Search

Your search keyword '"Smid, K."' showing total 242 results
Start Over Author "Smid, K."
242 results on '"Smid, K."'

10. Abstracts of poster presentations

Author

Agostinho, A. B., Rosi, F., Tabucchi, A., Carlucci, F., Pizzichini, M., Arnér, Elias S. J., Eriksson, Staffan, Barankiewicz, J., Trembacz, H., Zwierzchowski, L., Bergman, A. M., van Haperen, V. W. T. Ruiz, Veerman, G., Vermorken, J. B., Peters, G. J., Bory, C., Chantin, C., Rocca, J. L., Bzowska, A., Ananlev, A. V., Ramzaeva, N., Alksins, E., Maurins, J. A., Kulikowska, E., Shugar, D., Davies, P. M., Fairbanks, L. D., Simmonds, H. A., De Graaf, T. W., Van Dijk, W., de Jong D., Huysmans F., De Abreu R., Monnens L., Dijkman H., van Liebergen F., Assmann K., Duley, J. A., Hanefeld, F., Fabianowska-Majewska, K., Duley, A. J., Greger, J., Wasiak, T., Gathof, B. S., Ried, T., Zwieauer, K., Gresser, U., Griesmacher, A., Weigel, G., Müller, M. M., Gross, M., Empl, W., Guisan, B., Roch-Ramel, F., Harley, E. H., Baumgarten, I., Kaletha K., Nagel-Starczynowska G., Karlsson, Anna, Lambooy, L., Boerbooms, A., De Abreu, R., van de Putte, L., Stolk, J., vd Pulte, L., Komissarov, A. A., Romanova, D. V., Debabov, V. G., Kozlov, A. M., Sokolov, V. B., Aksinenko, A. Y., Fetisov, V. I., Komoriya, Keiji, Osada, Yoshio, Hasegawa, Masaichi, Kondo, Shiro, Couch, Ronald C., Griffin, Travis B., Lakaschus, G., Löffler, H. G., Löffler, M., Jiménez, M. López, Salinero, M. A., Guilarte, J. Sánchez, Matesanz, J. Perianes, Medina, L. Vigil, Galiana, J. Ruiz, Marlewski, M., Smolenski, R. T., Swierczynski, J., Rutkowski, B., Zydowo, M. M., Micheli, V., Pescaglini, M., Sestini, S., Jacomelli, G., Magagnoli, C., Pompucci, G., Hayek, G., Mimouni, M., Boptemps, F., Van den Berghe, G., Miranda, M. E., Mateos, F. A., Herrero, E., González, A., Puig, J. G., Miscetti, P., Minelli, A., Proietti, A., Moroni, M., Mezzasoma, I., Moro, J. F., Noam, I., Cameron, J. S., McBride, M. B., Mathew, C. G. P., Ogg, C. S., Puig, J. G., Miranda, M. E., Mateos, F. A., Luzi, L., Noordhuis, P., Kazemier, K., Kaspers, G. J. L., Overgaard-Hansen, K., Marcussen, M., Klenow, H., Pelatti, A., Quaratino, C. P., D'Amario, C., Tentarelli, R., Giacomello, A., Rocchigiani, M., Iacomelli, G., Pandolfi, M. L., Arezzini, L., Terzuoli, L., Pagani, R., Di Sciascio, N., Colosimo, A., Ranieri-Paggi, M., Ronca, F., Brown, P. E., Moir, A. J. G., Raggi, A., Schwendel A., Grune T., Siems W. G., Holzhuetter H. G., Sebesta, I., Krijt, J., Vondrak, K., Kmoch, S., Hrebicek, M., Senatore, G., Del Lucchese, G., Martini, C., Lucacchini, A., Siems, W. G., Mertsch, K., Blasig, I., Grune, T., Skladanowski, A. C., Hoffmann, C. S., Krass, J. D., Makarewicz, W., Jastorff, B., Slingerland, R. J., Bodlaender, J. M., Van Lenthe, H., Elzinga, L., Van Kuilenburg, A. B. P., Voûte, P. A., Van Gennip, A. H., Smid, K., van der Wilt, C. L., Aherne, G. W., Pinedo, H. M., Sorqi, M. L., Rucci, C., Zoppini, A., Staub M., Sasvári-Székely M., Spasokukockaja T., Hrabák A., Stolk, J. N., De Abreu, R. A., De Koning, D. G. M., Lambooy, L. H. M., Kerstens, P. J. S. M., Boerbooms, A. M. Th., van de Putte, L. B. A., Szüts, P., Szirovicza, éva, åbrahám, C. S., Havass, Z., Jezewska, M. M., Van Acker, K. J., Eyskens, F. J., Verkerk, R. H., Scharpé, S. S., van Kuppevelt, T. H., Veerkamp, J. H., Sabina, R. L., Van Laar J. A. M., Mayhew E., Durrani F. A., Peters G. J., Rustum Y. M., Wang, J. Z., Leoncini, R., Vannoni, D., and Marinello, E.

