sulindac has been researched along with Carcinoma-in-Situ* in 2 studies
2 other study(ies) available for sulindac and Carcinoma-in-Situ
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Efficacy of dimethylaminoparthenolide and sulindac in combination with gemcitabine in a genetically engineered mouse model of pancreatic cancer.
Pancreatic cancer remains one of the deadliest diseases, with limited surgical and treatment options. Two targets of interest include the transcription factor nuclear factor-κB and cyclooxygenase-2, which are constitutively activated and overexpressed, respectively, in human pancreatic adenocarcinoma. We have previously shown that dimethylaminoparthenolide (DMAPT), a bioavailable nuclear factor-κB inhibitor, and the cyclooxygenase inhibitors sulindac and celecoxib have potential chemotherapeutic efficacy. The current study evaluates the efficacy of intervention with DMAPT and sulindac in the LSL-Kras(G12D);Pdx-1-Cre genetically engineered mouse model. Gemcitabine, traditionally a chemotherapeutic agent, has relatively low toxicity; thus, combinations with low-dose gemcitabine were also explored.. LSL-Kras(G12D);Pdx-1-Cre mice at 7 months of age were randomized into placebo, DMAPT (40 mg/kg per day), sulindac (20 mg/kg per day), gemcitabine (50 mg/kg twice weekly), and combination treatment groups. After 3 months of treatment, the mice were killed.. The percentage of normal pancreatic ducts was significantly increased by the combinations of DMAPT/sulindac, DMAPT/gemcitabine, sulindac/gemcitabine, and DMAPT/sulindac/gemcitabine compared to placebo. Additionally, the percentage of mouse pancreatic intraepithelial neoplasia-2 lesions was significantly decreased by DMAPT/gemcitabine.. Intervention with DMAPT and sulindac in combination with gemcitabine may delay or prevent progression of premalignant pancreatic lesions in the LSL-Kras(G12D);Pdx-1-Cre mouse model of pancreatic cancer. Topics: Animals; Antineoplastic Combined Chemotherapy Protocols; Carcinoma in Situ; Cyclooxygenase 2; Cyclooxygenase 2 Inhibitors; Cytokines; Disease Progression; Genes, p53; Mice; Mice, Transgenic; Mutation; NF-kappa B; Pancreatic Neoplasms; Proto-Oncogene Proteins p21(ras); Sesquiterpenes; Sulindac | 2013 |
Bowen's disease (squamous cell carcinoma in situ) in immunosuppressed patients treated with imiquimod 5% cream and a cox inhibitor, sulindac: potential applications for this combination of immunotherapy.
Patients with chronic lymphocytic leukemia (CLL) often have a protracted course. However, all these patients are immunosuppressed and may have a high incidence of cutaneous malignancies.. To determine if combination therapy using topical imiquimod cream 5% and the oral cyclooxygenase (COX) inhibitor are useful in the therapy of squamous cell carcinoma in situ (SCC in situ)/Bowen's disease in patients with long-standing CLL.. Five CLL patients with head and neck cutaneous SCC in situ, which met criteria for Bowen's disease, were treated with topical 5% topical imiquimod cream and an oral COX inhibitor, sulindac 200 mg twice a day.. All patients showed clinical resolution and histologic clearing of the tumors after 16 weeks of therapy.. The local immune modulator, 5% imiquimod, in combination with a COX inhibitor, with its many potential antitumor effects may stimulate the innate and possibly the adaptive immune responses to clear these malignancies. Topics: Adjuvants, Immunologic; Administration, Topical; Aged; Aminoquinolines; Antineoplastic Agents; Bowen's Disease; Carcinoma in Situ; Cyclooxygenase Inhibitors; Drug Therapy, Combination; Female; Humans; Imiquimod; Immunosuppression Therapy; Immunotherapy; Leukemia, Lymphocytic, Chronic, B-Cell; Male; Middle Aged; Neoplasms, Second Primary; Ointments; Skin Neoplasms; Sulindac | 2001 |