Clinical features and prognosis of small cell carcinoma of the bladder: a single center retrospective analysis

Introduction

Small cell carcinoma of the bladder (SCCB) is a poorly differentiated and rapidly progressing neuroendocrine malignant tumor, with an incidence rate of less than 1% among bladder malignancies (1,2). SCCB predominantly affects males and is characterized by high malignancy. It is often diagnosed at an advanced stage, leading to a poor prognosis. The current knowledge of this rare disease is limited, and most studies are case reports or case series (3,4), with few studies focusing on prognostic factors. This paper retrospectively analyzes the clinical data of 41 patients with SCCB, exploring their clinical characteristics and prognostic factors. We present this article in accordance with the STROBE reporting checklist (available at https://tau.amegroups.com/article/view/10.21037/tau-2024-645/rc).

Methods

Study population and design

A retrospective analysis was performed on the case data of 41 patients with SCCB treated at Changhai Hospital, Navy Medical University, from November 2006 to November 2023, with all cases confirmed by pathological diagnosis. Clinical and pathological data encompassed age, gender, body mass index (BMI), histopathological classification, tumor location, tumor diameter, tumor count, clinical presentation, and surgical methods. Histopathological classification followed the 2016 World Health Organization (WHO) classification of urinary tract tumors (5), and tumor-node-metastasis (TNM) staging adhered to the 8^th edition by the Union for International Cancer Control (UICC) in 2017 (6). Pathological diagnoses were verified by two pathologists. Follow-up was conducted through outpatient visits or telephone calls, from the initial pathological confirmation of SCCB to May 1, 2024. The primary endpoint was overall survival (OS), defined as the duration from surgery to death from any cause or the last follow-up. To minimize selection bias, all cases diagnosed as SCCB were included, and data collection was standardized across all patients. Missing data were handled through listwise deletion to ensure consistency in statistical analyses.

In the analysis, quantitative variables were handled based on clinical relevance and statistical considerations. Continuous variables, such as age, BMI, and maximum tumor diameter, were categorized into groups to facilitate analysis and interpretation: age was grouped into <70 and ≥70 years to reflect clinically relevant age thresholds for prognosis. BMI was categorized into <24 and ≥24 kg/m² to assess the impact of nutritional status on survival. Maximum tumor diameter was divided into <4 and ≥4 cm based on clinical guidelines suggesting tumor size as a prognostic factor. Other variables, such as smoking history (yes/no) and tumor staging (T, N, M), were grouped according to standard clinical classifications. These groupings were chosen to simplify interpretation, highlight clinically meaningful differences, and align with established prognostic factors.

This is a retrospective study in which patient information was anonymized, and the study did not impact treatment or prognosis. The study was conducted in accordance with the Declaration of Helsinki (as revised in 2013) and was approved by the Ethics Committee of Changhai Hospital, Navy Medical University (approval No. CHEC2022-147). The requirement for written patient consent was waived due to the retrospective nature of the study.

Treatment methods

Among the 41 patients, 26 (63.41%) underwent radical cystectomy with urinary diversion, including 17 via laparoscopic surgery, 4 via robot-assisted laparoscopic surgery, and 5 via open surgery. Urinary diversion techniques included ureterocutaneostomy in 14 patients, ileal bladder in 8 patients, and neobladder reconstruction in 4 patients. Partial cystectomy was performed in 6 patients (14.63%), of whom 4 underwent laparoscopic partial cystectomy with ureteral reimplantation, and 2 underwent open partial cystectomy. Additionally, 6 patients (14.63%) received transurethral resection of bladder tumor (TURBT), 2 underwent debulking TURBT, and 1 underwent cystoscopic biopsy.

Postoperatively, 16 patients (39.02%) received chemotherapy (10 received cisplatin + etoposide and 6 received gemcitabine + cisplatin), while 9 patients (21.95%) received intravesical therapy [4 with gemcitabine, 4 with pirarubicin, and 1 with Bacillus Calmette-Guérin (BCG)]. Immunotherapy (toripalimab) and radiotherapy were administered to 3 patients each (7.31%).

