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)

Photodynamic therapy is achieved by a photodynamic reaction which is induced by excitation of photosensitizer exposed to light. This phenomenon was first reported by Raab et al in 1990. In 1960 Lipson et al reported hematoporphyrin derivative (HpD) by treating hematoporphyrin chloride with hydrochloric acid and sulfuric acid. The development of HpD established the basis of today's photodynamic therapy (PDT). Dougherty reported the treatment of skin tumors by PDT first with an argon dye laser in 1978. The author and his colleagues began basic studies of this treatment using HpD supplied by Dougherty and argon dye laser in canine lung cancer in 1978. These studies confirmed the effectiveness and safety of the method. Bronchofiberscopic PDT for early stage central type squamous cell carcinoma was performed by the authors in 1980 for the first time in the world and complete cure was obtained. Since then PDT has been attracted much attention. The photosensitizer and the laser with a specific wavelength are the key point of PDT. Photofrin, a porfimer sodium (Japan Lederle Co. Ltd., Tokyo, Japan) and excimer dye laser (Hamamatsu Photonics Co. Ltd., Hamamatsu, Japan) obtained governmental approval for clinical use in Japan in 1994, which is equivalent to FDA approval in the US. This method is now used clinically in Canada for certain indications and the Netherlands. In the US it is only approved for compassionate use in cancer of the esophagus. A total of more than 3,000 tumors in the various organs have been treated by PDT so far in 32 countries. The most frequently treated organ is the lung, with 808 cases. A phase II clinical study of PDT for early stage cancer cases of the lung, esophagus, stomach, cervix and urinary bladder was performed in 15 institutions from 1989 to early 1992. The results showed that PDT can successfully treat more than at least 50% of patients with early stage cancer cancer that would otherwise have to be treated by surgery and this means that PDT can contribute to their QOL. The cost effectiveness of PDT versus operation was estimated by the calculation based on QALY's (Quality Adjusted Life Year's saved) by Fujino of the Economics Department of Chuo University. According to this calculation PDT was estimated to be at least 30 percent less than the cost of operation. PDT is indicated in cases with superficial localized early stage lung cancer as a curative treatment and as a palliative treatment for opening stenotic or obstructed bronchi due to tumor prior to the combination therapy with surgery. Recent studies on photodynamic therapy (PDT) began just two decades ago, therefore there are still a large number of unsolved problems. However PDT will have many applications in a wide range of fields from preclinical to clinical medical science. In lung cancer, the indications will be extended for early stage lung cancer and improvement of therapeutic results will be achieved by the development of new photosensitizers such as chlorin, pheophorbide, phthalocyanin, ALA, benzoporphyrin, etc which can be excited by longer wavelength and new lasers such as pulsed excimer dye, YAG-OPO and diode lasers. Through these new developments the indications of this treatment for malignant will continue to expand.
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PMID:[History of photodynamic therapy--past, present and future]. 854 74

C-fibres probably represent the common final pathway in both ACE inhibitors and neoplastic cough. A recent report demonstrated that inhaled sodium cromoglycate is an effective treatment for ACE inhibitors' cough; this effect might be due to the suppression of afferent unmyelinated C-fibres. We tested the hypothesis that inhaled sodium cromoglycate might also be effective in lung cancer patients who presented with irritative neoplastic cough. Twenty non-small-cell lung cancer (NSCLC) patients complaining of cough resistant to conventional treatment were randomised to receive, in a double-blind trial, either inhaled sodium cromoglycate or placebo. Patients recorded cough severity daily, before and during treatment, on a 0 to 4 scale. The efficacy of treatment was tested with the Mann-Whitney U-test for non-parametric measures, comparing the intergroup differences in the measures of summary of symptom scores calculated in each patient before and after treatment. We report that inhaled sodium cromoglycate can reduce cough, also in NSCLC patients and that such reduction, observed in all patients treated, is statistically significant (P < 0.001). Inhaled sodium cromoglycate appears to be a cost-effective and safe treatment for lung cancer-related cough.
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PMID:Inhaled sodium cromoglycate to treat cough in advanced lung cancer patients. 868 42

