Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0242379 (lung cancer)
 71,905 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The alpha alpha form of S-100 protein (S-100a0), which is distributed mainly in the heart and striated muscles, and also in the brain and kidney, was determined in tumor tissues and sera of patients with renal cell carcinoma by employing an enzyme immunoassay system for bovine S-100a0 protein. The average content of S-100a0 in the renal cell carcinoma tissue (n = 10) was about 650 ng/mg protein, 4-fold higher than that in the kidney (n = 6, 160 ng/mg protein). Immunohistochemically, S-100a0 antigen was localized in such epithelial cells as proximal tubules, Bowman's capsules and collecting tubules of normal kidney, and in the cytoplasm, nucleus and occasionally plasma membrane of the tumor cells. The contents of S-100a0 protein in various lung carcinoma tissues were low (less than 10 ng/mg protein). Serum S-100a0 concentrations were less than 0.3 ng/ml in healthy subjects, but they were significantly increased in patients with renal cell carcinoma at diagnosis, showing greater than 0.5 ng/ml in 17/32 cases (53%). Serum S-100a0 levels were also enhanced in some patients with lung cancer (10/33, 30%), breast cancer (4/20, 20%) and other non-neoplastic diseases, indicating that S-100a0 protein in the serum is not a specific biomarker for renal cell carcinoma. However, serum S-100a0 concentrations in patients with renal cell carcinoma changed in parallel with the clinical course during treatment. These results suggest that serum S-100a0 may be a useful biomarker at least for monitoring the clinical course of renal cell carcinoma.
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PMID:High levels of S-100a0 (alpha alpha) protein in tumor tissues and in sera of patients with renal cell carcinoma. 393 85

Monoclonal antibodies with selectivity for human lung cancer were produced by immunizing BALB/c mice with an established line of human small cell lung cancer (NCI-H69) and fusing the mouse spleen cells to mouse myeloma line X63-Ag8.653. The resulting hybrid cells were initially screened by immunoautoradiography for production of antibodies that would react with NCI-H69 and another small cell lung cancer line (NCI-H128) but not its autologous B-lymphoblastoid line (NCI-H128BL). Stable monoclonal antibody-producing lines were isolated by repeated cloning. Three independently derived monoclonal antibodies, designated 525A5, 534F8, and 538F12, were found to react with three of the major types of human lung cancer (small cell, adenocarcinoma, and squamous carcinoma). They did not react with bronchioloalveolar and large cell lung cancers, myeloma, lymphomas, leukemias, osteogeneic sarcoma, mesothelioma, hypernephroma, malignant melanoma, simian virus 40-transformed human fetal lung cells, skin fibroblast lines, human B-lymphoblastoid lines, human erythrocytes, and rodent cells. Interestingly, these antibodies also bound to three out of three human neuroblastomas and two out of three breast cancers but failed to react with mouse neuroblastoma and rat pheochromocytoma. The monoclonal antibodies reacted with human small cell lung cancer tumors obtained at autopsy, but had insignificant reactions with normal human lung, liver, spleen, and skeletal muscle. We conclude that monoclonal antibodies have been generated that react with common antigenic determinants expressed on several human lung cancer types, neuroblastoma, and some breast cancers, but are not detectable by our current assays on a variety of other human tumors or normal adult human tissues. Such antibodies are of potential clinical and biological importance.
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PMID:Monoclonal antibodies that demonstrate specificity for several types of human lung cancer. 627 Jun 85

Two murine IgG2Ak monoclonal antibodies (703D4, 704A 1) were produced and characterized after immunization with a human large cell lung cancer line (NCI-H 157). These antibodies detect different epitopes on 31 kilodalton [35S]methionine incorporating protein(s). Radiobinding and immunohistochemical studies show these antibodies bind to most (11/13) human non-small cell lung cancer (adenocarcinoma, epidermoid, and large cell), but not to small cell lung cancer (0/11) tumors tested. The epitopes these antibodies recognized are also expressed on human melanomas (7/8), two other tumors (osteogenic sarcoma, renal cell carcinoma), but not on many other human tumors (breast, colon, neuroblastoma, lymphoid), and not on a panel of normal adult human tissues. Because the antigen(s) are preserved after fixation and because of their ability to distinguish lung cancer types from each other and normal tissues, they should be of clinical, as well as of biologic interest.
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PMID:Monoclonal antibodies that distinguish non-small cell from small cell lung cancer. 630 2

