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)

Oncogenic activation of myc genes in human cancer involves deregulated expression of myc proteins with no major structural alterations. Here two independent small cell lung carcinoma (SCLC) cell lines were found to express similar novel proteins antigenically related to L-myc. cDNAs corresponding to these proteins were cloned and shown to encode chimeric polypeptides with amino-terminal sequences from a novel gene named rlf joined to the L-myc protein. Although the chimeric mRNAs were shown to be identical, they result from distinct DNA rearrangements. The L-myc fusion protein may represent another activation mechanism of the myc proto-oncogenes.
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PMID:A fusion protein formed by L-myc and a novel gene in SCLC. 185 Oct 85

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

Lung cancer is the leading cause of death from cancer in Western countries. For improved diagnosis and refined therapeutical approaches it is of major importance to understand by what mechanisms carcinoma of the lung develop. The analysis of primary lung cancer revealed specific chromosomal alterations and allelic losses of the short arm of chromosome 3. Genetic aberrations have been observed in proto-oncogenes such as H-ras, K-ras, C-myc and raf-1 as well as in the tumor suppressor genes Rb and p53. Rearrangement of rlf and elevated expression in certain lung tumors have also been reported. The development of lung cancer also involves the altered activation of genes coding for growth factors such as TGF beta 2 and certain growth factor receptor genes such as c-erbB-2, HEK2 and FGFR-4.
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PMID:Oncogenic alterations in primary human lung-tumors (review). 2160 36