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  • 1
    Electronic Resource
    Electronic Resource
    Serotonin metabolism following platinum-based chemotherapy combined with the serotonin type-3 antagonist tropisetron (1995)
    Springer
    Cancer chemotherapy and pharmacology 36 (1995), S. 477-482 
    Details
    ISSN: 1432-0843
    Keywords: Serotonin metabolism ; Serotonin type-3 antagonist
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The administration of platinum-based chemotherapy induces serotonin release from the enterochromaffin cells, causing nausea and vomiting. This study was conducted to evaluate parameters of serotonin metabolism following platinum-based chemotherapy given in combination with the serotonin type-3 antagonist tropisetron as an antiemetic agent. In nine chemotherapy-naive patients with disseminated germ-cell tumors, parameters of serotonin metabolism in both blood and urine were evaluated during two consecutive courses of platinum-based chemotherapy. Serotonin concentrations in platelet-rich plasma and platelet-poor plasma as well as urinary 5-hydroxyindoleacetic acid (5-HIAA) and serotonin levels were measured during the full length of the courses. By means of comparison with the antiemetic agent chlorpromazine, used on day 1 of the first course only, the effect of the serotonin type-3 antagonist tropisetron, the antiemetic agent used during the rest of the courses, on these parameters was studied. Clinical effects were also recorded. No change in the parameters of serotonin metabolism could be demonstrated during either course by the serotonin type-3 antagonist tropisetron. Also in vitro, no effect of tropisetron on the active serotonin uptake by platelets was found. Serotonin levels in platelets showed no correlation with emetic response. However, the platelet serotonin content decreased significantly between the first and the second course (P〈0.01). The significant reduction in platelet serotonin content observed between the first and the second course indicates a depletion of total body serotonin. The role of a serotonin type-3 antagonist might be affected by the altered serotonin equilibrium during later courses of chemotherapy.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00685797
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  • 2
    Electronic Resource
    Electronic Resource
    Renal toxicity of the anticancer drug fostriecin (1998)
    Springer
    Cancer chemotherapy and pharmacology 42 (1998), S. 160-164 
    Details
    ISSN: 1432-0843
    Keywords: Key words Fostriecin ; Nephrotoxicity ; Topoisomerase II
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Purpose: Fostriecin is an inhibitor of topoisomerase II catalytic activity. In a phase I trial we observed renal toxicity, documented as a rise in serum creatinine, which was reversible and non-dose-limiting. The purpose of this study was a detailed analysis of this toxicity. Methods: A total of 20 patients received fostriecin as a 1-h i.v. infusion daily × 5 at doses ranging from 2 to 20 mg/m2 per day. Serum creatinine determination and urinalysis were performed daily during drug administration. Renal hemodynamics were measured by means of clearance studies using 125I-iothalamate and 131I-hippuran in eight patients at doses of ≥4 mg/m2 per day at baseline, on day 3 or 4 during the first course, and 3 weeks after the second course. Results: The rise in serum creatinine was maximal after one to two doses despite continued administration. This increase showed no correlation with the dose level at fostriecin doses of ≥4 mg/m2 per day. Urinary β2-microglobulin concentrations increased 150-fold (median), which is compatible with impaired tubular reabsorption. The median change in the glomerular filtration rate (GFR) was −36% (range −28% to −44%), that in effective renal plasma flow (ERPF) was −23% (range −11% to −36%), and the filtration fraction (FF) decreased in all patients during the first course of treatment. The values measured 3 weeks after the second course, however, did not differ from baseline. Conclusions: Fostriecin induces reversible renal hemodynamic changes compatible with renal tubular damage.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s002800050800
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  • 3
    Electronic Resource
    Electronic Resource
    HLA-Dr-expressing CD8bright cells are only temporarily present in the circulation during subcutaneous recombinant interleukin-2 therapy in renal cell carcinoma patients (1993)
    Springer
    Cancer immunology immunotherapy 36 (1993), S. 198-204 
    Details
    ISSN: 1432-0851
    Keywords: Renal cell carcinoma ; rIL-2 ; Lymphocyte phenotype ; HLA-Dr
