Library

feed icon rss

Your email was sent successfully. Check your inbox.

An error occurred while sending the email. Please try again.

Proceed reservation?

Export
Filter
  • non-small cell lung cancer  (2)
  • small cell lung cancer  (2)
  • 1
    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
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
  • 2
    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
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
  • 3
    ISSN: 0730-2312
    Keywords: non-small cell lung cancer ; small cell lung cancer ; drug resistance ; cell survival ; Life Sciences ; Molecular Cell Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: Clinical protocols for small cell lung cancer (SCLC) and non-small cell lung cancer (NSCLC) were devised to prospectively select individualized chemotherapy based on in vitro drug sensitivity testing (DST) of cell lines derived from the patient's SCLC tumor cell lines or the patient's fresh NSCLC tumor. DST data derived from SCLC tumor cell lines were available for 33/115 (29%) patients. The DST-selected chemotherapy regimen was administered to 21 (18%) patients, or 64% of patients with DST. In SCLC, the DST-selected chemotherapy was administered either during weeks 13-24 following 12 weeks of etoposide/cisplatin, or at relapse after complete response to etoposide/cisplatin. Several parameters of in vitro drug sensitivity were significantly associated (two-sided P 〈 0.05) with clinical response to primary therapy and also with response to the DST-selected chemotherapy regimen, but were not associated with survival (P = 0.24). Five patients treated with their DST-selected chemotherapy attained a complete or partial response, compared to 5 of 68 who received an empiric regimen (P = 0.057). A total of 36/165 (22%) NSCLC patients had DST successfully completed. These results directed management for 21/96 (22%) patients who eventually received chemotherapy, or 58% of patients with DST. Response to chemotherapy for the patients treated prospectively with their DST-selected chemotherapy regimen (2/21; 9%) was not significantly different than the response rate for patients treated empirically with etoposide/cisplatin (10/69; 14%) in the absence of in vitro results to direct chemotherapy (P = 0.73). There was no difference in survival by treatment group for the NSCLC patients. The correlation between in vitro and clinical response was not significant for any individual drug or for all drugs considered together, illustrating the poor predictive value of in vitro testing with currently available chemotherapy in NSCLC. © 1996 Wiley-Liss, Inc.
    Additional Material: 5 Ill.
    Type of Medium: Electronic Resource
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
Close ⊗
This website uses cookies and the analysis tool Matomo. More information can be found here...