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esophagitis/l tyrosine
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Markers of tyrosine kinase activity in eosinophilic esophagitis: a pilot study of the FIP1L1-PDGFRα fusion gene, pERK 1/2, and pSTAT5.
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The pathogenesis of eosinophilic esophagitis (EoE) is incompletely understood. In certain eosinophilic diseases, activation of tyrosine kinase after fusion of the Fip1-like-1 and platelet-derived growth factor receptor-α genes (F-P fusion gene) mediates eosinophilia via downstream effectors such as
Epidermal growth factor receptor tyrosine kinase inhibitor, erlotinib, and concurrent 5-fluorouracil, cisplatin and radiotherapy for patients with esophageal cancer: a phase I study.
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This phase I trial investigates the safety of combining radiation, 5-fluorouracil (5-FU) and cisplatin with the epidermal growth factor receptor tyrosine kinase inhibitor, erlotinib, in patients with esophageal carcinoma. From April 2000 to January 2005, 11 patients with squamous or adenocarcinoma
[Effect of FOY-305 on post-operative reflux esophagitis in rats (II). Analysis of mechanism in the pathogenesis of reflux esophagitis after total gastrectomy in rats].
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Esophagitis after total gastrectomy has been associated with biliary and pancreatic reflux into the esophagus. The purpose of this study is to clarify the effect of FOY-305 on these factors in the esophagitis. We initially produced esophagitis in rats with total gastrectomy followed by an
Recent research advances in eosinophilic esophagitis.
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OBJECTIVE
Eosinophilic esophagitis (EoE) is a chronic allergic disease triggered by food allergens with an increasing prevalence. This review highlights recent research advances in EoE with a focus on the literature of the past 18 months.
RESULTS
The incidence of EoE in the black population is
Severe Erosive Pill Esophagitis Induced by Crizotinib Therapy: A Case Report and Literature Review.
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Previous case reports have described esophagitis thought to be secondary to crizotinib, an oral tyrosine-kinase inhibitor used in the treatment of anaplastic lymphoma kinase- (ALK-) positive non-small cell lung cancer (NSCLC). In those reports, the interval development of esophagitis was between two
Crizotinib-induced erosive esophagitis in a pediatric patient with neuroblastoma.
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Crizotinib is an oral tyrosine kinase inhibitor, approved by the FDA in 2011, for use in anaplastic lymphoma kinase positive, metastatic, non-small cell lung cancer. Crizotinib inhibits oncogenic protein expression and impairs cellular proliferation in tumors with an overexpressed anaplastic
Prospective study of epidermal growth factor receptor tyrosine kinase inhibitors concurrent with individualized radiotherapy for patients with locally advanced or metastatic non-small-cell lung cancer.
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OBJECTIVE
To establish the safety profile and efficacy of epidermal growth factor receptor tyrosine kinase inhibitors (EGFR-TKIs) concurrent with individualized radiotherapy (RT) in patients with locally advanced or metastatic non-small-cell lung cancer (NSCLC).
METHODS
Between June 2007 and January
Severe Ulcerative Esophagitis Induced by Crizotinib Therapy.
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Crizotinib is an oral tyrosine-kinase inhibitor that inhibits anaplastic lymphoma kinase (ALK) in gene-rearranged non-small cell lung cancer (NSCLC). In 2011, the Food and Drug Administration approved crizotinib for treatment of locally advanced or metastatic ALK-positive NSCLC. The crizotinib
Neurotrophic tyrosine kinase receptor 1 is a direct transcriptional and epigenetic target of IL-13 involved in allergic inflammation.
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Although interleukin (IL)-13 and neurotrophins are functionally important for the pathogenesis of immune responses, the interaction of these pathways has not been explored. Herein, by interrogating IL-13-induced responses in human epithelial cells we show that neurotrophic tyrosine kinase receptor,
The esophagitis to adenocarcinoma sequence; the role of inflammation.
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Esophageal adenocarcinoma (EAC) is the eighth most common cancer worldwide, and approximately 15% of patients survive 5years. Reflux disease (GERD) and Barrett's esophagus (BE) are major risk factors for the development of EAC, and epidemiologic studies highlight a strong association with obesity.
Free radicals and antioxidant systems in reflux esophagitis and Barrett's esophagus.
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OBJECTIVE
Experimental studies suggest that free radicals are involved in acid and pepsin-induced damage of esophageal mucosa. The profile and balance between free radicals and antioxidant systems in human esophagitis are unknown.
METHODS
Superoxide anion and its powerful oxidant reaction with
Eosinophilic disorders in children.
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Many pediatric diseases demonstrate blood or tissue eosinophilia. Included among these disorders are common atopic diatheses such as asthma as well as the rarer conditions of hypereosinophilic syndrome and eosinophilic gastrointestinal disorders. Eosinophil trafficking and activation in target
17β-Estradiol protects the esophageal epithelium from IL-13-induced barrier dysfunction and remodeling.
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The mechanism of MAP kinase activation under acidic condition in feline esophageal smooth muscle cells.
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Reflux esophagitis results from repeated exposure of the esophagus to acidic gastric juice or bile-containing duodenal contents. In Barrett's adenocarcinoma, acid increases proliferation via ERK and p38 MAPK activation. This study was focused on determination of the mechanism(s) underlying MAPKs
Concurrent erlotinib and radiotherapy for chemoradiotherapy-intolerant esophageal squamous cell carcinoma patients: results of a pilot study.
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Concurrent chemoradiotherapy is the standard treatment for patients with locally advanced esophageal squamous cell carcinoma. However, a number of patients present intolerance to chemoradiotherapy because of advanced age or malnutrition. Erlotinib, an inhibitor of epidermal growth factor receptor
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