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  • 1
    Digitale Medien
    Digitale Medien
    New York, N.Y. : Wiley-Blackwell
    Journal of Cellular Biochemistry 63 (1996), S. 276-287 
    ISSN: 0730-2312
    Schlagwort(e): Ga nitrate ; transferrin ; transferrin receptors ; small cell lung cancer ; Life Sciences ; Molecular Cell Biology
    Quelle: Wiley InterScience Backfile Collection 1832-2000
    Thema: Biologie , Chemie und Pharmazie , Medizin
    Notizen: 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.
    Zusätzliches Material: 5 Ill.
    Materialart: Digitale Medien
    Bibliothek Standort Signatur Band/Heft/Jahr Verfügbarkeit
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  • 2
    ISSN: 0730-2312
    Schlagwort(e): non-small cell lung cancer ; small cell lung cancer ; drug resistance ; cell survival ; Life Sciences ; Molecular Cell Biology
    Quelle: Wiley InterScience Backfile Collection 1832-2000
    Thema: Biologie , Chemie und Pharmazie , Medizin
    Notizen: 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.
    Zusätzliches Material: 5 Ill.
    Materialart: Digitale Medien
    Bibliothek Standort Signatur Band/Heft/Jahr Verfügbarkeit
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