The Experts below are selected from a list of 198 Experts worldwide ranked by ideXlab platform
Ying-nan Chen - One of the best experts on this subject based on the ideXlab platform.
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β-Cyclodextrin tetradecasulfate/Tetrahydrocortisol±minocycline as modulators of cancer therapies in vitro and in vivo against primary and metastatic lewis lung carcinoma
Cancer Chemotherapy and Pharmacology, 1993Co-Authors: Beverly A. Teicher, Enrique Alvarez Sotomayor, Zhen Dong Huang, Sylvia Holden, Vrinda Khandekar, Ying-nan ChenAbstract:Tetrahydrocortisol, β-cyclodextrin tetradecasulfate, and minocycline used alone or in combination are not very cytotoxic toward EMT-6 mouse mammary tumor cells growing in monolayer. Tetrahydrocortisol (100 μ M , 24 h) and β-cyclodextrin tetradecasulfate (100 μ M , 24 h) protected EMT-6 cells from the cytotoxicity of CDDP, melphalan, 4-hydroperoxycyclophosphamide, BCNU, and X-rays under various conditions of oxygenation and pH. Minocycline (100 μ M , 24 h) either had no effect upon or was additive with the antitumor alkylating agents or X-rays in cytotoxic activity toward the EMT-6 cells in culture. The combination of the three modulators either had no effect upon or was to a small degree protective against the cytotoxicity of the antitumor alkylating agents or X-rays. The Lewis lung carcinoma was chosen for primary tumor growth-delay studies and tumor lung-metastases studies. Tetrahydrocortisol and β-cyclodextrin tetradecasulfate were given in a 1:1 molar ratio by continuous infusion over 14 days, and minocycline was given i.p. over 14 days, from day 4 to day 18 post tumor implantation. The combination of Tetrahydrocortisol/β-cyclodextrin tetradecasulfate diminished the tumor growth delay induced by CDDP and melphalan and produced modest increases in the tumor growth delay produced by cyclophosphamide and radiation. Minocycline co-treatment increased the tumor growth delay produced by CDDP, melphalan, radiation, bleomycin, and, especially cyclophosphamide, where 4 of 12 animals receiving minocycline (14×5mg/kg, days 4–18) and cyclophosphamide (3×150 mg/kg, days, 7, 9, 11) were long-term survivors. The 3 modulators given in combination produced further increases in tumor growth delay with all of the cytotoxic therapies, and 5 of 12 of the animals treated with the 3-modulator combination and cyclophosphamide were long-term survivors. Although neither Tetrahydrocortisol/β-cyclodextrin tetradecasulfate, minocycline, nor the three modulator combination impacted the number of lung metastases, there was a decrease in the number of large lung metastases. Treatment with the cytotoxic therapies alone reduced the number of lung metastases. Addition of the modulators to treatment with the cytotoxic therapies resulted in a further reduction in the number of lung metastases. These results indicate that agents that inhibit the breakdown of the extracellular matrix can be useful additions to the treatment of solid tumors.