Statistical analysis

Data sorting and statistical analysis were performed using R version 4.4.0 and GraphPad Prism 10.2.3 software. Missing data were addressed using listwise deletion, where cases with any missing values were excluded from the analysis. Differences between groups were deemed statistically significant at P<0.05. The Kaplan-Meier method was employed to generate survival curves and calculate survival rates, with group comparisons conducted using the log-rank test. Univariate Cox regression analysis was utilized to explore disease risk factors, and significant variables (P<0.05) were included in multivariate Cox regression to adjust for confounders and identify independent prognostic factors for SCCB, with results presented in a forest plot.

Results

Patients’ characteristics

A total of 41 patients were included in the final analysis. Among them, 39 patients completed follow-up, while 2 were lost to follow-up (follow-up rate: 95.1%). The cohort comprised predominantly male patients (n=38, 92.68%), with a male-to-female ratio of 12:1. The median age was 71 years (range, 41–89 years), and the average BMI was 24.45±3.29 kg/m² (range, 19.03–32.00 kg/m²). A total of 23 patients (56.10%) had a smoking history, all of whom were male, with 15 of the 23 smokers being heavy smokers (smoking index of 400). Table 1 lists the basic clinical characteristics of the 41 patients and their relationship with OS.

Pathological characteristics

Among the 41 patients, pathological diagnoses included 23 cases (56.1%) of pure SCCB, 16 cases (39.02%) of SCCB combined with urothelial carcinoma, 1 case (2.43%) of SCCB combined with adenocarcinoma, 1 case (2.43%) of SCCB combined with both urothelial carcinoma and adenocarcinoma, and 4 cases (9.75%) of SCCB combined with prostatic adenocarcinoma. Immunohistochemistry (IHC) was performed on 37 patients (Figure 1), revealing neuron-specific enolase (NSE) positivity in 20 cases (80%), synaptophysin (SYN) positivity in 25 cases (80.65%), chromogranin A (CGA) positivity in 8 cases (21.62%), and cluster of differentiation 56 (CD56) positivity in 26 cases (70.27%). Postoperative pathological staging was stage III or above in 23 cases (56.10%). Fourteen cases had lymph node metastasis, with 4 confirmed by postoperative pathology and the remaining 10 suggested by postoperative follow-up imaging. Among the 14 patients with distant metastasis, 3 had metastasis at initial diagnosis, 2 underwent debulking TURBT, and 1 underwent cystoscopy with biopsy, followed by chemotherapy. During follow-up, 11 patients developed distant metastasis. Postoperative metastasis sites primarily included the liver, bones, lungs, and pelvic and retroperitoneal lymph nodes. Subgroup analysis of prognostic factors for OS in M0 small cell bladder cancer patients undergoing radical surgery revealed a significant difference in OS based on T stage (P=0.005) (Table S1). The pathological characteristics of the patients and their relationship with OS are shown in Table 2. Treatment strategies and prognosis for patients with different pathological stages are shown in Table 3.

Figure 1 Immunohistochemical staining of CD56, NSE, CGA, and SYN in SCCB tissue. Tissue sections from different patients with SCCB, observed at 100× magnification. Each section is labeled with the corresponding immunohistochemical marker (CD56, NSE, CGA, or SYN) in the upper left corner, and the scale bar is located in the lower left corner, representing 50 µm. Each immunohistochemical section is magnified in a specific area, outlined in a box, to highlight the staining of the respective marker. These markers are used to identify specific cellular components, such as CD56, NSE, CGA, and SYN positive cells, in SCCB tissue. CD56, cluster of differentiation 56; NSE, neuron-specific enolase; CGA, chromogranin A; SYN, synaptophysin; SCCB, small cell carcinoma of the bladder.

