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)

Monoclonal antibodies KS1/4, KS1/9, and KS1/17 were developed in this laboratory from a fusion of the murine myeloma cell line P3X63Ag8 with spleens of BALB/c mice previously primed with UCLA P3 cells derived from a human adenocarcinoma of the lung. Monoclonal antibodies KS1/4 and KS1/17 seemed to recognize similar glycoprotein antigens on the lung carcinoma cells by indirect immunoprecipitation and sodium dodecyl sulfate-polyacrylamide gel electrophoresis analysis. However, mapping of [3H]lysine- and [3H]arginine-labeled tryptic peptides of antigens in specific immunoprecipitates of lung carcinoma cells by high-pressure liquid chromatography revealed a one peptide difference. Antibody KS1/9 did not immunoprecipitate any identifiable protein from detergent extracts of the immunizing cell line by routine methods and appears to detect a glycolipid antigen. Immunocytochemical analysis of tissue sections showed this monoclonal antibody to be reactive with adenocarcinomas of the lung and not with the other histological types of lung carcinoma or normal tissue. Monoclonal antibodies KS1/4 and KS1/17, however, reacted with 3 major histological types of lung cancer and minimally with the proximal tubules of normal kidney and the epithelium of bronchioles.
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PMID:Antigens associated with a human lung adenocarcinoma defined by monoclonal antibodies. 636 52

The effects of the ortho and para isomers of aryldimethyltriazeno carboxylic and benzensulfonic acids and amides have been examined in mice bearing subcutaneous Lewis lung carcinoma. The toxicity of these compounds varies widely and does not correlate with the effects on tumor progression. The growth of subcutaneous primary tumor is unaffected or only marginally inhibited by all the tested compounds, while a marked depression in the formation of spontaneous lung metastasis is observed, with the exception of the sodium salt of the ortho benzensulfonic acid. The compounds showing the greatest activity on metastasis are the hydrosoluble salts of the ortho and para carboxylic acid and the para sulfonamido derivative, indicating that, in addition to the activity reported for the potassium salt of the para carboxylic acid, also its ortho isomer and the para sulfonamido derivative possess selective and pronounced antimetastatic effects. No correlation can be found between the reported effects on tumor progression and physicochemical parameters of the triazenes tested.
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PMID:Effects of isomeric aryldimethyltriazenes on Lewis lung carcinoma growth and metastases in mice. 661 6

Experiments were made to investigate the effect of four anesthetic drugs that are commonly used in surgical practice on the postoperative growth of mouse tumors in syngeneic recipients. These experiments revealed that some of the anesthetics when applied for surgical excision of the local tumor, strongly accelerated postoperative progression of spontaneous lung metastases produced by the 3LL Lewis lung carcinoma and by the B16 melanoma. Some of the drugs caused the appearance of metastases in organs, such as the liver, in which spontaneous metastases are not usually produced by these tumors. A T10 sarcoma clone that does not produce detectable metastases in immune intact mice even following intravenous injection, did produce metastases when injected into animals treated with pentothal sodium.
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PMID:Anesthetic drugs accelerate the progression of postoperative metastases of mouse tumors. 727 67

During 1965 to 1968, 80 workers who had been engaged in the production of 2, 4, 5-sodium trichlorphenoxyacetate and butylester of trichlorphenoxyacetate acid became ill. The cause of the illness was 2, 4, 7, 8-tetrachlordibenzo-p-dioxin. A 10-yr study has been conducted for 55 exposed individuals. The majority of the patients developed chloracne, and 11 manifested porphyria cutanea tarda. Approximately one-half of the patients suffered from metabolic disturbances, i.e., pathologically elevated lipids with abnormalities in the lipoprotein spectrum, and two-fifths of the patients had pathological changes in the glucose tolerance test. One-third of the patients had biochemical deviations indicative of a mild liver lesion. Histological examination revealed light steatosis, or periportal fibrosis, or activation of Kupffer cells. Fluorescence of the liver tissues was present in ultraviolet light. In 17 persons symptoms of nervous system focal damage existed, with predominance of peripheral neuron lesion of the lower extremities (verified by EMG examination). The majority of patients suffered from various psychological disorders. As of this date, two patients have died of bronchogenic lung carcinoma; one of liver cirrhosis; one of a rapidly developed, extremely unusual type of atherosclerosis precipue cerebri; and two patients have died in traffic accidents. The conditions of most other patients have improved.
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PMID:The development and prognosis of chronic intoxication by tetrachlordibenzo-p-dioxin in men. 746 93

