Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0684249 (lung carcinoma)
 23,830 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The proto-oncogene c-src codes for two tyrosine kinases, pp60c-src and pp60c-srcN. The latter protein appears to be exclusively expressed in neurons and neuronally differentiated tumors. In cell lines derived from neuroblastoma and small-cell lung carcinoma, src expression correlates positively with neuroendocrine differentiation. However, pp60c-srcN is expressed only in highly differentiated neuroblastomas. Although c-src expression in neuroendocrine tumors probably reflects and is the result of the differentiation stage at which the tumors have been arrested, high c-src expression and kinase activities in non-neuroectodermal tumors, e.g., colon carcinoma, breast carcinoma, might instead be a part of the malignant phenotype and contribute to the development of these tumors.
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PMID:src expression in small-cell lung carcinoma and other neuroendocrine malignancies. 217 63

The c-fos proto-oncogene and H-2K class I major histocompatibility antigens are differentially expressed in low-metastatic Lewis lung carcinoma clones, but not in high-metastatic clones. Interferons induce mRNA expression of fos and H-2 in non-expressor cells and elevate mRNA steady state levels of expressor cells. Transfection of non-expressor cells by v-fos or c-fos genes induces the transcription of H-2K mRNA and elevates the levels of H-2 proteins, but not of other gene products. These results, correlated with observations in other cell systems, suggest that the c-fos proto-oncogene controls the expression of MHC genes coding for class 1 antigens.
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PMID:The c-fos proto-oncogene in murine 3LL carcinoma clones controls the expression of MHC genes. 245 11

Proto-oncogenes, which have been widely implicated in the pathogenesis of malignant human tumors, frequently demonstrate restriction fragment length polymorphism (RFLP). Population studies of such restriction alleles is of potential interest for genetic analysis of cancer susceptibility. Some of the initial date of Krontiris et al (1985) showing a significant increase of rare c-ha-ras-l alleles in individuals with tumors, have been confirmed in certain types of cancer (breast cancer, lung adenocarcinoma), whereas others have been refuted (myelodysplasia, melanoma, colon adenocarcinoma). Other significant associations have been found between other proto-oncogene RLFPs and tumors (c-mos and breast cancer, c-raf and non Hodgkins lymphoma, L-myc and lung carcinoma metastasis). Although they are controversial, these studies should be extended, in order to determine whether the presence of certain alleles is a contributing factor in the development of certain tumors.
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PMID:[Genetic polymorphism and susceptibility to cancer]. 289 51

The macrophage-specific colony stimulating factor CSF-1 is required for the growth and differentiation of monocytes. The cell surface receptor for CSF-1 is identical to the product of the c-fms proto-oncogene. The present studies have monitored CSF-1 and c-fms expression in human carcinoma cell lines. Two of three human ovarian carcinoma cell-lines expressed multiple species of CSF-1 mRNA. Furthermore, detection of CSF-1 transcripts was associated with secretion of CSF-1 protein that was increased after phorbol ester treatment. CSF-1 mRNA was also detectable in 4 breast and 2 lung carcinoma cell lines. In contrast, c-fms expression was found only in SK-Br-3 breast carcinoma cells. Similar studies in 2 human choriocarcinoma cell lines demonstrated the presence of c-fms, but not CSF-1, transcripts. While phorbol ester treatment was associated with increased c-fms mRNA levels in choriocarcinoma cells, this agent had no effect on CSF-1 expression. These findings indicate that: 1) CSF-1 expression is frequent in human ovarian, breast and lung carcinoma cells; and 2) coexpression of the CSF-1 and c-fms genes, as found in monocytes is infrequent in malignant epithelial and choriocarcinoma cell lines.
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PMID:CSF-1 and C-FMS gene expression in human carcinoma cell lines. 297 87

Twelve cell lines isolated from patients with small cell lung cancer have been studied for amplification of the three characterised members of the myc proto-oncogene family (c-myc, N-myc, and L-myc) and for abnormalities of chromosome 3. Ten of these lines were being studied for the first time. Ten of the 12 small cell lung cancer cell lines had amplification of one member of the myc proto-oncogene family. Amplification of c-myc was observed in only one small cell lung line--a "morphological variant". One "classic" small cell lung cancer line expressed c-myc but had no obvious amplification of the gene. N-myc and L-myc were more commonly amplified than c-myc. Chromosomal abnormalities (mainly deletions) in chromosome 3 were observed in all small cell lung carcinoma cell lines examined. When the small cell lung carcinoma lines were grouped according to "classic" or "variant" characteristics, it was found that the "classics" had deletions of the short arm of chromosome 3, whereas the "biochemical variants" had deletions of the long arm of chromosome 3. The extent of the deletions varied between cell lines. For the deletion in the short arm of chromosome 3 the minimum common region of overlap was assigned to bands 3p23-3p24.
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PMID:Oncogene amplification and chromosomal abnormalities in small cell lung cancer. 303 34