Survival outcomes and prognostic factors

Among the 41 patients, 39 were followed up, and 2 were lost to follow-up, with a follow-up period of 5–131 months and a median follow-up time of 41 months. Twenty patients died, with a median OS of 30 months, and 1- and 3-year OS rates of 74.8% and 41.4%, respectively. The median OS for patients with T3–T4 stage was 15 months, and for patients with distant metastasis, it was 8 months. Univariate Cox regression analysis identified T stage (P=0.002), lymph node metastasis (P<0.001), and distant metastasis (P<0.001) as prognostic risk factors. Multivariate Cox regression analysis indicated that T stage [HR: 3.69, 95% confidence interval (CI): 1.06–12.82, P=0.04] and distant metastasis (HR: 11.12, 95% CI: 3.18–38.93, P<0.001) were independent prognostic factors for SCCB, as shown in Figure 2, with the survival curve depicted in Figure 3. The results of univariate and multivariate Cox regression analyses are presented in Table 4.

Figure 2 Cox multivariate regression analysis. *, significant difference. HR, hazard ratio; CI, confidence interval; T, tumor; N, node; M, metastasis.

Figure 3 Kaplan-Meier survival curves for independent risk factor. (A) Patients with T1 or T2 tumors showed significantly better survival than patients with T3 or T4 tumors (P=0.001). (B) The presence of distant metastases significantly affected survival (P<0.001).

Discussion

Epidemiology, clinical presentation, and prognosis of SCCB

SCCB predominantly affects elderly males, with a male-to-female ratio of approximately 3:1. In this study, the median age was 71 years (38 males and 3 females), with the peak incidence observed in patients aged 70 to 80 years. Although survival rates in older patients (≥70 years) were lower than in younger patients, the difference was not statistically significant. SCCB typically occurs in the lateral walls and base of the bladder, with most tumors being solitary and around 50 mm in diameter (7). In our investigation, 48.78% of tumors were located in the lateral wall, with a median tumor size of 40 mm, and 65.85% of patients had solitary tumors. Survival analysis showed no significant correlation between tumor location, size, number, and prognosis.

Gross hematuria is the most common presenting symptom in SCCB, followed by dysuria, bladder irritation, and lower abdominal pain. In rare cases, patients may present with paraneoplastic syndromes such as ectopic adrenocorticotropic hormone (ACTH) secretion or hypercalcemia (8). In our study, 80.49% of patients presented with gross hematuria, and no cases of paraneoplastic syndrome were observed. Univariate analysis showed no significant association between presenting symptoms and prognosis. Most SCCB patients present at advanced stages (T3–T4) (8,9), as seen in 56.1% of our cases, and multivariate Cox regression confirmed T stage as an independent prognostic factor. In addition, our findings further demonstrate that T stage is a key prognostic factor influencing OS in M0 small cell bladder cancer patients undergoing radical surgery.

The prognosis of SCCB is generally poor, with previous studies reporting a median survival time of 4–23 months and 5-year survival rates ranging from 10% to 40% (10). In our study, the 1- and 3-year survival rates were 74.8% and 41.4%, respectively, with a median survival of 30 months, which is higher than that reported in the literature. This may be due to the small sample size and potential selection bias. SCCB primarily metastasizes via lymph nodes, and metastasis occurs earlier and more aggressively than in urothelial carcinoma (11). Studies have shown that SCCB patients with distant metastasis have a significantly worse prognosis compared to those without metastasis (12-14). In our cohort, 34.14% of patients had lymph node metastasis, and 34.14% had distant metastasis. Multivariate analysis confirmed distant metastasis as an independent prognostic factor, supporting the observation that advanced-stage SCCB has a poor prognosis.

