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  • 1
    ISSN: 1749-6632
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Natural Sciences in General
    Type of Medium: Electronic Resource
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  • 2
    ISSN: 1749-6632
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Natural Sciences in General
    Type of Medium: Electronic Resource
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  • 3
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Publishing Ltd
    Annals of the New York Academy of Sciences 547 (1988), S. 0 
    ISSN: 1749-6632
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Natural Sciences in General
    Type of Medium: Electronic Resource
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  • 4
    Electronic Resource
    Electronic Resource
    [s.l.] : Nature Publishing Group
    Nature 337 (1989), S. 406-406 
    ISSN: 1476-4687
    Source: Nature Archives 1869 - 2009
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Notes: [Auszug] PROTEIN chemistry, the demise of which was predicted in a News and Views article1 10 years ago, is still an essential technique for determining protein structure. Robert Anderegg and colleagues in the December 1988 issue2 of the Journal of Biological Chemistry, for example, report the struc-ture of ...
    Type of Medium: Electronic Resource
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  • 5
    ISSN: 1573-0646
    Keywords: dihydrolenperone ; drug evaluation ; drug screening assays ; antitumor ; carcinoma ; non-small cell lung carcinoma ; oat cell
    Source: Springer Online Journal Archives 1860-2000
    Topics: Chemistry and Pharmacology , Medicine
    Notes: Summary Antitumor activity of the butyrophenone dihydrolenperone in non-small cell lung cancer was initially suggested byin vitro screening against tumor cells derived from fresh surgical samples using the human tumor colony-forming assay. We have completed a directed phase I trial in patients with lung cancer. Thirty-two patients with lung cancer have completed 25 courses of therapy at doses of 10 to 60 mg/square meter orally on a twice daily schedule. Twenty-three men and 9 women with a median age of 55 (range 24–69) were entered. Twenty-four were performance status 0 or 1 and 8 were 2. The maximum tolerated dose was 50 mg/square meter orally twice daily and the dose limiting toxicity was somnolence. Of the 32 patients, 18 developed symptomatic hypotension (grade 1 or 2). There was no significant hematologic, renal, or hepatic toxicity.In vitro drug testing using the MTT [3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl-tetrazolium bromide (thiazolyl blue)] assay confirmed 50% inhibition of non-small cell and small cell lung cancer cell line growth at 70–450 micromolar concentrations. Plasma dihydrolenperone levels were at least 75-fold less than levels at whichin vitro activity was observed. We conclude: 1) the maximum tolerated dose in our study is 50 mg/square meter orally twice daily, 2) the dose-limiting side effect of dihydrolenperone is somnolence, and 3) the concentrations of dihydrolenperone observed in plasma are significantly lower than those associated within vitro activity.
    Type of Medium: Electronic Resource
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  • 6
    ISSN: 0730-2312
    Keywords: cell lines ; clinical correlation ; in vitro data ; polymorphic markers ; lung cancer ; Life Sciences ; Molecular Cell Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: The cell line data base described in this paper includes both clinical information about the patients from whom the cell line were derived and information about the in vitro analyses performed of the cell lines. The cell line data base has evolved as a part of a systematic effort by a research group at the NCI since 1976 to generate human cell lines as biological tools to study cancer and other diseases. The cell lines were generated from clinical specimens obtained as part of a series of Institutional Review Board-approved clinical protocols. The preponderance of the data is on lung cancer cell lines, though a broad range of other cancers are represented. A bank of over 300 human cell lines including cancer cell and in some instances autologous B-lymphoblastoid cells from the NCI-VA and NCI-Navy Medical Oncology Branch are reposited at the American Type Culture Collection. The cell lines are available for the research community. The entire data base is available on the American Type Culture Collection Web Site (///http://www.atcc.org/). © 1996 Wiley-Liss, Inc.This article is a US Government work and, as such, is in the public domain in the United States of America.
    Additional Material: 5 Tab.
    Type of Medium: Electronic Resource
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  • 7
    ISSN: 0730-2312
    Keywords: carcinogenesis ; chemoprevention ; intermediate end point ; biomarkers ; differentiation ; growth factors ; lung cancer ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: The need for validate intermediate end point markers to facilitate lung cancer chemointervention research is competing. Three major classes of lung markers are relevant for this application. Since lung cancer includes four distinct hitologies, markers that map degrees of histologic differentiation are important. Many of the markers for squamous differentiation overlap with the candidates for application in the study of head and neck cancer. Production of tissue-specific cell product especially for surfactant or CEA is of interest, because the gene structure is known and many differentiation-related polymorphisms exist. This strategy would be useful for adenomatous type of tissue. A second type of marker is the broad group of differentiation markers. The carbohydrates or blood group-like antigens comprise a representative example. Carbohydrate structures are expressed in a specific sequence during fetal processes, and this sequence appears to reverse with the development of a cancer. Retrodifferentiation of specific differentiation markers is the basis of a major effort to effect earlier lung cancer detection using sputum immunocytochemistry. The final class includes markers which affects either positive or negative aspects of growths. Candidates in this area include growth factors or their receptors or genes that regulate growth. If the intermediate end point marker reflects tumor biology and is in that casual path of tumor progression, serial observation of that parameter should indicate the success of the intervention. In all three of these examples the clinical material to be analyzed could be sputum specimens bonrchial biopsies or resected lung tissue. Systematic analysis of these markers in context of intervention trials required to validate their utility. Long term clinical follow up will demonstrate the degree of concordance between biomarkers and more traditional clinical trial end points and will establish if such tools can play a role in catalyzing the rate of prevention research. © 1992 Wiley-Liss, Inc.