Broad phase II trial of methylglyoxal-bi (guanylhydrazone) (MGBG) is under way at the Memorial Sloan-Kettering Cancer Center. Studies in renal cell carcinoma, lymphomas, and non-small-cell lung cancer are completed, and substantial numbers of patients with esophageal and head and neck cancer have been treated. Small numbers of patients with other solid tumors have also been entered into the study. MGBG has significant antineoplastic activity against lymphomas, with 16/40 heavily pretreated patients (40%) having partial remissions (PR) lasting 1 to 8+ months. MGBG has also demonstrated more modest activity in non-small-cell lung cancer, esophageal, and head and neck carcinoma; it appears to have little or no therapeutic value in renal cell cancer. Toxicities have been manageable, and included mild nausea and vomiting, diarrhea, mucositis, and myelosuppression. The dose-limiting toxicity, seen most frequently in those patients with impaired renal function, was lethargy and fatigue. MGBG has demonstrated activity in lymphomas, lung, esophageal, and head and neck cancer. Further trials of this agent are indicated, both alone and in combination.
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PMID:Phase II trials of methylglyoxal-bis (guanylhydrazone). 704 14

A comparative radioimmunologic study of changes in the ratio of calcitonin and parathyroid hormone secretion was carried out in healthy controls (young and older than 40 years), patients with benign tumors, inflammatory processes and malignancies of the stomach, kidney, breast, prostate and lung. A significant increase in the "calcitonin index" (ratio of molar concentrations of calcitonin and parathyroid hormone) was established in patients with cancer of the breast, prostate and skeletal metastases of lung cancer, irrespective of the presence of primary tumor. This index is irrelevant in cases of gastric and renal carcinoma and cannot be used a indication of skeletal dissemination because of the predominant level of parathyroid hormone secretion.
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PMID:[Calcitonin and parathyrin in the blood serum of cancer patients]. 710 29

The autopsy material of the USSR AMS Cancer Research Center for 1960--1977 was studied. Among 3327 patients dying of malignant tumours, secondary tumour involvement of the heart was revealed in 170 (5.1%) cases, in 119 patients the tumour metastasized into the heart, in 51 grew into the pericardium. Most frequently, tumour involvement of the heart occurred in lung cancer, systemic diseases of the hemopoietic tissue, melanoma, and mammary gland carcinoma. Growth of the tumour into the heart, as a rule, was found in systemic diseases and lung cancer. Melanoma, renal carcinoma, and carcinoma of the oral cavity were characterized by small- and large-nodular forms of metastasis. The tumour involvement was most frequently found in the pericardium followed by the myocardium. In outgrowths of the tumour, the outer layer of the pericardium and in small-nodular metastases the visceral layer (epicardium) were affected most frequently. Hemorrhagic pericarditis was frequently observed in tumour alterations of the heart. Metastases and outgrowths into the heart were always associated with progression of the tumour.
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PMID:[Secondary tumors of the heart (based on autopsy materials in the Oncology Research Center of the Academy of Medical Sciences of the USSR over the period of 1960-1977)]. 740 18

An extended YAC contig has been developed for the 3p14 region containing the hereditary renal carcinoma 3;8 translocation breakpoint and the 3p14.2 fragile site FRA3B. This region of chromosome 3 has been implicated by chromosomal translocation, deletion, and loss of heterozygosity in the pathogenesis of several malignant diseases. The contig allows accurate positioning of candidate genes, polymorphic markers, and other 3p rearrangements within this region. The contig, spanning approximately 6 Mb of DNA, contains 51 YACs identified by 27 markers, including a subset of CA repeats located in the 3p14.1-14.2 interval. The order of CA microsatellites, derived from marker content of the YACs, is in agreement with the order previously determined by genetic linkage studies. We find that the protein-tyrosine phosphatase gamma gene, PTPRG, is located minimally 1 Mb proximal to the t(3;8) breakpoint. The more proximal 3p homozygous deletion in the small-cell lung cancer cell line, U2020, is more than 5 Mb from the site of the 3;8 translocation. This integrated physical and genetic map provides a framework for further investigations of malignant diseases associated with proximal 3p loss. In addition, the positioning of separate 3p14.2 aphidicolin-induced breakpoints suggests that FRA3B may represent a region rather than a single site.
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PMID:Integrated YAC contig containing the 3p14.2 hereditary renal carcinoma 3;8 translocation breakpoint and the fragile site FRA3B. 753 24