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β cyclodextrin tetradecasulfate Tetrahydrocortisol minocycline as modulators of cancer therapies in vitro and in vivo against primary and metastatic lewis lung carcinoma
Cancer Chemotherapy and Pharmacology, 1993Co-Authors: Beverly A. Teicher, Enrique Alvarez Sotomayor, Zhen Dong Huang, Vrinda Khandekar, Gulshan Ara, Sylvia A Holden, Ying-nan ChenAbstract:Tetrahydrocortisol, β-cyclodextrin tetradecasulfate, and minocycline used alone or in combination are not very cytotoxic toward EMT-6 mouse mammary tumor cells growing in monolayer. Tetrahydrocortisol (100 μM, 24 h) and β-cyclodextrin tetradecasulfate (100 μM, 24 h) protected EMT-6 cells from the cytotoxicity of CDDP, melphalan, 4-hydroperoxycyclophosphamide, BCNU, and X-rays under various conditions of oxygenation and pH. Minocycline (100 μM, 24 h) either had no effect upon or was additive with the antitumor alkylating agents or X-rays in cytotoxic activity toward the EMT-6 cells in culture. The combination of the three modulators either had no effect upon or was to a small degree protective against the cytotoxicity of the antitumor alkylating agents or X-rays. The Lewis lung carcinoma was chosen for primary tumor growth-delay studies and tumor lung-metastases studies. Tetrahydrocortisol and β-cyclodextrin tetradecasulfate were given in a 1:1 molar ratio by continuous infusion over 14 days, and minocycline was given i.p. over 14 days, from day 4 to day 18 post tumor implantation. The combination of Tetrahydrocortisol/β-cyclodextrin tetradecasulfate diminished the tumor growth delay induced by CDDP and melphalan and produced modest increases in the tumor growth delay produced by cyclophosphamide and radiation. Minocycline co-treatment increased the tumor growth delay produced by CDDP, melphalan, radiation, bleomycin, and, especially cyclophosphamide, where 4 of 12 animals receiving minocycline (14×5mg/kg, days 4–18) and cyclophosphamide (3×150 mg/kg, days, 7, 9, 11) were long-term survivors. The 3 modulators given in combination produced further increases in tumor growth delay with all of the cytotoxic therapies, and 5 of 12 of the animals treated with the 3-modulator combination and cyclophosphamide were long-term survivors. Although neither Tetrahydrocortisol/β-cyclodextrin tetradecasulfate, minocycline, nor the three modulator combination impacted the number of lung metastases, there was a decrease in the number of large lung metastases. Treatment with the cytotoxic therapies alone reduced the number of lung metastases. Addition of the modulators to treatment with the cytotoxic therapies resulted in a further reduction in the number of lung metastases. These results indicate that agents that inhibit the breakdown of the extracellular matrix can be useful additions to the treatment of solid tumors.
Beverly A. Teicher - One of the best experts on this subject based on the ideXlab platform.
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β-Cyclodextrin tetradecasulfate/Tetrahydrocortisol±minocycline as modulators of cancer therapies in vitro and in vivo against primary and metastatic lewis lung carcinoma
Cancer Chemotherapy and Pharmacology, 1993Co-Authors: Beverly A. Teicher, Enrique Alvarez Sotomayor, Zhen Dong Huang, Sylvia Holden, Vrinda Khandekar, Ying-nan ChenAbstract:Tetrahydrocortisol, β-cyclodextrin tetradecasulfate, and minocycline used alone or in combination are not very cytotoxic toward EMT-6 mouse mammary tumor cells growing in monolayer. Tetrahydrocortisol (100 μ M , 24 h) and β-cyclodextrin tetradecasulfate (100 μ M , 24 h) protected EMT-6 cells from the cytotoxicity of CDDP, melphalan, 4-hydroperoxycyclophosphamide, BCNU, and X-rays under various conditions of oxygenation and pH. Minocycline (100 μ M , 24 h) either had no effect upon or was additive with the antitumor alkylating agents or X-rays in cytotoxic activity toward the EMT-6 cells in culture. The combination of the three modulators either had no effect upon or was to a small degree protective against the cytotoxicity of the antitumor alkylating agents or X-rays. The Lewis lung carcinoma was chosen for primary tumor growth-delay studies and tumor lung-metastases studies. Tetrahydrocortisol and β-cyclodextrin tetradecasulfate were given in a 1:1 molar ratio by continuous infusion over 14 days, and minocycline was given i.p. over 14 days, from day 4 to day 18 post tumor implantation. The combination of Tetrahydrocortisol/β-cyclodextrin tetradecasulfate diminished the tumor growth delay induced by CDDP and melphalan and produced modest increases in the tumor growth delay produced by cyclophosphamide and radiation. Minocycline co-treatment increased the tumor growth delay produced by CDDP, melphalan, radiation, bleomycin, and, especially cyclophosphamide, where 4 of 12 animals receiving minocycline (14×5mg/kg, days 4–18) and cyclophosphamide (3×150 mg/kg, days, 7, 9, 11) were long-term survivors. The 3 modulators given in combination produced further increases in tumor growth delay with all of the cytotoxic therapies, and 5 of 12 of the animals treated with the 3-modulator combination and cyclophosphamide were long-term survivors. Although neither Tetrahydrocortisol/β-cyclodextrin tetradecasulfate, minocycline, nor the three modulator combination impacted the number of lung metastases, there was a decrease in the number of large lung metastases. Treatment with the cytotoxic therapies alone reduced the number of lung metastases. Addition of the modulators to treatment with the cytotoxic therapies resulted in a further reduction in the number of lung metastases. These results indicate that agents that inhibit the breakdown of the extracellular matrix can be useful additions to the treatment of solid tumors.
