Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0024623 (gastric cancer)
 36,219 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Gastric cancer is one of the leading causes of cancer mortality in the world. Gastric adenocarcinomas account for more than 95% of gastric tumors, whereas gastrointestinal stromal tumors (GISTs) are the most common neoplasms of the rare gastric mesenchymal tumors. Although the incidence of mid-distal gastric adenocarcinomas is decreasing, the incidence of gastroesophageal junctional tumors and Barrett's adenocarcinomas is increasing for unknown reasons. The majority of gastric tumors are sporadic in nature. However, there are rare, inherited gastric cancer predisposition traits, such as germline p53 (Li-Fraumeni syndrome) as well as E-cadherin (CDH1) alterations in familial diffuse gastric cancers. Gastric cancer has been observed to be part of the spectrum of neoplasms associated with germline mismatch repair gene (MMR) alterations that give rise to the hereditary nonpolyposis colorectal cancer (HNPCC) entity. Comparative genomic hybridization analyses have identified several amplifications and losses of DNA copy numbers in gastric cancers. Loss of heterozygosity (LOH) studies have shown several chromosomal loci with significant allelic loss, thus indicating the possibility of harboring a tumor suppressor gene important in gastric tumorigenesis. Microsatellite instability (MIS) and associated alteration of the TGF-bIIR, IGFRII, BAX, E2F-4, hMSH3, and hMSH6 genes are found in a subset of gastric carcinomas. Cell adhesion molecule abnormalities such as those involving CDH1 may play an important role in diffuse-type gastric cancer development. Although, multiple somatic alterations have been described in gastric carcinomas at the molecular level, the significance of these changes in gastric tumorigenesis remains to be established in most instances. The critical molecular alterations in gastric cancers that may lead to advances in our armamentarium to combat this lethal disease remain to be fully characterized.
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PMID:Molecular biology of gastric cancer. 1197 14

Gastric cancer is one of the world's most common cancers and is a leading cause of cancer death worldwide. Neoplasia of the stomach is mainly composed of adenocarcinomas, which for more than 95% of cases. Although mesenchymal tumors (i.e., stromal tumors, leiomyomas and leiomyosarcomas, and schwannomas), primary lymphomas, and carcinoid tumors can also arise in the stomach, malignant tumors of these types occur much less often.
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PMID:Molecular and biologic basis of upper gastrointestinal malignancy. Gastric carcinoma. 1242 50

Topics discussed here include PTEN mutations and colonic polyps; WNT signaling, APC, beta-catenin, and gastrointestinal neoplasms; mismatch-repair genes (MLH1, MSH2, PMS1, MSH6) and hereditary nonpolyposis colorectal cancer; MYH mutations and autosomal recessive colorectal tumors; STK11 mutations and Peutz-Jeghers syndrome; TGFbeta and gastrointestinal cancer; BMPR1A mutations and juvenile polyposis; FGF/FGFR alterations in gastrointestinal neoplasms; PTCH mutations and gastrointestinal neoplasms; RUNX3 expression and gastric cancer; role of mucins in gastric carcinogenesis; KIT, PDGFRalpha, and gastrointestinal stromal tumors; intestinal neurofibromatosis; and gastrointestinal tumors in other disorders.
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PMID:Molecular dimensions of gastrointestinal tumors: some thoughts for digestion. 1451 68

