View clinical trials related to Gastric Cancer.
Filter by:There are four capital reconstructions after total gastrectomy which is widely used in China. Life quality is the only standard to evaluate postoperative results of different reconstructions. In order to determine the best reconstruction after total gastrectomy, we designed this study to compare life qualities of four reconstructions.
The purpose of this study is to assess the usefulness of laparoscopic surgery for gastric cancer in comparison with open gastrectomy.
The primary goal of this phase II trial is to evaluate the response rate of combination chemotherapy with S-1 and Irinotecan in patients with advanced gastric cancer as a first-line therapy.
Recently, cytokine polymorphisms are considered to play an important role in the pathogenesis of peptic ulcer and gastric cancer. We intended to clarify the association between polymorphisms of pro-inflammatory and anti-inflammatory cytokines, and the susceptibility to gastric cancer, gastric ulcer and duodenal ulcer in Japan, and to detect the individuals who have higher risks for gastrointestinal disease development.
S-1 is a novel oral fluorouracil antitumor drug that consists of tegafur which is a prodrug of 5-fluorouracil (5-FU); 5-chloro-2,4-dihydropyridine (CDHP), which inhibits dihydropyrimidine dehydrogenase (DPD) activity; and potassium oxonate (Oxo), which reduces gastrointestinal toxicity. 5-FU is metabolized by CYP2A6 and DPD. In this study, the researchers investigate the influences of differences in activities of CYP2A6 and DPD on pharmacokinetics and pharmacodynamics of S-1 and clinical outcomes in digestive organ cancer patients treated with S-1.
Thermal therapy (hyperthermia, or heat) increases chemotherapy cancer cell kill. By itself, thermal therapy can also kill cancer cells. Whole body thermal therapy is a systemic treatment; whole-body fever-range thermal therapy can safely treat cancer cells wherever they are throughout the entire body. In this study, we are testing the combination of fever-range heat treatment and chemotherapy to test 1) The response of three types of cancer (small-cell lung, neuroendocrine cancer, lung cancer, and gastric cancer) to the thermo-chemotherapy improves cancer response compared to the effect of only chemotherapy drugs in current use; 2) whether the thermo-chemotherapy treatment helps the person's own body fight the cancer cells; and 3) whether this treatment is safe and comfortable for the patient. This study does not offer heat treatment alone. Any patient with inoperable or metastatic small cell lung cancer, neuroendocrine cancer (any organ), gastric cancer, or lung cancer, can be treated with the Phase II protocol therapy; however, the patient will need to undergo selected medical tests to make sure this treatment would be safe for them.
Background: Gastric carcinoma (GC) remains among the most frequent malignancies in Taiwan as well as in the world and also one of leading causes of cancer-related death. Accumulating evidence shows that chronic inflammation leads to the occurrence of cancers, including GC, via multiple mechanisms. Cyclooxygenase-2 (COX-2) is a crucial enzyme in inflammatory process and is shown to be up-regulated in a variety of cancers. Therefore, COX-2 may play an important role in carcinogenesis. The hallmarks of cancer include continuing proliferation, evading apoptosis, prohibiting immunity, promoting angiogenesis, enhancing invasion and metastasis. We hypothesize that COX-2 induces carcinogenesis through multiple mechanistic strategies and interactions of multiple genes simultaneously. Laser capture microdissection (LCM) for obtaining pure cancer cells and microarray technology and analysis are now generally accepted as powerful tools in genomic research, providing reliable microdissection of cancer cells and simultaneous analysis of whole genome. Aim: Use microarray technology to investigate patterns of genomic change related to differential COX-2 expression and their clinicopathological association in GC. Materials: GC cell lines are transfected with COX-2-expressing vector to establish cell lines with differential levels of COX-2 expression. Clinical specimens are obtained from surgical resection of GC proved by pathology at the Surgical Department of National Taiwan University Hospital, which COX-2 expression is evaluated by Western blotting and immunohistochemical staining. Methods: The present project will use microarray for analysis of genome clustering patterns of surgical tissue (GC cells procured by LCM) and GC cell lines based on differential COX-2 expression levels, to discover significantly positively or negatively associated gene clusterings which contain candidate genes for studies of carcinogenesis mechanisms and establishment of animal experiment models in another component project. Execution: In the first year of this 3-year project, we will establish GC cell lines expressing differential COX-2 levels by transfection of COX-2-expressing vector and focus on analyzing their genomes by microarray. We also start to collect surgical specimens of GC, record clinicopathological characteristics, procure cells by LCM and assess RNA quality, perform microarray experiments. In the second year, we will continue LCM, RNA extraction, and microarray experiments. In the third year, microarray experiment of a total of 60 pairs, including 30 high-COX-2 cases and 30 low-COX-2 cases, of tumor and non-tumoral tissues are completed. Final analysis is carried out to identify clustering, to select candidate genes, and investigate their relationship to clinicopathological characteristics, according to COX-2 expression. These genes are to be subjected to mechanism and animal studies. We expect a better understanding of patterns of gene clustering in differential COX-2 gene expression.