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β cyclodextrin tetradecasulfate Tetrahydrocortisol minocycline as modulators of cancer therapies in vitro and in vivo against primary and metastatic lewis lung carcinoma
Cancer Chemotherapy and Pharmacology, 1993Co-Authors: Beverly A. Teicher, Enrique Alvarez Sotomayor, Zhen Dong Huang, Vrinda Khandekar, Gulshan Ara, Sylvia A Holden, Ying-nan ChenAbstract:Tetrahydrocortisol, β-cyclodextrin tetradecasulfate, and minocycline used alone or in combination are not very cytotoxic toward EMT-6 mouse mammary tumor cells growing in monolayer. Tetrahydrocortisol (100 μM, 24 h) and β-cyclodextrin tetradecasulfate (100 μM, 24 h) protected EMT-6 cells from the cytotoxicity of CDDP, melphalan, 4-hydroperoxycyclophosphamide, BCNU, and X-rays under various conditions of oxygenation and pH. Minocycline (100 μM, 24 h) either had no effect upon or was additive with the antitumor alkylating agents or X-rays in cytotoxic activity toward the EMT-6 cells in culture. The combination of the three modulators either had no effect upon or was to a small degree protective against the cytotoxicity of the antitumor alkylating agents or X-rays. The Lewis lung carcinoma was chosen for primary tumor growth-delay studies and tumor lung-metastases studies. Tetrahydrocortisol and β-cyclodextrin tetradecasulfate were given in a 1:1 molar ratio by continuous infusion over 14 days, and minocycline was given i.p. over 14 days, from day 4 to day 18 post tumor implantation. The combination of Tetrahydrocortisol/β-cyclodextrin tetradecasulfate diminished the tumor growth delay induced by CDDP and melphalan and produced modest increases in the tumor growth delay produced by cyclophosphamide and radiation. Minocycline co-treatment increased the tumor growth delay produced by CDDP, melphalan, radiation, bleomycin, and, especially cyclophosphamide, where 4 of 12 animals receiving minocycline (14×5mg/kg, days 4–18) and cyclophosphamide (3×150 mg/kg, days, 7, 9, 11) were long-term survivors. The 3 modulators given in combination produced further increases in tumor growth delay with all of the cytotoxic therapies, and 5 of 12 of the animals treated with the 3-modulator combination and cyclophosphamide were long-term survivors. Although neither Tetrahydrocortisol/β-cyclodextrin tetradecasulfate, minocycline, nor the three modulator combination impacted the number of lung metastases, there was a decrease in the number of large lung metastases. Treatment with the cytotoxic therapies alone reduced the number of lung metastases. Addition of the modulators to treatment with the cytotoxic therapies resulted in a further reduction in the number of lung metastases. These results indicate that agents that inhibit the breakdown of the extracellular matrix can be useful additions to the treatment of solid tumors.
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Antiangiogenic agents potentiate cytotoxic cancer therapies against primary and metastatic disease.
