gastrins and Intestinal-Neoplasms

Topics: Acute Kidney Injury; Adenoma, Islet Cell; Adult; Amines; Carboxy-Lyases; Dehydration; Endocrine Glands; Fluorescent Antibody Technique; Gastrins; Glucagon; Humans; Hyperplasia; Intestinal Neoplasms; Intestinal Secretions; Intestines; Male; Multiple Endocrine Neoplasia; Neurosecretory Systems; Pancreas; Paraneoplastic Endocrine Syndromes; Peptides; Zollinger-Ellison Syndrome

A patient with long-standing Crohn's disease of the large and small intestine was found to have extensive gastric metaplasia of the ileum. Most metaplastic glands were of the pyloric type, but numerous oxyntic glands with parietal and chief cells were also seen. By immunofluorescence the chief cells contained both the group I and group II pepsinogens, while the pyloric gland cells contained only the group II pepsinogens. Gastric-containing or other endocrine cells were not detected in the metaplastic pyloric and oxyntic glands. The latter findings are consistent with the concept expressed by Pearse that the endocrine and exocrine cells of the gastrointestinal mucosa may originate from different precursor elements during embryogenesis.

Topics: Choristoma; Crohn Disease; Female; Fluorescent Antibody Technique; Gastric Mucosa; Gastrins; Humans; Ileum; Intestinal Neoplasms; Metaplasia; Middle Aged; Pepsinogens; Pylorus; Stomach

Topics: Angiography; Biological Assay; Diarrhea; Duodenum; Endocrine System Diseases; Gastrectomy; Gastric Juice; Gastrins; Humans; Intestinal Neoplasms; Islets of Langerhans; Malabsorption Syndromes; Pancreatic Neoplasms; Peptic Ulcer; Prognosis; Radioimmunoassay; Stomach; Zollinger-Ellison Syndrome

With the widespread use of endoscopy, small and low-grade type 3 gastric neuroendocrine tumours (NETs) are increasingly being detected. The clinicopathological features, biological behaviour and appropriate treatment strategy for these NETs remain unclear.. Patients with biopsy-proven gastric NET and a normal fasting serum gastrin level were identified from a prospectively maintained database. Clinicopathological features and long-term outcome of local resection for type 3 NETs were reviewed retrospectively and compared according to tumour grade.. Some 32 patients with type 3 gastric NETs were included (25 patients with NET grade G1, 5 with G2 and 2 with G3). Pathological tumour size was 2·0 cm or less in 30 patients. All tumours were well differentiated, even G3 lesions, and all tumours but one were confined to the submucosal layer. G1 NETs were significantly smaller and had a significantly lower lymphovascular invasion rate than G2 and G3 NETs. Twenty-two patients with a G1 NET without lymphovascular invasion were treated with wedge or endoscopic resection. After a median follow-up of 59 (range 6-102) months, no patient with a G1 NET of 1·5 cm or smaller developed recurrence and one patient with a G1 NET larger than 1·5 cm had recurrence in a perigastric lymph node. Among seven patients with a G2 or G3 NET, two had lymph node metastasis and one had liver metastases.. Low-grade type 3 gastric NET has non-aggressive features and a favourable prognosis. Wedge or endoscopic resection may be a valid option for patients with type 3 gastric G1 NET no larger than 1·5 cm without lymphovascular invasion.

Topics: Adult; Aged; Biomarkers, Tumor; Biopsy; Endoscopy, Gastrointestinal; Female; Follow-Up Studies; Gastrectomy; Gastrins; Humans; Intestinal Neoplasms; Male; Middle Aged; Neoplasm Grading; Neoplasm Recurrence, Local; Neuroendocrine Tumors; Pancreatic Neoplasms; Prognosis; Prospective Studies; Stomach Neoplasms; Time Factors