Despite its decline in incidence in developed countries, gastric cancer is the second digestive cancer in France and remains the second most cause of cancer-related deaths in the world. Gastritis induced by H. pylori infection and food regimen are the most frequent precancerous gastric factors. However there is no definite clinical evidence of the benefit of eradication on cancer risk. By waiting for effective anti-H. pylorivaccine, H. pylori should be only eradicated in selected patients at the highest risk of cancer. The stake is to develop inexpensive tests for identification of individuals at high risk, depending on genotypic polymorphisms of both the bacterium and the host. The endoscopic diagnosis is currently made at an advanced stage, related to non-specific and late symptoms. The prognosis remains poor with 5 years overall survival rate less than 20%. Surgical resection with D1 lymphadenectomy is the gold standard curative treatment. An adjuvant therapy with chemoradiotherapy should be considered for patients at high risk for recurrence. Gastric cancer is considered to be a chemotherapy sensitive disease, but polychemotherapy regimens (fluorouraci +/- cisplatin +/- epirubicin) result in modest increased survival (median 9 months); yet, the promising effectiveness of new drugs (irinotecan, docetaxel, oxaliplatin, capecitabin, targeted biotherapies) makes us hope an improvement of results. A number of entities, linitis plastica, gastric MALT lymphoma and stromal tumors should be recognised, because must have a different treatment.
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PMID:[Stomach cancer]. 1582 91

Gastrointestinal stromal tumors (GISTs) are thought to originate from mesenchymal stem cells that differentiate toward the interstitial cells of Cajal (ICCs). The frequent occurrence of activating mutations involving exon 11 of c-Kit gene in sporadic GISTs indicates an important role in genesis of this tumor type. In the present study we examined c-Kit gene mutations in a series of GISTs and also in ICCs of surrounding normal tissues. Samples from 18 patients were monitored immunohistochemically for c-Kit expression and microdissected for sequencing analysis of exons 9, 11, 13, and 17 of the c-Kit gene. It was revealed to be mutated in exon 11 or adjacent introns in 9 out of the total of 18 (50.0%) GISTs. In 6 (33.3%) cases, mutations in ICCs were also detected in the same exon. With stomach GISTs, 8 of 16 (50.0%) cases harbored mutations and 4 had mutations in background ICCs (25.0%). In contrast counterpart ICCs in gastric cancer cases harbored no c-Kit gene mutations (0 out of 24=0%) (P<0.02). ICCs undergoing c-Kit mutation as a possible early initiation step in GIST tumorigenesis may thus have pre-neoplastic potential.
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PMID:Frequent c-Kit gene mutations not only in gastrointestinal stromal tumors but also in interstitial cells of Cajal in surrounding normal mucosa. 1629 6

The term gastrointestinal stromal tumors (GISTs) is defined diagnostically as the main group of mesenchymal tumors with spindle or epithelioid cells arising from the wall of the gastrointestinal tract with immunohistochemical reactivity for CD117 antibody. Previous studies revealed that cells in GISTs express a growth factor receptor with tyrosine kinase activity (termed c-kit), which is the product of the c-kit proto-oncogene. The most specific and practical diagnostic criteria for GISTs are: immunohistochemically determined c-kit (CD117) expression; mitotic score; and tumor size. A small GIST concomitant with early gastric cancer is rarely encountered clinically. Herein we have reported a case of a 1.1-cm GIST detected by esophagogastroduodenoscopy concomitant with a IIc type of early gastric cancer (signet ring cell type). It was detected during a routine physical health examination. To our knowledge, this is the first report of a small GIST concomitant with a signet ring cell type of early gastric cancer.
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PMID:Small gastrointestinal stromal tumor concomitant with early gastric cancer: a case report. 1652 Dec 3

Gastrointestinal stromal tumors (GISTs) are rare mesenchymal neoplasms with an annual incidence of approximately 10 to 20 per 1 million cases. Although pathologists have often observed incidental small GISTs in the stomach resected from patients with gastric cancer, no report on the real incidence of gastric GISTs is available. In this study, 100 whole stomachs resected from patients with gastric cancer were sectioned at 5-mm intervals and hematoxylin and eosin-stained slides (a mean of 130 slides for each case) were examined for microscopic GISTs. KIT (CD117), CD34, and desmin expression of the incidental tumors was evaluated by immunohistochemistry, and genomic DNA extracted from formalin-fixed and paraffin-embedded tumor tissues was analyzed for c-kit gene mutations in exon 11. In 35 of the 100 whole stomachs, we found 50 microscopic GISTs, all of which were positive for KIT and/or CD34 and negative for desmin. Most microscopic GISTs (45/50, 90%) were located in the upper stomach. Two of the 25 (8%) microscopic GISTs had c-kit gene mutations. Fifty-one leiomyomas with positive expression for desmin were observed in 28 of the 100 stomachs. Both leiomyomas and GISTs were found in 12 stomachs. These results indicate that microscopic GISTs are common in the upper portion of the stomach. Considering the annual incidence of clinical GISTs, only few microscopic GISTs may grow into a clinical size with malignant potential. Further studies are required to clarify the genetic events responsible for the transformation of microscopic GISTs to clinical GISTs.
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PMID:High incidence of microscopic gastrointestinal stromal tumors in the stomach. 1699 66