Cancer research, 1992Co-Authors: Beverly A. Teicher, Enrique Alvarez Sotomayor, Zhen Dong HuangAbstract:Abstract The formation of a blood supply (angiogenesis) is critical to the growth of solid tumors. The naturally occurring steroid Tetrahydrocortisol, the synthetic cyclodextrin derivative β-cyclodextrin tetradecasulfate, and the tetracycline derivative minocycline have antiangiogenic activity. Tetrahydrocortisol and β-cyclodextrin tetradecasulfate in a 1:1 molar ratio by continuous infusion over 14 days and minocycline administered i.p. over 14 days from day 4 to day 18 postimplantation of the Lewis lung carcinoma significantly increased the growth delay of the primary tumor after treatment with cis-diamminedichloroplatinum(II), melphalan, cyclophosphamide, Adriamycin, bleomycin, and radiation therapy administered in Standard regimens. Addition of the antiangiogenic agents to treatment with the cytotoxic therapies not only reduced the number of lung metastases formed from the primary tumor but also reduced the number of large metastases. Five of 12 animals treated with the antiangiogenic modulators and cyclophosphamide were long-term survivors (>120 days). Thus, antiangiogenic therapies can potentiate the efficacy of Standard anticancer therapies. The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked advertisement in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.
L E Panin - One of the best experts on this subject based on the ideXlab platform.
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Effect of DNA methylation on the interaction with Tetrahydrocortisol–apolipoprotein A-I complex
Nanotechnologies in Russia, 2016Co-Authors: P. A. Kuznetsov, O. I. Gimautdinova, B. N. Zaitsev, E. N. Demchenko, L E PaninAbstract:The effect of GCNGC site methylation on the DNA binding to Tetrahydrocortisol–apolipoprotein A-I complex was shown by atomic force microscopy and enzymatic analysis. Methylation of GCNGC sites alters the mechanism of interaction of Tetrahydrocortisol–apolipoprotein A-I complex with DNA and leads to the aggregation of the DNA-protein complexes. It was assumed that the involvement of complexes of steroid hormones with apolipoprotein A-I in the process of chromatin restructuring is associated with the processes of DNA methylation/demethylation.
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effect of dna methylation on the interaction with Tetrahydrocortisol apolipoprotein a i complex
Nanotechnologies in Russia, 2016Co-Authors: P. A. Kuznetsov, O. I. Gimautdinova, B. N. Zaitsev, E. N. Demchenko, L E PaninAbstract:The effect of GCNGC site methylation on the DNA binding to Tetrahydrocortisol–apolipoprotein A-I complex was shown by atomic force microscopy and enzymatic analysis. Methylation of GCNGC sites alters the mechanism of interaction of Tetrahydrocortisol–apolipoprotein A-I complex with DNA and leads to the aggregation of the DNA-protein complexes. It was assumed that the involvement of complexes of steroid hormones with apolipoprotein A-I in the process of chromatin restructuring is associated with the processes of DNA methylation/demethylation.
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Mechanisms of interaction of Tetrahydrocortisol and its complex with apolipoprotein A-I and DNA regulatory cis-elements of CC(GCC)5/GG(CGG)5 type
Biofizika, 2008Co-Authors: L E Panin, V G Kunitsyn, L M PoliakovAbstract:An IR-spectroscopy study of the mechanism of interaction between duplex CC(GCC)5/GG (CGG)5Li2 and Tetrahydrocortisol or Tetrahydrocortisol-apolipoprotein A-I complex revealed the formation of hydrogen bonds between the OH group of the Tetrahydrocortisol A-ring and the C=0 group of cytosine or guanine. Tetrahydrocortisol forms hydrogen bonds with the PO2-group of the duplex and with the OH-group of monosaccharide. The interaction of Tetrahydrocortisol and apolipoprotein A-I with the duplex occurs at the same active site, namely, with the C=O-group of bases. The order --> order structural transition takes place in the duplex under the action of Tetrahydrocortisol. The order --> disorder structural transition takes place in the duplex under the action of Tetrahydrocortisol-apolipoprotein A-I complex.
