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)

Cancer chemotherapy was purely palliative until the early sixties. Tumor cures have been since obtained, first in malignant trophoblastoma and Burkitt's lymphoma, and more recently in Hodgkin's disease, diffuse histiocytic lymphoma, acute lymphocytic leukemia in children, Wilms's tumor and osteosarcoma. Preliminary data are suggestive of tumor cures in testicular teratomas and, possibly, in small cell carcinoma of the lung. Five patients with trophoblastoma, Hodgkin's disease, melanoma, chronic myelocytic leukemia and anaplastic carcinoma of the lung are briefly presented, all without evidence of tumor relapse 3 years or more after chemotherapy. Theoretical bases for improvement of the curative effect of cancer chemotherapy are discussed, including the development of new agents, and new pharmacological problems concerning drug interactions, complexes of drugs with macromolecules or immunoglobulins and liposomes are considered.
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PMID:[Curability of malignant neoplasms: value and limitations of chemotherapy]. 21 68

The secretion of insulin-like growth-factor-binding proteins (IGFBPs) and expression of the genes encoding IGFBP-1, IGFBP-2 and IGFBP-3 have been studied in a panel of cell lines derived from breast carcinomas, Wilms' tumour, neuroblastoma, retinoblastoma, colon carcinoma, liver adenocarcinoma, Burkitt's lymphoma and a non-small-cell lung carcinoma. All cell lines, with the exception of the Burkitt's lymphoma cell line, secreted IGFBPs, as detected by affinity labelling. A 34-kDa BP was present in the conditioned media of all IGFBP-secreting cell lines, whereas BPs ranging from 18 kDa to 53 kDa were variably secreted. All IGFBP-secreting cell lines expressed the IGFBP-2 gene as determined by Northern blot analysis. The Wilms' tumour, the neuroblastoma and the retinoblastoma cell line expressed the IGFBP-2 gene only. All other cell lines, with the exception of the Burkitt's lymphoma, expressed the IGFBP-2 gene and, in addition, either the IGFBP-1 gene and/or the IGFBP-3 gene. IGFBP-1 gene expression could be detected by reverse transcriptase polymerase chain reaction only. IGFBP-3 gene expression was detected by Northern blot analysis, but transcripts were less abundant than IGFBP-2 mRNAs. These findings indicate that the expression of multiple BP genes and the secretion of BPs may be a common property of tumour cells.
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PMID:Insulin-like growth-factor-binding protein gene expression and protein production by human tumour cell lines. 137 87

Radiotherapy is one of the main therapeutic methods for malignant tumors, but on the other hand it can also induce new malignant tumors. Recently, we experienced a case of a 22-year-old woman with triple cancers (Wilms' tumor, thyroid cancer and mucoepidermoid carcinoma of the lung). She had been treated repeatedly for right-sided pulmonary metastases from the Wilms' tumor. The last cancer arose from a different organ in the field irradiated to treat the first cancer, after a latent period of about 20 years. Therefore, this case is classified as highly probable radiation-induced cancer (A-1 group) by the diagnostic criteria for radiation-induced cancer proposed by Sakai et al. Second cancers (radiation-induced cancers) mainly consist of soft tissue sarcomas, leukemias, skin cancers, urinary bladder cancers, large bowel cancers and other tumors. The occurrence of mucoepidermoid carcinoma of the lung as a radiation-induced tumor had not been reported. This patient also showed poor growth of the right breast and marked deformity of the right side of the thorax as late damage from irradiation. We must make efforts to decrease late damage from radiotherapy for pediatric cancers.
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PMID:[A case of radiation-induced mucoepidermoid carcinoma of the lung following radiotherapy for pulmonary metastasis of Wilms' tumor]. 196 24

Antigen expression in fourteen cases of Wilms' tumour was assessed with a panel of monoclonal antibodies. The panel included antibodies reactive with intermediate filament proteins and antibodies reactive with membrane markers originally reported to be associated with small cell lung carcinoma. The immunohistological findings in the tumours were compared to results obtained in adult and fetal kidney. The antigen profile in the blastemal tissue component of the tumours revealed both characteristics of embryonic tissue and signs of early epithelial differentiation. In addition, the histologically apparent transition between blastema and tubules was shown to be reflected in a concurrently occurring and gradual increase in the number of expressed epithelial antigens. Between different tumours, heterogeneity in the degree of epithelial differentiation in the blastema was found. In addition, one case showing foci of anaplasia proved to have an entirely different antigen profile when compared with the other thirteen, non-anaplastic cases. This result is discussed in relation to the different clinical behaviour of focally anaplastic tumours. It is concluded that immunohistology can confirm and extend the histological classification of Wilms' tumour. In addition, new subtypes may be identified in this way.
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PMID:Heterogeneity of Wilms' tumour blastema. An immunohistological study. 246 31