Minimally invasive surgery has become the preferred treatment strategy for most gastrointestinal diseases. Owing to specific anatomical reasons and in highly selected patients, gastric diseases offer the opportunity for an endogastric approach. In this setting, 2 different strategies may be used: (1) endogastric mucosectomy for superficial lesions such as highly selected early gastric cancer and (2) stapled wedge resection for intramural lesions such as gastric stromal tumors. A detailed description of this simple and radical treatment option is performed which requires standard laparoscopic instrumentation and basic laparoscopic skills. With the widespread of this approach, endogastric surgery is expected to become the preferred initial step in the management of various gastric diseases.
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PMID:Endogastric surgery for gastric diseases--simplifying technical aspects. 1804 2

Diagnostic and treatment strategies for gastrointestinal stromal tumors (GISTs) have evolved greatly since the introduction of molecularly targeted therapies. Although several clinical practice guidelines are extant, such as those published by the National Comprehensive Cancer Network and the European Society of Medical Oncology, it is not clear as to whether these are appropriate for clinical practice in Japan. Therefore, clinical practice guidelines for the optimal diagnosis and treatment of GIST tailored for the Japanese situation have often been requested. For this reason, the Japanese Clinical Practice Guideline for GIST was proposed by the GIST Guideline Subcommittee, with the official approval of the Clinical Practice Guidelines Committee for Cancer of the Japan Society of Clinical Oncology (JSCO), and was published after assessment by the Guideline Evaluation Committee of JSCO. The GIST Guideline Subcommittee consists of members from JSCO, the Japanese Gastric Cancer Association (JGCA), and the Japanese Study Group on GIST, with the official approval of these organizations. The GIST Guideline Subcommittee is not influenced by any other organizations or third parties. Revision of the guideline may be done periodically, with the approval of the GIST Guideline Subcommittee, either every 3 years or when important new evidence that might alter the optimal diagnosis and treatment of GIST emerges. Here we present the English version of the Japanese Clinical Practice Guideline for GIST prepared by the GIST Guideline Subcommittee.
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PMID:Clinical practice guidelines for gastrointestinal stromal tumor (GIST) in Japan: English version. 1894 52

The author reports a very rare case of sporadic primary multiple extragastrointestinal stromal tumors (EGISTs) of the omentum associated with different mutations of the exon 11 of the c-kit gene in a 75-year-old man with gastric cancer. During an operation for the cancer, two solid tumors (10 mm and 8 mm) were found in the omentum. Both tumors consisted of cellular spindle cells. Mitotic figures were two and three per 50 high power fields. The tumor cells were positive for KIT, CD34 and vimentin, but negative for desmin, S100 protein, alpha-smooth muscle actin and p53 protein. Ki67 labeling was 2% and 3%. The larger EGIST showed a deletion of codons 552-558 of exon 11 of the c-kit gene, while the smaller EGIST had a point mutation at codon 559 (GTT-->GAT) in exon 11 of the c-kit gene. Exons 9, 13, and 17 of the c-kit gene, and exons 12 and 18 of the platelet derived growth factor receptor alpha genes showed no mutations. The case shows that sporadic multiple EGISTs can occur in the omentum.
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PMID:Primary multiple extragastrointestinal stromal tumors of the omentum with different mutations of c-kit gene. 1908 44


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