A ras oncogene-amplified recombinant BHK-21 cell line (ras-rBHK-IgG) has been established, and was shown to hyperproduce the recombinant IgG chimeric human monoclonal antibody (hMAb) AE6F4, which recognizes lung cancer cells. We found that the ras-rBHK-IgG cell could be easily cultured in a protein-free ERDF medium supplemented with iron(III) nitrate, hydroxyethyliminodiacetic acid, and non-protein synthetic attachment factor as well as in a serum-free ERDF medium supplemented with insulin, transferrin, ethanolamine, and sodium selenite. The productivity of recombinant hMAb from the cells cultured in dishes at high cell densities was higher in protein-free medium than in serum-containing medium. True high density culture of the ras-rBHK-IgG cells was done in protein-free medium using the Tecnomouse, which is a novel hollow fiber bioreactor system. After culture for 30 days in protein-free culture, a total amount of about 14 mg of the recombinant hMAb AE6F4 was obtained, and was shown to be reactive against lung cancer cells in tissues.
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PMID:Production of recombinant human monoclonal antibody using ras-amplified BHK-21 cells in a protein-free medium. 870 11

Molecular mechanisms related to sodium retention have been implicated in the pathogenesis of hypertension. It is unclear how sodium retention leads to a rise in blood pressure, but ouabainlike compound may act as a final common pathway in sodium-induced hypertension. In ectopic corticotropin syndrome, hypertension has been attributed to cortisol inactivation overload, giving rise to mineralocorticoid-type hypertension. We sequentially measured plasma and urinary levels of ouabainlike compound over 2 months to evaluate its role in the hypertensive mechanisms in a 64-year-old man with this syndrome caused by lung cancer. His data included hypokalemia and increased cortisol concentrations, corticotropin levels, and urinary 17-hydroxycorticosteroid excretion. Plasma renin activity was suppressed. Plasma and urinary levels of ouabainlike compound were markedly increased concomitantly with high blood pressure. The maximum plasma level was 40-fold the normal range of the subject. After chemotherapy, ouabainlike compound levels gradually decreased in parallel with the decline in blood pressure and rise in potassium concentration. A correlation was observed between plasma and urinary levels of ouabainlike compound (P < .05). Plasma and urinary levels of ouabainlike compound correlated with systolic (P < .01) and diastolic (P < .05) pressures, respectively. The peak of ouabainlike compound in plasma and urine coincided with that of authentic ouabain on high-performance liquid chromatography. Ouabainlike compound derived from urine inhibited [3H]ouabain binding to human erythrocytes. These findings suggest that ouabainlike compound with biological activity could partly account for hypertension in ectopic corticotropin syndrome.
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PMID:Ouabainlike compound in hypertension associated with ectopic corticotropin syndrome. 879 27

In order to improve the diagnosis of lung carcinoma, in which a complicated histologic pattern is present, the immunohistochemistry of 119 adenocarcinomas, 65 squamous cell carcinomas, 12 small cell carcinomas, 18 large cell carcinomas, and 15 metastatic adenocarcinoma in the lung were evaluated using a monoclonal antibody, KM195, against lung carcinoma, and compared with the immunohistochemical results using anti-human cytokeratin (CAM 5.2) and other monoclonal antibodies. Formalin-fixed, paraffin-embedded tissues were stained using the labeled streptavidin-biotin method. Extracts from fresh tissue homogenate, after fractionation by sodium dodecyl sulfate-polyacrylamide gel electrophoresis, were transferred by Western blotting and stained with KM195. The anti-lung adenocarcinoma, murine, monoclonal antibody KM195 (IgG), was positive in 107 of 119 adenocarcinomas (90%), in 15 of 18 large cell carcinoma (83%), in three of 65 squamous cell carcinomas (5%), 13 of 15 (87%) metastatic adenocarcinoma in the lung, and was negative in 12 small cell carcinomas (P < 0.001). KM195-bound protein of primary and metastatic adenocarcinoma in the lung cases concentrated at about 40 kDa. In contrast, CAM 5.2 was positive in 52 of 67 (78%) adenocarcinomas, 10 of 62 (16%) squamous cell carcinomas, and was negative in six small cell carcinomas. These results suggest that the immunohistochemistry for KM195 may be a more useful marker over CAM 5.2 for the diagnosis of pulmonary adenocarcinoma.
Lung Cancer 1996 Aug
PMID:KM195 as an immunohistochemical marker of adenocarcinoma of the lung. 886 22

