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 level of c-Ki-ras-2-specific mRNA was found to be markedly enhanced (10- to 20-fold) in a human epidermoid lung carcinoma transplanted into nude mice, compared with that in other lung carcinomas. Analysis of DNA revealed that c-Ki-ras-2 gene was amplified approximately 10-fold in this carcinoma, while c-Ha-ras, c-myc and c-sis were not amplified. Chromosome abnormalities were also observed in this carcinoma.
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PMID:Amplification and enhanced expression of cellular oncogene c-Ki-ras-2 in a human epidermoid carcinoma of the lung. 392 99

68 cases of lung carcinoma, 3 carcinoids and 15 fibrosing alveolitis with foci of adenomatosis and bronchiolo-alveolar carcinoma were studied. Oncoproteins c-fos, c-jun, c-ets-1, c-myc L and L-myc were identified in the tumour and surrounding tissue. Expression of c-fos was revealed in 79 of 138(59.4%) of proliferative and dysplastic changes of lung epithelium; c-jun in 40 of 61 (65.6%), c-ets-1 in 22 of 41 (53.7%), c-myc in 41 of 96(42.7%) and L-myc in 15 of 61 (24.6%), mainly in altered bronchial epithelium with a positive reaction to the antibodies against neuron specific enolase and S100 protein. More pronounced expression of nuclear oncoproteins, heterogeneity of their location in tissues, frequent cytoplasmic location in tumour cells were typical for lung carcinoma.
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PMID:[Nuclear oncoprotein expression in lung precancer and cancer at various stages of tumor progression studies at the level of light- and electron-immunohistochemistry]. 760 17

The retinoblastoma (RB) tumour suppressor gene has been associated not only with retinoblastoma but also with several other tumours like osteosarcoma, small cell lung carcinoma and prostate and breast cancer. We have studied the incidence of RB gene alterations in 96 primary breast tumours using Southern blotting techniques. The outcome has been related with patient and tumour characteristics, oncogene amplifications, p53 mutations and prognosis. RB gene alterations were found to occur more frequently in estrogen receptor (ER)-positive than in ER-negative tumours and less frequently in tumours with oncogene amplification than in tumours without oncogene amplification of HER2/neu, c-myc or 11q13. RB gene alteration was observed in tumours both with and without a p53 gene mutation. Data on 87 patients (mean age, 59.6 years; median follow-up, 108 months) and RB gene alterations revealed a significant association between the frequency of RB gene alterations and node-negative patients (p < 0.01) or smaller (< 2 cm) tumours (p < 0.01), but no relation with age, differentiation grade or (relapse-free) survival. Patients with and without RB gene alterations showed the same relapse-free and overall survival.
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PMID:Association between RB-1 gene alterations and factors of favourable prognosis in human breast cancer, without effect on survival. 761 56

Five small-cell lung carcinoma (SCLC) cell lines were established from xenografted tumor lines. These tumor lines were established after transplantation into nude mice of primary tumors or metastatic foci obtained surgically, from untreated (IRSC-2M, IRSC6M, IRSC-10M and IRSC-61M) or treated patients (IRSC-74M). They were then set-up in culture as parallel cell lines. Histologically, these tumor lines were classified as being of the classic (IRSC-2M, IRSC-10M and IRSC-61M) or intermediate type (IRSC-6M and IRSC74M). Four of these 5 SCLC cell lines grew as floating cell aggregates, while one (IRSC6M) grew as an adherent cell monolayer. Growth rates were slow (doubling times ranged between 120 and 194 h) but could be accelerated (67 to 144 h) by cultivating cells in medium mixed (v/v) with self-conditioned medium. Electron microscopical examination revealed that all SCLC cell lines contained dense core granules, characteristic of their neuroendocrine origin. These cell lines formed colonies in agarose with colony forming efficiencies ranging from 0.02-0.36%. The classic-type cell lines retained their tumorigenic capacity when re-injected intracranially into naive nude mice, whereas the intermediatetype cells did not. Cytogenetic analysis confirmed the human origin of SCLC xenografts and cultured cell lines. Various numerical and structural chromosome abnormalities were found, with deletion in the short arm of chromosome 3 being the most common (4 of the 5 cell lines). Deletions in or loss of the chromosome 10 were also observed. Oncogene expression was studied in 3 representative cell lines (IRSC-10M, IRSC-2M and IRSC-74M). L-myc was overexpressed only in IRSC-74M, while the GRP gene was overexpressed in the classic (IRSC-2M and IRSC-10M) but not in the intermediate-type cells (IRSC-74M). The Ki-ras oncogene was overexpressed in the 3 cell lines, while c-myc, N-myc, Ha-ras, N-ras, erb B2 and sis were not detected in any of them. The 3 cell lines weakly expressed the MDR1 gene, while the GST-pi gene was not expressed. These cell lines constitute a multifaceted well-characterized in vitro model for studying the biology of these phenotypically diverse cancer cells.
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PMID:Establishment and characterization of five human small cell lung cancer cell lines from early tumor xenografts. 784 23