Published
1993
Full Text
View/download PDF

11. Abstracts of oral presentations

Author

Boulieu, R., Lenoir, A., Mornex, J. F., Bohman, C., Balzarini, J., Wigerinck, P., Van Aerschot, A., Herdewijn, P., De Clercq, Erik, Brosh, S., Zoref-Shani, E., Sperling, O., Danziger, E., Sidi, Y., Bromberg, Y., Burgemeister, Renate, Rötzer, Elke, Gutensohn, Wolf, Connolly, G. P., Harrison, P. J., Diasio, R. B., Lu, Z., Zhang, R., Gresser, U., Gutensohn, W., Resta, R., Thompson, L. F., Javaux, F., Vincent, M. F., Van den Berghe, G., Kamilli, I., Rauch, R., Hahn, D., Keuzenkamp-Jansen, C. W., De Abreu, R. A., Bökkerink, J. P. M., vd Heijden, M. A. H., Löffler, M., Becker, C., Wegerie, E., Marcussen, M., Overgaard-Hansen, K., Klenow, H., Marinaki, A. M., Harley, E. H., McBride, M. B., Simmonds, H. A., Moro, F., Cameron, J. S., Ogg, C. S., Williams, D. G., Rigden, S., Haycock, G., Miranda, M. E., Puig, J. G., Mateos, F. A., Vázquez, J. O., van Haperen, V. W. T. Ruiz, Veerman, G., Vermorken, J. B., Peters, G. J., van der Wilt, C. L., Noordhuis, P., Smid, K., Pinedo, H. M., Salerno, C., Lomonte, A., Giardini, O., Crifo, C., Smolenski, R. T., Yacoub, M. H., Seymour, A. M. -L., Stegmann, A. P. A., Honders, M. W., Willemze, R., Landegent, J. E., Stet, E. H., Vogels-Mentink, G. M., Lambooy, L. H. J., Trijbels, J. M. F., Torres, R. J., Tozzi, M. G., Pesi, R., Turriani, M., Allegrini, S., Camici, M., Ipata, P. L., van den Berg, A. A., Meinsma, J. R., van Lenthe, H., van Gennip, A. H., van Kuilenburg, A. B. P., Abeling, N. G. G. M., Bakker, H. D., Slingerland, R. J., Van den Bergh, F., and Sabina, R. L.

Published
1993
Full Text
View/download PDF

17. Cellular pharmacology of multi- and duplex drugs consisting of ethynylcytidine and 5-fluoro-2'-deoxyuridine

Author

Bijnsdorp, I.V., Schwendener, R.A., Schott, H., Fichtner, I., Smid, K., Laan, A.C., Schott, S., Losekoot, N., Honeywell, R.J., and Peters, G.J.