In a family with a constitutional translocation t(3;6), the oldest member carrying the translocation had developed multiple nonpapillary renal cell carcinomas (RCCs). The translocation breakpoint was positioned between 3p13 and 3p14.1. This is close to the region in which a t(3;8) breakpoint has been reported in a family with hereditary RCC. We defined the location of the t(3;6) and t(3;8) breakpoints by fluorescence in situ hybridization (FISH) analysis with yeast artificial chromosomes (YACs) from the 3p14-13 region. Both interphase nuclei and metaphase cells from translocation-carrying members of both families have been used, allowing the definition of flanking YACs for each breakpoint. We could thereby clearly confirm that the breakpoints are different, the t(3;8) breakpoint being most distal. In addition, we have shown that both translocation breakpoints are located distal to the homozygously deleted region in the U2020 lung cancer cell line.
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PMID:Defining the position of the breakpoint of the constitutional t(3;6) occurring in a family with renal cell carcinoma. 753 63

Alterations in the p53 tumor suppressor gene appear to be important in the development of many human tumors. The wild-type p53 gene has a polymorphism at codon 72 that presents the arginine (CGC) or proline (CCC) genotype, which recently has been reported to be associated with genetically determined susceptibility to smoking-related lung cancers. To determine whether this p53 genotype influences individual risk of urologic cancer and/or its progression, we used polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) analysis to assay the allelic frequencies of this polymorphism in 85 renal cell carcinoma patients, 151 urothelial cancer patients, 33 testicular cancer patients, 28 prostatic cancer patients and 56 patients without neoplastic disease. The allelic distributions of the three genotypes (Arg/Arg, Arg/Pro, Pro/Pro) in patients with renal cell carcinoma (29.4%, 55.3%, 15.3%), urothelial cancers (45.7%, 39.7%, 14.6%), testicular cancer (45.4%, 48.5%, 6.1%) or prostate cancer (42.9%, 50.0%, 7.1%) did not differ significantly from those in the normal controls. However, Pro/Pro genotype in renal cell carcinoma and urothelial cancer (smoking-related cancers) was more frequent than that in prostate cancer and testicular cancer (smoking-unrelated cancers) with borderline significance (P = 0.0881). There was no particular correlation between frequency of the three genotypes and grade or stage of each type of tumor. The association of genetic predisposition to urologic cancers with p53 gene codon 72 polymorphism is not so clear as the previous study of Japanese lung cancer patients, but this polymorphism may play some role in urothelial cancers and renal cell carcinoma, in which smoking is an epidemiological risk factor.
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PMID:Allelic frequency of p53 gene codon 72 polymorphism in urologic cancers. 755 95

Seventy nine advanced cancer patients in a clinical trial were treated with LAK/IL-2 combining with Lycium Barbarum polysaccharides (LBP). Initial results of the treatment from 75 evaluable patients indicated that objective regression of cancer was achieved in patients with malignant melanoma, renal cell carcinoma, colorectal carcinoma, lung cancer, nasopharyngeal carcinoma, malignant hydrothorax. The response rate of patients treated with LAK/IL-2 plus LBP was 40.9% while that of patients treated with LAK/IL-2 was 16.1% (P < 0.05). The mean remission in patients treated with LAK/IL-2 plus LBP also lasted significantly longer. LAK/IL-2 plus LBP treatment led to more marked increase in NK and LAK cell activity than LAK/IL-2 without LBP. The results indicate that LBP can be used as an adjuvant in the biotherapy of cancer.
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PMID:[Observation of the effects of LAK/IL-2 therapy combining with Lycium barbarum polysaccharides in the treatment of 75 cancer patients]. 772 Apr 97


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