    Additional Material: 1 Tab.
    Type of Medium: Electronic Resource
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  • 8
    Electronic Resource
    Electronic Resource
    New York, N.Y. : Wiley-Blackwell
    Journal of Cellular Biochemistry 59 (1995), S. 254-259 
    ISSN: 0730-2312
    Keywords: Breast cancer ; chemoprevention ; intervention ; lung cancer ; promotion ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: Improved molecular-based detection of early epithelial cancer creates an oupportunity for selective pharmacologic agents to arrest the development of emerging cancers. Developing a successful prevention approach to cancer control could eventually lead to a significant decline in cancer mortality rates; progress depends on the amount of resources committed to this area. Most major prevention trials are federally supported due to their size, duration, and cost. Much of the initial developmental cost for advanced cancer treatment agents was supported by the pharmaceutical industry. Developing a cancer treatment agent is perceived as more clearly defined and achievable than for prevention agents. Preliminary discussions with representatives of the pharmaceutical and biotech industry have identified a number of barriers to chemoprevention product development. Researchers agree that a number of promising agents are being passed over for expeditious development due to the uncertainty associated with chemoprevention drug development. The major factors affecting this circumstance are considered, including cost of clinical trials, absence of a positive model, and inability to project liability exposure.Similar problems were encountered in the area of childhood vaccine development. Insights from that process may have applicability to prevention drug development. Resolving these problems now can have a significant effect on the rate of progress in this promising new approach to cancer control.
    Additional Material: 2 Tab.
    Type of Medium: Electronic Resource
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  • 9
    Electronic Resource
    Electronic Resource
    New York, N.Y. : Wiley-Blackwell
    Journal of Cellular Biochemistry 63 (1996), S. 269-275 
    ISSN: 0730-2312
    Keywords: IGF-I ; non-small cell lung cancer ; monoclonal antibodies ; growth ; receptors ; Life Sciences ; Molecular Cell Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: The ability of monoclonal antibody (mAb) αI̊-3 to interact with non-small cell lung cancer (NSCLC) cells was investigated. MAb αI̊-3 inhibited specific binding of 125I-IGF-I and 125I-αI̊-3 to a panel of 8 NSCLC cell lines with high affinity (IC50 = 200 and 50 ng/ml, respectively). 125I-αI̊-3 bound with high affinity (Kd = 40 ng/ml) to a single class of sites (Bmax = 8,000/cell) using NCI-H838 cells. 125I-αI̊-3 was internalized when exposed to NCI-H838 or H1299 cells at 37°C but not 4°C. αI̊-3 immunoprecipitated major 90 and 130 kD proteins. IGF-I stimulated and αI̊-3 inhibited the clonal growth of NCI-H1299 cells. αI̊-3 slowed the growth of NCI-H157 and H838 xenografts in nude mice. In a biodistribution study 125I-αI̊-3 was preferentially localized to the tumor as opposed to other organs. These data suggest that IGF-I may be a regulatory agent in NSCLC. © 1996 Wiley-Liss, Inc.This article is a US Government work and, as such, is in the public domain in the United States of America.
    Additional Material: 6 Ill.
    Type of Medium: Electronic Resource
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  • 10
    Electronic Resource
    Electronic Resource
    New York, N.Y. : Wiley-Blackwell
    Journal of Cellular Biochemistry 63 (1996), S. 276-287 
    ISSN: 0730-2312
    Keywords: Ga nitrate ; transferrin ; transferrin receptors ; small cell lung cancer ; Life Sciences ; Molecular Cell Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: The effect of a combination of anti-transferrin receptor (TFR) antibody, 42/6, and Ga(No3)3 on cell growth was examined in small cell lung cancer (SCLC) cell lines: classic, NCl-H209, NCl-H345, NCl-H510; and variant, NCl-H82 and NCl-N417. The role of TFR and transferrin(TF) in Ga(No3)3 cellular uptake was also tested. Exogenous TF did not enhance the cytotoxicity of Ga. At 〉 3 μg/mL, Ga(No3)3 inhibited growth in all cell lines in TF-supplemented or deficient media. At 〈 3 μg/mL, Ga stimulated growth for all cells but this effect was eliminated by TF or 42/6. Classic SCLC lines required 3-4-fold less exogenous gallium than variant lines to reduce cell number by 50%. The mean Ga uptake (ng/106 cells) in H345 and H209 cell lines was 4-5-fold compared to H82 and N417 uptake (P 〈 0.001). 42/6 reduced exogenous TF-stimulated growth. Antibody plus Ga(No3)3 caused a slight further cell number decline in all cell lines in TF-supplemented or deficient media. These results suggest that the addition of 42/6 antibody treatment would not increase the effectiveness of Ga(No3)3 in patients. Both exogenous and endogenous TF and TFR play an important role in Ga uptake in these cells. © 1996 Wiley-Liss, Inc.
    Additional Material: 5 Ill.
    Type of Medium: Electronic Resource
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