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Query: UMLS:C0027627 (metastases)
 103,950 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

When gastric cancer patients' leucocytes were exposed to a panel of tumour extracts, leucocyte migration reactivity was "positive" before operation (90% of cases), it declined after surgery and it reappeared in patients with local recurrence or metastases. In patients with non-malignant gastric diseases, "positive" reactivity against tumour extracts was associated almost exclusively with atrophic gastritis with and without intestinal metaplasia (24/43 cases). "Positive" patients also showed a pathological migration index with an extract of normal gastric mucosa.
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PMID:A modified leucocyte migration assay as indicator of malignant and non-malignant gastric mucosal alteration. 89 59

Carcinoid tumors of the stomach are rare (0.4% of all malignancies of the stomach). Long-lasting hypergastrinemia, most often due to chronic atrophic gastritis, leads to hyperplasia of ECL-cells in the gastric fundic mucosa with consequent dysplasia or neoplasia. Between 1974 and 1988 four patients underwent surgical treatment after diagnosis of a gastric carcinoid tumor. One patient was treated by local excision, two by subtotal resection and one patient underwent complete gastrectomy. None of the patients had local or distant metastases or died in the follow-up period due to tumor progression. The different approaches to surgical therapy are discussed.
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PMID:[Carcinoid tumor of the stomach--aspects of surgical therapy]. 186 Mar 53

During recent decades an increasing number of case reports have pointed at a relation between atrophic gastritis type A and gastric carcinoid. This relation has now been quantitatively documented in endoscopic screening studies. Among patients with pernicious anaemia the prevalence of gastric carcinoid was 2-9%. Many of these carcinoids, however, remain subclinical. The majority are broadbased polypoid tumours. Most are situated in the gastric body or fundus. Of 95 patients with atrophic gastritis and gastric carcinoid reported in the literature, 60 (63%) had multicentric tumours and 13 (14%) lymph node and/or hepatic metastases. Microscopically, the tumours, which are frequently of the enterochromaffin-like cell type, show various structural differentiations, glandular differentiation indicating malignant potential. Purely intramucosal carcinoids have been described. The precurser lesion to such "early carcinoids", as well as to infiltrating carcinoids, is probably hyperplasia of endocrine cells in the atrophic fundic mucosa. Such hyperplasias, whether nodular or diffuse, are quantitatively related to hypergastrinaemia, which is a typical feature of antrum sparing (type A) atrophic gastritis. Most tumours can be treated endoscopically, although antrectomy with abolition of hypergastrinemia may be the definitive treatment. It seems that the risk of developing gastric carcinoid 'per se' does not justify regular gastric screening in patients with type A atrophic gastritis. However, as these patients also run an increased risk of developing several benign diseases, gastric adenocarcinoma, and probably also pancreatic malignancy, regular survey in selected cases is indicated.
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PMID:Atrophic gastritis and gastric carcinoid tumours. 278

Since 1984, an experimental and clinical study on the relation between PGE and gastric carcinoma has been performed by determining PGE content in the bioptic gastric mucosa and plasma. It is found the PGE content in the gastric mucosa and plasma is increased in all patients with gastric cancer, especially with signet ring cell carcinoma. It is higher in the regional lymph node metastasis than in the early cancer, extensive metastases and normal subjects. The PGE content in the plasma is reduced obviously 7-10 days after operation but is increased markedly in recurrent patients. There is no significant difference in extensive metastases, relapse free and normal subjects. The PGE content in the plasma is significantly higher in gastric carcinoma than in chronic atrophic gastritis, but no difference is present between chronic atrophic gastritis and normal subjects.
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PMID:[Prostaglandin E (PGE) and gastric carcinoma]. 303 44