We examined the effect of selective thromboxane A2 (TXA2) receptor antagonists, calcium 5(Z)-1R, 2S, 3S, 4S-7-[3-phenylsulphonylaminobicyclo [2.2.1] hept-2-yl]-5-heptonoate hydrate (S-1452) and +/- -7-(3,5,6,-trimethyl-1,4-benzoquinon-2-yl)-7-phenylhaptanoic acid (AA-2414), on sensitivity to cis-diamminedichloroplatinum (II) (CDDP) in non-small-cell lung cancer cell lines. IC50 values to CDDP using MTT assay were decreased 2.1- and 4.6-fold respectively by treatment with 250 or 500 microM S-1452, for a 2 h simultaneous drug exposure, and those of PC-9/CDDP, a CDDP-resistant cell line, were decreased 3.1- and 6.1-fold. Sensitivity to carboplatin was also enhanced by the treatment with S-1452. IC50 values to CDDP and carboplatin were decreased by treatment with AA-2414 in a dose-dependent manner. Isobologram analysis showed that the combination of CDDP with S-1452 or AA-2414 produced supra-additive or additive effects in each cell line. Neither glutathione content nor glutathione S-transferase activity was changed in either cell line by treatment with 500 microM S-1452. Accumulation of platinum into PC-9 and PC-9/CDDP was increased by the treatment in a dose-dependent manner. Na+, K+-ATPase activity of PC-9 and PC-9/CDDP was enhanced by the treatment of S-1452 in a dose-dependent manner. These data show that the TXA2 receptor antagonists may enhance the sensitivity of non-small-cell lung cancer cell lines to platinum agents. Increase in Na+, K+-ATPase activity induced by S-1452 may be the mechanism of its sensitising effect through increase in platinum accumulation.
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PMID:Modulation of sensitivity to cis-diamminedichloroplatinum (II) by thromboxane A2 receptor antagonists in non-small-cell lung cancer cell lines. 893 34

Imipenem/cilastatin sodium (IPM/CS) was administered to 102 patients with respiratory tract infections and lung cancer. Patients with other serious diseases were excluded and a total of 73 patients were enrolled. They were divided into 12 patients who underwent surgery (operated group) and 61 who did not (non-operated group); the latter group included 28 patients treated with anticancer agents or radiation therapy (treated group) and 33 untreated patients (untreated group). IPM/CS was effective in 75% of the patients, both with and without surgery. The drug was effective in 81% of the treated group, although many of the patients had Stage III or more advanced cancer, as well as bronchial occlusion. IPM/CS was also effective in 69% of the untreated group, although many of the patients have serious infections and a PS (Performance Status) of 3 or greater. Thus, IPM/CS treatment achieved good results. Bacteriological studies showed that 3 out of 4 strains in the operated group and 16 out of 18 in the non-operated group were eliminated. Safety was evaluated in all patients. Two patients (2%) experienced side effects and two others (2%) showed abnormal clinical findings, but the symptoms were mild and resolved after discontinuation or completion of therapy. In conclusion, IPM/CS was very effective for treating respiratory infections in patients with lung cancer.
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PMID:[Clinical efficacy of imipenem/cilastatin sodium for respiratory infections in patients with lung cancer]. 905 11

We have previously reported on the secretion of a family of high Mr plasminogen activators (PAs) by a human lung cancer cell line [Harvey et al. (1991) Biochim. Biophys. Acta 1078, 360-368]. We have now extended these studies to several human cancer cell lines and a human embryonic lung cell line. In the present study with HPL-SK-1 lung cancer, A431 epidermoid cancer, ovarian carcinoma, and embryonic lung cell lines, we show that the 900- and the 660-kDa PAs are disulfide-bonded multiprotein oligomeric complexes. They are functionally and immunologically related to human urinary PA (uPA). Their size and PA activity are not destroyed by strong denaturants such as 8 M urea or 2% sodium dodecyl sulfate (SDS), suggesting that the uPA moiety is covalently associated with the rest of the molecule. It is only under strong denaturing conditions with 1.4 M beta-mercaptoethanol and 2% SDS that the uPA moiety could be released as a 21- to 23-kDa fragment along with two major polypeptide chains of 70 and 40 kDa, respectively. The presence of the uPA active center in the reduced PA660 was demonstrated by [3H]diisopropylphosphorofluoridate labeling and by Western blot using a monoclonal antibody to uPA B chain. N-terminal amino acid sequencing of the 70- and 40-kDa polypeptides, respectively, showed homology to the neural cell adhesion molecule and the beta chain of haptoglobin. A minor fragment of 18 kDa obtained under strong reduction conditions was also sequenced and shown to share homology with the alpha chain of haptoglobin. Western blot analysis of the reduced PAs with monoclonal antibody to the neural cell adhesion molecule and rabbit anti-haptoglobin confirmed the homologies obtained by the sequence data. Further, immobilized monoclonal antibodies to the neural cell adhesion molecule, uPA B chain, and rabbit anti-haptoglobin bound the multiprotein complexes with uPA activity, from A431, ovarian cancer, and embryonic lung cell lines. The bound material, after dissociation, exhibited PA activity that was inhibited by monoclonal antibody to the uPA B chain. These data suggest that in tumor and embryonal cell lines, in addition to proper folding and assembly of proteins by intramolecular disulfide bond formation in the endomembrane compartment, intermolecular disulfide bonds could also occur, producing multiprotein oligomers as in the present case. Formation of such oligomers may have a selective advantage for such cells in the focalization of proteolytic activity through the interaction of the neural cell adhesion molecule domain with the extracellular matrix and in immunosuppression of lymphocytes by the haptoglobin portion of the complex.
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PMID:Cancer cells release a covalent complex containing disulfide-linked domains from urinary plasminogen activator, neural cell adhesion molecule, and haptoglobin alpha and beta chains. 930 1

