10 research outputs found

    Signet-Ring Cell-Like Amphicrine Cell Carcinoma of the Stomach

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    A poorly differentiated adenocarcinoma containing diverse components, tubular, signet-ring cell and neuroendocrine elements, in a 79-year-old man is described. Endoscopy examination revealed a Borrmann type IV tumor in the antrum. Histologically, scattered foci of tubular and signet-ring cells and a greater number of neuroendocrine elements were observed. The tumor cells were positive for chromogranin A, neuron specific enolase (NSE) and carcinoembryonic antigen (CEA). Furthermore, about one third of the tumor cells were demonstrated as amphicrine differentiation by double staining with chromogranin A and periodic acid-Schiff (PAS). Amphicrine cell carcinomas with exocrine and endocrine differentiation in the stomach is rare and poor prognosis. The present case suggests that amphicrine cell carcinomas can occur in signet-ring cell morphogenesis, and that a multipotential stem cell is an origin of this unusual variant of neuroendocrine carcinoma

    Role of Parathyroid Hormone/Parathyroid Hormone-Related Peptide on Cell Proliferation in the Gastric Mucosa

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    Parathyroid hormone-related peptide (PTHrP) is widely expressed in normal tissues and elicits various functions through the PTH/PTHrP receptor. Relaxation effects of PTHrP on gastrointestinal smooth muscle cells were well documented, but the physiological role on mucosal growth and differentiation is little known. The purpose of this study was to evaluate the expression of PTHrP and PTHPTHrP receptor in the rat gastric mucosa, and the role of PTHrP on mucosal cell proliferation. Male Wistar rats were used in this study. Localization of PTHrP and PTH/PTHrP receptor were observed by immunohistochemistry and in situ hybridization. Expression of PTH/PTHrP receptor mRNA were examined by RNase protection assay in control and stress condition. Double staining with BrDU incorporation was performed to differentiate cell cycle states. Cell proliferative effect by external PTHrP-(1-34) was evaluated by BrDU incorporation. PTHrP immunopositive cells were encountered in and around the mucosal neck area. PTH/PTHrP receptor immunoreactivity was observed in the gastric mucosa broadly. Cells with stronger expression for PTHrP and its cognate receptor were located in the vicinity of generative zone. But BrDU incorporating cells were negative for both PTHrP and PTH/PTHrP receptor. By RNase protection assay, PTH/PTHrP receptor mRNA expression was weak in a steady state, and the receptor expression increased at stress. External PTHrP-(1-34) did not show cell proliferative effect in a steady state. At stress BrDU incorporation was suppressed significantly, and PTHrP-(1-34) increased BrDU incorporation. These observations suggest that PTHrP and PTH/PTHrP receptor involve maintenance of mucosal growth and differentiation in the stomach

    Two Cases of Multiple Carcinoid Tumors and Gastric Enterochromaffin-like Cell Hyperplasia, Dysplasia and Neoplasia in Type A Gastritis

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    We describe two cases of multiple carcinoids and hyperplasia, dysplasia and neoplasia of enterochromaffin-like (ECL) cells associated with atrophic gastritis type A in the stomach. Multiple polypoid lesions measuring 1 cm showed upper gastroendoscopic features. They were all found in the upper body of the stomach. All polypoid lesions with carcinoid foci were observed from the deeper layers of the propria mucosa to the submucosa and were surrounded by ECL cells. In one case, the serum gastrin level which was as high as 1700 pg/mi, returned to normal range (17 pg/ml) after gastrectomy. It is suggested that longstanding hypergastrinemia may have played a causative role in the development of multiple gastric carcinoid tumors. A total gastrectomy was considered essential for treatment of aggressive multiple carcinoid tumors with hypergastrinemia

    Epstein-Barr virus-associated gastric carcinoma in Kazakhstan

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    Two Cases of Multiple Carcinoid Tumors and Gastric Enterochromaffin-like Cell Hyperplasia, Dysplasia and Neoplasia in Type A Gastritis

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    We describe two cases of multiple carcinoids and hyperplasia, dysplasia and neoplasia of enterochromaffin-like (ECL) cells associated with atrophic gastritis type A in the stomach. Multiple polypoid lesions measuring 1 cm showed upper gastroendoscopic features. They were all found in the upper body of the stomach. All polypoid lesions with carcinoid foci were observed from the deeper layers of the propria mucosa to the submucosa and were surrounded by ECL cells. In one case, the serum gastrin level which was as high as 1700 pg/mi, returned to normal range (17 pg/ml) after gastrectomy. It is suggested that longstanding hypergastrinemia may have played a causative role in the development of multiple gastric carcinoid tumors. A total gastrectomy was considered essential for treatment of aggressive multiple carcinoid tumors with hypergastrinemia

    The Influence of Alpha-fetoprotein on Natural Suppressor Cell Activity and Ehrlich Carcinoma Growth

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    The influence of alpha-fetoprotein (AFP) on the bone marrow (BM) natural suppressor (NS) cells of intact Ehrlich carcinoma -bearing CBA mice was studied. Bone marrow NS cells were fractionated into three fractions by isopycnic centrifugation on percoll gradients: NS1 (ρ=1.080 g/ml), NS2 (ρ=1.090 g/ml) and NS3 (1.100>ρ>1.090 g/ml). These fractions were highly different in their sensitivity to known NS cell inductors (interleukin (IL)-2, IL-3 or histamine). None of the NS fractions isolated from the intact mice spontaneously produced antiproliferative activity, however, they showed a high level of NS (antiproliferative and natural killer cell inhibitory) activity under the influence of AFP. A single injection of AFP to intact mice led to an increase of spontaneous NS activity and the inhibition of natural killer cell activity. NS activity, especially NS2, was increased in when tumor cells were subcutaneously inoculated three days after AFP injection. In the AFP-treated mice, the tumor mass at 14 days was 60% larger than that in the untreated mice. Our data confirmed that AFP is a tumor marker that can inhibit cancer immunity and plays a role in cancer pathogenesis
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