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Origins and morphogenesis of colorectal neoplasms.

Gastrointestinal stem cells are considered pivotal in colonic carcinogenesis. There is evidence to suggest that early microadenomas in the colon are polyclonal in origin. Adenomas, once initiated, enlarge by the process of crypt fission. It is also the main mechanism by which neoplastic clones spread through the colorectal epithelium. Both concepts are important for our understanding of the early events in colonic carcinogenesis.

Animals↗

Neoplasms of the upper gastrointestinal tract.

Neoplasms of the upper gastrointestinal tract are generally detected by barium studies or endoscopy. Computed tomography remains the primary imaging modality for staging. Magnetic resonance imaging and endoscopic ultrasonography may also play an increasing role in evaluating these tumors.

Barium Sulfate↗

Fibronectin and type III collagen in epithelial neoplasms of gastrointestinal tract and salivary gland.

The distribution of fibronectin (FN) and collagen type III (IIIC) have been compared in a series of epithelial neoplasms from the gastrointestinal tract and salivary gland. The difficulty of distinguishing between FN of epithelial and fibroblastic origin is emphasised and evidence is presented for the validity of this distinction. In carcinomas FN was sometimes, but not invariably, lost from epithelial cell surfaces. Both FN and IIIC were increased in reactive connective tissue stroma. It is concluded that loss of cell surface FN is unlikely to be a useful diagnostic marker for malignancy, but that the occurrence of this phenomenon in vivo as in vitro indicates that it is biologically significant.

Adenocarcinoma↗

Transgenic mice carrying a PSArasT24 hybrid gene develop salivary gland and gastrointestinal tract neoplasms.

BACKGROUND: Although prostate cancer is one of the most prevalent tumors in men, knowledge of its biology has been hindered by lack of animal models. We have attempted to develop a prostate cancer model utilizing transgenic mouse technology. EXPERIMENTAL DESIGN: Two lines of transgenic mice were derived from one cell stage embryos injected with a fusion gene consisting of a mutated (codon 12) ras gene driven by the human prostate specific antigen (PSA) promoter in an attempt to target the oncogene specifically to the mouse prostate gland. Nontransgenic FVB/N mice were used as controls. The animals were sacrificed for study between 4 and 55 weeks of age. RESULTS: All organs were normal except the salivary glands and gastrointestinal tracts, both of which developed carcinomas in animals older than 44 weeks. The salivary gland tumors were of ductal origin, exhibited a variable degree of differentiation, and were shown to contain abundant PSAras mRNA by in situ hybridization. The gastrointestinal tract tumors were undifferentiated but appeared to be of stromal origin. Both salivary gland and gastrointestinal tumors occasionally metastasized. No transgene expression could be demonstrated in the prostate gland by either reverse transcription-polymerase chain reaction or in situ hybridization. CONCLUSIONS: Lack of transgene expression by the prostate can be explained on the basis of the apparent species specificity previously observed for PSA. Expression in salivary gland is best attributed to identity between the nucleotide sequences of the PSA promoter and of a mouse glandular kallikrein normally secreted by the salivary gland.

Animals↗

Targeting of iodine-123-labelled tumour-associated monoclonal antibodies to ovarian, breast, and gastrointestinal tumours.

Two tumour-associated monoclonal antibodies, HMFG1 and HMFG2, were labelled with iodine-123 and used to detect primary and metastatic ovarian, breast, and gastrointestinal neoplasms by external body scintigraphy in twenty patients with advanced disease. Tumours became visible 3 min to 18 h after injection of labelled antibody. The presence of antibody in the tumours was confirmed by autoradiography and immunoperoxidase staining of surgically removed tissues. The mean tumour uptake of radiolabel was 0.6% of the injected amount. These antibodies can therefore localise specifically to tumours and successful imaging can thus be achieved. This method can complement existing diagnostic techniques and also provide a basis for a selective therapeutic approach to malignant disease.

Adenocarcinoma↗

Primary lymphoma of the gastrointestinal tract.

