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M T Taylor et al.
Cancer research, 60(23), 6607-6610 (2000-12-16)
Both the sulfide and sulfone metabolites of sulindac, a nonsteroidal anti-inflammatory drug, display anticarcinogenic effects in experimental models. Sulindac sulfide inhibits cyclooxygenase (COX) enzyme activities and has been reported to suppress ras-dependent signaling. However, the mechanisms by which sulindac sulfone
The developmental toxicity of indomethacin and sulindac.
A Lione et al.
Reproductive toxicology (Elmsford, N.Y.), 9(1), 7-20 (1995-01-01)
Jason L Liggett et al.
Biochimica et biophysica acta, 1840(1), 322-331 (2013-10-02)
Nonsteroidal anti-inflammatory drugs (NSAIDs) are well known for treating inflammatory disease and have been reported to have anti-tumorigenic effects. Their mechanisms are not fully understood, but both cyclooxygenase (COX) dependent and independent pathways are involved. Our goal was to shed
Konstantinos Katoumas et al.
Cancer prevention research (Philadelphia, Pa.), 8(7), 642-649 (2015-05-06)
The antineoplastic properties of the NSAID sulindac have long been studied. The purpose of this study was to explore sulindac's in vivo effects on oral squamous cell carcinoma (SCC) oncogenesis using the hamster cheek pouch oral carcinogenesis model (HOCM). Thirty
Stephen P Fink et al.
Carcinogenesis, 36(2), 291-298 (2014-12-17)
Non-steroidal anti-inflammatory drugs prevent colorectal cancer by inhibiting cyclooxygenase (COX) enzymes that synthesize tumor-promoting prostaglandins. 15-hydroxyprostaglandin dehydrogenase (15-PGDH) is a tumor suppressor that degrades tumor-promoting prostaglandins. Murine knockout of 15-PGDH increases susceptibility to azoxymethane-induced colon tumors. It also renders these
Wan-Ling Liu et al.
Journal of chromatography. A, 1395, 32-40 (2015-04-15)
In this study, an organic polymer monolithic columns, which were prepared via in situ polymerization of alkyl methacrylate-ester (AMA), divinylbenzene (DVB) and vinylbenzyl trimethylammonium chloride (VBTA, charged monomer), were developed as adsorbent for solid-phase microextraction (SPME). Different parameters affecting the
L Saso et al.
Archives of pharmacal research, 24(2), 150-158 (2001-05-08)
The activity of nonsteroidal antiinflammatory drugs (NSAIDs) in rheumatoid arthritis is not only due to the inhibition of the production of prostaglandins, which can even have beneficial immunosuppressive effects in chronic inflammatory processes. Since we speculated that these drugs could
Jigar Pravinchandra Modi et al.
Brain research, 1576, 91-99 (2014-06-27)
The present study analyzed whether administration of sulindac, a non-steroidal anti-inflammatory drug (NSAID) would prevent, attenuate or repair ischemia induced brain injury and reverse functional impairment in a focal ischemia model of stroke. Male Sprague-Dawley rats (weight 250-300 g) were
F M Giardiello
Cancer metastasis reviews, 13(3-4), 279-283 (1994-12-01)
Sulindac is useful in regression of adenomatous polyps. In addition to orally administered sulindac, rectal preparations also appear to be efficacious [32]. However, further studies are necessary to determine whether regression of adenomas, the precursor of colorectal cancer, will cause
Paul J Limburg et al.
Lung cancer (Amsterdam, Netherlands), 79(3), 254-261 (2012-12-25)
Sulindac represents a promising candidate agent for lung cancer chemoprevention, but clinical trial data have not been previously reported. We conducted a randomized, phase II chemoprevention trial involving current or former cigarette smokers (≥30 pack-years) utilizing the multi-center, inter-disciplinary infrastructure
Zhichao Liu et al.
PLoS computational biology, 7(12), e1002310-e1002310 (2011-12-24)
Drug-induced liver injury (DILI) is a significant concern in drug development due to the poor concordance between preclinical and clinical findings of liver toxicity. We hypothesized that the DILI types (hepatotoxic side effects) seen in the clinic can be translated
Shigeru Tatebe et al.
Biochemical and biophysical research communications, 290(5), 1427-1433 (2002-02-01)
Nonsteroidal anti-inflammatory drugs (NSAIDs) have been demonstrated to suppress colorectal tumorigenesis. NSAIDs have also been used to treat inflammatory illnesses. However, the underlying mechanisms of action by NSAIDs have not been completely elucidated. In this study, we reported that among
Stephen X Skapek et al.
Pediatric blood & cancer, 60(7), 1108-1112 (2013-01-03)
Desmoid fibromatosis (desmoid tumor, DT) is a soft tissue neoplasm prone to recurrence despite complete surgical resection. Numerous small retrospective reports suggest that non-cytotoxic chemotherapy using tamoxifen and sulindac may be effective for DT. We evaluated the safety and efficacy
Minjun Chen et al.
Drug discovery today, 16(15-16), 697-703 (2011-06-01)
Drug-induced liver injury (DILI) is a leading cause of drugs failing during clinical trials and being withdrawn from the market. Comparative analysis of drugs based on their DILI potential is an effective approach to discover key DILI mechanisms and risk
Haonan Li et al.
