mobic has been researched along with Carcinoma--Squamous-Cell* in 5 studies
1 trial(s) available for mobic and Carcinoma--Squamous-Cell
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The effects of a COX-2 inhibitor meloxicam on squamous cell carcinoma of the esophagus in vivo.
Our previous study showed that aspirin induced apoptosis of esophageal cancer cells in vitro by inhibiting the pathway of NF-kappaB downstream regulation of cyclooxygenase-2. The purpose of this study was to determine if similar changes occurred in vivo in the tumors of patients with SCC of the esophagus who were given a preferential COX-2 inhibitor, meloxicam. Fifty-three patients who had an esophagectomy for SCC were allocated randomly to either a Treatment group (n = 25) or a control group (n = 28). Patients in the Treatment group were given 7.5 mg/day of meloxicam, for between 10 and 14 days before surgery. Patients in the control group did not take any type of NSAID during this time interval. Samples of the tumor taken from the resected specimens were collected. Proliferation and apoptosis were measured by flow cytometry. The concentration of 6-keto-prostaglandin F(1)alpha in cancer tissue was determined by radio-immuno-assay. Expression of COX-2 mRNA was measured with RT-PCR and COX-2 protein levels with Western blot analysis. Nuclear NF-kappaB and cytoplasmic I kappaB protein levels were determined by electrophoretic mobility shift assay and Western blot, respectively. There were significantly more apoptotic cells in the tumors of patients who were using meloxicam. It also decreased the levels of COX-2 mRNA, COX-2 protein and nuclear NF-kappaB protein and increased the cytoplasmic I kappaB protein in the cancer. We conclude that meloxicam induces apoptosis in SCC of the esophagus in vivo by inhibiting the pathway of NF-kappaB downstream regulation of COX-2. Topics: 6-Ketoprostaglandin F1 alpha; Adult; Aged; Anti-Inflammatory Agents, Non-Steroidal; Apoptosis; Blotting, Western; Carcinoma, Squamous Cell; Cell Proliferation; Cyclooxygenase 2; Cyclooxygenase 2 Inhibitors; Electrophoretic Mobility Shift Assay; Esophageal Neoplasms; Esophagectomy; Female; Flow Cytometry; Gene Expression Regulation, Enzymologic; Gene Expression Regulation, Neoplastic; Humans; I-kappa B Proteins; Male; Meloxicam; Middle Aged; NF-kappa B; NF-KappaB Inhibitor alpha; Radioimmunoassay; Reverse Transcriptase Polymerase Chain Reaction; Signal Transduction; Thiazines; Thiazoles | 2008 |
4 other study(ies) available for mobic and Carcinoma--Squamous-Cell
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Frontal sinus carcinoma in forty-one dogs (2001-2022).
Reports on canine frontal sinus carcinomas (FSCs) are scarce. This retrospective review of 41 dogs with FSC (2001-2022) describes demographic and clinical characteristics of canine FSC and reports the clinical experience and overall survival following treatment with toceranib phosphate (TOC) and meloxicam in 10 cases. Median age at diagnosis was 10.6 years (range: 6.5-15.4 years). There was a male-to-female-ratio of 2.4:1. The most common breeds were Jack Russell Terriers (JRT) (n = 7; 17.1%) and Rottweilers (n = 3, 7.3%). Mesocephalic breeds (70.6%) were most commonly affected, brachycephalics accounted for 8.8%. The most frequent clinical signs included skull deformation dorsomedial to the eye (87.5%), pain/head-shyness (40.0%), ocular (22.5%)/nasal (17.5%) discharge, and exophthalmos (17.5%). Duration of symptoms prior to diagnosis varied from a few days to 9 months. There were no neurological signs at initial presentation despite imaging evidence of osteolysis of the lamina interna of the frontal bone in most dogs (69.4%). In 11.5%, pulmonary changes suggestive of metastasis or concurrent primary pulmonary neoplasia were present. Tumour types included squamous cell carcinoma (58.5%), unspecified carcinoma (29.3%), and adenocarcinoma (9.8%). Ten dogs were treated with TOC (median 2.8 mg/kg EOD or three times per week) and meloxicam (0.1 mg/kg, EOD) (TOC-M), resulting in subjective regression of skull deformity in 8/10 (80.0%) patients. Overall median survival time with TOC-M was 183.5 days (range: 120-434 days). FSCs typically present with skull deformation, but no overt neurological signs. Male dogs and JRT may be overrepresented. The use of TOC-M in FSC appears promising and warrants further prospective evaluation. Topics: Animals; Carcinoma, Squamous Cell; Dog Diseases; Dogs; Female; Frontal Sinus; Male; Meloxicam; Mouth Neoplasms; Paranasal Sinus Neoplasms; Pyrroles; Retrospective Studies | 2023 |
Squamous cell carcinoma of the anal sacs in three dogs.
