Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:6.3.5.5 (CPS)
 1,262 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The changes of carbamyl phosphate synthetase I (CPS 1) in diethylnitrosamine-(DEN)-induced enzyme-altered liver cells were studied by means of immunohistochemical (PAP) and in situ cDNA-mRNA hybridization methods. The experimental rats were treated with DEN, 2-acetylaminofluorene (2-AAF) and 2/3 hepatectomy according to Solt-Farber's protocol and were further promoted by oral daily administration of 0.05% phenobarbital in drinking water. The results showed that the average number of lesions showing abnormal expression of CPS 1 was relatively constant over the course of the experiment (8 months), while the number of normally expressing lesions gradually decreased. The former lesions were also larger in volume than the latter ones. We conclude that in DEN-initiated lesions the abnormally expressed CPS 1 lesions may grow continuously, thus leading to the formation of larger nodules. We also suspect that some of these lesions have increased tendencies to develop into tumors.
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PMID:The immunohistochemistry and in situ cDNA-mRNA hybridization of carbamyl phosphate synthetase I in enzyme-altered liver cells during carcinogenesis. 237 Dec 60

In order to study the changes of phenotype and gene expression of carbamyl phosphate synthetase I (CPS 1) in preneoplastic altered liver cells in situ, serial cryostat sections of rat liver initiated by diethylnitrosamine (DENO) and promoted by phenobarbital (PB) were hybridized with 35S-GPS 1 cDNA probe by in situ hybridization, and immunohistochemical demonstration (PAP) of CPS 1 were made simultaneously. The results showed that abnormal expression of CPS 1 in the altered foci and nodules increased much more rapidly than that in normal ones, and consequently they might be more susceptable to develop into tumor.
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PMID:[An immunohistochemical and in situ hybridization study of carbamyl phosphate synthetase I in altered liver cells during carcinogenesis]. 238 10

In this report, 141 patients with gastric cancer were studied histochemically. Tissue CEA was stained by the CEA-PAP method and the gastric cancer was classified into CEA-producing (96 cases, 68.1%) and CEA non-producing gastric cancer (45 cases, 31.9%). Histologically, CEA-producing gastric cancer was well differentiated adenocarcinoma and CEA non-producing gastric cancer was chiefly undifferentiated carcinoma. PAS, pH 2.5 Alcian-blue, High Iron Diamine, Alkaline-PAS, and Concanavalin A paradoxical stain were applied to specimens from each type of gastric carcinoma. Mucosubstances of CEA-producing gastric cancer were positive for A-B, HID, AL-PAS and CPS III-1; those of CEA non-producing gastric cancer were positive for PAS and CPS III-s, but negative for A-B, HID and A1-PAS. These results suggest that CEA-producing gastric cancer arises from intestinal metaplasia of gastric mucosa and that CEA non-producing gastric cancer arises from the gastric mucosa itself.
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PMID:[Mucohistochemical studies of CEA producing and non-producing stomach cancers]. 619 17