Personal dose monitoring of fluorouracil and metabolites of capecitabine(XELODA)in patients with colorectal cancer patients (PersonaX)
Ontology highlight
ABSTRACT:
DISEASE(S): Colorectal Cancer
PROVIDER: 2624254 | ecrin-mdr-crc |
REPOSITORIES: ECRIN MDR
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Project description:Interventions: Blood samples(10 points) are collected after the first administration of capecitabine for pharmacokinetic analysis and cytidine deaminase activity measurement.
Primary outcome(s): To evaluate the correlation AUC of 5-DFUR/AUC of 5-DFCR ratio and cytidine deaminase activity.
Study Design: Single arm Non-randomized
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Project description:CoMet, a fully automated Computational Metabolomics method to predict changes in metabolite levels in cancer cells compared to normal references has been developed and applied to Jurkat T leukemia cells with the goal of testing the following hypothesis: up or down regulation in cancer cells of the expression of genes encoding for metabolic enzymes leads to changes in intracellular metabolite concentrations that contribute to disease progression. Nine metabolites predicted to be lowered in Jurkat cells with respect to normal lymphoblasts were examined: riboflavin, tryptamine, 3-sulfino-L-alanine, menaquinone, dehydroepiandrosterone, α-hydroxystearic acid, hydroxyacetone, seleno-L-methionine and 5,6-dimethylbenzimidazole. All, alone or in combination, exhibited antiproliferative activity. Of eleven metabolites predicted to be increased or unchanged in Jurkat cells, only two (bilirubin and androsterone) exhibited significant antiproliferative activity. These results suggest that cancer cell metabolism may be regulated to reduce the intracellular concentration of certain antiproliferative metabolites, resulting in uninhibited cellular growth and have the implication that many other endogenous metabolites with important roles in carcinogenesis are awaiting discovery. Keywords: cell type
2008-08-04 | GSE9648 | GEO
Project description:MCF7 cells were treated during 90 minuts with 5'DFUR 250uM in presence or absence of NBTI 100nM. RNA from two independent experiments was isolated and hybridization was performed in duplicate in all cases, using reciprocal labelling Keywords: 5'DFUR effect. Time 24h
2006-07-13 | GSE2931 | GEO
Project description:MCF7 cells were treated during 90 min with 5'DFUR 250 uM in presence or absence of NBTI 100nM. The effect was analyzed 4 hours after the beginning of treatment. RNA from two independent experiments was isolated and hybridization was performed in duplicate in all cases, using reciprocal labelling. Keywords: 5'DFUR effect. Time 4h
2006-07-13 | GSE2930 | GEO
Project description:Intervention1: Capecitabine (CJSC Biocad) tablets 500mg: The study will involve patients who receive capecitabine monotherapy. In a monotherapy regimen, capecitabine is administered 1250 mg/m2 twice a day in the morning and evening (total daily dose of 2500 mg/m2) for two weeks followed by 7 days break. Within this study, Capecitabine will be administered orally in the morning of Day 1/Day 2 in the dose of 1250 mg/m2. The drug will be taken within 30 minutes after the meal (breakfast).
Control Intervention1: Xeloda (Capecitabine)tablets 500mg: The study will involve patients who receive capecitabine monotherapy. In a monotherapy regimen, capecitabine is administered 1250 mg/m2 twice a day in the morning and evening (total daily dose of 2500 mg/m2) for two weeks followed by 7 days break. Within this study, Xeloda will be administered orally in the morning of Day 1/Day 2 in the dose of 1250 mg/m2. The drug will be taken within 30 minutes after the meal (breakfast).
Primary outcome(s): Assessment of pharmacokinetic parameters after single administration of the Test drug and the reference drug:
Area under capecitabine «concentration-time» curve at the time of the drug administration up to 12 hours (AUC(0-12))
Timepoint: 0 min, 15 mins, 30 mins, 45 mins, 1hr, 1hr 30 mins, 2 hrs, 3 hrs, 4 hrs, 5 hrs, 6 hrs, 8 hrs, 10 hrs and 12 hrs after administration of the test or reference drug.