Evidence is rapidly accumulating that chronic inflammation may contribute to carcinogenesis through multiple mechanisms in a number of malignancies, including gastric carcinoma (GC). Cyclooxygenase-2 (COX-2), an inducible enzyme pivotal in the inflammatory response, converts arachidonic acid to the prostaglandins (PGs) required in initiating and maintaining reactions during the inflammatory process. Over-expression of COX-2 has been reported in a wide variety of cancers and is therefore implicated to play an important role in carcinogenesis. COX-2 can be blocked by non-steroidal anti-inflammatory drugs (NSIADs) and is currently the most studied therapeutic target of NSAIDs. Clinically, NSAIDs have long been used to treat various inflammatory or rheumatologic disorders. Earlier clinical studies have confirmed an association between COX-2 over-expression and GC occurrence. The known mechanisms by which COX-2 promotes carcinogenesis include evasion from apoptosis, suppression of immunity, promotion of angiogenesis, and facilitation of invasiveness. However, inflammation-associated factors mediating the effects of COX-2 on carcinogenesis remain largely unknown. Interleukin-6 (IL-6) is a pro-inflammatory cytokine associated with gastritis and GC. Our earlier works has disclosed that IL-6 can promote angiogenic and anti-apoptotic ability of GC. However, the relationship between COX-2 and IL-6 in GC remains unknown. The present study aims to investigate the clinical association between COX-2 and IL-6 in GC, to use a GC cell model for experimental study on causation and mechanism, and to verify the in vivo effect of COX-2 on IL-6 by an animal model. We will collect 100 consecutive surgical samples of GC from the pathology archive of National Taiwan University Hospital and use immunohistochemical stain to compare protein expression in GC. The clinical study is to define certain subgroups of GC exhibiting an association between COX-2 and IL-6. In experimental study, we will clarify the causal relationship by the dose- and time-dependent experiments of COX-2 transient transfection in a GC cell line. COX-2 acts mainly via PGs, like PGE2. Therefore, we also stimulate GC cells with exogenous stimulation of PGE2 and EP receptor 1-4 agonists to determine the possible way(s) by which COX-2 induces IL-6 expression. A selective COX-2 inhibitor NS-398 and various inhibitors of PGE2 receptors are used as well to block COX-2 for determining the signaling pathway of COX-2 on IL-6. Finally, we will establish a stable COX-2 over-expressing transfectant of GC cells and its control vector transfectant for xenograft implantation study on mice. A COX-2 selective agent, celecoxib, will be administered orally to mice and tumor blocks will be harvested for determination of IL-6 expression. The present study will provide clearer understanding of the role of COX-2 on the pro-inflammatory cytokine IL-6 in GC in both clinical and basic aspects. It might also stand for a model capable of systemically investigating the role of COX-2 on various cytokines implicated in GC.