Eighty-five patients undergoing single lung transplantation have been studied to determine the presence of anti-epithelial cell antibodies (AECA) prior to transplantation using the human lung carcinoma epithelial cell line A549 in a microcytotoxicity assay. In addition, 29 healthy volunteers were also assayed for the presence of AECA. Twenty-seven of the 85 recipients exhibited AECA prior to transplantation compared to none of the 29 control subjects (p = 0.0001). Actuarial graft survival at 1 year was 78% for the AECA negative group compared to 56% for AECA positive recipients (p = 0.01). No correlation was seen between the presence of AECA and graft rejection as determined by transbronchial biopsy. However, there was an association between AECA and post-transplant infection (p = NS) where 16 (64%) of the AECA positive recipients had postoperative infection episodes compared to 25 (47%) of the negative recipients. Sodium dodecylsulphate polyacrylamide gel electrophoresis and Western blotting was also performed for 68 of the recipients and antibody reactivity was detected in 22 patients compared to 26 patients exhibiting AECA detectable by microcytotoxicity. The presence of AECA demonstrable by Western blotting did not correlate with graft survival, rejection or infection. In conclusion, AECA detectable prior to single lung transplantation are associated with a decrease in graft survival and with postoperative infections.
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PMID:Pre-transplant anti-epithelial cell antibodies and graft failure after single lung transplantation. 755 82

Sodium D-glucaro-delta-lactam (ND2001) inhibited spontaneous pulmonary metastases of the highly metastatic B16 melanoma variant with a maximal inhibition rate of 99.5%, and 6 of 7 animals remained metastasis-free. Likewise, ND2001 inhibited the spontaneous pulmonary metastases of both Lewis lung carcinoma (3LL) with a rate of 98.0% (3 of 5 animals remaining metastasis-free) and rat KDH-8 liver carcinoma with a rate of 82.5% (3 of 7 animals remaining metastasis-free), although it was unable to inhibit the metastases of mouse BMT-11 fibrosarcoma and rat SST-2 breast carcinoma. Pretreatment with ND2001 in vitro inhibited the pulmonary metastases of the B16 variant and 3LL cells, which indicates direct action upon the cancer cells. When the invasive activity of cancer cells was measured by the Boyden chamber method, the number of invading B16 variant or 3LL cells was reduced with maximal inhibition rates of 93.0% or 89.9%, respectively, but pretreatment with ND2001 failed to reduce the invasive activity of BMT-11 or SST-2 cells. ND2001 showed neither cytocidal nor antitumor activity. These results suggest that ND2001 inhibited pulmonary metastases at the invasive step into the basement membrane by directly changing some property of the tumor cells.
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PMID:Inhibition of pulmonary metastases and tumor cell invasion in experimental tumors by sodium D-glucaro-delta-lactam (ND2001). 773 8

Three patients with small cell carcinoma of the lung presented with a persistent unpleasant sweet taste as their initial and only symptom. On further evaluation, they were found to have hyponatremia secondary to the syndrome of inappropriate secretion of antidiuretic hormone. In each case, resolution of the sweet taste paralleled an increase in serum sodium concentration after water restriction alone. Linkage of the sweet taste with a low serum sodium concentration strongly implicates hyponatremia--rather than tumor, antidiuretic factor, medications, or chemotherapy--as the central mechanism responsible for this previously unreported (to our knowledge) sentinel symptom of small cell carcinoma of the lung.
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PMID:Sweet taste (dysgeusia). The first symptom of hyponatremia in small cell carcinoma of the lung. 777 65

Previous reports have demonstrated that beta-endorphin stimulates the clonal growth of human small cell lung carcinoma (SCLC) cell lines. In this study, the human SCLC lines, NCI-H69, NCI-H345, and NCI-N417, were observed to be highly-enriched in saturable, high-affinity binding sites which are labeled by [125I]beta-endorphin. In contrast to conventional opioid receptors, [125I]beta-endorphin SCLC binding was insensitive to naloxone and other mu, delta, or kappa opioid ligands. Further analysis of the NCI-H69 cells demonstrated that specific (naloxone-insensitive) binding was dependent on receptor concentration, reversible, sensitive to sodium ion, but insensitive to the GTP analogue, Gpp(NH)p. These results suggest a role for naloxone-insensitive beta-endorphin in modulating SCLC metabolism.
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PMID:Human small cell lung cancer cells express high affinity naloxone-insensitive [125I]-endorphin binding sites. 783 28