Study Design: Randomized, Crossover Trial
Method of generating randomization sequence:Computer generated randomization Method of allocation concealment:Sequentially numbered, sealed, opaque envelopes Blinding and masking:Open Label
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Project description:Transcriptomic analysis of S. maltophilia D457 after one-hour induction with the antibiotic fosfomycin, the intermediate metabolites phosphoenolpyruvate or glyceraldehyde-3-phosphate
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Project description:We found that ERY974 shows only moderate antitumor efficacy in MKN45 non-inflamed tumor in huNOG mice. We also observed that ERY974 + capecitabine increases antitumour efficacy in non-inflamed MKN45 tumours. To identify a mechanism of combination effect, we compared RNA expression of MKN45 tumors treated with ERY974, capecitabine, or combination.
2022-08-21 | GSE211373 | GEO
Project description:This model is from the article:
Restriction point control of the mammalian cell cycle via the cyclin E/Cdk2:p27 complex.
Conradie R, Bruggeman FJ, Ciliberto A, Csikász-Nagy A, Novák B, Westerhoff HV, Snoep JL
FEBS J.2010 Jan; 277(2): 357-67
20015233,
Abstract:
Numerous top-down kinetic models have been constructed to describe the cell cycle. These models have typically been constructed, validated and analyzed using model species (molecular intermediates and proteins) and phenotypic observations, and therefore do not focus on the individual model processes (reaction steps). We have developed a method to: (a) quantify the importance of each of the reaction steps in a kinetic model for the positioning of a switch point [i.e. the restriction point (RP)]; (b) relate this control of reaction steps to their effects on molecular species, using sensitivity and co-control analysis; and thereby (c) go beyond a correlation towards a causal relationship between molecular species and effects. The method is generic and can be applied to responses of any type, but is most useful for the analysis of dynamic and emergent responses such as switch points in the cell cycle. The strength of the analysis is illustrated for an existing mammalian cell cycle model focusing on the RP [Novak B, Tyson J (2004) J Theor Biol230, 563-579]. The reactions in the model with the highest RP control were those involved in: (a) the interplay between retinoblastoma protein and E2F transcription factor; (b) those synthesizing the delayed response genes and cyclin D/Cdk4 in response to growth signals; (c) the E2F-dependent cyclin E/Cdk2 synthesis reaction; as well as (d) p27 formation reactions. Nine of the 23 intermediates were shown to have a good correlation between their concentration control and RP control. Sensitivity and co-control analysis indicated that the strongest control of the RP is mediated via the cyclin E/Cdk2:p27 complex concentration. Any perturbation of the RP could be related to a change in the concentration of this complex; apparent effects of other molecular species were indirect and always worked through cyclin E/Cdk2:p27, indicating a causal relationship between this complex and the positioning of the RP.
The rate constants presented in the paper have units [per tenth of an hour] and have been changed here to [per hour] (e.g. k16 = 0.25 not 0.025); for further confirmation of the correctness of this change, see the original model (Novak, J Theor Biol 2004 230:563).
2024-09-02 | BIOMD0000000265 | BioModels
Project description:This is a prospective time-and-motion study to document and compare the time used in preparation, dispensing and administration for capecitabine/oxaliplatin (XELOX) versus IV 5-FU/leucovorin/oxaliplatin (FOLFOX4) regimens in colorectal cancer (CRC) patients.
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Project description:This is a multi-centre prospective non-interventional study designed to evaluate the effects of patient age on the pharmacokinetics of capecitabine and its metabolites 5’DFCR, 5’DFUR, and 5-FU. In addition, the study will assess the correlation between the pharmacokinetic parameters calculated and cytidine deaminase, biomarkers of aging, clinical frailty, treatment outcome, and toxicity. To be enrolled, patients must have breast or colorectal cancer and be eligible to receive capecitabine monotherapy in accordance with its approved clinical usage in the UK. Treatment will be administered according to NICE guidelines as well as the clinical judgement of the prescribing physician. One hundred patients (50 breast cancer patients, 50 colorectal cancer patients) who are about to start treatment with capecitabine monotherapy will be recruited to the study and undergo study procedures within the first week of treatment.
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