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91.
Ross?J.?Mason Igor?Frank Bimal?Bhindi Matthew?K.?Tollefson R.?Houston?Thompson R.?Jeffrey?Karnes Robert?Tarrell Prabin?Thapa Stephen?A.?BoorjianEmail author 《World journal of urology》2017,35(12):1879-1884
Purpose
To evaluate perioperative and oncologic outcomes of patients undergoing radical cystectomy (RC) for recurrence of urothelial carcinoma (UC) after prior partial cystectomy (PC), and to compare these outcomes to patients undergoing primary RC.Methods
Patients who underwent RC for recurrence of UC after prior PC were matched 1:3 to patients undergoing primary RC based on age, pathologic stage, and decade of surgery. Perioperative and oncologic outcomes were compared using Wilcoxon sign-rank test, McNemars test, the Kaplan–Meier method, and Cox proportional hazards regression analyses.Results
Overall, the cohorts were well matched on clinical and pathological characteristics. No difference was noted in operative time (median 322 versus 303 min; p = 0.41), estimated blood loss (median 800 versus 700 cc, p = 0.10) or length of stay (median 9 versus 10 days; p = 0.09). Similarly, there were no differences in minor (51.7 versus 44.3%; p = 0.32) or major (10.3 versus 12.6%; p = 0.66) perioperative complications. Median follow-up after RC was 5.0 years (IQR 1.5, 13.1 years). Notably, CSS was significantly worse for patients who underwent RC after PC (10 year—46.8 versus 65.9%; p = 0.03). On multivariable analysis, prior PC remained independently associated with an increased risk of bladder cancer death (HR 2.28; 95% CI 1.17, 4.42).Conclusions
RC after PC is feasible, without significantly adverse perioperative outcomes compared to patients undergoing primary RC. However, the risk of death from bladder cancer may be higher, suggesting the need for careful patient counseling prior to PC and the consideration of such patients for adjuvant therapy after RC.92.
93.
Non-cirrhotic portal fibrosis in children. 总被引:3,自引:0,他引:3
U Poddar B R Thapa P Puri C S Girish K Vaiphei R K Vasishta K Singh 《Indian journal of gastroenterology》2000,19(1):12-13
BACKGROUND AND OBJECTIVES: Non-cirrhotic portal fibrosis (NCPF) is an infrequent cause of portal hypertension in children. We report 11 children with NCPF, from among 338 with portal hypertension, seen over 6.5 years. METHODS: The diagnosis was based on patent splenoportal axis on ultrasonography and/or splenoportal venography and liver biopsy showing no evidence of cirrhosis or other diagnosis, in children with portal hypertension. Those with variceal bleed were managed with endoscopic sclerotherapy and/or shunt surgery. RESULTS: The median age was 11 years (range 5 to 14), and 8 were boys. Presentation was with variceal bleed in 6, lump in left upper abdomen in 5 (though all children had splenomegaly) and esophageal varices on endoscopy. The median spleen enlargement was 8.5 cm; 8 also had hepatomegaly. Hypersplenism was present in 7, and two had developed ascites after bleed. Of 6 children presenting with bleed, variceal obliteration was achieved on sclerotherapy (average 5.6 sessions) in 4 while two underwent shunt surgery for associated hypersplenism. After median follow up of 57.5 months (range 12-78) all are alive and well. CONCLUSION: NCPF is an uncommon cause of portal hypertension in Indian children. Presentation with variceal bleed is less common than in adults; sclerotherapy is effective. 相似文献
94.
Adam Lauko Bicky Thapa Vyshak Alva Venur Manmeet S. Ahluwalia 《Current neurology and neuroscience reports》2018,18(10):70
Purpose of the Review
Brain metastasis is a common complication of advanced malignancies, especially, lung cancer, breast cancer, renal cell carcinoma, and melanoma. Traditionally surgery, when indicated, and radiation therapy, either as whole-brain radiation therapy or stereotactic radiosurgery, constituted the major treatment options for brain metastases. Until recently, most of the systemic chemotherapy agents had limited activity for brain metastases. However, with the advent of small molecule tyrosine kinase inhibitors and immunotherapy agents, there has been renewed interest in using these agents in the management of brain metastases.Recent Findings
Immune checkpoint inhibitors have revolutionized the treatment of metastatic melanoma, lung cancer, kidney cancer, and bladder cancer among others. They modulate the immune system to recognize tumor antigens as “non-self” antigens and mount an immune response against them.Summary
Initial studies of using immune checkpoint inhibitors in brain metastases have shown promising activity, and several clinical trials are currently underway. Studies are also assessing the combination of radiation therapy and immunotherapy in brain metastases. The results of these ongoing clinical trials have the potential to change the therapeutic paradigm in patients with brain metastases.95.
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98.
Ovarian molar pregnancy, though a very rare entity, behaves like any other molar pregnancy. After surgical management, close follow‐up with β‐hCG surveillance is invariable to detect progression to persistent gestational trophoblastic disease. 相似文献
99.
Nonsteroidal anti-inflammatory drug-activated gene-1 (NAG-1) expression is upregulated not only by NSAIDs such as sulindac
sulfide, but also by several antitumorigenic dietary compounds, suggesting that NAG-1 is a specific target for the development
of effective anticancer agents. Despite being a downstream target of p53, NAG-1 induction is both p53-dependent and p53-independent.
It is not clear whether NAG-1 induction is the responsible factor in cancer cell apoptosis with mutated p53. In this study,
we report that NAG-1 induction alone cannot determine apoptotic cell fate in colon cancer cells. Although docetaxel induced
an increase in NAG-1 and apoptosis in both HCT-116 (wild-type p53) and HT-29 (mutant p53) colon cancer cells, NAG-1 knockdown
with siRNA prevented docetaxel-induced cell death in only HCT-116 cells. Docetaxel decreased Bcl-2 in HCT-116 cells, which
have functionally active p53, according to luciferase reporter gene analyses, and docetaxel-induced cell death and changes
in Bcl-2 and NAG-1 expression were blocked by PFT-α, a p53 inhibitor. In HT-29 cells with functionally inactive p53, the docetaxel-induced
Bcl-xL decrease, NAG-1 increase, and cell death were not blocked by PFT-α. On the other hand, sulindac sulfide at concentrations
that significantly induced NAG-1 did not decrease cell viability comparable to docetaxel, and it did not affect the level
of p53, Bax, Bcl-2, and Bcl-xL in either cell line. The present study demonstrates that p53-dependent NAG-1 induction is linked
to cell death and that NAG-1 induction without accompanying alteration of antiapoptosis protein Bcl-2 family members may not
lead to cancer cell death. 相似文献
100.