Subjects
Cancer Research
Abstract

Prodrugs can have the advantage over parent drugs in increased activation and cellular uptake. The multidrug ETC-L-FdUrd and the duplex drug ETC-FdUrd are composed of two different monophosphate-nucleosides, 5-fluoro-2'deoxyuridine (FdUrd) and ethynylcytidine (ETC), coupled via a glycerolipid or phosphodiester, respectively. The aim of the study was to determine cytotoxicity levels and mode of drug cleavage. Moreover, we determined whether a liposomal formulation of ETC-L-FdUrd would improve cytotoxic activity and/or cleavage. Drug effects/cleavage were studied with standard radioactivity assays, HPLC and LC-MS/MS in FM3A/0 mammary cancer cells and their FdUrd resistant variants FM3A/TK(-). ETC-FdUrd was active (IC(50) of 2.2 and 79 nM) in FM3A/0 and TK(-) cells, respectively. ETC-L-FdUrd was less active (IC(50): 7 nM in FM3A/0 vs 4500 nM in FM3A/TK(-)). Although the liposomal formulation was less active than ETC-L-FdUrd in FM3A/0 cells (IC(50):19.3 nM), resistance due to thymidine kinase (TK) deficiency was greatly reduced. The prodrugs inhibited thymidylate synthase (TS) in FM3A/0 cells (80-90%), but to a lower extent in FM3A/TK(-) (10-50%). FdUMP was hardly detected in FM3A/TK(-) cells. Inhibition of the transporters and nucleotidases/phosphatases resulted in a reduction of cytotoxicity of ETC-FdUrd, indicating that this drug was cleaved outside the cells to the monophosphates, which was verified by the presence of FdUrd and ETC in the medium. ETC-L-FdUrd and the liposomal formulation were neither affected by transporter nor nucleotidase/phosphatase inhibition, indicating circumvention of active transporters. In vivo, ETC-FdUrd and ETC-L-FdURd were orally active. ETC nucleotides accumulated in both tumor and liver tissues. These formulations seem to be effective when a lipophilic linker is used combined with a liposomal formulation.

Published
2011

20. Modulation of both endogenous folates and thymidine enhance the therapeutic efficacy of thymidylate synthase inhibitors

Author

Wilt, C. L., Backus, H. H. J., Smid, K., Comijn, L., Veerman, G., Wouters, D., Voorn, D. A., Priest, D. G., Bunni, M. A., Mitchell, F., Jackman, A. L., Jansen, G., Godefridus J Peters, Medical oncology, Laboratory Medicine, Rheumatology, CCA - Cancer biology and immunology, CCA - Imaging and biomarkers, CCA - Cancer Treatment and quality of life, AII - Inflammatory diseases, and Medical oncology laboratory

Abstract

Plasma levels of folates and thymidine in mice are about 10-fold higher than in humans and may influence the therapeutic efficacy of thymidylate synthase (TS) inhibitors, such as 5-fluorouracil (5FU) and the antifolates pemetrexed (MTA) and raltitrexed (RTX). Therefore, we tested their therapeutic efficacy in various murine tumor models, grown in mice on a normal and a folate-depleted diet, with high and low thymidine kinase (TK) levels. MTA and RTX were inactive against Colon-26-10 [doubling times gained by treatment; growth delay factor (GDF), 0.5 and 0.3, respectively], whereas 5FU was very active (GDF, >10; complete cures). Colon-26-10/F, grown in mice on a folate-depleted diet, was more sensitive to RTX and MTA (GDF, 2.1 and 1.3, respectively) but not to 5FU (GDF, 1.2); however, leucovorin reversed the effect leading to cures. Folate depletion did not reverse resistance of Colon-26A and Colon-26G (low TK) to MTA and RTX, whereas leucovorin only enhanced the 5FU effect in Colon-26A and Colon-26A/F. Folic acid at 15 mg/kg did not improve the therapeutic efficacy of MTA in folate-deficient mice. The folate-depleted diet decreased the reduced folates in Colon-26A/F and Colon-26-G/F tumors less (4-5-fold; P < 0.01) than in Colon-26-10/F tumors (8-fold; P < 0.001). Folate depletion increased TS levels 2-3-fold in all of the models and TK levels 6-fold (P < 0.01) in Colon-26G/F, explaining the lack of activity of MTA and RTX in Colon-26G/F. In contrast, TK-deficient FM3A/TK tumors were much more sensitive to RTX, MTA, and 5FU than parent FM3A tumors, which have comparable TS levels. The rate of thymidine phosphorylysis varied considerably in all of the tumors without a clear relation to antitumor activity. In conclusion, tumor folates may potentiate (5FU) or protect (antifolates). Murine tumor models should combine low folates and low thymidine rescue to optimize preclinical testing of antifolates.

Published
2001

21. End-joining deficiency and radiosensitization induced by gemcitabine

Author

Putten, J. W. G., Groen, H. J. M., Smid, K., Godefridus J Peters, and Kampinga, H. H.