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The effect of subcutaneous recombinant interleukin-2 (rIL-2) therapy on the “activation status” of peripheral blood lymphocytes (PBL) of 17 renal cell carcinoma patients was investigated in a longitudinal study. The expression of the activation markers HLA-Dr and CD25 on cytotoxic T cells, helper T cells, and natural killer (NK) cells, was analysed using two-colour flow cytometry of whole-blood samples. In addition, the ability of isolated PBL to proliferate in vitro in response to various stimuli was investigated. The absolute amounts of NK cells and HLA-DR-expressing NK cells increased continuously during the whole course of therapy. The absolute amounts of T cells and HLA-Dr-expressing T cells, however, showed an early increase only during the first 1 or 2 weeks of therapy, after which the absolute amounts of HLA-Dr-expressing T cells decreased. In particular, the absolute amount of HLA-Dr-expressing CD8bright+ T cells was significantly lowered in the second half of therapy. PBL collected on day 7 of therapy (post-cycle-1 PBL) showed, as compared to those collected prior to therapy (pretherapy PBL), a decreased proliferative response in vitro after stimulation with phytohaemagglutinin, concanavalin A, soluble CD3 mAb (WT32) or rIL-2. This decreased in vitro response of post-cycle-1 PBL was also reflected in a decrease in the percentage of CD8bright+ T cells expressing HLA-Dr in cultures with rIL-2 or CD3 mAb, in contrast to cultures of pretherapy PBL, which showed an increase of this percentage. We conclude that T cells are the predominantly stimulated subpopulation during the first 2 weeks of subcutaneous rIL-2 therapy. The significant decrease in the absolute amounts of HLA-Dr-expressing T cells in the peripheral blood during the second half of therapy may partly be explained by a decreased responsiveness to rIL-2, but a selective redistribution of HLA-Dr-expressing cells may also be involved.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01741092
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  • 4
    Electronic Resource
    Electronic Resource
    The role of methoxymorpholino anthracycline and cyanomorpholino anthracycline in a sensitive small-cell lung-cancer cell line and its multidrug-resistant but P-glycoprotein-negative and cisplatin-resistant counterparts (1995)
    Springer
    Cancer chemotherapy and pharmacology 35 (1995), S. 345-348 
    Details
    ISSN: 1432-0843
    Keywords: Key words Morpholino anthracyclines ; MRP ; Cisplatin resistance
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract  The cytotoxic action of two morpholino anthracyclines, methoxymorpholino anthracycline (MRA-MT, FCE 23762) and cyanomorpholino anthracycline (MRA-CN), was compared with the cytotoxicity of doxorubicin (DOX), the topoisomerase II inhibitor etoposide (VP-16), the topoisomerase I inhibitor camptothecin, methotrexate, and cisplatin in GLC4, a human small-cell lung-cancer cell line, in GLC4-Adr, its P-glycoprotein (Pgp)-negative, multidrug-resistant (MDR; 100-fold DOX-resistant) subline with overexpression of the MDR-associated protein (MRP) and a lowered topoisomerase II activity, and in GLC4-CDDP, its cisplatin-resistant subline. GLC4-Adr was about 2-fold cross-resistant for the morpholino anthracyclines and GLC4-CDDP was, relative to GLC4, more resistant for the morpholino anthracyclines than for DOX. Overall, MRA-CN was about 2.5-fold more cytotoxic than MRA-MT. The cytotoxicity profile of the morpholino anthracyclines in these cell lines mimicked that of camptothecin.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00689457
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  • 5
    Electronic Resource
    Electronic Resource
    The role of methoxymorpholino anthracycline and cyanomorpholino anthracycline in a sensitive small-cell lung-cancer cell line and its multidrug-resistant butP-glycoprotein-negative and cisplatin-resistant counterparts (1995)
    Springer
    Cancer chemotherapy and pharmacology 35 (1995), S. 345-348 
    Details
    ISSN: 1432-0843
    Keywords: Morpholino anthracyclines ; MRP ; Cisplatin resistance
