Nonmuscle-Invasive Bladder Cancer: What's Changing and What has Changed

2017 ◽  
Vol 84 (1) ◽  
pp. 1-8 ◽  
Author(s):  
Ramanitharan Manikandan ◽  
Oscar Rodriguez ◽  
Rubén Parada ◽  
Joan Palou Redorta

Purpose Nonmuscle-invasive bladder cancer (NMIBC) is a challenging disease to manage primarily due to its varied clinical course. The management of NMIBC has witnessed a widespread change with respect to its diagnosis and treatment. Although transurethral resection (TUR) and adjuvant bacillus Calmette–Guerin (BCG) stills remain the cornerstone, newer protocols has come into vogue to achieve optimal care. On the basis of a literature review, we aimed to establish ‘what changes has already occurred and what is expected in the future’ in NMIBC. Methods A Medline search was performed to identify the published literature with respect to diagnosis, treatment and future perspectives on NMIBC. Particular emphasis was directed to determinants such as the quality of TUR and the newer modifications, Re-TUR, current status of newer macroscopic and microscopic imaging, role of urinary biomarkers, clinical, histologic and molecular predictors of high-risk disease, administration of intravesical agents, salvage therapy in BCG recurrence and the current best practice guidelines were analyzed. Results and Conclusions Optimal TUR, restaging in select group, incorporation of newer endoscopic imaging and judicious administration of intravesical chemo-immunotherapeutic agents can contribute to better patient care. Although there is a plethora of urinary markers, there is insufficient evidence for their use in isolation. The future probably lies in identification of genetic markers to determine disease recurrence, nonresponders to standard treatment and early institution of alternative/targeted therapy.

2015 ◽  
Vol 2015 ◽  
pp. 1-6 ◽  
Author(s):  
Andres F. Correa ◽  
Katherine Theisen ◽  
Matthew Ferroni ◽  
Jodi K. Maranchie ◽  
Ronald Hrebinko ◽  
...  

Background. Thirty to forty percent of patients with high grade nonmuscle invasive bladder cancer (NMIBC) fail to respond to intravesical therapy with bacillus Calmette-Guerin (BCG). Interferon-α2B plus BCG has been shown to be effective in a subset of patients with NMIBC BCG refractory disease. Here we present a contemporary series on the effectiveness and safety of intravesical BCG plus interferon-α2B therapy in patients with BCG refractory NMIBC.Methods. From January of 2005 to April of 2014 we retrospectively found 44 patients who underwent induction with combination IFN/BCG for the management of BCG refractory NMIBC. A chart review was performed to assess initial pathological stage/grade, pathological stage/grade at the time of induction, time to IFN/BCG failure, pathological stage/grade at failure, postfailure therapy, and current disease state.Results. Of the 44 patients who met criteria for the analysis. High risk disease was found in 88.6% of patients at induction. The 12-month and 24-month recurrence-free survival were 38.6% and 18.2%, respectively. 25 (56.8%) ultimately had disease recurrence. Radical cystectomy was performed in 16 (36.4%) patients.Conclusion. Combination BCG plus interferon-α2B remains a reasonably safe alternative treatment for select patients with BCG refractory disease prior to proceeding to radical cystectomy.


2009 ◽  
Vol 23 (6) ◽  
pp. 983-988 ◽  
Author(s):  
Eleanor R. Ray ◽  
Kathryn Chatterton ◽  
Kay Thomas ◽  
M. Shamim Khan ◽  
Ashish Chandra ◽  
...  

Cancer ◽  
2012 ◽  
Vol 118 (22) ◽  
pp. 5525-5534 ◽  
Author(s):  
Francis Thomas ◽  
Derek J. Rosario ◽  
Naomi Rubin ◽  
John R. Goepel ◽  
Maysam F. Abbod ◽  
...  

2021 ◽  
Vol 39 (6_suppl) ◽  
pp. 490-490
Author(s):  
Ruben Carmona ◽  
Alan Pollack ◽  
Zachary L Smith ◽  
Jeff M. Michalski ◽  
Hiram Alberto Gay ◽  
...  

490 Background: Integrating molecular subtypes, gene transcripts associated with disease recurrence (DR), and clinicopathologic features may help risk stratify muscle-invasive bladder cancer (MIBC) patients & guide therapy selection. We hypothesized that combined transcriptomic & clinical data would improve risk stratification for DR (local or distant) after cystectomy +/- adjuvant chemotherapy. Methods: We identified 401 MIBC patients (pT2-4 N0-N3 M0) in The Cancer Genome Atlas with detailed demographic, clinical, pathologic, and treatment-related data. We split the data into training (60%) & testing (40%) sets. We produced RNA gene expression scores for molecular subtype using 48 established, relevant genes (PMID 28988769). In the training set, we performed feature selection by conducting random forest modeling of an additional 108 genes associated with DR. We kept genes of highest importance based on the evaluation of increasing mean-squared error & node purity. We excluded highly correlated genes & used the false discovery rate method for multiple hypotheses testing. We performed univariable analyses on genes of highest importance, molecular subtype, & clinicopathologic variables. Using adjusted multivariable analyses (MVA), we built two models: with & without transcriptomic data. Using the testing set, we compared the final models' performance to predict DR, using receiver operating characteristics & area under the curve (AUC). Results: Median follow-up was 18 months (range 1-168). 104 patients recurred with a 5-yr cumulative incidence of 34.6%[28.6-40.5%]. Using the training set, we identified 6 genes significantly associated with DR (VEGFA, TRMT1, FGFR2B, ERBB2, MMP14, PDGFC). The final MVA showed that the new 6-gene signature (HR 1.61, 95% CI 1.27-2.05, p < 0.001); immune molecular subtype [increased expression of PD-L1, PD-1, IDO1, CXCL11, L1CAM, SAA1] (HR 0.52, 95% CI 0.29-0.94, p = 0.03); smoking status (HR 1.17 per 10 pack-years, 95% CI 1.05-1.29, p = 0.005); and local failure risk factors [≥pT3 with negative margins & ≥10 nodes removed (HR 1.63, 95% CI 1.15-2.32, p = 0.006); ≥pT3 and positive margins OR < 10 nodes removed (HR 3.26, 95%CI 2.43 to 4.09, p = 0.007)], were all significantly associated with DR. This combined model outperformed a stand-alone clinicopathologic model (AUC 0.75 vs. 0.66) in the testing set. The combined model stratified patients based on DR risk into 3 groups with 5-yr cumulative incidences of 19.8%[7.7-31.9%] (low-risk); 34.5%[26.1-42.8%] (intermediate); and 49.8%[37.7-61.9%] (high), Gray’s Test p < 0.0001. Conclusions: To our knowledge, this study is the first to integrate clinicopathologic & transcriptomic information (including molecular subtype) to better stratify MIBC patients by risk of recurrence. This stratification may help guide decision-making for adjuvant treatment. Further validation is warranted.


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