SCCB often coexists with other histological types of bladder cancer, such as urothelial carcinoma, squamous cell carcinoma, and adenocarcinoma, which can complicate diagnosis. Therefore, pathological examination remains the “gold standard” for diagnosis (15). A study suggests that pure SCCB has a worse prognosis than mixed SCCB (13). However, in our study, pure SCCB accounted for 56.1% of cases and mixed SCCB for 43.9%, with no significant difference in survival rates between these two groups. IHC plays an important role in diagnosing SCCB, with common neuroendocrine markers including NSE, Syn, CgA, and CD56. The reported positive expression rates for NSE, CgA, and Syn range from 25–100%, 22–89%, and 67–76%, respectively (13). Elevated serum NSE levels (>25 ng/mL) have been associated with poor prognosis (16). In our study, 37 patients underwent IHC testing, and while the presence of neuroendocrine markers confirmed the tumor’s origin, there was no association between these markers and patient prognosis.

T staging and distant metastasis were identified as independent prognostic factors in our multivariate analysis, findings consistent with previous literature (17,18). Additionally, studies have also shown that lymph node positivity is associated with poor prognosis (19). While the significance of T staging and metastasis as prognostic factors is well-established in oncology, our study adds to the body of evidence specific to SCCB, which remains poorly understood due to its rarity. The diversity of treatment strategies observed in the study by Lu et al. (20) further reflects the lack of standardized protocols for SCCB, irrespective of whether the disease is localized or locally advanced. Our findings highlight the aggressive nature of advanced SCCB and reinforce the need for early and aggressive treatment strategies.

Treatment and prognosis of SCCB

Due to the rarity of SCCB, there is no established standard treatment regimen. Given its histological and biological similarities to small cell lung cancer (SCLC), SCCB treatment often follows the protocols used for SCLC. Surgical interventions for SCCB include radical cystectomy, partial cystectomy, and TURBT, typically supplemented by chemotherapy, radiotherapy, or immunotherapy. Although radical cystectomy is the standard surgical approach for muscle-invasive SCCB and has been associated with better survival outcomes, patient-specific factors often necessitate alternative approaches. In our cohort, 63.41% (26/41) of patients underwent radical cystectomy, while the remaining patients underwent partial cystectomy or TURBT.

TURBT is commonly used for localized SCCB but has a high recurrence rate postoperatively (10). It has been reported that the median survival of just 11 months for patients who underwent TURBT or biopsy alone (21). More than half of SCCB patients undergo radical cystectomy, which has been shown to significantly improve survival (7,22,23). In our analysis, the use of partial cystectomy and TURBT in some cases reflects patient-specific considerations such as advanced age, significant comorbidities, or limited surgical tolerance, which made them unfit for radical surgery. Additionally, certain patients presented with localized disease or declined more extensive surgery due to personal preference. However, these limited surgical approaches may have contributed to poorer outcomes due to incomplete tumor resection. Survival analysis showed that patients who underwent radical cystectomy had higher survival rates than those with other surgical methods, but the difference was not statistically significant (P=0.15).

Chemotherapy, particularly cisplatin-based regimens, has been demonstrated to significantly improve survival in SCCB patients (22,24,25). Neoadjuvant chemotherapy (NACT) not only reduces tumor stage but also improves long-term survival (26). Recent studies have demonstrated that T1 SCCB patients undergoing upfront surgery (i.e., without NACT) face a high risk of pathological upstaging to pT2+ (71%). This finding further underscores the importance of early systemic therapy, even in patients with seemingly low-stage disease (17). Another study of 203 patients with neuroendocrine carcinoma of the urinary tract (NEC-URO) found that NACT significantly improved downstaging rates compared with initial surgery alone (49.6% vs. 14.5%, P<0.0001), particularly when using an ifosfamide plus doxorubicin/etoposide plus cisplatin (IA/EP) regimen (65% downstaging) versus EP (39%), methotrexate, vinblastine, doxorubicin, and cisplatin/gemcitabine plus cisplatin (MVAC/GC) (27%), or other regimens (36%). Furthermore, patients treated with NACT followed by surgery had significantly better 5-year OS (57%) compared with surgery alone (22%) or surgery followed by adjuvant chemotherapy (30%) (27). These findings highlight the critical role of NACT, particularly NEC-specific regimens, in improving outcomes for NEC-URO and SCCB patients.