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Interaction of apolipoproteins A-I and E in the regulation of DNA, RNA, and protein biosynthesis in cultured rat hepatocytes
Bulletin of Experimental Biology and Medicine, 2007Co-Authors: L E Panin, D. V. Sumenkova, R. A. Knyazev, L. M. PolyakovAbstract:Experiments on hepatocyte culture showed that apolipoprotein A-I—Tetrahydrocortisol complex increases the rate of DNA, RNA, and protein biosynthesis measured by radioactive label incorporation. Apolipoprotein E acted as competitor of the apolipoprotein A-I—Tetrahydrocortisol complex and abolished biological activity of the latter. We hypothesize that this mechanism of regulation plays an important role in processes of intracellular regeneration and proliferation.
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Effect of glucocorticoids and their complexes with apolipoprotein A-I on the secondary structure of eukaryotic DNA
International Journal of Quantum Chemistry, 2004Co-Authors: L E Panin, V G Kunitsyn, F. V. TusikovAbstract:The Tetrahydrocortisol–apolipoprotein A-I complex specifically interacts with eukaryotic DNA isolated from rat liver. This interaction is highly cooperative and of a saturating nature. One DNA molecule binds about 54 molecules of the complex. Small-angle X-ray scattering has shown that hydrogen bonds between nitrous bases are destroyed and that single-stranded structures are formed at the interaction of the Tetrahydrocortisol–apolipoprotein A-I complex with eukaryotic DNA. The most probable site of binding the Tetrahydrocortisol–apolipoprotein A-I complex with DNA is the sequence of the CC(GCC)n type entering the structure of many genes, among them the structure of the human apolipoprotein A-I gene. Oligonucleotide of this type has been synthesized. The association constant (Kass) of its complexation was shown to be 1.66 · 106 M−1. Substitution of Tetrahydrocortisol for cortisol in the complex results in a considerable decrease of Kass. IR-spectroscopy study has shown that the interaction of Tetrahydrocortisol with oligonucleotide CC(GCC)3–5 is accompanied by the formation of hydrogen bonds via the CO-NH, PO2, and OH groups of desoxycytidinephosphate. The Tetrahydrocortisol–apolipoprotein A-I complex alters the DNA secondary structure formed at the interaction with the hormone, causing the structural transition “order tangle.” It is assumed that in the GC-pairs of the given DNA sequence, Tetrahydrocortisol initiates the rupture of hydrogen bonds, while the hydrophobic interactions between nitrous bases and apoA-I intensify this process. © 2004 Wiley Periodicals, Inc. Int J Quantum Chem, 2005
Zhen Dong Huang - One of the best experts on this subject based on the ideXlab platform.
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β-Cyclodextrin tetradecasulfate/Tetrahydrocortisol±minocycline as modulators of cancer therapies in vitro and in vivo against primary and metastatic lewis lung carcinoma
Cancer Chemotherapy and Pharmacology, 1993Co-Authors: Beverly A. Teicher, Enrique Alvarez Sotomayor, Zhen Dong Huang, Sylvia Holden, Vrinda Khandekar, Ying-nan ChenAbstract:Tetrahydrocortisol, β-cyclodextrin tetradecasulfate, and minocycline used alone or in combination are not very cytotoxic toward EMT-6 mouse mammary tumor cells growing in monolayer. Tetrahydrocortisol (100 μ M , 24 h) and β-cyclodextrin tetradecasulfate (100 μ M , 24 h) protected EMT-6 cells from the cytotoxicity of CDDP, melphalan, 4-hydroperoxycyclophosphamide, BCNU, and X-rays under various conditions of oxygenation and pH. Minocycline (100 μ M , 24 h) either had no effect upon or was additive with the antitumor alkylating agents or X-rays in cytotoxic activity toward the EMT-6 cells in culture. The combination of the three modulators either had no effect upon or was to a small degree protective against the cytotoxicity of the antitumor alkylating agents or X-rays. The Lewis lung carcinoma was chosen for primary tumor growth-delay studies and tumor lung-metastases studies. Tetrahydrocortisol and β-cyclodextrin tetradecasulfate were given in a 1:1 molar ratio by continuous infusion over 14 days, and minocycline was given i.p. over 14 days, from day 4 to day 