Morphologic transformation of NIH 3T3 mouse cells occurs upon transfection of these cells with large amounts (greater than or equal to 10 micrograms) of recombinant DNA molecules carrying the normal human H-ras-1 proto-oncogene. We provide experimental evidence indicating that transformation of these NIH 3T3 cells results from the combined effect of multiple copies of the H-ras-1 proto-oncogene rather than from spontaneous mutation of one of the transfected H-ras-1 clones (E. Santos, E.P. Reddy, S. Pulciani, R.J. Feldman, and M. Barbacid, Proc. Natl. Acad. Sci. USA 80:4679-4683, 1983). Levels of H-ras-1 RNA and p21 expression are highly elevated in the NIH 3T3 transformants, and in those cases examined, these levels correlate with the malignant properties of these cells. We have also investigated the presence of amplified ras genes in a variety of human carcinomas. In 75 tumor biopsies, we found amplification of the human K-ras-2 locus in one carcinoma of the lung. These results indicate that ras gene amplification is an alternative pathway by which ras genes may participate in the development of human neoplasia.
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PMID:ras gene Amplification and malignant transformation. 391 35

We determined a complete nucleotide sequence of an activated form of the c-H-ras-1 proto-oncogene cloned from the human cell line (QG56), using the DNA transfection technique and NIH3T3 cells as recipients. This cell line was established from a squamous-cell lung carcinoma of a Japanese patient, and the activated gene had 2 nucleotide substitutions. One substitution of a thymidine for an adenosine was found at position 1069 of the 2898 nucleotide sequence in a restriction endonuclease (SacI) fragment, which corresponds to the second base of the 61st codon of the gene encoding P21 protein. This nucleotide replacement was assumed to be responsible for the transforming activity. Another substitution of a guanosine for an adenosine which was detected at position 746 in the first intron was thought to be a genetic polymorphism unassociated with the transforming activity. Comparison of the various lengths of restricted fragments suggested that the activity was markedly influenced by certain sequences flanking the c-H-ras-1 gene.
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PMID:Isolation and characterization of an activated C-H-ras-1 gene from a squamous-cell lung carcinoma cell line. 400 2

The c-kit proto-oncogene encodes a tyrosine kinase receptor for stem cell factor and plays a critical role in the growth and differentiation of various types of cells including hematopoietic stem cells. To investigate the mechanisms of its transcriptional regulation, we isolated the 5' flanking region of the human c-kit gene and characterized its promoter activity in hematopoietic cells. Nucleotide sequence analysis revealed that the 1.2 kb 5' flanking region lacked a typical "TATA box," but had a relatively high G + C content and four potential Sp1-binding sites. Putative binding sites for AP-2, basic helix-loop-helix proteins, Ets-domain proteins, Myb and GATA-1 were also found. Primer extension and S1 nuclease protection analyses of hematopoietic cells indicated that the major transcription start sites are 62 bp and 58 bp upstream of the translation start site. Essentially the same start sites were detected in non-hematopoietic cells such as small cell lung carcinoma and glioblastoma: this single promoter in c-kit is different from the multiple promoter system of c-fms, a c-kit-related gene, in which at least two promoters are differently used in hematopoietic and non-hematopoietic cells. An analysis of the c-kit 5' flanking region using the bacterial chloramphenicol acetyltransferase gene (CAT assay) in human erythroleukemia HEL cells, which express the endogenous c-kit mRNA at high levels, showed that a region from -180 to -22 is important for the expression of the c-kit gene. In addition, a negative regulatory element(s) is suggested to be involved in the regulation of the c-kit gene expression in mammals.
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PMID:Characterization of the promoter region of the human c-kit proto-oncogene. 750 48

Rearrangements of the L-myc proto-oncogene with the cellular gene rlf occur in a subset of human small cell lung carcinoma (SCLC) resulting in the expression of a fusion protein. To investigate whether expression of such a rlf/L-myc fusion protein could contribute to the development of SCLC we constructed a chimeric minigene where the rlf first exon and the L-myc second and third exon are under the control of the rlf promoter thereby recapitulating the events of the rearrangement. Attempts to generate transgenic mice with this minigene showed that mouse embryos containing high copy numbers of the rlf/L-myc minigene fail to develop, suggesting that the expression of a rlf/L-myc fusion protein interferes with early differentiation processes. To investigate the nature of this potential embryonic lethality further, we transfected the rlf/L-myc construct stably into embryonic stem (ES) cells. Transfected ES lines that express the rlf/L-myc construct do not show a higher proliferation rate than the parental ES line but fail to properly develop embroid bodies. In addition, outgrowth and differentiation of cells from embroid bodies was severely impaired in ES cells expressing the rlf/L-myc construct when compared to normal ES cells, again suggesting an interference of rlf/L-myc expression with proper differentiation. Expression of a rlf/L-myc fusion may therefore be of critical importance in tumorigenesis by blocking differentiation and thereby allowing continued proliferation of cells and the acquisition of further mutations leading to a fully malignant tumor.
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PMID:Expression of a rlf/L-myc minigene inhibits differentiation of embryonic stem cells and embroid body formation. 797 Jul 11

By successive screenings of cDNA libraries prepared from human tumours and from human foreskin keratinocytes, we have isolated overlapping cDNAs coding for a novel protein which we call Ron, with sequence characteristics of a receptor protein tyrosine kinase. Ron is a 1400 amino acid protein structurally similar to the 1408 amino acid product of the C-MET proto-oncogene, the receptor for hepatocyte growth factor and scatter factor. The two proteins have 63% overall sequence identity in their intracellular regions. We have localised the RON gene to human chromosome region 3p21, a region frequently deleted in small cell carcinoma of the lung and in renal cell carcinoma, and which is believed to harbour unidentified tumour suppressor genes. Interestingly, normal lung tissue contains transcripts of the RON gene.
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PMID:A novel putative receptor protein tyrosine kinase of the met family. 838 24


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