Follow-up examinations were carried out in 55 patients with small carcinoid tumours in the stomach (diameter 0.5-1.7 cm). For the most part, the tumours were located within the body and fundus of the stomach, with only 3 being found in the antrum. Thirty-five of the 55 patients (63.6%) had multiple gastric carcinoids, while in 46 patients (83.6%) concomitant chronic atrophic gastritis was also present. Eight patients were treated surgically, while 47 patients were merely kept under endoscopic/bioptic surveillance. In 34 out of 40 patients in whom the diagnosis had been established more than 6 months previously (longest observation period 13 years), follow-up findings were available (7 surgical patients, 27 non-operated patients). The patients submitted to surgery (average follow-up period 3.5 years) are alive and free of complaints between 1 and 9 years post-op; no metastases have occurred, but a recurrent tumour has developed in a single patient. Among the 27 non-operated patients (average follow-up period 3.6 years), 3 have died of diseases unrelated to the carcinoid tumours, in none of the other patients has there been any change in the findings. On the basis of these results it is concluded that, in carcinoid tumours of the stomach with a diameter of less than 1.0 cm, surgical treatment is not absolutely necessary, and that, in comparison with the risks represented by surgical mortality and post operative morbidity, regular endoscopic/bioptic follow-up can be considered to be adequate.
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PMID:[The prognosis of carcinoid tumors of the stomach]. 305 76

Neoplastic proliferations of neuroendocrine cells (NE) may occur throughout the entire GI tract but affect particularly appendix and ileum ("midgut carcinoids"), rectum ("hindgut carcinoids"), as well as stomach and the duodenum ("foregut carcinoids"). Only more exceptionally, they arise in the esophagus, jejunum and colon. The NE tumors encompass a heterogeneous gross and microscopic structural spectrum, ranging from inconspicuous microproliferations ("mucous membrane nevi") to bulky tumor masses. Their growth patterns are usually characteristic and easily recognized. In doubtful cases their NE differentiation becomes established by a characteristic silver affinity, by the ultrastructurally observed presence of characteristic "endocrine" secretion granules, and by immunohistochemically detectable occurrence of "pan-NE markers" (neuron-specific enolase, chromogranins, and synaptophysin), biogenic amines (mainly serotonin), and neurohormonal peptides. Foregut carcinoids usually contain serotonin, gastrin, and somatostatin, midgut carcinoids often only serotonin and tachykinins, whereas the hindgut carcinoids as a rule are multihormonal with a wide spectrum of hormonal peptides, including even insulin. Most GI NE tumors are found in the appendix (50%) and the ileum (30%). Practically all (98%) of the appendiceal NE tumors are benign. They have recently been proposed as arising from apparently Schwann-cell-related NE cells in the submucosa, whereas the ileal--and probably also all the other non-appendiceal NE tumors--are derived from the totipotential cells in epithelial crypts of the mucosa. Among the ileal NE neoplasms a large number can metastasize and result in a fatal outcome. The ability to metastasize is related to the size and to the multiplicity of the primary tumors at the time of initial diagnosis and, to some extent, to their histopathologic growth pattern. Now, some relationship between the prognosis and the cytochemically assessed nuclear DNA content of the NE tumor cells has also been established; not less than about 1/4 to 1/3 seem to be aneuploid. Almost 90% of the rectal carcinoids are benign. Exceptionally, a highly malignant NE neoplasms can arise from the colon/rectum--as well as from the esophagus--composed of NE cells of small and intermediate size. The NE tumors of the stomach are often composed of ECL (enterochromaffin-cell-like) cells; such ECL cell carcinoids are related to atrophic gastritis with pernicious anemia; experimentally, they can be induced by hypergastrinemia in rats. Duodenal carcinoids often contain psammoma bodies and can be associated with neurofibromatosis.
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PMID:Neuroendocrine tumors of the gastrointestinal tract. 329 Aug 66

