No abstract available.
Heart Failure* ; Heart* ; Learning* ; Urinary Bladder*

Even with advances in perioperative medical care, anesthetic management, and surgical techniques, radical cystectomy (RC) which remains the gold standard therapy for the treatment of muscle-invasive bladder cancer, yet is still associated with a high morbidity rate as well as a prolonged length of hospitalization (LOH). Recently, there has been a great deal of interest in developing multimodal and multidisciplinary strategies that might aid in the acceleration postoperative convalescence by decreasing variance in perioperative care for patients having complex operations. Many patient series have shown that Enhanced Recovery After Surgery (ERAS) protocols can improve outcomes in patients having RC by reducing the incidence of gastrointestinal complications and the LOH without increasing readmissions or overall morbidity. Many studies are going to evaluate and incorporate scientific data in ERAS program to modify as many of the variables leading to RC morbidity, as well as to enhance how patients are cared for before and after operation. In this review, we offer a summary of the preoperative, intraoperative, and postoperative key components of undergoing an ERAS protocol for patients undergoing RC, as well as future research prospects.

Radical cystectomy (RC) is the gold standard treatment option for muscle invasive bladder cancer (MIBC). However, up to 25% of patients who undergo RC show metastatic lymph node deposits during the procedure. In such cases, the 5-year survival rate is reported to be 25%–30%. Pelvic lymph node dissection (PLND) can also provide useful prognostic information, including data regarding the disease burden, lymph node density, and extracapsular extension of metastatic lymph nodes. Accordingly, the National Comprehensive Cancer Network guidelines recommend that PLND that includes the common iliac lymph node should be performed at the time of RC to allow reliable staging of MIBC. In addition to its diagnostic role, many studies have reported the potential therapeutic role of PLND. Data from clinical trials indicate a substantial oncological advantage in PLND cohorts compared to non-PLND cohorts, regardless of pathological nodal status, as a result of removal of metastatic and micrometastatic tumor cells nested in lymph nodes. As such, despite the diagnostic and therapeutic role of PLND in MIBC, the optimal PLND template remains controversial. Currently, extended PLND (E-PLND) is recommended for diagnostic purposes, however, E-PLND did not show therapeutic effectiveness in some recent preliminary randomized controlled trials. In this review, we will discuss the appropriate range of PLND for RC in terms of its diagnostic and therapeutic importance, and propose an appropriate range of PLNDs based on the evidence and randomized trials so far.

In the past decade, the treatment of metastatic urothelial cancer (mUC), including bladder cancer (BC), has transformed significantly with the introduction of diverse therapies, such as immune checkpoint inhibitors, targeted therapies, and antibody-drug conjugates.This change is partly due to advancements in genomic understanding, particularly nextgeneration sequencing, which has identified numerous mutations in UC. Among these therapies, erdafitinib, a pan-fibroblast growth factor receptor (FGFR) inhibitor for specific FGFR2 and FGFR3 alterations, is the only targeted therapy approved till now. In 2019, erdafitinib became pivotal for the treatment of mUC, particularly in patients with specific FGFR alterations. Recent studies have highlighted the benefits of combining erdafitinib with immunotherapy, thereby broadening the treatment options. Ongoing investigations exist on its use in non-muscle-invasive BC and in combination with drugs such as enfortumab vedotin in mUC. Other FGFR-targeted agents are under development; however, overcoming FGFR resistance and ensuring the safety of combination therapies remain major hurdles.FGFR3 mutations are particularly prevalent in BC, a heterogeneous form of UC, and account for a considerable proportion of new cancer diagnoses annually. Approximately half of these cancers have FGFR3 mutations, with gene rearrangements being a common feature. These FGFR3 genomic alterations often occur independently of mutations in other BC oncogenes, such as TP53 and RB1. This review emphasizes the importance of FGFR inhibition in UC and the optimization of its use in clinical practice. Moreover, it underscores the ongoing efforts to evaluate combination strategies and early treatment testing to enhance the effectiveness of targeted therapies for UC.

In the past decade, the treatment of metastatic urothelial cancer (mUC), including bladder cancer (BC), has transformed significantly with the introduction of diverse therapies, such as immune checkpoint inhibitors, targeted therapies, and antibody-drug conjugates.This change is partly due to advancements in genomic understanding, particularly nextgeneration sequencing, which has identified numerous mutations in UC. Among these therapies, erdafitinib, a pan-fibroblast growth factor receptor (FGFR) inhibitor for specific FGFR2 and FGFR3 alterations, is the only targeted therapy approved till now. In 2019, erdafitinib became pivotal for the treatment of mUC, particularly in patients with specific FGFR alterations. Recent studies have highlighted the benefits of combining erdafitinib with immunotherapy, thereby broadening the treatment options. Ongoing investigations exist on its use in non-muscle-invasive BC and in combination with drugs such as enfortumab vedotin in mUC. Other FGFR-targeted agents are under development; however, overcoming FGFR resistance and ensuring the safety of combination therapies remain major hurdles.FGFR3 mutations are particularly prevalent in BC, a heterogeneous form of UC, and account for a considerable proportion of new cancer diagnoses annually. Approximately half of these cancers have FGFR3 mutations, with gene rearrangements being a common feature. These FGFR3 genomic alterations often occur independently of mutations in other BC oncogenes, such as TP53 and RB1. This review emphasizes the importance of FGFR inhibition in UC and the optimization of its use in clinical practice. Moreover, it underscores the ongoing efforts to evaluate combination strategies and early treatment testing to enhance the effectiveness of targeted therapies for UC.