18 post tumor implantation. The combination of Tetrahydrocortisol/β-cyclodextrin tetradecasulfate diminished the tumor growth delay induced by CDDP and melphalan and produced modest increases in the tumor growth delay produced by cyclophosphamide and radiation. Minocycline co-treatment increased the tumor growth delay produced by CDDP, melphalan, radiation, bleomycin, and, especially cyclophosphamide, where 4 of 12 animals receiving minocycline (14×5mg/kg, days 4–18) and cyclophosphamide (3×150 mg/kg, days, 7, 9, 11) were long-term survivors. The 3 modulators given in combination produced further increases in tumor growth delay with all of the cytotoxic therapies, and 5 of 12 of the animals treated with the 3-modulator combination and cyclophosphamide were long-term survivors. Although neither Tetrahydrocortisol/β-cyclodextrin tetradecasulfate, minocycline, nor the three modulator combination impacted the number of lung metastases, there was a decrease in the number of large lung metastases. Treatment with the cytotoxic therapies alone reduced the number of lung metastases. Addition of the modulators to treatment with the cytotoxic therapies resulted in a further reduction in the number of lung metastases. These results indicate that agents that inhibit the breakdown of the extracellular matrix can be useful additions to the treatment of solid tumors.
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β cyclodextrin tetradecasulfate Tetrahydrocortisol minocycline as modulators of cancer therapies in vitro and in vivo against primary and metastatic lewis lung carcinoma
Cancer Chemotherapy and Pharmacology, 1993Co-Authors: Beverly A. Teicher, Enrique Alvarez Sotomayor, Zhen Dong Huang, Vrinda Khandekar, Gulshan Ara, Sylvia A Holden, Ying-nan ChenAbstract:Tetrahydrocortisol, β-cyclodextrin tetradecasulfate, and minocycline used alone or in combination are not very cytotoxic toward EMT-6 mouse mammary tumor cells growing in monolayer. Tetrahydrocortisol (100 μM, 24 h) and β-cyclodextrin tetradecasulfate (100 μM, 24 h) protected EMT-6 cells from the cytotoxicity of CDDP, melphalan, 4-hydroperoxycyclophosphamide, BCNU, and X-rays under various conditions of oxygenation and pH. Minocycline (100 μM, 24 h) either had no effect upon or was additive with the antitumor alkylating agents or X-rays in cytotoxic activity toward the EMT-6 cells in culture. The combination of the three modulators either had no effect upon or was to a small degree protective against the cytotoxicity of the antitumor alkylating agents or X-rays. The Lewis lung carcinoma was chosen for primary tumor growth-delay studies and tumor lung-metastases studies. Tetrahydrocortisol and β-cyclodextrin tetradecasulfate were given in a 1:1 molar ratio by continuous infusion over 14 days, and minocycline was given i.p. over 14 days, from day 4 to day 18 post tumor implantation. The combination of Tetrahydrocortisol/β-cyclodextrin tetradecasulfate diminished the tumor growth delay induced by CDDP and melphalan and produced modest increases in the tumor growth delay produced by cyclophosphamide and radiation. Minocycline co-treatment increased the tumor growth delay produced by CDDP, melphalan, radiation, bleomycin, and, especially cyclophosphamide, where 4 of 12 animals receiving minocycline (14×5mg/kg, days 4–18) and cyclophosphamide (3×150 mg/kg, days, 7, 9, 11) were long-term survivors. The 3 modulators given in combination produced further increases in tumor growth delay with all of the cytotoxic therapies, and 5 of 12 of the animals treated with the 3-modulator combination and cyclophosphamide were long-term survivors. Although neither Tetrahydrocortisol/β-cyclodextrin tetradecasulfate, minocycline, nor the three modulator combination impacted the number of lung metastases, there was a decrease in the number of large lung metastases. Treatment with the cytotoxic therapies alone reduced the number of lung metastases. Addition of the modulators to treatment with the cytotoxic therapies resulted in a further reduction in the number of lung metastases. These results indicate that agents that inhibit the breakdown of the extracellular matrix can be useful additions to the treatment of solid tumors.