Eight species of novel recombinant tumor necrosis factor-S (rTNF-SAM group) were constructed in which N-terminal amino acid sequences were based on that of TNF-S from THP-1 cells with higher basicity than conventional rTNF-alpha. Two of this rTNF-SAM group, denoted as rTNF-SAM1 and rTNF-SAM2, showed more cytocidal activity on A549 lung carcinoma cells and G401 Wilm's tumor cells than did rTNF-alpha. In addition to these cell lines, rTNF-SAM1 revealed strong cytocidal activity on T24 bladder carcinoma cells, which are resistant to rTNF-alpha. Moreover, possible cachectin activity of rTNF-SAM2 seemed to be lower than that of conventional rTNF-alpha, suggesting that rTNF-SAM2 has less side effects. Actually, toxicity as expressed by LD50 value of rTNF-SAM2 as well as others of the rTNF-SAM group was significantly lower than that of conventional rTNF-alpha. Thus, newly constructed rTNF-SAM1 and rTNF-SAM2 should be more promising antitumor reagents for clinical use, since they were shown to be superior to conventional rTNF-alpha both in antitumor effect and in less side effects.
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PMID:Biological activities of novel recombinant tumor necrosis factor having N-terminal amino acid sequences derived from cytotoxic factors produced by THP-1 cells. 285 Oct 34

Loss of genes at specific chromosomal loci is a characteristic of retinoblastoma, Wilms' tumour, transitional cell carcinoma of the bladder, embryonal tumours and small cell carcinoma of the lung. The significance of nonrandom gene loss in these neoplasms is that gene loss on one chromosome may uncover null mutations at corresponding loci of the homologous chromosome. Loss of specific gene products from somatic cells may be critical in the origin or evolution of certain human tumours. Clues to identification of new loci of gene loss in common adult solid tumours may be found in literature that describes chromosomal abnormalities in rare heritable cancers. Karyotypes of tumours in two families with hereditary renal carcinoma showed translocations involving the short arm of chromosome 3 (refs 10 and 11). We have examined tumours from 18 patients with non-hereditary renal cell carcinomas and found loss of alleles at loci on the short arm of chromosome 3 in all eleven of the patients who could be evaluated.
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PMID:Loss of alleles of loci on the short arm of chromosome 3 in renal cell carcinoma. 288 53

Histological description of human cancer strains (lung carcinoma, laryngeal cancer, Jewing's sarcoma, fibrosarcoma, Wilms' tumor, renal carcinoma) transplanted into 6- to 8-week-old nude mice and 4- to 6-week old nude rats is presented. Human origin of these strains is proved by an analysis of lactate dehydrogenase isoenzymes. The growth rate of human cancer strains in rats is considerably higher than in mice.
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PMID:[Human tumor lines transplantable to athymic mice and rats]. 397 Oct 37

The use of radiocolloid liver scanning as a routine diagnostic procedure to detect liver metastases has been declining as the most effective uses of this test have become better appreciated. Liver scanning to detect hepatic metastases appears to have the greatest efficacy in two circumstances. The first is as a staging procedure in malignancies that metastasize to the liver early, before being suspected clinically or liver function parameters alter. Such malignancies include gastric carcinoma, Wilms' tumor, small cell carcinoma of the lung, and rhabdomyosarcoma. The second effective use of liver scanning is as a confirmatory test in patients with known malignancy who develop abnormal levels of serum liver enzymes, carcinoembryonic antigen titer, hepatomegaly, ascites, or jaundice.
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PMID:Efficacy of liver scanning in malignant diseases. 609 64

A new class of fragile sites termed common fragile sites is induced by aphidicolin, an inhibitor of DNA polymerase alpha. Analysis of these common fragile sites and cancer chromosome breakpoints indicates that eight fragile sites are in bands with cancer breakpoints. This is unlikely to be due to chance (p less than 0.01). Common fragile sites are in both bands where breaks occur in carcinoma of the lung and in carcinoma of the ovary. Common fragile sites are in bands with breaks leading to constitutional chromosome abnormalities associated with cancer: hereditary renal cell carcinoma and aniridia-Wilms' tumor complex. Common fragile sites, thus, may predispose to chromosome breaks and rearrangements in cancer.
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PMID:Cancer chromosome breakpoints and common fragile sites induced by aphidicolin. 643 79

Although it is widely accepted that tumor suppressor genes play an important role in the genesis and progression of human cancer, little is known about genetic events that accumulate during multistage lung carcinogenesis. Thus, to determine a subset of tumor suppressor genes that are involved in the genesis and progression of non-small cell lung carcinoma (NSCLC), 22 brain metastases and 23 stage I primary lung tumors were examined for allelic losses at 40 loci on 10 chromosomes including the loci of 5 tumor suppressor genes, APC, WT1, RB, p53, and DCC. The incidence of allelic losses on chromosomes 3p, 13q, and 17p was high (> 60%) in both primary tumors and brain metastases. In brain metastases, a high incidence of allelic losses (> 60%) was also observed at loci on chromosomes 2q, 18q, and 22q, and the incidence of allelic losses on these chromosomes in brain metastases was significantly higher than that in primary tumors (P < 0.05). In two cases of brain metastases with corresponding primary lung tumors, sequential accumulation of allelic losses during progression of primary lung tumors was observed on several chromosomes including chromosomes 2q and 18q. These results indicate that, besides loss of heterozygosity for chromosomes 3p, 13q, and 17p, loss of heterozygosity for chromosomes 2q, 18q, and 22q also occurs frequently in advanced NSCLCS. Thus, it is possible that loss of heterozygosity on chromosomes 2q, 18q, and 22q occurs late in the progression of NSCLC and/or causes phenotypic alterations of NSCLC cells into more aggressive ones.
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PMID:Frequent allelic losses on chromosomes 2q, 18q, and 22q in advanced non-small cell lung carcinoma. 792 10


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