In the past decade, the treatment of metastatic urothelial cancer (mUC), including bladder cancer (BC), has transformed significantly with the introduction of diverse therapies, such as immune checkpoint inhibitors, targeted therapies, and antibody-drug conjugates.This change is partly due to advancements in genomic understanding, particularly nextgeneration sequencing, which has identified numerous mutations in UC. Among these therapies, erdafitinib, a pan-fibroblast growth factor receptor (FGFR) inhibitor for specific FGFR2 and FGFR3 alterations, is the only targeted therapy approved till now. In 2019, erdafitinib became pivotal for the treatment of mUC, particularly in patients with specific FGFR alterations. Recent studies have highlighted the benefits of combining erdafitinib with immunotherapy, thereby broadening the treatment options. Ongoing investigations exist on its use in non-muscle-invasive BC and in combination with drugs such as enfortumab vedotin in mUC. Other FGFR-targeted agents are under development; however, overcoming FGFR resistance and ensuring the safety of combination therapies remain major hurdles.FGFR3 mutations are particularly prevalent in BC, a heterogeneous form of UC, and account for a considerable proportion of new cancer diagnoses annually. Approximately half of these cancers have FGFR3 mutations, with gene rearrangements being a common feature. These FGFR3 genomic alterations often occur independently of mutations in other BC oncogenes, such as TP53 and RB1. This review emphasizes the importance of FGFR inhibition in UC and the optimization of its use in clinical practice. Moreover, it underscores the ongoing efforts to evaluate combination strategies and early treatment testing to enhance the effectiveness of targeted therapies for UC.

In the past decade, the treatment of metastatic urothelial cancer (mUC), including bladder cancer (BC), has transformed significantly with the introduction of diverse therapies, such as immune checkpoint inhibitors, targeted therapies, and antibody-drug conjugates.This change is partly due to advancements in genomic understanding, particularly nextgeneration sequencing, which has identified numerous mutations in UC. Among these therapies, erdafitinib, a pan-fibroblast growth factor receptor (FGFR) inhibitor for specific FGFR2 and FGFR3 alterations, is the only targeted therapy approved till now. In 2019, erdafitinib became pivotal for the treatment of mUC, particularly in patients with specific FGFR alterations. Recent studies have highlighted the benefits of combining erdafitinib with immunotherapy, thereby broadening the treatment options. Ongoing investigations exist on its use in non-muscle-invasive BC and in combination with drugs such as enfortumab vedotin in mUC. Other FGFR-targeted agents are under development; however, overcoming FGFR resistance and ensuring the safety of combination therapies remain major hurdles.FGFR3 mutations are particularly prevalent in BC, a heterogeneous form of UC, and account for a considerable proportion of new cancer diagnoses annually. Approximately half of these cancers have FGFR3 mutations, with gene rearrangements being a common feature. These FGFR3 genomic alterations often occur independently of mutations in other BC oncogenes, such as TP53 and RB1. This review emphasizes the importance of FGFR inhibition in UC and the optimization of its use in clinical practice. Moreover, it underscores the ongoing efforts to evaluate combination strategies and early treatment testing to enhance the effectiveness of targeted therapies for UC.

Prostate cancer (PC) treatment has reached a milestone with the introduction of poly(ADP-ribose) polymerase (PARP) inhibitors. PARP inhibitors (PARPi) induce breaks in single-stranded and/or double-stranded DNA, resulting in synthetic lethality in cancer cells lacking functional homologous recombination genes. Around 20% to 25% of patients with metastatic castrationresistant prostate cancer harbor mutations in DNA damage repair genes, either somatic or germline. The success of PARPi in these patients has prompted studies exploring its potential in tumors classified as "BRCAness," which refers to tumors without germline BRCA1 or BRCA2 mutations. Additionally, there is a proposed connection between androgen receptor signaling and synthetic lethality of PARPi. The inclusion of genetic mutation tests in the treatment algorithm for PC is a significant step towards precision and personalized medicine, marking a first in the field. The objectives of this review encompass understanding the mechanism of action of PARPi in both monotherapy and combination therapy, exploring patient selection criteria, discussing pivotal studies that led to its approval, and offering future prospects. However, numerous unanswered questions remain, including the identification of the patient population that could benefit most from PARPi, determining whether to use PARPi as monotherapy or in combination, and finding the optimal timing of PARPi administration in advanced or localized disease. To address these questions, several ongoing clinical trials are being conducted.

The standard management for patients with muscle invasive bladder cancer (MIBC) involves radical cystectomy and pelvic lymph node dissection. Although this treatment may be curative, a large proportion of patients will develop recurrence and will ultimately die of metastatic disease. Prospective, randomized clinical trial data demonstrate a survival advantage for those patients who receive neoadjuvant chemotherapy (NAC) prior to radical cystectomy and this concept was confirmed by meta-analysis. The administration of cisplatin-based combination NAC has consistently demonstrated a survival benefit of 5%. The pathologic downstaging is used as a surrogate end point. The efficacy of NAC for MIBC was established primarily with methotrexate, vinblastine, doxorubicin, and cisplatin (MVAC), with complete response rates (pT0) as high as 38%. Dose dense M-VAC (DDMAVC) is preferred over standard MVAC, and gemcitabine/cisplatin is a reasonable alternative to standard M-VAC for NAC. In Korea, while NAC use has slowly increased over time, it remains an underutilized therapeutic approach in Korean clinical practice.
Biomarkers ; Cisplatin ; Cystectomy ; Doxorubicin ; Drug Therapy* ; Humans ; Korea ; Lymph Node Excision ; Methotrexate ; Neoadjuvant Therapy ; Prospective Studies ; Recurrence ; Standard of Care* ; Urinary Bladder Neoplasms ; Vinblastine

No abstract available.
Animals ; Models, Animal