We have performed a comprehensive analysis of the DNA copy number changes that occur in 18 small cell lung carcinoma cell lines using comparative genomic hybridization (Kallioniemi et al., Science (Washington DC). 258: 818-821, 1992). DNA copy number abnormalities detected in this study include previously identified increases at 1p22-32 (L-myc), 2p24-25 (N-myc), and 8q24 (c-myc) and decreases at 17p13 (p53), 13q14 (RB), and 3p. In addition, novel DNA copy number increases were detected at 5p, 1q24, and Xq26, and novel decreases were found at 22q12.1-13.1, 10q26, and 16p11.2. Many of the most common DNA copy number changes revealed are at loci not previously recognized to be important in small cell lung cancer. In addition, a number of the DNA copy number changes, including increases at 1p22-32, 2p24-25, and 3q22-25 and a decrease on 18p, were found to occur preferentially in small cell lung carcinoma lines of the "variant" phenotype. This correlation suggests that genes may reside at these loci whose overexpression or inactivation contributes to the radiation resistance or aggressive growth phenotypes characteristic of this subtype of small cell lung carcinoma.
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PMID:Identification of frequent novel genetic alterations in small cell lung carcinoma. 792 22

The N-myc gene is amplified and overexpressed in neuroblastoma, retinoblastoma and small cell lung carcinoma, and is considered to be related to cell proliferation and/or differentiation. The transcriptional regulatory sequences of the c-myc gene have been already identified, while those of N-myc have remained obscure for a long time. In this report, we have identified several positive and negative transcriptional regulatory elements in the upstream region of the mouse N-myc gene. Among them, an activating sequence spanning -860 to -797 bp (63 bp) could be reduced to a functional core of 21 bp from -846 to -826. This sequence, termed N21 box, worked as a positive transcriptional element when linked directly upstream (but not downstream) of the putative N-myc promoter in HeLa, not in IMR32 cells. At least two proteins, of 42 kDa and 100 kDa, bound to the double-stranded N21 box, and were expressed in HeLa as well as in IMR32 cells. Moreover, the plus strand of N21 box could be specifically bound by a species of 42 kDa from either cell type and by a 37 kDa protein found only in HeLa cells. These proteins may be factors binding to positive transcriptional regulatory elements and may have a role in the regulation of N-myc expression.
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PMID:Transcriptional regulation of the N-myc gene: identification of positive regulatory element and its double- and single-stranded DNA binding proteins. 824 Dec 68

Tumor progression is a complex process involving many alternative molecular pathways that are often tissue and/or species specific. The c-myc oncogene has been implicated in malignant progression in a variety of human tumors. In many instances, amplification and/or elevated expression of the c-myc gene have been associated with poor prognosis or decreased survival; in other cases, correlations have been demonstrated between c-myc activation and specific parameters of advanced neoplastic stage such as hormone independence, transplantability, invasiveness, etc. The tumor types exhibiting c-myc as a "progressor" gene include breast, colon, small cell lung carcinoma, as well as ovarian cancer, lymphomas, and squamous cell carcinomas. The c-myc oncogene has been implicated in a number of experimental animal tumor models, especially rat liver. Several studies have found that c-myc often functions in rodent tumor progression. For example, rat skin carcinomas induced by ionizing radiation show c-myc amplification to be related directly to tumor size and age.
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PMID:The c-myc oncogene in tumor progression. 835 42

