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)

A method of measuring pulmonary arterial transit time (PATT), from the pulmonary valve to the precapillary vessels, using the gamma-emitting isotope technetium-99m and external counting probes, has been applied in patients coming to cardiac catheterization. The method was successfully applied in 36 of 39 patients. The dose of 99Tc for a single determination was 1 mc. Agreement between right and left lung transit times was good, average difference between the two lungs being less than 7% of mean PATT. Reproducibility between duplicate injections was 9.4 +/- 1.2% (SEM). Pulmonary arterial volume (PAV) was calculated as the product of PATT and flow. In 11 normal patients average PAV was 92 ml . m-2 and constituted 30% of total pulmonary blood volume (PBV). In ten patients with pulmonary hypertension secondary to lung disease average PAV was 129 ml . m-2, constituting 38% of PBV, while, in seven patients with left ventricular disease and a similar degree of pulmonary hypertension, PAV was also 129 ml . m-2, but constituted only 29% of PBV. Thus, in pulmonary hypertension secondary to lung disease the pulmonary arteries are enlarged out of proportion to the remainder of the pulmonary vascular bed. In seven patients with carcinoma of the lung, in whom one main branch of the pulmonary artery was occluded with a balloon catheter, PAV fell significantly less than would be predicted, indicating a distension of the unoccluded portion of the arterial tree. Distensibility in the unoccluded part of the arterial tree was calculated to be 4.5% per cmH2O pressure.
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PMID:Measurement of human pulmonary arterial volume in vivo. 50 85

Histochemistry, SEM-EDX and X-ray fluorescence analysis were applied to detect the distribution of iron, arsenic and other related elements in the pulmonary tissues of tin miners in Yunnan. Lesions obtained in human beings could be reproduced in rats subjected to intratracheal injection of arsenic containing ore dust, which was prepared in order to study the deposition, dissociation and release of inhaled less-soluble arsenic containing ors dust in the lungs and the process of development of different ferruginous bodies. Data obtained in the pulmonary tissues provided also the evidence about the role of arsenic as the etiological factor of lung carcinoma in the tin miners of Yunnan province.
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PMID:[Study of deposition and translocation of mineral dust in lungs of tin miners in Yunnan by X-ray microanalysis]. 149 71

The thymidylate synthase inhibitor N10-propargyl-5,8-dideazafolic acid (CB3717) inhibits the growth of human lung carcinoma A549 cells. The cytotoxicity of CB3717 is potentiated by the nucleoside transport inhibitor dipyridamole (DP), which not only inhibits the uptake and therefore salvage of thymidine but also inhibits the efflux of deoxyuridine, thereby enhancing the intracellular accumulation of deoxyuridine nucleotides. Measurement of intracellular deoxyuridine triphosphate (dUTP) pools, by sensitive radioimmunoassay, demonstrated a large increase in response to CB3717, in a dose- and time-related manner, and this accumulation was enhanced by coincubation with DP. In untreated cells and those treated with DP alone, dUTP was close to or below the limit of detection of the assay. In cells treated for 24 h with 3 microM CB3717 (concentration producing 50% growth inhibition) the intracellular dUTP was 46.1 +/- 9.6 (SEM) pmol/10(6) cells and after 24 h exposure to 30 microM CB3717, 337.5 +/- 37.9 pmol dUTP/10(6) cells was detected. There was significant enhancement by DP of the accumulation of dUTP in cells treated with CB3717; coincubation of cells with 1 microM DP + 3 microM CB3717 for 24 h resulted in intracellular dUTP levels of 174.7 +/- 57.7 pmol/10(6) cells. Accumulation of DNA strand breaks, measured by alkaline elution, also increased in response to CB3717 concentration and exposure period. Newly synthesized (nascent) DNA was more sensitive to damage by CB3717 than was mature DNA. As with the accumulation of dUTP, coincubation with DP also enhanced the accumulation of strand breaks, whereas DP alone had little or no effect on DNA fragmentation. When data for cells treated with CB3717 alone and CB3717 in combination with DP were combined, there was a significant correlation of intracellular dUTP levels with the level of DNA strand breaks. This strongly suggests that growth inhibition following thymidylate synthase inhibition is mediated through an increase in intracellular dUTP, leading to uracil misincorporation into DNA, its subsequent excision, and resultant strand breakage.
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PMID:Mechanism of cell death following thymidylate synthase inhibition: 2'-deoxyuridine-5'-triphosphate accumulation, DNA damage, and growth inhibition following exposure to CB3717 and dipyridamole. 201 98

