Currently, we are further looking into enhancement of reaction kinetics and exploitation of tandem crDA in vivo. (C) 2009 Elsevier Inc. All rights reserved.”
“Introduction: The mouse monoclonal antibody MOv18, directed against the alpha-isoform of folate receptor (FR), was investigated to identify the optimal radioconjugate for radioimmunotherapy APR-246 supplier of minimal residual disease in ovarian cancer.
Methods:
Pharmacokinetics, biodistribution, long-term therapeutic efficacy and toxicity of MOv18, labeled with the beta-emitters I-131, Y-90 and Lu-177, were compared in a xenografted mouse model, composed by two cell lines, A431FR and A431MK, differing only for FR expression.
Results: A shorter blood clearance and a higher tumor uptake were observed for Y-90- and Lu-177- compared to I-131-MOv18, and a shorter blood pharmacokinetics was recorded in A431FR-bearing animals. At equitoxic maximum tolerable doses, the general irradiation by I-131- and Y-90-MOv18 gives rise to strong targeted effects on A431FR and nontargeted effects on A431MK tumors, while Lu-177-MOv18 was able to eradicate small size tumor masses expressing the antigen of interest exerting only mild non-targeted effects.
Conclusion: Lu-177-MOv18 at the maximal tolerated dose
is the immunoradioconjugate this website with the best therapeutic window in experimental conditions of small tumor volume. (C) 2009 Elsevier Inc. All rights reserved.”
“Introduction: [1-(11)C]Acetate positron emission tomography (PET) is used for myocardial studies. In the myocardium, mitochondrial acetylCoA synthetase (ACSS1) mainly contributes to the radiopharmaceutical
uptake. [1-(11)C]Acetate PET is also used for tumor diagnosis; however, the uptake mechanism of radiolabeled acetate in tumors remains unclear. Our previous study reported that cytosolic acetyl-CoA synthetase (ACSS2) Nintedanib (BIBF 1120) was expressed in tumor cells and up-regulated under hypoxia, whereas expression of ACSS1 was negligible regardless of the oxygen conditions. We also indicated that ACSS2 is a bidirectional enzyme that controls acetyl-CoA/acetate metabolism in tumor cells. In this study, to elucidate the basic mechanism Of tumor acetate uptake, we focused oil ACSS2 and investigated the role of ACSS2 in the uptake of radiolabeled acetate in tumor cells.
Methods: [1-(14)C]Acetate uptake and ACSS2 expression were examined in four tumor cell lines under normoxia or hypoxia. An ACSS2 knockdown study was also performed.
Results: [1-(14)C]Acetate uptake was increased in the tumor cells under hypoxia. This pattern followed that of ACSS2 expression. The incorporated (14)C was mostly distributed in the lipid-soluble fractions, and this tendency increased under hypoxia. ACSS2 knockdown led to a corresponding reduction in [1-(14)C]acetate uptake in all tumor cell lines examined under normoxia and hypoxia.