Prompted by the lack of knowledge of the distribution of gastric lymphatics and the discrepancy between the incidence of lymph node metastases from intramucosal gastric carcinoma versus intramucosal colonic carcinoma, we undertook a study of the distribution of lymphatics in normal, abnormal non-neoplastic, and neoplastic gastric mucosas. The study involved the histologic, immunocytochemical, and electron microscopic evaluation of a total of 47 gastric biopsy, polypectomy, and resection specimens and showed that the gastric lymphatics normally begin as a plexus of vessels immediately superficial to, within, and below the muscularis mucosae. The upper two-thirds of the gastric lamina propria is normally devoid of lymphatics. This distribution is maintained throughout the cardia, fundus, and antrum and is also maintained in hyperplastic and neoplastic tissues. However, in patients with severe atrophic gastritis in which the overall height of the gastric mucosa is markedly decreased, lymphatic capillaries may be found near the surface epithelium. The relevance of these findings to the behavior of early gastric cancer is discussed.
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PMID:Lymphatic distribution of the stomach in normal, inflammatory, hyperplastic, and neoplastic tissue. 330 16

Records of the 30 cases of gastric carcinoid at the Mayo Clinic showed that the gastric mucosa was normal, hyperplastic, or atrophic (nonantral) in 12, 2, or 16 patients, respectively. In the atrophic group, the tumors were in the gastric body and fundus; small, polypoid, and multicentric; and associated with fundal argyrophil cell hyperplasia. In immunocytochemical studies, minor tumor cell populations stained positively for 5-hydroxytryptamine, gastrin, and somatostatin in 1 case and for 5-hydroxytryptamine in 3 others. Metastasis occurred in 3 patients. Twelve patients had pernicious anemia. Parietal cell or intrinsic factor antibodies or both were present in all 12 patients tested. Each of the 7 patients with an intact antrum had massive hypergastrinemia. No common HLA-A, -B, or -DR antigen pattern was detected among the 10 patients tested. The results suggest that nonantral gastric atrophy predisposes to gastric carcinoid as well as to gastric carcinoma.
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PMID:The syndrome of gastric argyrophil carcinoid tumors and nonantral gastric atrophy. 619 1

A method for measurement of gastrin in human antral mucosa or in extragastric tissue has been developed and validated. Tissue gastrin was extracted by boiling followed by homogenization at neutral pH. Extractable gastrin immunoreactivity was measured by radioimmunoassay using an antiserum with equal affinity towards G-17 I, G-17 II, G-34 I and G-34 II molecular forms. Almost all extractable gastrin immunoreactivity was recovered after a single extraction and no significant interference by other peptides and/or substances present in tissue was found. The mean gastrin concentration in antral mucosa of healthy subjects was similar to that observed in duodenal ulcer patients, while patients with type A chronic atrophic gastritis or with antral gastrin cell hyperplasia had mean values significantly higher. Gastrin concentration in all specimens from gastrinoma or its metastases was above the upper limit of the range of control tissue. Measurement of tissue gastrin seems to be a valuable tool in the diagnosis of antral gastrin cell hyperplasia and Zollinger-Ellison syndrome.
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PMID:Measurement of immunoreactive gastrin in tissue. 650 40

A series of 60 patients with early gastric cancer (EGC) operated on from 1.1.1971 to 31.5.1983 is reviewed; since three cases had two and another case even had three synchronous primitive neoplastic lesions, a total of 65 EGC are reported. A prevalence of the "ulcerated" types, a large variability of lesion size and a prevalence of location along the lesser curvature and the antrum was observed; 38 EGC (58.46%) were confined to the mucosa (m), 27 (41.54%) also involved the submucosa; histologically, 53 EGC (81.54%) were of the intestinal type, and 12 (18.46%) were of the diffuse type. Associated lesions, above all chronic atrophic gastritis, intestinal metaplasia and adenomatous gastric polyps were often found. Clinical symptoms were not very specific (epigastric pain, abdominal distension, vomit, dyspepsia, GI hemorrhage) whereas x-ray and endoscopic evaluation had a very high diagnostic accuracy. Our policy is to perform curative resection for gastric cancer, in the form of partial or total gastrectomy with the removal of first level (n1) and second level (n2) lymph node groups and occasionally additional resection of enlarged lymph nodes in the tertiary (n3) group when metastases are suspected. All our patients have been followed up in order to detect any recurrences or metastases.
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PMID:Early gastric cancer: evaluation of diagnostic, clinicopathologic and therapeutic aspects in 60 cases. 652 25


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