Subjects
V(D)J RECOMBINATION, CHEF ELECTROPHORESIS, TUMOR-CELLS, DNA-REPAIR, CELL-CYCLE, SCID MUTATION, PROTEIN-KINASE ACTIVITY, IN-VITRO, DOUBLE-STRAND BREAKS, 2',2'-DIFLUORO-2'-DEOXYCYTIDINE
Abstract

The mechanism of radiosensitization by gemcitabine (2',2'-dinuoro-2'-deoxycytidine, dFdC) is not exactly known. We investigated the possible role of inhibition of the repair of DNA double-strand breaks by dFdC by measuring the extent of radiosensitization in different cell lines deficient and proficient in components of nonhomologous end-joining and in the parental cell lines. Different cell lines were incubated with 0.5 and 5 muM dFdC for 4 h. Cells deficient in DNA-dependent protein-kinase catalytic subunit (V3) showed sensitization similar to that of wild-type cells (AA8) and complemented cells (V3+YAC). Ku80-deficient cells (xrs5 and xrs6) showed even more radiosensitization by dFdC as compared with wild-type CHO-K1. However, Ku80-complemented cell lines (xrs5+huKu80 and xrs6+haKu80) did not show radiosensitization. The differences in dFdC-mediated radiosensitization were not attributable to different changes in deoxynucleotide triphosphate levels and cell cycle distribution. We conclude that a functional nonhomologous end-joining pathway is not required for dFdC-mediated radiosensitization.

Published
2001

22. Personeelsbeleid op MKB-boomkwekerij : belangrijke zaken op gebied van instroom, doorstroom en uitstroom

Author

Smid, K. and Smid, K.

Abstract

Dat grote bedrijven een afdeling Personeelszaken hebben is logisch. Zij moeten wel beleid maken, vanwege de grote aantallen medewerkers. Personeelsplanning, opleidingen- en scholingsbeleid, ziekteverzuimbeleid, protocollen over veiligheid of alcoholmisbruik enzovoorts. Veel werkgevers in het MKB beschouwen dat als typische onderwerpen voor de afdeling Personeelszaken van grotere bedrijven. Heeft een MKBondernemer werkelijk geen personeelsbeleid nodig?

Published
2011

23. Cellular pharmacology of multi- and duplex drugsconsisting of ethynylcytidine and 5-fluoro-2'-deoxyuridine

Author

Bijnsdorp, I V, Schwendener, R A, Schott, H, Fichtner, I, Smid, K, Laan, A C, Schott, S, Losekoot, N, Honeywell, R J, Peters, G J, Bijnsdorp, I V, Schwendener, R A, Schott, H, Fichtner, I, Smid, K, Laan, A C, Schott, S, Losekoot, N, Honeywell, R J, and Peters, G J

Abstract

Prodrugs can have the advantage over parent drugs in increased activation and cellular uptake. The multidrug ETC-L-FdUrd and the duplex drug ETC-FdUrd are composed of two different monophosphate-nucleosides, 5-fluoro-2'deoxyuridine (FdUrd) and ethynylcytidine (ETC), coupled via a glycerolipid or phosphodiester, respectively. The aim of the study was to determine cytotoxicity levels and mode of drug cleavage. Moreover, we determined whether a liposomal formulation of ETC-L-FdUrd would improve cytotoxic activity and/or cleavage. Drug effects/cleavage were studied with standard radioactivity assays, HPLC and LC-MS/MS in FM3A/0 mammary cancer cells and their FdUrd resistant variants FM3A/TK(-). ETC-FdUrd was active (IC(50) of 2.2 and 79 nM) in FM3A/0 and TK(-) cells, respectively. ETC-L-FdUrd was less active (IC(50): 7 nM in FM3A/0 vs 4500 nM in FM3A/TK(-)). Although the liposomal formulation was less active than ETC-L-FdUrd in FM3A/0 cells (IC(50):19.3 nM), resistance due to thymidine kinase (TK) deficiency was greatly reduced. The prodrugs inhibited thymidylate synthase (TS) in FM3A/0 cells (80-90%), but to a lower extent in FM3A/TK(-) (10-50%). FdUMP was hardly detected in FM3A/TK(-) cells. Inhibition of the transporters and nucleotidases/phosphatases resulted in a reduction of cytotoxicity of ETC-FdUrd, indicating that this drug was cleaved outside the cells to the monophosphates, which was verified by the presence of FdUrd and ETC in the medium. ETC-L-FdUrd and the liposomal formulation were neither affected by transporter nor nucleotidase/phosphatase inhibition, indicating circumvention of active transporters. In vivo, ETC-FdUrd and ETC-L-FdURd were orally active. ETC nucleotides accumulated in both tumor and liver tissues. These formulations seem to be effective when a lipophilic linker is used combined with a liposomal formulation.