Neuroendocrine tumors in the pancreas and the gastrointestinal tract may secrete hormones which cause specific syndromes. Well-known examples are gastrinomas, glucagonomas, and insulinomas. Cholecystokinin-producing tumors (CCKomas) have been induced experimentally in rats, but a CCKoma syndrome in man has remained unknown until now.. Using a panel of immunoassays for CCK peptides and proCCK as well as for chromogranin A, we have examined plasma samples from 284 fasting patients with gastroenteropancreatic neuroendocrine tumors. In hyperCCKemic samples, plasma CCK was further characterized by chromatography.. One of the patients displayed gross hyperCCKemia. She was a 58-year old woman with a pancreatic endocrine tumor, liver metastases, 500-1000-fold elevated basal CCK concentration in plasma, diarrhea, severe weight loss, recurrent peptic ulcer and bilestone attacks from a contracted gallbladder. The CCK concentrations in plasma were not affected by resection of the pancreatic tumor, but decreased to normal after hemihepatectomy with removal of the metastases.. A CCKoma syndrome with severe hypersecretion of CCK exists in man. The duodenal ulcer disease and diarrhea with permanently low gastrin in plasma suggest that CCKomas may mimic gastrinoma-like symptoms, because CCK peptides are full agonists of the gastrin/CCK-B receptor.

Topics: Adolescent; Adult; Aged; Aged, 80 and over; Animals; Child; Cholecystokinin; Denmark; Female; Gastrinoma; Gastrins; Humans; Intestinal Neoplasms; Liver Neoplasms; Male; Middle Aged; Neuroendocrine Tumors; Pancreas; Pancreatic Neoplasms; Rats; Stomach Neoplasms; Young Adult

Many neuroendocrine gastrointestinal and lung tumors express sst2A somatostatin receptors. Because the cellular location of sst2A in the corresponding non-neoplastic tissue is unknown, we searched for sst2A immuno-reactive cells and characterized their type in these tissues using a highly specific sst2A antibody (R2-88). Epithelial sst2A cells, identified as neuroendocrine, gastrin-producing cells, were found in large numbers in the antrum and the duodenum, but not in the gastric corpus. They were also present in the proximal jejunum, rarely noted in the distal jejunum and ileum, and absent in the large intestine and the appendix vermiformis. Moreover, sst2A cells were found abundantly in the neural plexus. sst2A receptors on antral gastrin cells could mediate somatostatin inhibition on gastrin secretion, whereas those in the neural plexus could mediate somatostatin effects on motility and ion transport in the lower gastrointestinal tract. Rare sst2A cells in bronchi and bronchioles located basally and parabasally in the gastrointestinal epithelium were detected that could represent stem/progenitor cells. It is currently not clear whether and which of the identified sst2A cells are at the origin of sst2A-positive neuroendocrine gut or lung tumors.

Topics: Gastrins; Humans; Immunohistochemistry; Intestinal Mucosa; Intestinal Neoplasms; Lung Neoplasms; Neuroendocrine Tumors; Receptors, Somatostatin; Respiratory Mucosa

To investigate the incidence of neuroendocrine (NE) cells and their hormone products in adenocarcinomas and evaluate their significance in clinical pathology and prognosis.. By using tissue sectioning and immunocyto-chemistry, 356 cases of adenocarcinomas were studied to examine the presence of chromorgranin and polypeptide hormones in adenocarcinoma samples from our hospital.. The positive rate of NE cells and hormone products was 41.5 % (54/130) and 59.3 % (32/54), respectively in large intestinal adenocarcinoma cases; 39.6 % (38/96) and 36.8 % (14/38), respectively in gastric cancer cases; 38.1 % (8/21) and 50.0 % (4/8), respectively in prostatic cancer cases; 21.0 % (17/81) and 17.6 % (3/17), respectively in breasr cancer cases; 17.9 % (5/28) and 60.0 % (3/5), respectively in pancreatic cancer cases. Among carcinomas of large intestine, pancreas and breast, the highly differentiated NE cell numbers were higher than the poorly differentiated NE cell numbers; while the gastric carcinoma cases had more poorly differentiated NE cells than highly differentiated NE cells. The higher detection rate of NE cells and their hormone products, the higher 5-year survival rate among the large intestine cancer cases.. Close correlation was observed between NE cells and their hormone products with the cancer differentiations. For colorectal carcinomas, there is a close correlation of the presence of NE cells and their hormone products with the tumor staging and prognosis.

