View clinical trials related to Stomach Neoplasms.
Filter by:This study is for people with advanced gastric or gastroesophageal cancer. This study is being done to find out how long it takes tumors to grow after patients take the drugs capecitabine, oxaliplatin and cetuximab. Capecitabine (also called Xeloda) is a drug that has been approved by the Food and Drug Administration (FDA). Capecitabine has been approved for treatment of cancer of the colon and rectum. Oxaliplatin is another drug approved by the FDA. Oxaliplatin is also approved for treatment of cancer of the colon and rectum. Cetuximab is also a drug approved by the FDA for the treatment of cancer of the colon and rectum, as well as cancer of the head and neck. Capecitabine, oxaliplatin and cetuximab are not approved for gastric or gastroesophageal cancer. They are considered experimental drugs for this study. The purpose of this study is to see how long it takes patients' tumors to progress when they are taking oxaliplatin and capecitabine. Another purpose is to see how many tumors respond to this drug combination. The investigators also want to see how long people live when taking these drugs. The side effects of this drug combination will also be evaluated. This study will also measure the levels of certain genes (the cell's blueprint) in tumors. These genes affect how peoples' bodies react to the cancer drugs. Genes will also be measured in the blood. The investigators want to see how these genes can predict response to these study drugs.
This study is for people with advanced gastric or gastroesophageal cancer. This study is being done to find out how long it takes tumors to grow after receiving treatment with the drugs irinotecan (also known as CPT-11) and docetaxel (also known as Taxotere). Irinotecan is a drug that has been approved by the Food and Drug Administration (FDA). Irinotecan has been approved for treatment of cancer of the colon and rectum. Docetaxel is another drug approved by the FDA. Docetaxel is approved for treatment of breast, prostate and lung cancer. However, the FDA has authorized the use of irinotecan and docetaxel in this study. This study will evaluate the effects of these drugs on participant's tumors. The side effects of the combination of irinotecan and docetaxel will also be evaluated. This study will also measure the levels of certain substances in participant's tumors. These substances, called genes (which are the cell's blueprint), affect how people's bodies react to the cancer drugs. Genes will also be measured in participant's blood. The researchers want to see if these substances can predict response to the study drugs.
RATIONALE: Drugs used in chemotherapy, such as S-1 and cisplatin, work in different ways to stop the growth of tumor cells, either by killing the cells or by stopping them from dividing. Giving more than one drug (combination chemotherapy) may kill more tumor cells. Giving chemotherapy before surgery may shrink the tumor so that it can be removed. It is not yet known whether giving S-1 together with cisplatin before surgery is more effective than surgery followed by S-1 in treating stomach cancer. PURPOSE: This randomized phase III trial is studying how well giving S-1 together with cisplatin before surgery works compared to surgery followed by S-1 in treating patients with stage III stomach cancer.
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.
In this study, the investigators will use P-HDFL, a regimen with high tumor remission rate (~ 60-70%) and with only modest treatment-associated toxicities, as induction chemotherapy for patients with non-resectable gastric cancer. For those patients who have achieved complete response (CR) or partial response (PR), DI will be used to "consolidate" the remission. For those patients who fail to achieve remission by P-HDFL, DI will be used as salvage chemotherapy. The efficacy and toxicities of DI in these two settings will be evaluated in this prospective study.
Phase I study: To investigate primary objective (maximal tolerated dose and dose-limiting toxicity) and secondary objectives (pharmacokinetics, safety, estimation of a recommended dose, and anti-tumor effect by evaluable case) of E7070 in patients with gastric cancer who are extensive or intermediate metabolizer type (EM/IM) to CYP2C9 and CYP2C9 by intravenously administering once every 3 weeks. Phase IIa study: To investigate primary objective (response rate for efficacy assessment) and secondary objectives (frequency and severity of adverse drug reactions, and pharmacokinetics) of E7070 in patient with gastric cancer who are EM/IM type by intravenously administering once every 3 weeks.
This is a phase II study of taxotere, cisplatin and irinotecan (CPT-11) used in combination to treat metastatic esophageal and gastric cancer in an effort to see what effects (good and bad) the combination may have on the patients cancer.
The purpose of this study is to investigate the effect of selective COX-II inhibitor in patients with regionally disseminated stomach cancer treated by palliative resection (so called R1 or R2 gastrectomy).