Selenium is an essential trace element, the deficiency of which is associated with an increased incidence of some human cancers. Dietary supplementation with selenium has been reported to produce a decrease in the incidence of some cancers in humans. Thioredoxin reductase (TR) is a newly discovered homodimeric selenocysteine (SeCys)-containing protein that catalyzes the NADPH-dependent reduction of the redox protein thioredoxin (Trx). Trx is overexpressed by a number of human tumors, and experimental studies have shown that Trx contributes to the growth and to the transformed phenotype of some human cancer cells. Thus, TR, by reducing Trx, could play a role in regulating the growth of normal and cancer cells. We have investigated mechanisms by which selenium, in the form of sodium selenite, added to serum-free growth medium regulates TR activity in cancer cell lines. Selenium caused a dose-dependent increase in cellular TR activity. The increase in TR activity produced by 1 microM Se compared to medium with no added selenium was: for MCF-7 breast cancer cells, 37-fold; for HT-29 colon cancer cells, 19-fold; and for A549 lung cancer cells, 8-fold. In contrast, Jurkat and HL-60 leukemia cells showed no increase in TR activity. The half-life of the time course of induction of TR in HT-29 cells after adding selenium was 10 h. The increase in TR activity was accompanied by an increase in TR protein levels up to 3-fold and an increase in the specific activity of the enzyme of 5-32-fold, depending on the cell line. Studies using 75Se showed that the amount of selenium incorporated into TR increased with increasing selenium concentration up to a ratio of 1 selenium per TR monomer. There was an increase in TR mRNA levels of 2-5-fold at 1 microM selenium and an increase in the stability of TR mRNA with a half-life for degradation of 21 h compared to 10 h in the absence of selenium. Trx mRNA and protein levels and Trx mRNA stability were not affected by selenium. The results of the study show that the increase in TR activity caused by selenium is specific and due to several effects, including an increase in the stability of TR mRNA leading to increased TR mRNA levels, an increase in TR protein, but predominantly to an increase in the specific activity of TR associated with increased incorporation of selenium into the enzyme.
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PMID:Mechanisms of the regulation of thioredoxin reductase activity in cancer cells by the chemopreventive agent selenium. 935 64

This study was undertaken to define the impact of arginine vasopressin (AVP) and atrial natriuretic peptide (ANP) on sodium homeostasis in patients with lung cancer. Patients had their serum and urine electrolytes and osmolality determined before and after a saline infusion of 500 ml. The plasma hormones, AVP, ANP, plasma renin activity (PRA), angiotensin II, and aldosterone were determined by radioimmunoassay every 15 min before, during and after the saline infusion. Fifty patients, 31 with small cell lung cancer and 19 with non-small cell lung cancer participated in this trial. All 11 patients (10 patients with small cell lung cancer and one patient with non-small cell lung cancer) who presented with hyponatremia had inappropriately elevated levels of AVP. Elevated plasma AVP levels were highly correlated with the presence of hyponatremia (p < 0.00001). Initial plasma ANP levels were not associated with hyponatremia (p = 0.73). Urinary sodium concentration increased during the saline infusion proportional to the initial plasma level of ANP (p = 0.0045). AVP appears to be elevated in nearly all patients with hyponatremia of malignancy. ANP plasma levels in patients with lung cancer are associated with the ability to excrete a sodium load but do not appear to downregulate renin, angiotensin II, and aldosterone production.
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PMID:A prospective study of patients with lung cancer and hyponatremia of malignancy. 937 92


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