Topics: Adenocarcinoma; Adrenocorticotropic Hormone; Biomarkers; Calcitonin; Gastrins; Glucagon; Humans; Intestinal Neoplasms; Lymph Node Excision; Lymphatic Metastasis; Norepinephrine; Retrospective Studies; Serotonin; Somatostatin; Stomach Neoplasms

The effect of food restriction (FR) on spontaneous intestinal carcinogenesis in multiple intestinal neoplasia (Min) mice was examined. Thirty male Min mice were allotted to ad libitum feeding control and 20% FR groups from six weeks of age until the end of the 13-week experimental period. Although the total number of visible intestinal polyps in the FR group was not significantly different from the control group value, a significant decrease in large-sized polyps (>2 mm) and an increase in small-sized polyps (< or =2 mm) were observed in the distal small intestine. In this segment, the percentage of apoptotic cells counted in intestinal polyps in the FR group was significantly higher than in the control group, the percentage of proliferating cell nuclear antigen (PCNA)-positive cells not being significantly different. These results indicate that the FR may inhibit the growth of intestinal polyps in the Min mouse, and that apoptosis contributed in part to the inhibitory effect.

Topics: Animals; Apoptosis; Body Weight; Cell Division; Energy Intake; Food Deprivation; Gastrins; Genes, APC; Immunoenzyme Techniques; Intestinal Neoplasms; Intestinal Polyps; Male; Mice; Mice, Inbred C57BL; Mice, Knockout; Proliferating Cell Nuclear Antigen

Gastrointestinal carcinoids are derived from the diffuse intestinal endocrine system and may produce amines and many peptides, including serotonin, chromogranin A (CGA), and tachykinins. Most peptide hormones are synthesized as bigger prohormones, which are processed to smaller active hormones by prohormone convertases (PCs). A total of 35 cases of gastrointestinal carcinoids, including gastric, duodenal, small intestinal, appendiceal, and large intestinal carcinoids, were immunocytochemically stained for serotonin, CGA, and PC 1/3 and 2, in order to colocalize CGA and PCs in the carcinoids. All carcinoids were positive for CGA and PCs. Carcinoids that stained strongly for CGA were generally weakly stained for PCs and those weakly staining for CGA were more strongly stained for PCs in the majority of the small and large intestinal tumors. Gastrointestinal carcinoids were positive for CGA and PCs, and the presence of PCs may suggest that the conversion of peptide prohormones to smaller peptide hormones occurs in gastrointestinal carcinoids. PCs immunocytochemistry may be added as a new phenotypic characterization for gastrointestinal carcinoids.

Topics: Adult; Aged; Appendiceal Neoplasms; Aspartic Acid Endopeptidases; Carcinoid Tumor; Child; Chromogranin A; Chromogranins; Duodenal Neoplasms; Female; Gastrins; Gastrointestinal Neoplasms; Humans; Immunohistochemistry; Intestinal Neoplasms; Intestine, Large; Intestine, Small; Male; Middle Aged; Proprotein Convertase 2; Proprotein Convertases; Serotonin; Stomach Neoplasms; Subtilisins

We investigated whether a relationship exists in terms of growth pattern and hormone sensitivity in 18 gastrointestinal neoplastic cell lines. Hormones studied included gastrin, epidermal growth factor, estradiol and luteinizing hormone-releasing hormone.. The growth patterns were assessed by means of computer-assisted microscope analysis of Feulgen-stained nuclei combined with the mathematical Delaunay triangulation and Voronoi paving techniques. This methodology enabled four variables characterizing the cell colony patterns to be computed. The information contributed by these variables was analyzed by means of discriminant analysis and the decision tree technique.. Each phenotype (sensitivity level) exhibited distinct growth pattern (or cell colony) characteristics in the case of each hormone and/or growth factor under study. Furthermore, the sensitivity of the gastrointestinal cell lines to a given hormone (or growth factor) appeared to be peculiar to the hormone (or growth factor).. A direct relationship seems to exist between growth pattern and hormone sensitivity levels in gastrointestinal cancers, particularly colorectal.

