Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:4.1.1.6 (CAD)
 4,420 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Carotid duplex ultrasonography is the noninvasive procedure of choice for evaluating ECAD. However, carotid angiography should be performed before doing carotid endarterectomy. Multivariate logistic regression analysis showed that significant prognostic variables for ECAD in an elderly population are (1) cigarette smoking, (2) serum total cholesterol, (3) serum HDL cholesterol (inverse association), (4) diabetes mellitus, and (5) prior CAD. Patients with 80-100% ECAD develop a higher incidence of ABI and TIA than patients with 40-80% ECAD. Patients with 40-80% ECAD develop a higher incidence of ABI and TIA than patients with 0-40% ECAD. Patients with ECAD have a higher prevalence of prior CAD and develop a higher incidence of new coronary events than patients without ECAD. In patients with ECAD, significant prognostic variables for new coronary events are (1) silent ischemia, (2) prior CAD, (3) serum HDL cholesterol (inverse association), and (4) cigarette smoking. Risk factors for ECAD and CAD should be treated in patients with ECAD. Cigarette smoking must be stopped. Hypertension, dyslipidemia, and diabetes mellitus should be treated. Aspirin, 325 mg/d, should be administered to patients with ECAD. Ticlopidine hydrochloride, 250 mg two times per day should be considered in patients with ECAD who are unable to tolerate aspirin or who develop cerebrovascular events on aspirin. Carotid endarterectomy should be considered in symptomatic patients with 70-99% ECAD.
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PMID:Extracranial carotid arterial disease. 818 62

Gene silencing due to DNA hypermethylation is a major mechanism for loss of tumor suppressor genes function in colorectal cancer. Activating V600E mutation in BRAF gene has been linked with widespread methylation of CpG islands in sporadic colorectal cancers. The aim of the present study was to evaluate the methylation status of three cancer-related genes, APC2, p14ARF, and ECAD in colorectal carcinogenesis and their association with the mutational status of BRAF and KRAS among Iranian colorectal cancer patients. DNA from 110 unselected series of sporadic colorectal cancer patients was examined for BRAF V600E mutation by PCR-RFLP. Promoter methylation of genes in tumors was determined by methylation specific PCR. The frequency of APC2, E-CAD, and p14 methylation was 92.6%, 40.4% and 16.7%, respectively. But, no V600E mutation was identified in the BRAF gene in any sample. No association was found in cases showing epigenetic APC, ECAD, and p14 abnormality with the clinicopathological parameters under study. The association between KRAS mutations and the so called methylator phenotype was previously reported. Therefore, we also analyzed the association between the hot spot KRAS gene mutations in codons of 12 and 13 with genes' promoter hypermethylation in a subset of this group of patients. Out of 86 tumors, KRAS was mutated in 24 (28%) of tumors, the majority occurring in codon 12. KRAS mutations were not associated with genes' methylation in this tumor series. These findings suggest a distinct molecular pathway for methylation of APC2, p14, and ECAD genes from those previously described for colorectal cancers with BRAF or KRAS mutations.
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PMID:High frequency of genes' promoter methylation, but lack of BRAF V600E mutation among Iranian colorectal cancer patients. 2145 33