Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0030305 (pancreatitis)
 16,014 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

microRNAs are functional, 22 nt, noncoding RNAs that negatively regulate gene expression. Disturbance of microRNA expression may play a role in the initiation and progression of certain diseases. A microRNA expression signature has been identified that is associated with pancreatic cancer. This has been accomplished with the application of real-time PCR profiling of over 200 microRNA precursors on specimens of human pancreatic adenocarcinoma, paired benign tissue, normal pancreas, chronic pancreatitis and nine pancreatic cancer cell lines. Hierarchical clustering was able to distinguish tumor from normal pancreas, pancreatitis and cell lines. The PAM algorithm correctly classified 28 of 28 tumors, 6 of 6 normal pancreas and 11 of 15 adjacent benign tissues. One hundred microRNA precursors were aberrantly expressed in pancreatic cancer or desmoplasia (p < 0.01), including microRNAs previously reported as differentially expressed in other human cancers (miR-155, miR-21, miR-221 and miR-222) as well as those not previously reported in cancer (miR-376a and miR-301). Most of the top aberrantly expressed miRNAs displayed increased expression in the tumor. Expression of the active, mature microRNA was validated using a real-time PCR assay to quantify the mature microRNA and Northern blotting. Reverse transcription in situ PCR showed that three of the top differentially expressed miRNAs (miR-221, -376a and -301) were localized to tumor cells and not to stroma or normal acini or ducts. Aberrant microRNA expression may offer new clues to pancreatic tumorigenesis and may provide diagnostic biomarkers for pancreatic adenocarcinoma.
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PMID:Expression profiling identifies microRNA signature in pancreatic cancer. 1714 98

The objective of this study is to investigate the functions of parotid and pancreatic glands in response to intoxication with parathion-methyl (PM) and the effects of treatment in rats. Seventy-five male Wistar rats were divided equally into five groups: Group I, control; group II, received atropine and pralidoxime (2-PAM) for 24 h, but no PM; group III, oral PM but no atropine and 2-PAM; group IV, PM and atropine for 24 h and 2-PAM; group V, PM and atropine for 96 h and 2-PAM. After the administration of the chemicals, blood samples were drawn to test for amylase, lipase, acetylcholinesterase (AChE), and butyrylcholinesterase (BChE), while pancreatic and parotid glands of each rat were removed for light microscopic examination. Amylase levels were found significantly elevated in groups II, III, IV, and V, whereas lipase levels were supranormal in groups III, IV, and V. The blood levels of AChE were decreased in groups III and IV and BChE were decreased in II, III, IV, and V. No evidence of pancreatitis and parotitis was identified in the histopathologic evaluation in any group in 96 h; however, hyperchromasia, irregularity in nuclei, and binuclear cells were observed in all parotid glands in group V. Parotitis and pancreatitis were not evident; however, hyperamylasemia and hyperlipasemia were found, whereas various histologic changes in parotid glands were documented in the groups that were administered organophosphate and treatment.
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PMID:The effect of parathion-methyl and antidotes on parotid and pancreatic glands: a pilot experimental study. 1796 25