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Antiangiogenic agents potentiate cytotoxic cancer therapies against primary and metastatic disease.
Cancer research, 1992Co-Authors: Beverly A. Teicher, Enrique Alvarez Sotomayor, Zhen Dong HuangAbstract:Abstract The formation of a blood supply (angiogenesis) is critical to the growth of solid tumors. The naturally occurring steroid Tetrahydrocortisol, the synthetic cyclodextrin derivative β-cyclodextrin tetradecasulfate, and the tetracycline derivative minocycline have antiangiogenic activity. Tetrahydrocortisol and β-cyclodextrin tetradecasulfate in a 1:1 molar ratio by continuous infusion over 14 days and minocycline administered i.p. over 14 days from day 4 to day 18 postimplantation of the Lewis lung carcinoma significantly increased the growth delay of the primary tumor after treatment with cis-diamminedichloroplatinum(II), melphalan, cyclophosphamide, Adriamycin, bleomycin, and radiation therapy administered in Standard regimens. Addition of the antiangiogenic agents to treatment with the cytotoxic therapies not only reduced the number of lung metastases formed from the primary tumor but also reduced the number of large metastases. Five of 12 animals treated with the antiangiogenic modulators and cyclophosphamide were long-term survivors (>120 days). Thus, antiangiogenic therapies can potentiate the efficacy of Standard anticancer therapies. The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked advertisement in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.
Piero Salvadori - One of the best experts on this subject based on the ideXlab platform.
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recent advances in the assessment of the ratios of cortisol to cortisone and of some of their metabolites in urine by lc ms ms
Journal of Mass Spectrometry, 2009Co-Authors: Alessandro Saba, Andrea Raffaelli, Claudio Marcocci, Adamasco Cupisti, Antonella Petri, Piero SalvadoriAbstract:A previously reported method for the assessment of the ratio of Tetrahydrocortisol (THF) + allo-Tetrahydrocortisol (A-THF) to tetrahydrocortisone (THE) by HPLC-MS-MS has been significantly improved, in order to increase either ruggedness and reliability. That was achieved by the introduction of an on-line sample cleanup stage, which made use of a perfusion column as a solid phase microextraction (SPE) cartridge. The set of analytes was expanded, by introducing cortisol and cortisone, whose ratio supply additional diagnostic information. The response factors of both THF and A-THF has been checked, resulting almost identical, as well as the influence of the matrix on the calibration curves which, although different for water and urine, had similar effect on the ratios of interest. As a consequence, the calibration solutions can be prepared in pure water. The influence of several different storage procedures has also been tested, resulting in no substantial effect on the final result. Finally, the improved method has been used to run real samples from healthy volunteers, with satisfactory results.
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Recent advances in the assessment of the ratios of cortisol to cortisone and of some of their metabolites in urine by LC‐MS‐MS
Journal of mass spectrometry : JMS, 2008Co-Authors: Alessandro Saba, Andrea Raffaelli, Claudio Marcocci, Adamasco Cupisti, Antonella Petri, Piero SalvadoriAbstract:A previously reported method for the assessment of the ratio of Tetrahydrocortisol (THF) + allo-Tetrahydrocortisol (A-THF) to tetrahydrocortisone (THE) by HPLC-MS-MS has been significantly improved, in order to increase either ruggedness and reliability. That was achieved by the introduction of an on-line sample cleanup stage, which made use of a perfusion column as a solid phase microextraction (SPE) cartridge. The set of analytes was expanded, by introducing cortisol and cortisone, whose ratio supply additional diagnostic information. The response factors of both THF and A-THF has been checked, resulting almost identical, as well as the influence of the matrix on the calibration curves which, although different for water and urine, had similar effect on the ratios of interest. As a consequence, the calibration solutions can be prepared in pure water. The influence of several different storage procedures has also been tested, resulting in no substantial effect on the final result. Finally, the improved method has been used to run real samples from healthy volunteers, with satisfactory results.