Radiotherapy, either alone or in combination with chemotherapy, is another treatment option for localized SCCB. A study by Chau et al. showed no significant difference in median OS between patients treated with surgery and those treated with radiotherapy (1). However, some studies have reported recurrence of urothelial carcinoma in patients undergoing bladder-preserving treatment for SCCB, which may necessitate salvage cystectomy (28). Immunotherapy, particularly immune checkpoint inhibitors, may offer a promising treatment for SCCB, especially in patients with programmed cell death 1 (PD-1) or programmed death-ligand 1 (PD-L1) positivity who have relapsed after surgery (3,29). A recent report described a patient with SCCB who progressed on cisplatin/etoposide and nivolumab/ipilimumab showed a prolonged response to lurbinectedin. Genomic analysis identified a TP53 mutation and amplifications in E2F3 and MYCL. Following lurbinectedin resistance, a repeat biopsy revealed an actionable ERBB2 alteration, suggesting a resistance mechanism and potential therapeutic target (30). These findings highlight the role of molecular profiling in guiding personalized treatment for SCCB.

In our study, none of the patients received NACT, reflecting the historical evolution of clinical practice. This is primarily due to the long study period, spanning nearly two decades, during which treatment protocols for SCCB were not standardized. NACT was not widely adopted as a standard approach in the earlier years, which may have influenced treatment outcomes and limits comparisons with contemporary treatment regimens that include NACT. Sixteen patients received adjuvant chemotherapy postoperatively, seven of whom died due to disease progression. Among the 26 patients who underwent radical cystectomy, 17 were classified as M0. Of these, 7 received adjuvant chemotherapy, while 10 did not. Subgroup analysis of these localized patients suggests that adjuvant chemotherapy may provide a survival benefit, though the small sample size limits statistical significance. Univariate analysis showed no statistically significant association between adjuvant chemotherapy and OS (P=0.57), possibly due to this limitation. Importantly, we found that 56% of cases that underwent upfront surgery were stage 3 or above, underscoring the need for neoadjuvant therapy in muscle-invasive disease. This is consistent with the National Comprehensive Cancer Network (NCCN) guidelines, which recommend concurrent chemoradiotherapy or NACT followed by local treatment (cystectomy or radiotherapy) for SCCB patients with limited stage disease. Three patients received immunotherapy, all of whom were PD-1-positive. Two patients remained tumor-free during follow-up, while one patient relapsed and died of distant metastasis 4 months after starting immunotherapy. These findings suggest that immunotherapy may offer a new treatment avenue for patients who are unresponsive or intolerant to chemotherapy.

Study limitations

The primary limitation of this study is the small sample size, which is a consequence of the clinical rarity of SCCB. This may introduce selection bias and limit the statistical power of the analysis. Larger sample sizes or multicenter randomized controlled trials are needed to strengthen the reliability and generalizability of these findings.

Conclusions

SCCB is a highly malignant and aggressive urinary system tumor predominantly affecting males, commonly diagnosed at an advanced stage, and prone to metastasis. There is currently no standardized treatment protocol. Radical cystectomy is the preferred treatment for localized SCCB, and NACT and immunotherapy can extend OS. T stage and distant metastasis are independent prognostic factors for SCCB patients. Early diagnosis and treatment are crucial for improving prognosis.

Acknowledgments

We thank all the patients and the institutions for supporting these studies.

Footnote

Reporting Checklist: The authors have completed the STROBE reporting checklist. Available at https://tau.amegroups.com/article/view/10.21037/tau-2024-645/rc

Data Sharing Statement: Available at https://tau.amegroups.com/article/view/10.21037/tau-2024-645/dss

Peer Review File: Available at https://tau.amegroups.com/article/view/10.21037/tau-2024-645/prf

Funding: This study was supported by the National Natural Science Foundation of China (Nos. 82172871 and 82272950), Basic Research Project of Naval Medical University (No. 2024MS013), the Shanghai Municipal Health Commission (No. 2022YQ010), and the Changhong Program of Changhai Hospital (2024).