Topics: Cell Count; Cell Division; Decision Trees; Discriminant Analysis; Epidermal Growth Factor; Estradiol; Gastrins; Gonadotropin-Releasing Hormone; Humans; Intestinal Neoplasms; Tumor Cells, Cultured

The effects of combined administration of bombesin (40 micrograms/kg body weight) and the ornithine decarboxylase (ODC) inhibitor, 1,3-diaminopropane (DAP), on the development of large and small intestinal tumors and the incidence of their metastasis to the peritoneum induced by azoxymethane (AOM, 7.4 mg/kg body weight), the ODC activity of the intestinal wall, and the labeling index of the intestinal mucosa and tumor were investigated in inbred Wistar rats. Rats received weekly s.c. injections of AOM for 10 weeks, s.c. injections of bombesin every other day, and drinking water containing DAP (2.5 g/l) until the end of the experiment at week 40. Administration of bombesin significantly increased the incidence of intestinal tumors at week 40. It had no influence on the location, size, histological features or depth of involvement of intestinal adenocarcinomas, but significantly increased the incidence of their metastasis to the peritoneum. It also resulted in a significant increase in the intestinal ODC activity and labeling index. Administration of DAP with bombesin significantly reduced the enhancement of intestinal carcinogenesis by bombesin. Although the combined use of DAP with bombesin had little or no influence on the location, size, histological features, or depth of involvement of intestinal cancers, the incidence of their metastasis was significantly reduced. DAP significantly attenuated bombesin enhancement of the intestinal ODC activity and labeling index. These findings indicate that ODC inhibition attenuated the enhancement of intestinal carcinogenesis and metastasis to the peritoneum.

Topics: Adenocarcinoma; Animals; Azoxymethane; Body Weight; Bombesin; Cell Division; Diamines; Drug Synergism; Gastrins; Intestinal Mucosa; Intestinal Neoplasms; Male; Neoplasm Metastasis; Ornithine Decarboxylase Inhibitors; Peritoneal Neoplasms; Rats; Rats, Wistar

We have evaluated the peripheral blood natural killer (NK) cell activity and the in vitro effect of recombinant gamma-interferon (r gamma-IFN) on NK cell activity in 23 patients with a neuroendocrine tumour of the pancreas, small intestine or liver, and 23 healthy controls. Patients with a gastrinoma showed a NK cell activity which was not different from that of the control group, whereas patients with another type of neuroendocrine tumour had a decreased NK cell activity compared to the controls (p less than 0.05) and the gastrinoma patients (p less than 0.02). The impaired NK cell activity in these patients was as such not related to the presence of liver metastasis or performance status of the patients. r gamma-IFN significantly stimulated the NK cell activity in patients and controls. However, the cytotoxic response of the patients with a hormone production other than gastrin remained lower than in the two other groups. Follow-up studies in 8 patients showed NK cell activities not to vary with stable disease, to decrease with progressive disease, and to increase with regression of disease. In conclusion, NK cell activity is suppressed in patients with neuroendocrine tumours that produce hormones other than gastrin. This impairment is not related to the presence of metastasis but seems to be related to the course of the disease.

