Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0007095 (carcinoid)
 6,990 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In order to determine the topographical distribution of the K-ras codon 12 mutations in carcinoma and preneoplastic lesions of the lung, selective ultraviolet radiation fractionation, as well as microdissection followed by polymerase chain reaction-restriction fragment length polymorphism (PCR-RELP), was performed. Fourteen of 61 samples amplified (23.0%) had a mutation in the K-ras codon 12. Of 41 adenocarcinoma, 12 samples (29.3%) had a mutation, whereas none of the squamous cell carcinomas had a mutation. One of six large-cell carcinomas, one of three carcinoid tumours and none of three other carcinomas had a mutation. Direct sequencing revealed that K-ras codon 12 of six samples were TGT (Cys), five samples were GTT (Val), two samples were GCT (Ala) and one sample was TTT (Phe). A total of 113 lesions of 13 cases covered by dot were amplified after UV radiation. All of 74 carcinoma lesions had the mutation, and intratumour heterogeneity was not observed. Of 39 non-malignant lesions, one type II cell hyperplasia had the mutation, which suggests that the K-ras mutation occurs in the early stage of carcinogenesis. The lack of intratumour heterogeneity supports the hypothesis.
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PMID:K-ras point mutation occurs in the early stage of carcinogenesis in lung cancer. 951 49

The mechanism of progression from gastric endocrine cell hyperplasias (ECHs) to carcinoid tumor (GCT) is still unknown. In these lesions, the distribution of metaplastic Paneth, gastrin and pancreatic acinar cells developing due to consequences of corporal mucosal atrophy has not been investigated in detail. In this study, 33 gastric endoscopic biopsies with endocrine cell lesions were examined. In all cases except 6 with solitary GCT, complete-type (small intestine) intestinal metaplasia (IM) with Paneth cells was observed. The density of lysozyme-positive Paneth cells in IMs in cases with GCTs was less than those in ECH alone. The density of gastrin-positive cells in IMs and average number of micronodules of ECHs were similar. Pancreatic acinar metaplasia (PAM) was observed in 6 cases of GCTs with ECH. The size of GCTs with ECH was smaller than those without ECH. By image analysis, the percentage of Ki67 (MIB-1, proliferation marker) expressing cells of GCTs with ECH was 5.1+/-0.6%, and GCT without ECH 7.8+/-1%. Our results indicate that few Paneth cells and many PAMs in atrophic corporal mucosa are seen more frequently in cases of GCTs with ECH, compared to those in ECH alone. Gastrin-positive cells in the corporal IM may stimulate enterochromaffin-like (ECL) cells, which may induce hyperplasia, dysplasia or neoplasia by augmenting the effects of hypergastrinemia through a paracrine mechanism on local gastrin-sensitive cells.
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PMID:Altered distribution of metaplastic Paneth, gastrin and pancreatic acinar cells in atrophic gastritic mucosa with endocrine cell lesions. 1473 20