Conflicts of Interest: All authors have completed the ICMJE uniform disclosure form (available at https://tau.amegroups.com/article/view/10.21037/tau-2024-645/coif). The authors have no conflicts of interest to declare.

Ethical Statement: The authors are accountable for all aspects of the work in ensuring that questions related to the accuracy or integrity of any part of the work are appropriately investigated and resolved. The study was conducted in accordance with the Declaration of Helsinki (as revised in 2013). The study was approved by the Ethics Committee of Changhai Hospital, Navy Medical University (approval No. CHEC2022-147) and individual consent for this retrospective analysis was waived due to the retrospective nature.

Open Access Statement: This is an Open Access article distributed in accordance with the Creative Commons Attribution-NonCommercial-NoDerivs 4.0 International License (CC BY-NC-ND 4.0), which permits the non-commercial replication and distribution of the article with the strict proviso that no changes or edits are made and the original work is properly cited (including links to both the formal publication through the relevant DOI and the license). See: https://creativecommons.org/licenses/by-nc-nd/4.0/.

References

1. Chau C, Rimmer Frcr Y. Treatment Outcomes for Small Cell Carcinoma of the Bladder: Results From a UK Patient Retrospective Cohort Study. Int J Radiat Oncol Biol Phys 2021;110:1143-50. [Crossref] [PubMed]
2. Akbulut D, Al-Ahmadie H. Updates on Urinary Bladder Tumors With Neuroendocrine Features. Adv Anat Pathol 2024;31:169-77. [Crossref] [PubMed]
3. Kou Z, Wang P, Jia D, et al. Clinical analysis of small-cell carcinoma of the urinary bladder: A case report and review of literature. Asian J Surg 2024;47:1602-3. [Crossref] [PubMed]
4. Liu Y, Xu H, Wu B, et al. Small cell carcinoma of the bladder with coexisting prostate adenocarcinoma: two cases report and literature review. BMC Urol 2020;20:134. [Crossref] [PubMed]
5. Humphrey PA, Moch H, Cubilla AL, et al. The 2016 WHO Classification of Tumours of the Urinary System and Male Genital Organs-Part B: Prostate and Bladder Tumours. Eur Urol 2016;70:106-19. [Crossref] [PubMed]
6. Kandori S, Kojima T, Nishiyama H. The updated points of TNM classification of urological cancers in the 8th edition of AJCC and UICC. Jpn J Clin Oncol 2019;49:421-5.
7. Choong NW, Quevedo JF, Kaur JS. Small cell carcinoma of the urinary bladder. The Mayo Clinic experience. Cancer 2005;103:1172-8. [Crossref] [PubMed]
8. Ismaili N. A rare bladder cancer--small cell carcinoma: review and update. Orphanet J Rare Dis 2011;6:75. [Crossref] [PubMed]
9. Abrahams NA, Moran C, Reyes AO, et al. Small cell carcinoma of the bladder: a contemporary clinicopathological study of 51 cases. Histopathology 2005;46:57-63. [Crossref] [PubMed]
10. Church DN, Bahl A. Clinical review - small cell carcinoma of the bladder. Cancer Treat Rev 2006;32:588-93. [Crossref] [PubMed]
11. Trias I, Algaba F, Condom E, et al. Small cell carcinoma of the urinary bladder. Presentation of 23 cases and review of 134 published cases. Eur Urol 2001;39:85-90. [Crossref] [PubMed]
12. Koay EJ, Teh BS, Paulino AC, et al. A Surveillance, Epidemiology, and End Results analysis of small cell carcinoma of the bladder: epidemiology, prognostic variables, and treatment trends. Cancer 2011;117:5325-33. [Crossref] [PubMed]