Topics: Adult; Aged; Carcinoid Tumor; Cell Line; Female; Gastrinoma; Gastrins; Gastrointestinal Hormones; Humans; Interferon-gamma; Intestinal Neoplasms; Killer Cells, Natural; Lipoma; Liver Neoplasms; Male; Middle Aged; Pancreatic Neoplasms; Recombinant Proteins; Somatostatinoma; Tumor Cells, Cultured

The effect of daily parenteral administration of a long-acting analogue of somatostatin (SMS 201-995) on the development of intestinal tumours and the rate of crypt cell proliferation in azoxymethane-treated rats has been studied. SMS 201-995 had no significant effect on the number of colonic tumours induced. In the duodenum, SMS 201-995 administration was associated with a change in the number of tumours from 1.4/rat in saline-treated animals to 2.4/rat in animals treated for the last third of the study and 2.8/rat in animals treated with SMS for the entire duration of the study (P less than 0.02). SMS had no significant effect on the rate of cell proliferation in the duodenum, ileum or colon. The inhibition of release of gastrointestinal trophic hormones by this analogue of somatostatin thus does not appear to reduce the number of tumours in the intestine of azoxymethane-treated rats.

Topics: Animals; Antineoplastic Agents; Azoxymethane; Cell Division; Gastrins; Glucagon-Like Peptides; Intestinal Neoplasms; Intestines; Male; Octreotide; Rats; Rats, Inbred Strains; Somatostatin

The effects of tetragastrin and histamine on the incidence and histology of tumors induced in the small intestine by N-methyl-N'-nitro-N-nitrosoguanidine [(MNNG) CAS: 70-25-7] were investigated in male W rats. Animals were given MNNG at 150 micrograms/ml in their drinking water for 25 weeks and then 300 micrograms tetragastrin or 4 mg histamine dihydrochloride sc per day in depot form. Administration of tetragastrin or histamine after MNNG treatment resulted in a significant increase in gastric acid secretion and a significant reduction in the incidence of tumors in the duodenum; however, only histamine decreased the incidence of tumors in the jejunum. Histologically, the tumors induced in the small intestine were mostly adenocarcinomas, and their histologic type was not affected by either tetragastrin or histamine.

Topics: Adenocarcinoma; Animals; Drug Antagonism; Duodenum; Gastric Acidity Determination; Gastrins; Histamine; Intestinal Neoplasms; Jejunum; Male; Methylnitronitrosoguanidine; Rats; Stomach Neoplasms; Tetragastrin

Neuroendocrine tumours of the lung and gut are known to possess bombesin-like immunoreactivity. The recent observation that gastrin releasing peptide (GRP), a 27 amino acid peptide isolated from the porcine intestine, may be the mammalian analogue of bombesin led us to look for this peptide in a variety of human neoplasms. Formalin-fixed tissues from 85 tumours were examined by the immunoperoxidase technique, using specific antisera to the GRP molecule (1-27) and the GRP fragment (1-16). Intense cytoplasmic GRP immunoreactivity was seen in thyroid medullary carcinomas (3/3), carcinoids of lung, pancreas, and intestine (22/36), and paragangliomas (2/3). Less frequent staining was present in pulmonary small cell (oat cell) carcinomas (1/8) and pituitary adenomas (1/6). Complete absence of immunoreactivity was observed in three phaeochromocytomas, five Merkel cell tumours, six neuroblastomas and 15 non-neuroendocrine tumours. Normal neuroendocrine cells of the thyroid (C-cells) and bronchial mucosa (Kulchitsky cells) exhibited GRP immunoreactivity; nerve fibres from all sites failed to demonstrate staining for GRP. In each positive case, the pattern of staining for GRP (1-27) and GRP (1-16) was identical, although the GRP (1-16) immunostaining was weaker. These findings indicate that bombesin immunoreactivity in human neuroendocrine cells and tumours is attributable to GRP-like molecules and that GRP is a useful marker of neuroendocrine differentiation in many tumours.