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The cytotoxic action of two morpholino anthracyclines, methoxymorpholino anthracycline (MRA-MT, FCE 23 762) and cyanomorpholino anthracycline (MRA-CN), was compared with the cytotoxicity of doxorubicin (DOX), the topoisomerase II inhibitor etoposide (VP-16), the topoisomerase I inhibitor camptothecin, methotrexate, and cisplatin in GLC4, a human small-cell lung-cancer cell line, in GLC4-Adr, its P-glycoprotein (Pgp)-negative, multidrug-resistant (MDR; 100-fold DOX-resistant) subline with overexpression of the MDR-associated protein (MRP) and a lowered topoisomerase II activity, and in GLC4-CDDP, its cisplatin-resistant subline. GLC4-Adr was about 2-fold cross-resistant for the morpholino anthracyclines and GLC4-CDDP was, relative to GLC4, more resistant for the morpholino anthracyclines than for DOX. Overall, MRA-CN was about 2.5-fold more cytotoxic than MRA-MT. The cytotoxicity profile of the morpholino anthracyclines in these cell lines mimicked that of camptothecin.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00689457
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  • 6
    Electronic Resource
    Electronic Resource
    A phase II study of carboplatin and vincristine in previously treated patients with small-cell lung cancer (1989)
    Springer
    Cancer chemotherapy and pharmacology 25 (1989), S. 202-204 
    Details
    ISSN: 1432-0843
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary A total of 28 previously treated patients with small-cell lung cancer were treated at relapse with 400 mg/m2 carboplatin and 2 mg vincristine on days 1 and 8, every 4 weeks. Ten partial responses (PRs) (37%) but no complete responses (CRs) were seen. Median survival after the start of second-line treatment was 120 days (range, 39–503 days). Toxicity of this regimen was moderate, including WHO grade 3/4 myelosuppression in 26% of courses (n=66). Eight PRs were seen in a subgroup of 22 patients who relapsed 〈3 months after firstline treatment. The responses seen in this group of patients may be due to the absence of cross-resistance between the regimens used.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00689583
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  • 7
    Electronic Resource
    Electronic Resource
    Differential effects of all-trans-retinoic acid, docosahexaenoic acid, and hexadecylphosphocholine on cisplatin-induced cytotoxicity and apoptosis in a cisplantin-sensitive and resistant human embryonal carcinoma cell line (1998)
    Springer
    Cancer chemotherapy and pharmacology 41 (1998), S. 469-476 
    Details
    ISSN: 1432-0843
    Keywords: Key wordscis-Diamminedichloroplatinum(II) ; Differentiation ; Embryonal carcinoma
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Apart from modulation of tumor-cell drug sensitivity, induction of differentiation might be an alternative in the treatment of tumors resistant to cytotoxic drugs. In this report the capacity to induce differentiation and to modulate the cis-diamminedichloroplatinum(II) (CDDP) sensitivity of all-trans-retinoic acid (RA), docosahexaenoic acid (DCHA), and hexadecylphosphocholine (HePC) is examined in human germ-cell tumor cell lines. In the embryonal carcinoma cell line Tera-2 and its 3.7-fold CDDP-resistant subline Tera2-CP, we evaluated the effects of 96 h of pretreatment with RA (0.1 μM ), DCHA (23 μM ), and HePC (25 μM ) on differenctiation induction and on CDDP-induced cytotoxicity, DNA platination (4-h incubation), and apoptosis (continuous incubation). Without drug treatment, Tera2-CP showed less apoptosis than Tera-2. Pretreatment with RA decreased the cytotoxicity and apoptosis induced by CDDP without resulting in decreased DNA platination and increased differentiation in both cell lines. DCHA enhanced CDDP-induced cytotoxicity and apoptosis and did not affect the embryonal character of either cell line. HePC did not affect CDDP cytotoxicity or differentiation in either cell lines. Effects of the modulators on differentiation and on CDDP-induced cytotoxicity, DNA platination, and apoptosis did not differ between Tera-2 and Tera2-CP. RA can be applied for differentiation induction in CDDP-resistant germ-cell tumor models. However, in this model, RA reduced the apoptotic susceptibility. DCHA potentiated CDDP cytotoxicity in vitro; its in vivo modulatory capacity in germ-cell tumor cells deserves further study.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s002800050769
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  • 8
    Electronic Resource
    Electronic Resource
    Lack of cross-resistance to fostriecin in a human small-cell lung carcinoma cell line showing topoisomerase II-related drug resistance (1991)
    Springer
    Cancer chemotherapy and pharmacology 28 (1991), S. 461-464 
    Details
    ISSN: 1432-0843
