Henry Woo

Henry Woo is the Head of the Department of Urology at Blacktown Hospital in Sydney, Australia, He is also the Director of Uro-Oncology at the Chris O'Brien Lifehouse Comprehensive Cancer Centre. He is an Honorary Professor at the Australian National University and a Conjoint Professor at the Western Sydney University. His clinical practice is focussed on prostate cancer and the management of male LUTS/BPH. He has authored over 200 peer reviewed publications with many in high impact journals. He currently serves on the editorial boards of multiple journals including the Asian Journal of Urology, Prostate International, World Journal of Men's Health, European Urology Open Science, World Journal of Urology and Prostate Cancer and Prostatic Diseases. He is an Associate Editor of the SIU Journal.

15th August 2025

Time Session
12:00
13:00
Collaborative Care: Mastering Techniques and Cardiovascular Considerations
TICC - 1F 101A

16th August 2025

Time Session
10:30
12:00
  • Ju-Chuan HuTaiwan Facilitator Trans-Vaginal Repair for VV Fistula
    Jian-Hua HongTaiwan Facilitator
    Chung-Cheng WangTaiwan Commenter Ureteral Stent and SelectionUreteral stents are widely used in urology for the management of obstructive uropathies, including urologic or non-urologic malignancy, radiation therapy, ureteral calculus, infection, surgical or nonsurgical trauma, or congenital factors. An untreated ureteral obstruction could result in urinary tract infection, abdominal or flank pain, and a deterioration of renal function. Despite their widespread utility, the selection of an appropriate ureteral stent remains a complex clinical decision involving multiple variables including patient-specific factors, disease pathology, duration of stenting, and the desired balance between drainage efficacy and patient comfort. Advancements in stent technology have led to the development of a variety of stent types, distinguished by their material composition (e.g., polyurethane, silicone, and hydrophilic-coated polymers), design features (e.g., double-J, multi-length, tail stents), drug-eluting capabilities, reinforced metallic stent, and biodegradable stents. Each design aims to optimize certain aspects of performance such as resistance to encrustation, migration, infection, and stent-related symptoms. Key considerations in stent selection include indwelling time, risk of infection or encrustation, patient anatomy, and comorbidities or prior urologic surgery. For short-term use, polyurethane or co-polymer stents are often preferred due to their balance of flexibility and cost-effectiveness. In contrast, silicone stents may be more appropriate for long-term indwelling due to their superior biocompatibility and reduced encrustation rates. Drug-eluting stents are emerging as promising options in cases of recurrent infection or tumor-associated obstruction. Softer materials, tapered tips, and biodegradable stents aim to reduce stent-related lower urinary tract symptoms. Recently, we reported the efficacy and safety of Allium metallic ureteral stents in treating 13 patients with refractory ureteral strictures. The median (IQR) age of the patients was 63 (46–76) years. The median (IQR) follow-up was 15 (13.5–21) months. Treatment success and improvement were noted in 9 (69.2%) and 3 (23.1%) patients, respectively. Compared to the preoperative levels, the median (IQR) serum creatinine levels were significantly improved at 3 months after the operation [1.6 (1.25–2.85) vs. 1.2 (1.05–2.05), p = 0.02] and at the last visit [1.6 (1.25–2.85) vs. 1.2 (1.05–1.8), p = 0.02]. Stent migration and encrustation were noted in three (23.1%) and one (7.7%) patients, respectively. The preliminary results showed that Allium ureteral stents were safe and effective for patients with refractory ureteral strictures. In conclusion, as technology continues to evolve, the future of ureteral stenting lies in personalized device selection based on real-time patient feedback, predictive analytics, and enhanced biomaterials. Further clinical trials and comparative studies are essential to establish evidence-based guidelines that can assist clinicians in making the most appropriate stent choices for optimal outcomes Fixed and Adjustable Male Slings: Key Techniques for Primary Implantation and Troubleshooting in Challenging CasesMale slings have emerged as an effective surgical solution for stress urinary incontinence (SUI) following radical prostatectomy, offering an alternative to artificial urinary sphincters, particularly in patients with mild to moderate incontinence. Among the available options, fixed and adjustable male slings represent two major categories, each with distinct mechanisms of action, implantation techniques, and postoperative management considerations. Fixed male slings work by repositioning and compressing the bulbar urethra against the pubic ramus to restore continence. These slings rely on proper patient selection—typically individuals with preserved sphincter function, low-volume leakage, and no prior pelvic radiation. Key technical considerations include precise dissection of the perineal space, adequate urethral mobilization, tension-free sling placement, and symmetric anchoring of the arms. Avoidance of over-tensioning is crucial to prevent postoperative urinary retention and perineal discomfort. Adjustable male slings offer intraoperative or postoperative modification of sling tension to accommodate varying degrees of incontinence or suboptimal initial outcomes. These slings are particularly useful in patients with higher degrees of incontinence, previous pelvic surgery, or radiation. The implantation techniques vary but generally involve positioning a cushion or compressive element under the urethra, with external or subcutaneous access ports for saline adjustment. Mastery of device calibration, port placement, and infection prevention are critical to long-term success. Challenging cases—such as those involving prior sling failure, prior pelvic radiation, fibrosis, or altered anatomy—require tailored strategies. In irradiated patients, tissue integrity and healing potential are compromised, often necessitating the use of adjustable systems with minimal tissue dissection or the combination of sling and bulking agents. In reoperative fields, precise identification of tissue planes and modified dissection techniques are required to prevent urethral injury or inadequate compression. Troubleshooting sling failure involves assessing continence status, sling positioning via imaging or endoscopy, and determining whether revision, adjustment, or conversion to an artificial urinary sphincter is most appropriate. Postoperative complications including infection, urethral erosion, urinary retention, and persistent incontinence can be mitigated by proper surgical technique, patient education, and regular follow-up. Management of these complications should be proactive and individualized, balancing intervention timing with patient expectations and functional goals. In this topic, we will share our experiences to avoid these complications and increase the successful outcome.
    Steffi YuenHong Kong, China Speaker The Power of Powerbend in Management of Lower Pole and Complex StonesThe management of lower pole stones (LPS) and complex renal calculi remains one of the most challenging aspects of contemporary urolithiasis treatment, with the deflection capability of flexible ureteroscopes serving as the critical determinant of surgical success. Modern flexible ureteroscopes achieve impressive bidirectional deflection angles of 270° or even more, representing a significant advancement from earlier generation instruments. However, this “working deflection” capacity becomes substantially compromised when therapeutic instruments, such as laser fibers or stone baskets, are inserted through the working channel. The anatomical challenges of lower pole access, particularly steep infundibulopelvic angles, necessitate prolonged maximal deflection during lithotrispy that significantly increases the risk of ureteroscope damage and surgeon fatigability. Deflection deterioration is also directly proportional to instrument usage, with newer single-use scopes coming to the rescue. The introduction of flexible and navigable suction access sheaths (FANS) has revolutionized lower pole stone management allowing direct access to performing lithotriopsy and stone fragments retrieval, reducing the need for stone basket in stone relocation and fragment retrieval. Recent multicenter studies demonstrate comparable stone-free rates (<2mm) between lower pole and non-lower pole locations (96.6% vs 98.4%) when using FANS, with minimal complications and low reintervention rates. With current technological advancements, combined with improved surgical techniques and the strategic choice of single-use ureteroscopes with good deflection power, one can significantly achieve high stone-free rates with low infectious complications and reinterventions with FANS flexible ureteroscopy in the treatment of complex lower pole stones. FANs in Endourology: Finding the Best Combination with Lasers and Scopes for Optimal Outcomes
TICC - 1F 102
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