Topics: Adenoma; Adrenal Gland Neoplasms; Amino Acid Sequence; Bombesin; Carcinoid Tumor; Carcinoma, Small Cell; Gastrin-Releasing Peptide; Gastrins; Humans; Intestinal Neoplasms; Lung Neoplasms; Neoplasms; Neurosecretory Systems; Pancreatic Neoplasms; Peptides; Pheochromocytoma; Pituitary Neoplasms; Thyroid Neoplasms

Gut endocrine cells in a total of 122 intestinal-tract adenocarcinomas induced in inbred Wistar rats by 1,2-dimethylhydrazine dihydrochloride were examined histologically, ultrastructurally, and immunohistochemically for gastrin, somatostatin, vasoactive-intestinal polypeptide (VIP), and glicentin (enteroglucagon). Of the 122 tumors, argyrophil cells were detected in 42 tumors (34.3%) comprising 15 tumors of the well differentiated type and 27 tumors of the poorly differentiated type, including signet-ring-cell carcinomas. Of the 27 tumors of the poorly differentiated type, 12 were regarded as endocrine-cell carcinomas composed of numerous argyrophil or argentaffin cells and mucus-containing cells. Immunohistochemically, 7 of the 12 tumors had glicentin and two of these seven tumors also had gastrin and argentaffin cells synchronously. None of the tumors showed immunoreactivity for somatostatin and VIP. Nine of the 12 tumors metastasized to the lung, pancreas, liver, mesenterium, omentum, and lymph nodes. The metastatic foci of these tumors were also shown to have glicentin and argentaffin cells. Ultrastructurally, four types of endocrine granule were found in the tumor cells and amphicrine cells containing endocrine granules and mucous granules were noted. These endocrine-cell tumors were assumed to develop from totipotent immature cells of endodermal origin.

Topics: 1,2-Dimethylhydrazine; Adenocarcinoma; Animals; Carcinogens; Chromaffin System; Dimethylhydrazines; Enterochromaffin Cells; Female; Gastrins; Glucagon-Like Peptides; Intestinal Neoplasms; Male; Microscopy, Electron; Neoplasm Metastasis; Neoplasms, Experimental; Rats; Rats, Inbred Strains; Somatostatin; Vasoactive Intestinal Peptide

The trophic effect of chronic endogenous hypergastrinemia is compared with that of short term injected pentagastrin on colon mucosa of rats. Hypergastrinemia was achieved by antral exclusion. Pentagastrin (2 mg/kg) was administered to a group of sham operated rats every 12 hr for 48 hr prior to sacrifice. Normogastrinemic antrectomized and sham operated animals were studied as controls. Tissue content and synthesis of DNA, RNA, and protein were all markedly increased by both endogenous gastrin and exogenous pentagastrin. The stimulation by gastrin was significantly stronger than that of pentagastrin at the chosen schedule of administration.

Topics: Animals; Colon; DNA; Gastrins; Intestinal Mucosa; Intestinal Neoplasms; Male; Pentagastrin; Protein Biosynthesis; Rats; Rats, Inbred Strains; RNA

Pancreas and gut hormones are involved in many endocrine and gastrointestinal diseases. Radioimmunoassays for these hormones have proved particularly valuable in diagnosis, localisation and control of treatment of endocrine tumours, of which many are mixed. An estimate based on ten years experience in a homogenous population of 5 million inhabitants (Denmark) suggests, that endocrine gut tumour-syndromes on an average appear with an incidence of 1 patient per year/syndrome/million. At present six different syndromes are known: 1) The insulinoma syndrome, 2) The Zollinger-Ellison syndrome.3) The Verner-Morrison syndrome. 4) The glucagonoma syndrome. 5) The somatostatinoma syndrome, and 6) the carcinoid syndrome. Accordingly diagnostically valuable RIAs for pancreas and gut hormones include those for insulin, gastrin, VIP, HPP, glucagon, somatostatin, and presumably also substance P. It is probably safe to predict that the need for gut and pancreas hormone RIAs within the next decade will increase greatly in order to assure proper management of tumours producing gastroentero-pancreatic hormones.

