Cancers starting in different sections of the stomach may cause different symptoms and tend to have different outcomes. For example, cancers that start at the GE junction are staged and treated the same as cancers of the esophagus. A cancer that starts in the cardia of the stomach but then grows into the GE junction is also staged and treated like a cancer of the esophagus.
For more information, see Esophagus Cancer. A stomach cancer or gastric cancer almost always is an adenocarcinoma. These cancers develop from the cells that form the innermost lining of the stomach the mucosa.
These are cancers of the immune system tissue that are sometimes found in the wall of the stomach. The treatment and outlook depend on the type of lymphoma. For more detailed information, see Non-Hodgkin Lymphoma. These rare tumors start in very early forms of cells in the wall of the stomach called interstitial cells of Cajal. Germinal mutation Gastric fundic gland polyps are observed as an extracolonic feature of FAP.
Occasional malignant transformation has been reported. Somatic mutation Whilst somatic APC mutations are common in gastric cancers, their significance with regards to tumorigenesis remains unclear. It has been postulated that APC mutations play a role in adenoma formation and dysplasia, rather than the promotion of malignant progression.
Case reports exist of familial gastric cancer in Japanese and Korean families with germ line p53 mutations. It has been suggested that LFS may give rise familial clustering of gastric cancer in regions with high gastric cancer incidence. Somatic mutation Loss of functional p53 has been reported in virtually all human cancers including gastric cancers. Data on the significance of p53 mutations in SGC development, progression, and prognosis are conflicting.
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COX2 expression is particularly high in early gastric cancers suggesting that it may play an important role in early events in tumorigenesis. There is conflicting evidence on the association between H. Protein Cyclo-oxygenase 2 is an inducible enzyme responsible for regulating prostaglandin biosynthesis. COX2 activity is normally undetectable in gastric mucosa. The protein is involved in regulation of cell cycle progression in he G1 phase. Inactivation of PTEN is observed in multiple advanced cancers and cancer cell lines.
Germinal mutation Gastric hyperplastic polyps are a recognised feature of Cowden's syndrome although these are generally considered non-neoplastic. Germinal mutation Gastric adenocarcinoma is a recognised part of the hereditary nonpolyposis colon cancer HNPCC spectrum of tumours. Recent data suggest that mutations in known MMR genes in SGCs are uncommon and likely arise as a result of the mutator phenotype, rather than cause it.
Anticancer Res. World J Gastroenterol. J Clin Pathol. Epub May Virchows Arch. J Cell Biol.
What to Know About Stomach Cancer Surgery
Epub Oct El-Omar EM. Best Pract Res Clin Gastroenterol. Am Surg. Int J Cancer. Am J Pathol. Clin Cancer Res. Br Med Bull. Epub Feb Miettinen M, Lasota J. Arch Pathol Lab Med. Cancer Epidemiol Biomarkers Prev.
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J Gastroenterol. Genes Chromosomes Cancer. Pathol Res Pract. Epub May 6. Cancer Res. The vast majority of both benign and malignant tumours of the stomach are of epithelial origin, with mesenchymal and neuroendocrine tumours being much less common. Sarcomas, neuroendocrine carcinoma, primary squamous cell carcinoma and adenoacanthomas. Helicobacter pylori H. Gastric cancer is the second most common cause of cancer-related death globally. Early gastric cancer is most likely asymptomatic in most patients, or may produce non-specific dyspeptic symptoms. Resection with curative intent is the only treatment that will result in long-term survival from gastric adenocarcinoma.
The vast majority of primary lymphomas arising in the stomach are of non-Hodgkin's B-cell type. The gastric mucosa is normally devoid of lymphoid tissue. Patients with primary gastric lymphoma may present with non-specific dyspeptic symptoms, early satiety, or evidence of gastrointestinal haemorrhage due to ulcerating disease.
MALT lymphomas display cellular heterogeneity. Eradication of H. Gastric GISTs are highly cellular and tend to be of either spindle cell or epithelioid subtypes. Surgical resection is the treatment of choice for GISTs. Gastric carcinoid tumours are rare, comprising only 0. Numerous abnormalities of chromosome structure and number have been reported in gastric cancer series although no specific aberration has yet been identified.
Stomach cancer statistics
Comparative genomic hybridization has been used to screen for abnormalities of copy number in gastric cancers. Genes involved and Proteins. CDH1 cadherin 1, type 1, E-cadherin epithelial.
CDH1 encodes E-cadherin, a member of the cadherin superfamily of calcium-dependent cell adhesion molecules. MYC v-myc myelocytomatosis viral oncogene homolog avian. The C-MYC proto-oncogene encodes a transcription factor involved in activation of a number of genes involved in cell proliferation. MET met proto-oncogene hepatocyte growth factor receptor. The MET proto-oncogene encodes a transmembrane high affinity receptor for hepatocyte growth hormone. A small number of case reports exist of germ line mutations in MET predisposing to gastric cancer.
Overexpression of C-MET has been reported in both histological subtypes of gastric cancer and is associated with poor prognostic features. APC adenomatous polyposis coli. Gastric fundic gland polyps are observed as an extracolonic feature of FAP. Whilst somatic APC mutations are common in gastric cancers, their significance with regards to tumorigenesis remains unclear. TP53 Tumour protein p53 Li-Fraumeni syndrome. The transcription factor p53 plays a critical role in cell cycle arrest, senescence, DNA repair and apoptosis.
Loss of functional p53 has been reported in virtually all human cancers including gastric cancers. FGFR2 fibroblast growth factor receptor 2. Cyclo-oxygenase 2 is an inducible enzyme responsible for regulating prostaglandin biosynthesis. RUNX3 runt related transcription factor 3. SPEN spen family transcriptional repressor. The phosphate and tensin homolog acts as a tumour suppressor.
Gastric hyperplastic polyps are a recognised feature of Cowden's syndrome although these are generally considered non-neoplastic. Gastric adenocarcinoma is a recognised part of the hereditary nonpolyposis colon cancer HNPCC spectrum of tumours. PMID Interrelationship between chromosome 8 aneuploidy, C-MYC amplification and increased expression in individuals from northern Brazil with gastric adenocarcinoma. Molecular pathology of familial gastric cancer, with an emphasis on hereditary diffuse gastric cancer.
Evidence for two modes of allelic loss: multifocal analysis on both early and advanced gastric carcinomas. Helicobacter pylori CagA protein targets the c-Met receptor and enhances the motogenic response. Combination of gastric atrophy, reflux symptoms and histological subtype indicates two distinct aetiologies of gastric cardia cancer. Gastric adenocarcinoma arising from fundic gland polyps in a patient with familial adenomatous polyposis syndrome. Inverse relationship between APC gene mutation in gastric adenomas and development of adenocarcinoma.