In our effort to delineate factors that govern the ability of non-small cell lung carcinoma (NSCLC) to form monolayer cell lines, we have attempted to derive monolayer cell lines from the primary cultures of 29 unselected human NSCLCs. Eight new lines were obtained. Cell lines were easier to establish from poorly differentiated tumors, especially adenocarcinomas. One cell line was from a large cell neuroendocrine carcinoma. All cell lines were aneuploid, and they exhibited heterogeneous nutritional requirements for growth in vitro. Cell line-forming primary tumors demonstrated higher mean messenger RNA expression levels for transforming growth factor-alpha and c-met proto-oncogene than did tumors that failed to form cell lines. Although a high level of c-myc expression was correlated with the ability of NSCLC cell lines to form xenograft tumors in nude mice, it was not correlated with the ability of primary tumors to establish cell lines. The results suggest that autocrine growth loops play important roles in the ability of NSCLC cells to proliferate continuously in monolayer culture. The fact that the overexpression of transforming growth factor-alpha in NSCLCs has been negatively correlated with patient survival and that most cell lines can be established only from poorly differentiated carcinomas may provide the explanation for a previous report that the capability for cell line establishment constitutes a negative prognostic indicator for patient survival. However, when the genotype and phenotype of the cell lines were compared with those of their corresponding primary or xenograft tumors, the tumor cells that grew continuously as a cell line often represented a selective subpopulation of the heterogeneous neoplastic cells in the primary tumors. This finding should be taken into consideration when cell lines are used to evaluate the chemo- and radiosensitivity of tumor cells.
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PMID:Proto-oncogene and growth factor/receptor expression in the establishment of primary human non-small cell lung carcinoma cell lines. 838 8

Non-small cell lung carcinoma specimens of 173 previously untreated patients were analyzed for the expression of proteins encoded by the oncogenes c-myc, c-fos, c-jun, c-erbB-1, c-erbB-2, c-H-ras, c-K-ras and c-N-ras. Forty-six per cent of the tumors were positive for the c-MYC protein, 60% for c-FOS, 50% for c-JUN, 80% for c-ERBB-1, 55% for c-ERBB-2, 12% for c-H-RAS, 5% for c-K-RAS and 71% for c-N-RAS. Proteins encoded by c-fos and c-jun are overexpressed more frequently in carcinomas of smokers (c-fos: P < 0.005; c-jun: P < 0.01). When we grouped the patients according to their tumor histology the results became more evident. Squamous cell lung carcinomas of smokers showed a higher incidence of c-FOS (P = 0.01), c-JUN (P < 0.01) and c-ERBB-1 (P = 0.01) proteins than squamous cell lung carcinomas of non-smokers. The expression rate and the intensity of staining proved not to be influenced either by the number of cigarettes smoked daily or by cessation of smoking. In adenocarcinomas, however, we only found a trend for a more frequent overexpression of c-fos (P = 0.07) and c-jun (P = 0.14) encoded proteins in carcinomas of smokers and no correlation between the expression of c-erbB-1 products and smoking. No correlation was found between the expression of c-MYC, c-ERBB-2, c-H-RAS, c-K-RAS and c-N-RAS proteins and the smoking habits of the patients, neither in squamous cell carcinomas nor in adenocarcinomas of the lung.
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PMID:Overexpression of oncoproteins in non-small cell lung carcinomas of smokers. 838 72

A transplantable tumor and an in vitro culture cell line (GK-T3) were established from metastatic liver tissue of human small cell lung carcinoma (SCLC). Southern blot analysis revealed about 30-fold amplification of c-myc gene in the tumor cells in liver, xenografts, and in vitro cell line. The degree of c-myc amplification was essentially conserved through serial passages in nude mice and cultivation in vitro. The level of c-myc mRNA was significantly increased in these cells. Cytogenetically, numerical and complex structural abnormalities were observed in GK-T3 cells, including t(3p;6p), t(12q;17p), two homogeneously staining regions (hsrs) and several double minutes (dmins). These results suggest that activation of c-myc gene and alteration of gene(s) around these chromosomal breakpoints may play a role in tumorigenesis of GK-T3 SCLC.
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PMID:Establishment of a human small cell lung carcinoma cell line carrying amplification of c-myc gene and chromosomal translocation of t(3p;6p) and t(12q;17p). 839 Apr 24


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