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direct determination of the ratio of Tetrahydrocortisol allo Tetrahydrocortisol to tetrahydrocortisone in urine by lc ms ms
Journal of Chromatography B, 2006Co-Authors: Andrea Raffaelli, Alessandro Saba, Edda Vignali, Claudio Marcocci, Piero SalvadoriAbstract:The 11beta-hydroxysteroid dehydrogenase (11beta-HSD) is responsible for the interconversion of both the hormonally inactive cortisone and the active cortisol. This enzyme activity, which has implications in the pathogenesis of numerous diseases, is reflected in the ratio of tetrahydrometabolites of cortisol (allo-Tetrahydrocortisol and Tetrahydrocortisol) to those of cortisone (tetrahydrocortisone). Several methods have been proposed in the literature to determine such a ratio in urine. Most of them require tedious and extensive extraction and derivatization steps and make use of gas-chromatographic techniques, including gas chromatography coupled to mass spectrometry (GC-MS). We present here an alternative approach for the direct determination of such a ratio in urine by using liquid chromatography-electrospray ionization-tandem mass spectrometry (LC-ESI-MS-MS), based on a minimal sample treatment. Actually, the limit of detections (LODs) for pure standards in water permitted a simple dilution of the urine samples prior to the analysis, hence, an accurate optimization of the high performance liquid chromatography (HPLC) separation was needed in order to get rid of the severe influence of the urine matrix on the ionization efficiency. Besides, the nature of some interfering species was deeply investigated, as well as the suitability of some commercial deuterated steroids as internal standards. All these led to the final method, which was based on a HPLC separation on a C8 column and a ternary gradient water/methanol/acetonitrile. In parallel, an appropriate sample preparation was set up, which consisted of an enzymatic hydrolysis of the conjugated species and a followed 1:20 dilution. Preliminary measurements on real urine samples were performed as well.
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Direct determination of the ratio of Tetrahydrocortisol+allo-Tetrahydrocortisol to tetrahydrocortisone in urine by LC-MS-MS.
Journal of chromatography. B Analytical technologies in the biomedical and life sciences, 2005Co-Authors: Andrea Raffaelli, Alessandro Saba, Edda Vignali, Claudio Marcocci, Piero SalvadoriAbstract:The 11beta-hydroxysteroid dehydrogenase (11beta-HSD) is responsible for the interconversion of both the hormonally inactive cortisone and the active cortisol. This enzyme activity, which has implications in the pathogenesis of numerous diseases, is reflected in the ratio of tetrahydrometabolites of cortisol (allo-Tetrahydrocortisol and Tetrahydrocortisol) to those of cortisone (tetrahydrocortisone). Several methods have been proposed in the literature to determine such a ratio in urine. Most of them require tedious and extensive extraction and derivatization steps and make use of gas-chromatographic techniques, including gas chromatography coupled to mass spectrometry (GC-MS). We present here an alternative approach for the direct determination of such a ratio in urine by using liquid chromatography-electrospray ionization-tandem mass spectrometry (LC-ESI-MS-MS), based on a minimal sample treatment. Actually, the limit of detections (LODs) for pure standards in water permitted a simple dilution of the urine samples prior to the analysis, hence, an accurate optimization of the high performance liquid chromatography (HPLC) separation was needed in order to get rid of the severe influence of the urine matrix on the ionization efficiency. Besides, the nature of some interfering species was deeply investigated, as well as the suitability of some commercial deuterated steroids as internal standards. All these led to the final method, which was based on a HPLC separation on a C8 column and a ternary gradient water/methanol/acetonitrile. In parallel, an appropriate sample preparation was set up, which consisted of an enzymatic hydrolysis of the conjugated species and a followed 1:20 dilution. Preliminary measurements on real urine samples were performed as well.