13. Ismaili N, Heudel PE, Elkarak F, et al. Outcome of recurrent and metastatic small cell carcinoma of the bladder. BMC Urol 2009;9:4. [Crossref] [PubMed]
14. Wang G, Xiao L, Zhang M, et al. Small cell carcinoma of the urinary bladder: a clinicopathological and immunohistochemical analysis of 81 cases. Hum Pathol 2018;79:57-65. [Crossref] [PubMed]
15. Sved P, Gomez P, Manoharan M, et al. Small cell carcinoma of the bladder. BJU Int 2004;94:12-7. [Crossref] [PubMed]
16. Naito A, Taguchi S, Nakagawa T, et al. Prognostic significance of serum neuron-specific enolase in small cell carcinoma of the urinary bladder. World J Urol 2017;35:97-103. [Crossref] [PubMed]
17. Myers AA, Fang AM, Moussa MJ, et al. Impact of systemic therapy on clinical T1 small-cell neuroendocrine carcinoma of the bladder. ESMO Open 2024;9:103964. [PubMed]
18. Ismail U, Killeen RB. Taxane Toxicity. StatPearls. Treasure Island (FL) ineligible companies. Copyright © 2025, StatPearls Publishing LLC.; 2025.
19. Liveringhouse C, Sim AJ, Zhang J, et al. A Single Institution Experience in the Management of Localized Neuroendocrine Carcinoma of the Bladder. Clin Genitourin Cancer 2024;22:102222. [PubMed]
20. Lu J, Zhou J, Liu Y, et al. Treatment and survival of non-metastatic small cell carcinoma of the bladder from multiple centers in China. Sci Rep 2024;14:24652. [PubMed]
21. Schreiber D, Rineer J, Weiss J, et al. Characterization and outcomes of small cell carcinoma of the bladder using the surveillance, epidemiology, and end results database. Am J Clin Oncol 2013;36:126-31. [Crossref] [PubMed]
22. Siefker-Radtke AO, Dinney CP, Abrahams NA, et al. Evidence supporting preoperative chemotherapy for small cell carcinoma of the bladder: a retrospective review of the M. D. Anderson cancer experience. J Urol 2004;172:481-4. [Crossref] [PubMed]
23. Cheng L, Pan CX, Yang XJ, et al. Small cell carcinoma of the urinary bladder: a clinicopathologic analysis of 64 patients. Cancer 2004;101:957-62. [Crossref] [PubMed]
24. Quek ML, Nichols PW, Yamzon J, et al. Radical cystectomy for primary neuroendocrine tumors of the bladder: the university of southern california experience. J Urol 2005;174:93-6. [Crossref] [PubMed]
25. Mackey JR, Au HJ, Hugh J, et al. Genitourinary small cell carcinoma: determination of clinical and therapeutic factors associated with survival. J Urol 1998;159:1624-9. [Crossref] [PubMed]
26. Siefker-Radtke AO, Kamat AM, Grossman HB, et al. Phase II clinical trial of neoadjuvant alternating doublet chemotherapy with ifosfamide/doxorubicin and etoposide/cisplatin in small-cell urothelial cancer. J Clin Oncol 2009;27:2592-7. [Crossref] [PubMed]
27. Alhalabi O, Wilson N, Xiao L, et al. Comparative Effectiveness Analysis of Treatment Strategies for Surgically Resectable Neuroendocrine Carcinoma of the Urinary Tract. Eur Urol Oncol 2023;6:611-20. [Crossref] [PubMed]
28. Lohrisch C, Murray N, Pickles T, et al. Small cell carcinoma of the bladder: long term outcome with integrated chemoradiation. Cancer 1999;86:2346-52. [Crossref] [PubMed]
29. Hatayama T, Hayashi T, Matsuzaki S, et al. Successful treatment of recurrent small cell carcinoma of urinary bladder with pembrolizumab. IJU Case Rep 2020;3:252-6. [Crossref] [PubMed]
30. Moussa MJ, Khandelwal J, Wilson NR, et al. Durable Objective Response to Lurbinectedin in Small Cell Bladder Cancer with TP53 Mutation: A Molecular-Directed Strategy. Curr Oncol 2024;31:3342-9. [Crossref] [PubMed]