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)

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

The specific activity of carbamoyl phosphate synthetase (glutamine-hydrolyzing), the first and rate-limiting enzyme of de novo uridine 5'-triphosphate biosynthesis, was increased in 13 transplantable hepatomas, particularly in the rapidly growing tumors (5.7- to 9.5-fold), and the rise was correlated with tumor growth rates. Thus, synthetase activity was linked with both hepatic neoplastic transformation and progression. Synthetase specific activity was so elevated in a transplantable sarcoma (18-fold) and a kidney adenocarcinoma (5-fold). The increased activity should enhance the capacity of the pathway and should confer selective advantages to cancer cells.
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PMID:Carbamoyl phosphate synthetase (glutamine-hydrolyzing): increased activity in cancer cells. 720 43

Programmed death-1 ligand (PD-L1) expression has been used as a predictive marker for response to immune checkpoint inhibitors and has been reported to have prognostic value. Its prevalence and significance in endocervical adenocarcinoma (ECA) remain underinvestigated. We evaluated PD-L1 expression and CD8 tumor-infiltrating lymphocyte density in whole tissue sections of 89 ECAs. PD-L1 expression was observed in 68% of ECAs by combined positive score (CPS, cutoff 1) and 29% of ECAs by tumor proportion score (TPS, cutoff 1%). Using CPS, PD-L1 expression was seen in 11%, 78%, and 72% of pattern A, B, and C tumors, respectively, with significantly higher expression in tumors with destructive-type invasion (B and C) (P=0.001 [A vs. B], 0.0006 [A vs. C], 0.0002 [A vs. B+C]). Using TPS, no significant difference in PD-L1 expression was seen between tumors with different invasion patterns (0%, 22%, and 32% in tumors with pattern A, B, and C, respectively; P=0.27 [A vs. B], 0.053 [A vs. C], 0.11 [A vs. B+C]). PD-L1-positive ECAs demonstrated significantly higher CD8 tumor-infiltrating lymphocyte density (CPS: P=0.028; TPS: P=0.013) and worse progression-free survival when compared with PD-L1-negative ECAs (CPS: hazard ratio [HR]=4.253 vs. 0.235, P=0.025; TPS: HR=4.98 vs. 0.2; P=0.004). When invasion patterns were separately assessed, pattern C tumors similarly showed worse progression-free survival in PD-L1-positive tumors (CPS: HR=6.15 vs. 0.16, P=0.045; TPS: HR=3.78 vs. 0.26, P=0.027). In conclusion, our data show frequent PD-L1 expression in ECA with destructive-type invasion, supporting the role of the PD-1/PD-L1 pathway as a therapeutic target for these tumors. Our data also support PD-L1 as a negative prognostic marker associated with a potentially unfavorable outcome.
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PMID:PD-L1 Expression in Endocervical Adenocarcinoma: Correlation With Patterns of Tumor Invasion, CD8+ Tumor-infiltrating Lymphocytes, and Clinical Outcomes. 3329 32