Topics: Adenoma, Islet Cell; Carcinoid Tumor; Cholecystokinin; Gastric Inhibitory Polypeptide; Gastrins; Gastrointestinal Hormones; Glucagon; Glucagon-Like Peptides; Humans; Insulin; Intestinal Neoplasms; Motilin; Pancreatic Hormones; Pancreatic Neoplasms; Pancreatic Polypeptide; Radioimmunoassay; Secretin; Somatostatin; Substance P; Vasoactive Intestinal Peptide; Zollinger-Ellison Syndrome

A case of malignant endocrine tumour of the jejunum, associated with severe duodenal ulcer is described. The tumour and a local metastasis were examined by immunohistochemistry and found to contain abundant somatostatin-immunoreactive cells together with less numerous cells displaying gastrin immunoreactivity. This is to our knowledge the first case of intestinal somatostatinoma. The presence of gastrin cells in the tumour may explain the ulcer diathesis.

Topics: Duodenal Ulcer; Female; Gastrins; Humans; Intestinal Neoplasms; Jejunum; Middle Aged; Neoplasm Metastasis; Somatostatin

Immunocytochemical techniques using antigastrin antibody were employed to localize G cells in ectopic gastric mucosa of metaplastic and congenital origins and to compare their distribution with that in normal gastric mucosa. Five examples of Barrett's esophagus, 8 Meckel's diverticula, and 2 small bowel duplications were studied. Although G cells were absent in the gastric mucosa from all cases of Barett's esophagus, four Meckel's diverticula and one small bowel duplication contained G cells. In all instances of congenitally derived ectopic gastric mucosa where G cells were demonstrable, the gastric mucosa showed areas of antropyloric differentiation, whereas in the remaining cases the ectopic gastric mucosa was exclusively of the body-fundic type. It is concluded that the presence of G cells within ectopic gastric mucosa of Meckel's diverticula and small bowel duplications in foci of antropyloric differentiation reflects their developmental origin, whereas the absence of G cells in Barrett's esophagus is in keeping with its metaplastic derivation.

Topics: Choristoma; Esophageal Diseases; Esophagus; Gastric Mucosa; Gastrins; Histological Techniques; Humans; Intestinal Neoplasms; Intestine, Small; Meckel Diverticulum; Metaplasia

Topics: Animals; Carcinoid Tumor; Cholecystokinin; Dogs; Enterochromaffin Cells; Gastric Inhibitory Polypeptide; Gastric Mucosa; Gastrins; Gastrointestinal Hormones; Glucagon; Glucagon-Like Peptides; Humans; Intestinal Mucosa; Intestinal Neoplasms; Pancreatic Polypeptide; Rats; Secretin; Somatostatin; Stomach Neoplasms; Vasoactive Intestinal Peptide

1. Due to their common origin from the neural crest the hormonogenic cells of the intestinal tract show similar cyto-chemical and ultra-structural characteristics. 2. Hyperplasiae and tumors of these cells lead to excessive hormone production with its consequences on the reacting organs. 3. Hormone producing tumors can be confined to one organ only, but as multiple endocrine adenomatosis they can afflict several organs. 4. Diagnosis of most hormone producing tumors is possible with the adequate radio-immunologic tests. Radiologic and endoscopic examinations can contribute to the localization of the tumor. 5. Surgical resection of the tumor or of the reacting organs impaired by the overproduction of hormones from the tumor is the indicated therapy. Medicamentous therapy is rarely successful. 6. The growth of most hormonogenic tumors is relatively slow. Rates of survival of up to 30 years have been known, even after formation of metastases of the tumor. Effects of hormone overproduction on other organs can reduce the prognosis.

Topics: Adenoma; Carcinoid Tumor; Diarrhea; Gastrectomy; Gastrins; Humans; Hypokalemia; Intestinal Neoplasms; Multiple Endocrine Neoplasia; Pancreas; Paraneoplastic Endocrine Syndromes; Syndrome; Zollinger-Ellison Syndrome

Topics: Gastrins; Humans; Intestinal Neoplasms