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)

To examine a potential contribution of protooncogene abnormalities other than point-mutational activation of the K-ras protooncogene in the classification of non-small cell lung cancer, amplification of cellular protooncogenes was studied in 47 lung tumour specimens obtained at thoracotomy and in four lung tumour cell lines. The primary tumours included 21 adenocarcinomas, nine large-cell carcinomas, 13 epidermoid carcinomas, one carcinoid and three metastases of primaries outside the lung. The copy numbers per haploid genome of 11 protooncogenes in every tumour sample were determined: H-ras, K-ras, N-ras, c-myc, N-myc, L-myc, erbB, mos, myb, ncu (erbB-2) and ral amplifications. The c-myc gene was amplified 5-7-fold in two adenocarcinomas, the H-ras gene 3 5-fold in one adenocarcinoma, while the K-ras and the neu gene were amplified in lung metastases from a colorectal and a breast cancer primary respectively. None of the tumours with an amplified protooncogene simultaneously harboured a mutationally activated K-ras gene. We conclude that amplification of the investigated protooncogenes is a rare event in non-small cell lung cancer. In view of the two c-myc amplifications detected, a systematic study of c-myc expression levels in non-small cell lung cancers appears worthwhile.
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PMID:Cellular protoonocogenes are infrequently amplified in untreated non-small cell lung cancer. 254 15

The cell line COLO 320 DM, derived from an untreated human colon carcinoid tumor, was subcloned to obtain a population (Cl 11) with an average of 37 double minutes (DM) per cell. Fractionation of the chromosomes by differential centrifugation yielded a fraction enriched in DM. DNA isolated from the DM-enriched fraction was inserted into the Pst I site of pBR322. One clone, p446, representative of a number of similar clones, contained a region complementary to genomic unique sequences (region p446U). Southern blot analysis using COLO 320 DNA, and DNA from two other cell lines derived from the same biopsy, COLO 320 HSR and COLO 321 HSR, demonstrated amplification and rearrangement of sequences complementary to p446U when compared with 28 different tumor and normal cell lines, some of which contained DM or homogeneously staining regions (HSR). COLO 320 DM Cl 11 had approximately 110 copies per cell of the p446U sequence, or three copies per DM. COLO 320 HSR, which contained one HSR, had 35 copies per cell, while COLO 321 HSR, which contained two HSR, had 700 copies. In addition, p446U did not hybridize with insert sequences of recombinant plasmid pHM(E + H), which includes the human c-myc coding region, 3 kb of upstream flanking sequences and 0.5 kb of downstream flanking sequences, or with an exon 3 probe, pMYC RI-CLA. Amplification of p446U was also not seen in cell lines containing amplified c-myc or N-myc genes. These results indicate that more than one sequence may be amplified in DM or HSR containing tumor cells, but that they need not be amplified together in other tumors.
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PMID:Cloning of a non-c-myc DNA fragment from the double minutes of a human colon carcinoid cell line. 302 9

Somatostatin receptors are expressed on certain neural crest-derived tumors, including pancreatic islet cell and carcinoid tumors, medullary thyroid carcinomas, pheochromocytomas, and paragangliomas. The authors evaluated the expression of high affinity somatostatin receptors in childhood neuroblastoma using autoradiography techniques with the somatostatin analogue 125I-octreotide or 125I-[Leu8,D-Trp22,Tyr25]-SS-28 as the radioligand. Thirty tumors from 30 children with neuroblastoma were analyzed. Twenty-three of 30 tumors that were tested expressed somatostatin receptors. Correlation of somatostatin receptor expression with survival was statistically significant. The survival of those patients whose tumors expressed somatostatin receptors was of longer duration than that of patients whose tumors did not. This was an independent prognostic factor. Somatostatin receptors were expressed more frequently in tumor tissue from patients with lower stages of disease and in those with no evidence of N-myc amplification. Tumoral somatostatin receptors are expressed in a subgroup of patients with childhood neuroblastoma. Survival analysis in this group of patients indicates that somatostatin receptor expression is a favorable prognostic factor. This finding may have important implications for the therapy of children with this malignancy.
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PMID:Expression of somatostatin receptors in childhood neuroblastoma. 780 87