Primary gastrointestinal lymphoma represents approximately 1% of all gastrointestinal neoplasms. Gastric involvement is more common than small or large intestine and carries a better prognosis. Abdominal pain and weight loss may be the only manifestations and may be present for months or years before the diagnosis is made. Perforation and obstruction occur infrequently. Multiple tumors constitute 8% of cases. Although barium studies and endoscopy reveal the lesion in a high percentage of cases, exploratory celiotomy is not infrequently required for diagnosis. Only one-third of lymphomas are confined to the bowel at laparotomy. Histologically one-third are reticulum cell sarcomas and the remainder lymphosarcoma or lymphocytic lymphoma. Five year survival overall was 38%. Curative resections yielded a survival of 60% regardless of site while palliative resections offered only a 17% chance of cure. As expected, survival was inversely proportional to extent of nodal spread. Postoperative radiotherapy is recommended for residual disease.

Adolescent↗

Genetics and cancer of the gastrointestinal system. Annual oration in honor of Herbert M. Stauffer, M.D., 1914-1970.

Familial aggregations of tumors may occur in virtually all organ systems. The gastrointestinal tract is a frequent site for the development of cancers having an hereditary basis. Their recognition has important relevance to cancer control and prevention. In addition, detailed clinical and laboratory studies of inherited tumors may throw light upon the cause of the more common forms of gastrointestinal neoplasms. Radiologists must have a working knowledge of the genetic and diagnostic elements of each in order to fulfill their responsibilities to the patient, the patient's family and the referring physician.

Adenocarcinoma↗

Endoscopic diagnosis of duodenal neoplasms causing upper gastrointestinal bleeding.

Duodenal neoplasms are a rare and not often considered cause of massive upper gastrointestinal bleeding. During a 4-year period, 859 endoscopies in patients with upper gastrointestinal bleeding revealed a duodenal tumor to be the cause of bleeding in eight patients. Three patients had a primary duodenal neoplasm, two had metastatic involvement, and in three others pancreatic tumors had invaded the duodenum. In view of our findings, we recommend careful endoscopic scrutiny of all parts of the duodenum in patients with upper gastrointestinal bleeding especially when the cause of bleeding is not found in the esophagus, stomach, or duodenal bulb.

Adenocarcinoma↗

Primary Hodgkin's disease of the sigmoid colon: a case report and review of the literature.

We report the case of an 81-year-old man who underwent a segmental resection of the sigmoid colon for severe diverticular disease. Histopathologic diagnosis revealed extranodal Hodgkin's disease, and the diagnosis was confirmed by immunohistochemistry. The incidence of extranodal Hodgkin's disease is rare and represents an infrequent occurrence as a gastrointestinal neoplasm and primary gastrointestinal lymphoma. A review of the literature for gastrointestinal lymphomas with emphasis on the occurrence of Hodgkin's disease, the diagnostic features, and the site of gastrointestinal tract involvement is reported.

Aged↗

The expression of Lewis antigens in neoplasms of the gastrointestinal tract.

The indirect immunoperoxidase technique has been used to demonstrate Lea and Leb antigens in paraffin sections of both morphologically normal gastric and colonic mucosae and their neoplastic counterparts. Expression differed in various regions of the gastrointestinal tract: Leb occurred most frequently in the stomach and Lea most frequently in the colon. Coexpression of Lea and Leb occurred in only 5% of cases of normal mucosa, in 65% of gastric carcinomas and in 82% of carcinomas of the colon. Furthermore, 75% of cases of intestinal metaplasia in gastric mucosa and 30% of tubular adenomas, 50% of villous adenomas and 70% of tubulovillous adenomas in the colon co-expressed Lea and Leb antigens. In this study, the expression of Lewis antigens in carcinoma was found to differ from that of adjacent normal mucosa in 95% of cases of gastric carcinoma and 100% of cases of colonic carcinoma. The differences were shown by antigen acquisition and/or deletion. Similar changes were shown in 88% of cases of intestinal metaplasia in gastric mucosa, 20% of cases of tubular adenomas and 57% of cases of villous and tubulovillous adenomas of colon.

Adenoma↗