Carcinogenesis, 34(9), 2090-2098 (2013-05-22)
Sulindac has been identified as a competitive inhibitor of aldo-keto reductase 1B10 (AKR1B10), an enzyme that plays a key role in carcinogenesis. AKR1B10 is overexpressed in pancreatic ductal adenocarcinoma (PDAC) and exhibits lipid substrate specificity, especially for farnesyl and geranylgeranyl.
W R Waddell et al.
Journal of surgical oncology, 58(4), 252-256 (1995-04-01)
A putative explanation of the effect of sulindac on adenomatous colon and duodenal polyps from clinical observations and related in vitro experiments is presented. In cells with mutant APC genes, persistent high prostaglandin content of polyps leads to desensitization, downregulation
S Flis et al.
Anticancer research, 26(4B), 3033-3041 (2006-08-05)
The development of colon cancer is probably angiogenesis-dependent. Recently, sulindac sulfide was shown to possess anti-angiogenic activity. In the present work, the question of whether this activity reflects a specific interaction with angiogenesis or is secondary to the effect of
Nathaniel S Rial et al.
Expert review of gastroenterology & hepatology, 6(4), 507-517 (2012-08-30)
To reduce the morbidity and mortality from colorectal cancer (CRC), current clinical practice focuses on screening for early detection and polypectomy as a form of secondary prevention, complemented with surgical interventions when appropriate. No pharmaceutical agent is currently approved for
W R Waddell
Clinical science (London, England : 1979), 95(3), 385-388 (1998-09-09)
1.Sulindac, cis-5-fluoro-2-methyl-1-(p-methylsulphinylbenzylidene)indene-3-ace tic acid, inhibits growth of colon polyps and cancers. This effect has been attributed to inhibition of prostaglandin synthesis but more recent observations indicate that, in vitro, cells that do not have cyclo-oxygenase nor RNA for synthesis of
Silvia Castrignanò et al.
Biochimica et biophysica acta, 1820(12), 2072-2078 (2012-10-06)
Nanosized particles of gold are widely used as advanced materials for enzyme catalysis investigations. In some bioanalytical methods these nanoparticles can be exploited to increase the sensitivity by enhancing electron transfer to the biological component i.e. redox enzymes such as
D E Duggan
Drug metabolism reviews, 12(2), 325-337 (1981-01-01)
Sulindac is a prodrug which, following absorption, rapidly attains a metabolic equilibrium with its active pharmacophore, the sulfide metabolite. At the level of the whole body, the reversible interconversion sulindac in equilibrium sulfide, and the differing distributional and excretory properties
Mohanad Zbidah et al.
Cellular physiology and biochemistry : international journal of experimental cellular physiology, biochemistry, and pharmacology, 30(4), 1072-1082 (2012-12-04)
Sulindac sulfide, a non-steroidal anti-inflammatory drug (NSAID), stimulates apoptosis of tumor cells and is thus effective against malignancy. In analogy to apoptosis of nucleated cells, erythrocytes may undergo eryptosis, an apoptosis-like suicidal erythrocyte death, characterized by cell shrinkage and cell
Xue Zhou et al.
Journal of cellular and molecular medicine, 19(5), 1103-1113 (2015-02-24)
Pulmonary fibrosis (PF) is a disease with an unknown cause and a poor prognosis. In this study, we aimed to explore the pathogenesis of PF and the mechanism of sulindac in attenuating bleomycin (BLM)-induced PF. The rat PF model was
Yinghua Zhang et al.
International journal of molecular medicine, 35(1), 263-270 (2014-11-12)
Accumulating evidence suggests that anti-inflammatory agents and antioxidants have neuroprotective properties and may be beneficial in the treatment of neurodevelopental disorders, such as autism. In the present study, the possible neuroprotective properties of sulindac, a non-steroidal anti-inflammatory drug (NSAID), were
Loretta Aureli et al.
Journal of medicinal chemistry, 48(7), 2469-2479 (2005-04-02)
A novel class of 2-(R)-phenylpropionamides has been recently reported to inhibit in vitro and in vivo interleukin-8 (CXCL8)-induced biological activities. These CXCL8 inhibitors are derivatives of phenylpropionic nonsteroidal antiinflammatory drugs (NSAIDs), high-affinity ligands for site II of human serum albumin
Isaac T Schiefer et al.
Journal of medicinal chemistry, 54(7), 2293-2306 (2011-03-17)
Poor blood-brain barrier penetration of nonsteroidal anti-inflammatory drugs (NSAIDs) has been blamed for the failure of the selective amyloid lowering agent (SALA) R-flurbiprofen in phase 3 clinical trials for Alzheimer's disease (AD). NO-donor NSAIDs (NO-NSAIDs) provide an alternative, gastric-sparing approach
[Sulindac--drug therapy for familial adenomatous polyposis?].
J Zundler et al.
Medizinische Klinik (Munich, Germany : 1983), 88(1), 35-38 (1993-01-15)
[A case of sulindac induced acute pancreatitis].
M Uchihara et al.
Nihon Shokakibyo Gakkai zasshi = The Japanese journal of gastro-enterology, 89(9), 2073-2076 (1992-09-01)
Howard S Moskowitz et al.
Oral oncology, 48(11), 1136-1145 (2012-06-27)
Targeting the epidermal growth factor receptor (EGFR) using the tyrosine kinase inhibitor (TKI) erlotinib has demonstrated activity in aerodigestive tract malignancies. Co-targeting of the G-protein-coupled receptor cyclooxygenase (COX) with EGFR inhibitors has shown promise in preclinical models and early phase
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