The multidrug resistance (MDR) modulators amiodarone (AM), cyclosporin A (CsA), and PSC 833 were tested for their potential to modulate cytotoxicity of doxorubicin (DOX), vincristine (VCR), and mitoxantrone (MX) in a sensitive human small cell lung carcinoma cell line GLC4, in its DOX-resistant non-P-glycoprotein subline GLC4-Adr, and in its cisplatin-resistant subline GLC4-CDDP. GLC4-Adr, in which overexpression of the so-called multidrug resistance-associated protein has been demonstrated, is 91-fold resistant for DOX, 22-fold for VCR, and 7.5-fold for MX, compared with its sensitive cell line. AM previously modulated DOX and VCR resistance in the P-glycoprotein-positive human colon cancer cell line COLO 320. Cytotoxicity was studied in the microtiter well tetrazolium assay. In the small cell lung carcinoma cell lines described above, AM did not increase cytotoxicity of DOX, but increased VCR cytotoxicity; moreover, AM was shown to be a potent modulator of MX cytotoxicity. CsA did not potentiate DOX cytotoxicity, but, at a concentration of 4 microM, it modestly increased VCR cytotoxicity in GLC4. However, 0.8 and 4.0 microM CsA protected against MX cytotoxicity in GLC4 and GLC4-CDDP, but no effect was observed in GLC4-Adr. At the much higher ID10 concentration CsA modulated MX cytotoxicity 1.6-fold in GLC4-Adr and slightly in GLC4 and GLC4-CDDP. PSC 833, a nonimmunosuppressive CsA analogue, did not alter the cytotoxicity of DOX or MX in these cell lines, but potentiated VCR cytotoxicity in GLC4-Adr at a concentration of 0.4 microM. The modulation of MX cytotoxicity by AM and the protection by CsA was confirmed in a clonogenic assay. In the colony-forming unit granulocyte-monocyte assay, no additional MX toxicity on normal bone marrow by AM was observed. Flow cytometry of cellular MX fluorescence was performed in order to elucidate the mechanism behind the AM-induced increased MX cytotoxicity. This revealed an increase in cellular MX after 1-h incubation of MX combined with AM and an inhibition of efflux from GLC4 and GLC4-Adr; CsA and PSC 833 had no effect on MX efflux. An increase in MX-induced cleavable complexes by AM in GLC4 was observed using the K+/sodium dodecyl sulfate coprecipitation assay, but no effect of CsA was found. In conclusion, AM enhances MX and VCR cytotoxicity in these sensitive, non-P-glycoprotein DOX and cisplatin-resistant small cell lung carcinoma cell lines. It also inhibits efflux of MX and causes more MX-induced cleavable complexes.
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PMID:Effects of amiodarone, cyclosporin A, and PSC 833 on the cytotoxicity of mitoxantrone, doxorubicin, and vincristine in non-P-glycoprotein human small cell lung cancer cell lines. 792 67

Small cell lung carcinoma (SCLC) represents about 25% of all lung cancers. Human SCLC shows neuroendocrine features such as the production of neural peptide hormones, marker enzymes and neurosecretory granules, and the expression of neural cell adhesion molecules (NCAMs). Although SCLC is sensitive to both chemotherapy and radiation, prognosis remains poor due to the appearance of post-treatment chemo- and radioresistant variants. Monoclonal antibodies (MAbs) have been developed that bind to SCLC tumor antigens. We have used similar technology to define another SCLC marker designated gP94/115. The MAb CR101 binds to a highly glycosylated, cell-surface antigen associated with SCLC. In vitro expression of the antigen appears to be restricted to cell lines of SCLC origin. Enzymatic removal of the sugars resolves the antigen into two proteins of 94 and 115 kD by sodium dodecyl sulfate-polyacrylamide gel electrophoresis (SDS-PAGE). Fluorescence-activated cell sorting (FACS) analysis confirms the antibody's specificity. These results indicate that CR101 may recognize a novel protein expressed by SCLC.
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PMID:A novel antigen defined by monoclonal antibody CR101 is associated with small cell lung carcinoma. 792 66


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