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Von Pawel J.,Asklepios Fachkliniken Munich Gauting | Harvey J.H.,Alabama Oncology | Spigel D.R.,Sarah Cannon Research Institute | Dediu M.,Institute Of Oncology Prof Dr Alexandru Trestioreanu | And 5 more authors.
Clinical Lung Cancer | Year: 2014

Background This phase II study examined the efficacy of mapatumumab in combination with paclitaxel and carboplatin in patients with non-small-cell lung cancer (NSCLC). Patients and Methods Patients with stage IIIB or stage IV advanced primary NSCLC were randomly assigned (1:1:1) to receive up to 6 courses of standard-dose paclitaxel and carboplatin or a combination of paclitaxel, carboplatin, and mapatumumab (10 mg/kg or 30 mg/kg). Primary efficacy end points were overall response rate and median progression-free survival (PFS). Secondary efficacy end points included disease control rate, overall survival (OS), time to response, and duration of response. Exploratory studies included evaluation of historical biopsy materials for TRAIL-R1 expression by immunohistochemical analysis and serum levels of M30, a marker of apoptosis, before and after the first 2 doses of mapatumumab. Safety parameters, including adverse events (AEs), laboratory tests, and immunogenicity, were assessed. Results The majority of patients had stage IV disease (79%) and an Eastern Cooperative Oncology Group (ECOG) performance status of 0 (58%); baseline characteristics were similar across treatment arms. No improvements in response or disease control rates, PFS, or OS were gained from the addition of mapatumumab. Adverse events in the mapatumumab arms were generally consistent with toxicities seen in the carboplatin and paclitaxel control arm. Levels of M30 were highly variable, and consistent patterns were not seen across treatment arms. Conclusion This study showed no clinical benefit from adding mapatumumab to carboplatin and paclitaxel in unselected patients with NSCLC. The combination was generally well tolerated. The possibility of subgroups sensitive to mapatumumab is discussed. © 2014 Elsevier Inc. All rights reserved. Source

Aldea A.,Coltea Clinical Hospital | Negoita V.,Institute Of Oncology Prof Dr Alexandru Trestioreanu | Panait M.,Institute Of Oncology Prof Dr Alexandru Trestioreanu | Gruia M.I.,Institute Of Oncology Prof Dr Alexandru Trestioreanu | Anghel R.,Institute Of Oncology Prof Dr Alexandru Trestioreanu
Archives of the Balkan Medical Union | Year: 2013

Background: The aim of our paper is to identify if the free radicals of oxygen plays an important role in the development and growth of malignant tumors and also in the signaling pathway for the apoptotic transformations. Materials and methods: Our in vivo studies were performed in RS-1 hepatoma bearing Wistar rats. The assays started at 7 days from the tumor graft and was performed in dynamics the biochemical oxidative status parameters (such as lipid peroxides level, total thiol-groups level and the apoptosis) by flow-cytometry. The biological samples are represented by serum and total tissues homogenates removed from tumoral, peri tumoral and normal liver tissues. Results: The results show an increase of the oxidative status and the free radicals of oxygen production during the development and growth of tumor, also the modification of the apoptotic status suggesting an increased proliferative potential of the tumour. Conclusions: The purpose of the present study was to create an experimental model that could stand as a useful tool for clinical studies. Oxidative stress in tissues and blood comes from an increased free radicals production due to the decrease of endogenous antioxidants, as a consequence of the tumour's presence. The obtained results make a case for a dual relation between the tumoral cell and installed oxidative stress, more precisely the latter can be a cause or a consequence of malignant transformation. Source

Lazescu A.V.D.,University of Bucharest | Gruia M.I.I.,Institute Of Oncology Prof Dr Alexandru Trestioreanu | Anghel R.M.,University of Bucharest | Glavan D.A.,Institute Of Oncology Prof Dr Alexandru Trestioreanu
Revista Romana de Medicina de Laborator | Year: 2013

Purpose: To identify sialic acid as a tumor marker to be used in experimental models. Obtained data will be extrapolated to humans, so that this marker can be used in clinical practice. Materials and methods: We used B16 melanoma cells. The lot was composed of 30 male C57Bl6 mice, which received subcutaneous injections of 5x105 B16 melanoma cells into the right flank. Tumor volume was measured with a vernier caliper. Sialic acid was determined from the serum obtained by cardiac puncture. The second step of our research was performed on a number of 25 patients with cutaneous melanoma. Determination of sialic acid was performed using the Kattermann colorimetric method. The correlation between sialic acid and disease progression was exemplified in two clinical cases. Sialic acid determination was performed dynamically from diagnosis, following disease progression. Results: In murine models tumors increased after a lag period of up to 10 days. Tumor growth was recorded by measuring the tumor's diameters and calculating its volume. We observed a progressive increase of sialic acid in parallel with tumor volume. In human subjects, sialic acid levels increase in metastatic disease and are common in localized disease. In the two clinical cases there was a very strong correlation between sialic acid and disease progression. Con clusions: B16 melanoma cells are highly metastatic. Sialic acid level was increased in metastatic tumor animals compared to normal animals. Higher levels of sialic acid have been shown to correlate with the metastatic potential of tumor cells. For humans, determination of total serum sialic acid would be more useful for diagnosis of advanced melanoma stage rather than for early detection and screening. Source

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