through neuroregeneration, angiogenesis, anti-apoptotic signaling, and fibrosis inhibition. Once introduced into the target tissue, stem cells can differentiate into specific cell types or exert paracrine effects via secretion of growth factors and extracellular vesicles. Among the various sources studied, bone marrow-derived mesenchymal stem cells (BM-MSCs), adipose-derived stem cells (ADSCs), and umbilical cord-derived MSCs (UC-MSCs) have been most extensively explored. Preclinical studies consistently demonstrate that MSC-based therapies enhance cavernous nerve regeneration, suppress fibrosis, and preserve endothelial integrity. In rat models of diabetes- or nerve-injury-induced ED, intracavernosal injections of ADSCs or BM-MSCs significantly restore intracavernosal pressure (ICP) and improve corpus cavernosum histology. Phase I/II clinical trials also support the safety and preliminary efficacy of stem-cell approaches. For example, in men with diabetic ED treated with autologous BM-MSCs, significant improvements in International Index of Erectile Function-5 (IIEF-5) scores and penile arterial flow have been reported without major adverse events. Similarly, ADSC therapy in post-prostatectomy ED has shown encouraging short-term results. However, large-scale trials are needed to clarify long-term efficacy, immune responses, and safety profiles. Human amniotic fluid stem cells (hAFSCs) represent a promising alternative, offering characteristics that bridge embryonic and adult stem-cell profiles. These include broad multipotency, high proliferation, and low immunogenicity—traits ideal for allogeneic use and neuroregenerative purposes. Notably, hAFSCs secrete potent regenerative mediators such as brain-derived neurotrophic factor (BDNF), vascular endothelial growth factor (VEGF), and insulin-like growth factor-1 (IGF-1), all of which support neurovascular repair and smooth muscle integrity. Our recent studies demonstrate, for the first time, that hAFSCs persist long-term in penile tissue and can differentiate into cavernous smooth-muscle cells, effectively replacing damaged tissue and improving erectile function even in chronic neurogenic ED models. Despite these advantages, our findings did not reveal in-vivo homing of hAFSCs to nerve injury sites or differentiation into neural tissue. This suggests a need for future studies to identify the specific microenvironmental cues required to induce such responses. Additionally, combining hAFSCs with platelet-rich plasma (PRP) may provide synergistic benefits—enhancing stem-cell homing, paracrine signaling, and in-vivo differentiation—thereby advancing a more effective, scalable, and safe therapeutic strategy.
    Yu-Ching WenTaiwan Moderator
  • Chun-Te WuTaiwan Speaker 健保各領域審查共識及討論-泌尿腫瘤
  • Chih-Chieh LinTaiwan Speaker Vesico-Vaginal Fistula: General Concept and Patient Preparation健保各領域審查共識及討論-功能性
  • Cheng-Chia LinTaiwan Speaker DISS plus FANS used in RIRSNew technologies and techniques are constantly emerging, but the most important part of our discussions is how to use them most effectively. Through this surgical demonstration, we hope to share the procedure and our experience with everyone.健保各領域審查共識及討論-結石
  • 黃智賢Taiwan Speaker 開業沒資金怎麼辦? 專家教您如何降低創業初期的負擔!
  • 李維仁Taiwan Speaker 診所開業萬萬稅? 會計師教您認識醫療稅務核心觀念!
TICC - 2F 201BC
12:00
13:00
The Role of Immunotherapy in adj./mRCC, Updated Evidence and Clinical Practice
TICC - 2F 201DE