Plasma pancreastatin (PST)-like immunoreactivity in normal subjects and patients with various diseases was estimated by a RIA, using antiserum raised against a synthetic C-terminal peptide of human PST deduced from the sequence of human chromogranin-A. The mean level +/- SEM was 13.2 +/- 0.6 pmol/L in normal subjects, but was significantly higher in patients with chronic renal failure (526.7 +/- 48.5). An immunoreactive form corresponding to a human PST-like sequence [human chromogranin-A-(250-301)] and a larger form were detected by gel filtration of plasma from these patients, suggesting accumulation of the larger molecular form in these patients. A significant increase in PST-like immunoreactivity was also found in patients with liver cirrhosis (20.8 +/- 3.0 pmol/L), but not in patients with noninsulin-dependent diabetes mellitus, chronic pancreatitis, or pancreatic cancer. Elevated levels were found in 16 of the 21 patients with small cell lung carcinoma examined. High levels were also found in 3 of 11 patients with islet cell tumor.
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PMID:Plasma pancreastatin-like immunoreactivity in various diseases. 255 88

Eighteen patients with small cell carcinoma of the lung received high dose cyclophosphamide (180-200 mg/kg) intensification following five pulses of 'CHOP' chemotherapy (cyclophosphamide 750 mg/m2 i.v., adriamycin 50 mg/m2 i.v., vincristine 1.4 mg/m2 i.v., prednisolone 40 mg orally for 5 d). They received infusions of autologous bone marrow which had been stored at 4 degrees C for 34 h. Pancytopenia was predictable in onset and its duration acceptable. Recovery of neutrophils to greater than 1.0 x 10(9)/l was achieved in 17.5 +/-0.9 d (mean +/- SEM) and platelets to greater than 100 x 10(9)/l in 17.5 +/- 0.8 d. Four patients with acute myeloid leukaemia in complete remission received intensification with the supralethal combination of cyclophosphamide and total body irradiation followed by infusion of autologous marrow which had been stored at 4 degrees C for 54 h. Haematological reconstitution in these patients was acceptable but slower (greater than 1.0 x 10(9)/l neutrophils between days 26 and 40; greater than 20 x 10(9)/l platelets between days 23 and 77). Except in one case, normal peripheral counts were attained in all patients. It is concluded that bone marrow stored at 4 degrees C for up to 54 h is a simple and practical source of viable stem cells which have the capacity for acceptable haematological reconstitution.
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PMID:Haematological reconstitution following high dose and supralethal chemo-radiotherapy using stored, non-cryopreserved autologous bone marrow. 630 83

This paper reports the first case of skin metastases from small-cell carcinoma of the lung with electron microscopic confirmation. The 2 to 3-cm cutaneous lesions present on the chest and limbs were hard, nontender, smooth-surfaced, freely moveable nodules with normal appearing overlying skin. Characteristic dense-core granules 1562 +/- 123 A (SEM) in diameter were detected by electron microscopy. The detection by electron microscopy of dense-core granules may assist in confirming the diagnosis of small-cell carcinoma in cutaneous lesions with equivocal histologic findings.
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PMID:Skin metastases from small-cell carcinoma of the lung. 630 67

An animal model system was established for immunotherapy of lung cancer using line-1 lung carcinoma in Balb/cR mice and xenogeneic lymphocytes from New Zealand white (N2W) rabbits. The immunization schedule consisted of footpad and subcutaneous injections of 1 X 10(8) viable line-1 cells into two rabbits, twice at a weekly interval. Two other rabbits were maintained as source of unsensitized lymphocytes. All rabbits were bled on day 14 at which time 45 mice were divided into three groups of 15 for both transplantation of 1 X 10(4) viable line-1 cell (subcutaneously) and treatment with 1) control saline, 2) 2.5 X 10(6) unsensitized lymphocytes, and 3) 2.5 X 10(6) sensitized lymphocytes. These treatments were repeated twice at weekly intervals. Results were evaluated four weeks after transplant and initial treatment. Tumor developed in 13/15 control mice, 15/15 treated with unsensitized lymphocytes, and 7/15 with sensitized-lymphocyte injection. The mean tumor weight for group 1 (control mice) was 1.38 +/- 0.22 gm (SEM), group 2 was 2.09 +/- 0.25 gm, and 0.56 +/- 0.28 gm for group 3. There was a statistically significant difference between control and group 3 for both tumor appearance (P = 0.014) and tumor weight (P = 0.026).
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PMID:An animal model system for the immunotherapy of lung carcinoma using sensitized lymphocytes: a preliminary study. 742 Dec 67

