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2.
Onkologie ; 27(5): 441-6, 2004 Oct.
Article in English | MEDLINE | ID: mdl-15585973

ABSTRACT

OBJECTIVES: Aim of this study was to evaluate the clinical benefit and the toxicity of pegylated liposomal doxorubicin. PATIENTS AND METHODS: Patients with metastatic breast cancer (n = 30) who failed a prior chemotherapy regimen for metastatic disease received 45 mg/m2 pegylated liposomal doxorubicin (PLD) every 4 weeks following prophylactic administration of metoclopramide (10 mg) and dexamethasone (8 mg). RESULTS: 29 of 30 patients were assessed for clinical benefit and time to progression. All patients were assessed for toxicity and analysis of overall survival. 9 patients (31%) had a partial response, and 16 patients (55%) responded with stable disease, resulting in a clinical benefit rate of 86% (n = 25). Median time to progression was 4 months (95% CI: 2.8-5.2), median duration of response was 7 months (95% CI: 4.7-8.2), and median survival was 12 months (95% CI: 6.7-17.2). Skin toxicity was the most common adverse event (30%, all < or = grade 2). Other toxicities were remarkably low in occurrence. CONCLUSION: PLD is a well-tolerated, second-line monotherapy with a high rate of clinical benefit.


Subject(s)
Bone Neoplasms/drug therapy , Bone Neoplasms/mortality , Breast Neoplasms/drug therapy , Breast Neoplasms/mortality , Doxorubicin/administration & dosage , Liver Neoplasms/drug therapy , Liver Neoplasms/mortality , Adult , Aged , Antibiotics, Antineoplastic/administration & dosage , Austria/epidemiology , Bone Neoplasms/diagnosis , Bone Neoplasms/secondary , Breast Neoplasms/diagnosis , Delayed-Action Preparations/administration & dosage , Disease-Free Survival , Female , Humans , Liver Neoplasms/diagnosis , Liver Neoplasms/secondary , Lymphatic Metastasis , Middle Aged , Polyethylene Glycols , Survival Analysis , Treatment Outcome
3.
Eur J Cell Biol ; 48(1): 79-87, 1989 Feb.
Article in English | MEDLINE | ID: mdl-2526018

ABSTRACT

Trisomy 21 (Down's syndrome, DS) is the most frequent chromosomal aberration. Triplication of a small region of chromosome 21, the fragment 21q22 is sufficient to cause the DS phenotype including immunodeficiency, premature aging, neurodegenerations, mental retardation and an increased risk of leukemia. Chromosomal aberrations caused by X-ray irradiation were observed in DS lymphocytes and DS fibroblasts, but the correlation to cell death or repair deficiency was not clear. We approached this problem and report here on a profound X-ray repair deficiency of DS cells. With a colorimetric viability assay we observed an UV sensitivity of DS fibroblasts at doses beyond 14 Jm-2 but no significant X-ray sensitivity. By the nucleoid sedimentation technique, a deficient restoration of nucleoids in DS cells after X-ray irradiation was demonstrated. The same features apply for cells, which contain an overexpressed Cu/Zn-superoxide dismutase (SOD-1) gene. Radiation sensitivity of DS cells and SOD-1 overexpressing cells resemble those of ataxia telangiectasia (AT) fibroblasts. Additionally, DS and AT cells exert lack of inhibition of DNA synthesis after X-ray irradiation.


Subject(s)
Down Syndrome/pathology , Fibroblasts/radiation effects , Superoxide Dismutase/genetics , Cell Line , Cells, Cultured , Copper/metabolism , Down Syndrome/etiology , Down Syndrome/genetics , Gene Expression Regulation/radiation effects , Humans , Superoxide Dismutase/metabolism , Superoxide Dismutase/radiation effects , Transfection/radiation effects , Ultraviolet Rays/adverse effects , X-Rays/adverse effects , Zinc/metabolism
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