Anal sac squamous cell carcinoma is rare in dogs. Five cases have been previously reported, treatment of which involved surgery alone. This report describes three further cases of canine anal sac squamous cell carcinoma which underwent medical (meloxicam) management alone, resulting in survival of up to seven months. No metastases were identified. Squamous cell carcinoma, although extremely uncommon, should be considered as a possible differential diagnosis when a dog is presented for investigation of an anal sac mass. Topics: Anal Gland Neoplasms; Anal Sacs; Animals; Anti-Inflammatory Agents, Non-Steroidal; Carcinoma, Squamous Cell; Diagnosis, Differential; Dog Diseases; Dogs; Female; Male; Meloxicam; Thiazines; Thiazoles | 2015 |
A selective cyclooxygenase-2 inhibitor prevents inflammation-related squamous cell carcinogenesis of the forestomach via duodenogastric reflux in rats.
Duodenal reflux causes inflammation-related squamous cell carcinogenesis in the forestomach of rats without any carcinogens. The aim of this study was to investigate the efficacy of a selective cyclooxygenase (COX)-2 inhibitor, meloxicam, in preventing this carcinogenesis.. A series of 188 rats underwent a surgical duodenogastric reflux procedure and were divided into 2 groups. One group was given commercial chow (control group), and the other was given experimental chow containing meloxicam (0.3 mg/kg body weight/day) (meloxicam group). The animals were sequentially sacrificed at Weeks 20, 30, 40, 50, and 60 after surgery. The forestomach was examined for the presence of carcinoma, the incidence of reflux-related morphological changes, COX-2 expression, and its activity.. At Week 60, squamous cell carcinoma developed in 8 of 21 animals (38%) in the control group, but none of 20 (0%) in the meloxicam group (P<.05). In addition, basal cell dysplasia developed in 19 of 21 (90%) animals in the control group, but only 4 of 20 (20%) in the meloxicam group (P<.01). COX-2 immunoreactivity was predominantly detected in macrophages in the epithelial stroma. Compared with nonsurgical rats, RNA expression of COX-2 in the epithelium was up-regulated, reaching peak at an early stage of Week 20 in both groups (P<.005). The expression of microsomal prostaglandin E synthase-1 was lower in the meloxicam group than in the control group. PGE2 production was significantly suppressed throughout the experiment in the meloxicam group compared with the control group (P<.005).. Meloxicam was effective in preventing reflux-induced squamous cell carcinogenesis via an inflamed squamous epithelium. Topics: Animals; Carcinoma, Squamous Cell; Cyclooxygenase 2; Cyclooxygenase 2 Inhibitors; Dinoprostone; Duodenogastric Reflux; Immunohistochemistry; Inflammation; Male; Meloxicam; Random Allocation; Rats; Rats, Inbred F344; Stomach Neoplasms; Thiazines; Thiazoles | 2009 |
What is your diagnosis? Squamous cell carcinoma of the uropygial gland.
Topics: Animals; Anti-Infective Agents, Local; Anti-Inflammatory Agents, Non-Steroidal; Antineoplastic Agents; Bird Diseases; Carcinoma, Squamous Cell; Chlorhexidine; Diagnosis, Differential; Enrofloxacin; Female; Fluoroquinolones; Immunohistochemistry; Meloxicam; Parrots; Sebaceous Gland Neoplasms; Thiazines; Thiazoles; Treatment Outcome | 2007 |