Expression of cell surface antigens of the neural cell adhesion molecule (N-CAM) class was recently shown to be shared by both fetal and neoplastic neuroendocrine cells, including those of the lung. We investigated the expression and localization of MOC-1 antigen on small-cell (neuroendocrine) lung carcinoma cell lines with immunohistochemical methods at the light (LM) and electron microscopy (EM) level and by Western blot. At LM level, using monoclonal antibody (MAb) MOC-1 with the ABC method and immunofluorescence, positive staining was observed on surfaces of cells from all tumor lines examined. Strongest immunostaining was found on cell surfaces of pulmonary small-cell carcinoma-derived cell line NCI-H69 with the majority of cells showing positive staining. An adherent variant of NCI-H69 cell line, H69V, exhibited positive staining in about 60% of cells, whereas only occasional cells of NCI-H727 cell line derived from pulmonary carcinoid tumor were positive for MOC-1 antigen. Western blot analysis confirmed these findings, showing a strong MOC-1-specific band in cell extracts of NCI-H69, with weaker band densities for H69V and NCI-H727. Immunoelectron microscopy (IEM) revealed that MOC-1 was not uniformly distributed on the outer surface of plasma membrane; immunogold particles appeared concentrated in areas of thick cell surface "fuzz" coating, surface microvilli, and in areas of cell-cell contact. In some cells, areas of plasma membrane invaginations and a few intracytoplasmic vesicles were also labeled, suggesting endocytosis. Surface labeling for SEM confirmed the finding of more dense labeling over the microvilli, cell membrane folds, and in areas of cell-cell contact. The cell lines derived from pulmonary neuroendocrine cell tumors can provide a useful model to study the role and function of neural adhesion molecules in pulmonary neoplasia and during lung development.
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PMID:Localization of MOC-1 cell surface antigen in small-cell lung carcinoma cell lines: an immunohistochemical and immunoelectron microscopic study. 839 53

This investigation was effected to determine the levels of the two antioxidant enzymes, superoxide dismutase (SOD) (EC 1.15.1.1) and catalase (CAT) (EC 1.11.1.6) in lung cancerous tissues and to compare with normal lung tissue in order to evaluate the antioxidant status in lung cancer. Fifteen lung carcinoma tissue samples and the normal counterparts from the same cases were homogenized and the cytosols obtained by ultracentrifugation (100,000 x g). SOD was assayed using a modification of the indirect nitroblue tetrazolium assay method, while CAT was measured by a spectrophotometric method. The data obtained are as follows: 1.42 +/- 0.24 U/mg protein (means +/- SEM) of SOD in lung cancer and 3.13 +/- 0.51 U/mg protein in normal lung tissue and 33.53 +/- 6.09 U/mg protein of CAT in lung cancer and 71.33 +/- 14.38 in normal lung tissue. The differences were found to be significant at the level of P < 0.01 for both enzymes. These low levels of the antioxidant enzymes in lung cancerous tissues can lead to elevated levels of reactive oxygen metabolites, resulting in damage to the key subcellular structures such as DNA, cell membranes, and other vital cellular components.
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PMID:Evaluation of some antioxidant enzymes in lung carcinoma tissue. 863 62

Ectopic tumoral production of intact parathyroid hormone (PTH) is rare. The PTH-related protein is the common cause of hypercalcemia in most solid tumors, particularly squamous and renal carcinomas. We report the case of a 71-yr-old man with a PTH-producing squamous cell lung carcinoma. Immunocytochemical analysis of the tumor tissue as well as of cultured tumor cells revealed PTH positive staining. Cultured tumor cells released PTH and were calcium sensitive, producing 122 +/- 16 pg/microgram DNA of intact PTH (mean +/- SEM) at 0.5 mmol/L calcium compared with 26 +/- 2 pg/microgram DNA at 3.0 mmol/L calcium. Somatostatin analogues have been used in the treatment of humoral hypercalcemia of malignancy (HHM). However, we found that somatostatin (0.1 microgram/L) in cultured tumor cells increased the release of intact PTH (123 +/- 19 versus 82 +/- 1 pg/microgram DNA, P < 0.05) and thus might have a negative effect on the HHM. This report is the first to describe a true ectopic PTH-producing squamous cell lung carcinoma associated with HHM.
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PMID:Ectopic production of intact parathyroid hormone by a squamous cell lung carcinoma in vivo and in vitro. 885 39


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