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Cells exhibiting decreased topoisomerase II (Topo II) activity are resistant to several drugs that require Topo II as an intermediate. These drugs are cytotoxic due to the formation of a cleavable complex between the drug, Topo II and DNA. Fostriecin belongs to a new class of drugs that inhibit Topo II without inducing the formation of this cleavable complex. We tested fostriecin in three human small-cell lung carcinoma cell lines. GLC4 is the parent line. GLC4/ADR is the P-glycoprotein-negative multidrug-resistant subline, which is resistant to several Topo II inhibitors due to its decreased Topo II activity. GLC4/cDDP is the cisplatin-resistant subline, which displays increased Topo II activity. Topo II activity proved to be 100% in GLC4, 35% in GLC4/ADR and 130% in GLC4/cDDP. The fostriecin concentration causing inhibition of the growth of 50% of the cells (IC50) in the microculture tetrazolium assay following continous incubation was 11.2, 4.1 and 14.9 μm, respectively. After 1-h incubations, the IC50 was 117.8, 101.3 and 219.8 μm, respectively. Our results indicate a relationship between Topo II activity and fostriecin sensitivity in these closely related cell lines. At least in vitro, fostriecin displayed the capacity to kill cells showing resistance to drugs due to decreased Topo II activity. There was no relationship between this capacity and an increase in the activity of the reduced-folate carrier system, the proposed machanism for cellular entry of fostriecin, since we found no correlation between the cytotoxity of fostriecin and that of methotrexate.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00685823
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  • 9
    Electronic Resource
    Electronic Resource
    Renal dysfunction following high-dose carboplatin treatment (1988)
    Springer
    Journal of cancer research and clinical oncology 114 (1988), S. 212-214 
    Details
    ISSN: 1432-1335
    Keywords: Autologous bone marrow transplantation ; Carboplatin ; Renal dysfunction
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary A case history is reported or renal failure during and after treatment with carboplatin for 3 days, total dose 750 mg/m2, in a conditioning regimen prior to autologous bone marrow transplantation. Pretreatment renal function was compromised after nephrectomy and chemotherapy with cisplatin. A decrease in glomerular filtration rate concurred with a decreased in excretion of platinum in the urine and an increase in urinary beta 2 microglobulin. Treatment with high-dose carboplatin in patients with impaired renal function and previous treatment with cisplatin may lead to further loss of renal function.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00417840
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  • 10
    Electronic Resource
    Electronic Resource
    Effect of Ultrafilterable Platinum Concentration on Cisplatin and Carboplatin Cytotoxicity in Human Tumor and Bone Marrow Cells in Vitro (1994)
    Springer
    Pharmaceutical research 11 (1994), S. 1265-1269 
    Details
    ISSN: 1573-904X
    Keywords: cisplatin ; carboplatin ; ultrafllterable platinum concentration ; cytotoxicity ; myelotoxicity ; protein binding
    Source: Springer Online Journal Archives 1860-2000
    Topics: Chemistry and Pharmacology
    Notes: Abstract The importance of the ultrafilterable platinum (fPt) fraction of cisplatin (CDDP) and carboplatin (CBDCA) for cytotoxicity and myelotoxicity was studied in vitro. By incubating CDDP or CBDCA with fetal calf serum (PCS) various fractions of fPt were prepared and determined by atomic absorption spectroscopy. A relation of % fPt fraction and incubation time (h) of 87e-1123t(r = −0.99) and 101e-o.oo87t (r = −0.99) were determined for CDDP and CBDCA, respectively. Cytotoxicity in the human small cell lung carcinoma cell line GLC4 and fPt fraction were closely related for CDDP (r = 0.99) and for CBDCA r = 0.97). However, at a similar fPt fraction the concentrations inhibiting cell survival by 50% (IC50) of CBDCA exceeded that of CDDP by a factor of 10-18 with 4 h exposure and a factor of 5 with continuous exposure. Tested in the range of peak concentrations in plasma of patients and at a clinically relevant fPt fraction of 10%, CDDP was not toxic for human bone marrow cells in the CFU-GM assay, whereas it was toxic at fPt fractions of 50% and 90%. However, CBDCA was myelotoxic at a (clinically relevant) fPt fraction of 50%, and also at 75% and 90%. The use of different fPt fractions, produced by the incubation method described in this study, permits the study of platinum drugs in vitro while approximating in vivo conditions might be used to evaluate myelotoxicity of new platinum drugs prospectively. For CDDP and CBDCA the fraction fPt determines cytotoxicity on tumor cells, and their different fPt fraction in patients account at least partly for their difference in myelotoxicity.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1023/A:1018934209719
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