Published
2011

26. Expression microarray analysis and oligo array comparative genomic hybridization of acquired gemcitabine resistance in mouse colon reveals selection for chromosomal aberrations

Author

van de Wiel, M.A., Costa, J.L., Smid, K, Oudejans, C.B.M., Bergman, A., Meijer, G.J., Peters, Gons, Ylstra, B., van de Wiel, M.A., Costa, J.L., Smid, K, Oudejans, C.B.M., Bergman, A., Meijer, G.J., Peters, Gons, and Ylstra, B.

Abstract

Gemcitabine is a commonly used therapy for many solid tumors. Acquired resistance to this nucleoside analogue, however, diminishes the long-term effectiveness in a majority of patients. To better define the molecular background of gemcitabine resistance, a mouse colon tumor was selected during successive rounds of transplantation with continued treatment of gemcitabine. Expression microarray analysis was applied to determine which genes are consistently and highly overexpressed or underexpressed in the resistant versus the nonresistant tumor. For the statistical interpretation of the microarray data, a parametric model was implemented, which returns model-based differential gene expression (log-) ratios and their uncertainties. This defined a set of 13 genes, putatively responsible for the gemcitabine resistance in solid tumors. One of these, RRM1, was previously identified as an important marker for gemcitabine resistance in human cell lines. Five of the 13 genes, including RRM1, are located within a 3 Mb region at chromosome 7E1 of which four are highly overexpressed, suggesting a chromosomal amplification. Therefore, chromosomal copy number changes were measured, using oligo array comparative genomic hybridization. A narrow and high amplification area was identified on 7E1 that encompassed all five genes. In addition, reduced RNA expression of two other genes at 8E1 encoding COX4I1 and RPL13 could be explained by a decrease in chromosomal copy number on chromosome 8. In conclusion, the array comparative genomic hybridization biologically validates our statistical approach and shows that gemcitabine is capable to select for chromosomally aberrant tumor cells, where changed gene expression levels lead to drug resistance.

Published
2005
Full Text
View/download PDF

29. Preclinical emergence of vandetanib as a potent antitumour agent in mesothelioma: molecular mechanisms underlying its synergistic interaction with pemetrexed and carboplatin

Author

Giovannetti, E, primary, Zucali, P A, additional, Assaraf, Y G, additional, Leon, L G, additional, Smid, K, additional, Alecci, C, additional, Giancola, F, additional, Destro, A, additional, Gianoncelli, L, additional, Lorenzi, E, additional, Roncalli, M, additional, Santoro, A, additional, and Peters, G J, additional

Published
2011
Full Text
View/download PDF

40. Prognostic role of thymidylate synthase, thymidine phosphorylase/platelet-derived endothelial cell growth factor, and proliferation markers in colorectal cancer

Author

Triest, B. van, Pinedo, H.M., Blaauwgeers, J.L., Diest, P.J. van, Schoenmakers, P.S., Voorn, D.A., Smid, K., Hoekman, K., Hoitsma, H.F., Peters, G.J., Triest, B. van, Pinedo, H.M., Blaauwgeers, J.L., Diest, P.J. van, Schoenmakers, P.S., Voorn, D.A., Smid, K., Hoekman, K., Hoitsma, H.F., and Peters, G.J.

Abstract

Item does not contain fulltext

Published
2000

48. Antiproliferative Activity and Mechanism of Action of Fatty Acid Derivatives of Gemcitabine in Leukemia and Solid Tumor Cell Lines and in Human Xenografts

Author

Bergman, A. M., primary, Kuiper, C. M., additional, Noordhuis, P., additional, Smid, K., additional, Voorn, D. A., additional, Comijn, E. M., additional, Myhren, F., additional, Sandvold, M. L., additional, Hendriks, H. R., additional, Fodstad, Ø., additional, Breistøl, K., additional, and Peters, G. J., additional

Published
2004
Full Text
View/download PDF

Catalog

Books, media, physical & digital resources
See catalog results