mobic and Carcinoma-in-Situ

We reviewed the outcomes of metastatic renal cell carcinoma patients with the primary tumor in situ who initially underwent interferon-α-based immunotherapy to evaluate the effect of this therapy on metastatic sites as well as primary kidney tumor and survival.. Thirty-one patients, for whom upfront cytoreductive nephrectomy was considered to be inappropriate because of poor performance status and far-advanced disease, were the subject of the present study. Tumor response and reduction in the size of metastatic sites and primary kidney tumor were assessed. Overall survival distributions were estimated using the Kaplan-Meier method with the significance determined using the log-rank test.. Partial response was observed in 11 patients, yielding an overall response rate of 35%. Seventeen patients had regression or stabilization of metastatic sites, while progression of metastatic sites was observed in the remaining 14 patients. Regarding the maximum response of primary kidney tumor, a reduction in kidney primary tumor size was observed in 42% of the patients and the mean reduction rate in these patients was 18.2% (range: 3-36%). Furthermore, the reduction in the size of metastatic sites was significantly associated with that in the size of primary kidney tumor (R(2)= 0.432, P< 0.0001). The median survival for the 31 patients was 17 months. The median survival was 42 months in patients with regression or stabilization of metastatic sites and 7 months in those without (P< 0.001).. The present study suggests that metastatic sites as well as primary kidney tumor respond to interferon-α-based immunotherapy in metastatic renal cell carcinoma patients with primary tumor in situ.

Topics: Adult; Aged; Aged, 80 and over; Antineoplastic Combined Chemotherapy Protocols; Carcinoma in Situ; Carcinoma, Renal Cell; Chemotherapy, Adjuvant; Cimetidine; Dexamethasone; Female; Humans; Immunotherapy; Interferon-alpha; Kaplan-Meier Estimate; Kidney Neoplasms; Male; Meloxicam; Middle Aged; Neoadjuvant Therapy; Nephrectomy; Thiazines; Thiazoles; Treatment Outcome

Pancreaticobiliary maljunction (PBM) is a high risk factor in biliary tract carcinoma. The chemopreventive action of a cyclooxygenase (COX)-2 inhibitor (meloxicam) on N-nitrosobis (2-oxopropyl) amine (BOP)-induced gallbladder cancer in hamster PBM models was investigated. In 7-week-old female Syrian golden hamsters, the extrahepatic bile duct at the distal end of the common duct was ligated and cholecystoduodenostomy was performed (group I). In group II, the same surgery was performed and from week 4 after surgery, 10 mg/kg of BOP was injected subcutaneously once a week with a 1-week interval. In group III, in addition to the measures employed in group II, 5 mg/kg/day of meloxicam was administered once a day, every weekday. Pathological findings in the gallbladder in week 20 after surgery were as follows. In group I, proper epithelium (PE) was predominant and there was no cancer. In group II, PE was predominant, but there was also hyperplasia and atypical epithelium (AE) recognized in 8 of 11 cases (72.7%); the area of AE was more extensive than that in group I. Carcinoma in situ (CIS) was recognized in 4 of 11 cases (36.4%) in group II. Group III showed the same pathological findings as group I. However, compared with group II, the incidence of AE decreased to 27.3% and no cancerous lesion was observed. In week 20 after surgery, the proliferative cell nuclear antigen labeling index in group III was statistically significantly lower than in group II (P = 0.045). No statistically significant differences were noted among the groups in terms of apoptosis labeling index in week 20 after surgery. In conclusion, it was confirmed that meloxicam suppresses carcinogenesis in hamster PBM models and its mechanism may be based on the suppression of cell growth.

Topics: Animals; Apoptosis; Carcinogens; Carcinoma in Situ; Cell Proliferation; Cell Transformation, Neoplastic; Cricetinae; Cyclooxygenase 2; Cyclooxygenase Inhibitors; Disease Models, Animal; Epithelium; Female; Gallbladder; Gallbladder Neoplasms; Hyperplasia; Meloxicam; Mesocricetus; Nitrosamines; Proliferating Cell Nuclear Antigen; Thiazines; Thiazoles