A single-arm, prospective, multicenter, real-world study of efficacy and safety of fuquinitinib combined with capecitabine in maintenance therapy after first-line chemotherapy in metastatic colorectal cancer
Ontology highlight
ABSTRACT:
DISEASE(S): Colorectal Cancer
PROVIDER: 89641 | ecrin-mdr-crc |
REPOSITORIES: ECRIN MDR
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Project description:Interventions: Experimental group:Apatinib 250mg po, qd, continuous taken; XELOX: Oxaliplatin 135 mg/m2 Ivgtt d1, Capecitabine 1000mg/m2 d1-14, q3w;Control group:Bevacizumab 7.5mg/kg, q3w; XELOX: Oxaliplatin 135 mg/m2 Ivgtt d1, Capecitabine 1000mg/m2 d1-14, q3w
Primary outcome(s): Progress-free survival (PFS)
Study Design: Non randomized control
| 2687981 | ecrin-mdr-crc
Project description:Interventions: Experiment group:Kangai injection 60ml ivgtt D1-14 Q21d, combined with chemotherapy: Eloxatin 130mg/m2 2h ivgtt d1, Xeloda 1000mg/m2 bid po d1-14 Q21d;Control group:Chemotherapy: Eloxatin 130mg/m2 2h ivgtt d1, Xeloda 1000mg/m2 bid po d1-14 Q21d
Primary outcome(s): Adverse Reactions
Study Design: Randomized parallel controlled trial
| 2674808 | ecrin-mdr-crc
Project description:Interventions: Group A:Capecitabine 1g/m2 bid d1-14 q3w;Group B:Observation
Primary outcome(s): Time to progression
Study Design: Randomized parallel controlled trial
| 2673059 | ecrin-mdr-crc
Project description:To examine the effects of GSK199 treatment on antibody responses, a synovial antigen array analysis was performed using day 35 sera derived from mice with CIA treated with 30 mg/kg qd, 30 mg/kg bid GSK199 or saline. The synovial antigen arrays contain nearly 200 peptides and proteins, both citrullinated and uncitrullinated, representing candidate antigens in RA. Significance Analysis of Microarrays identified 7 and 14 autoantibody reactivities that were statistically decreased in CIA mice treated with 30 mg/kg qd or 30 mg/kg bid GSK199 respectively, compared to PBS treatment. By comparison, over 150 native and citrullinated epitopes on the arrays did not exhibit significant differences in reactivity. Sera from mice treated with 30 mg/kg GSK199 qd exhibited decreased IgG reactivity to native epitopes such as peptides from human fibrinogen alpha and beta chains and keratin while sera from mice treated with 30 mg/kg bid GSK199 demonstrated decreased IgG reactivity to native epitopes including collagen IV, heat shock protein 65, peptides from human fibrinogen alpha and beta chains (two of which match those that were decreased in the 30 mg/kg qd group), and vimentin as compared to saline controls (q < 0.1%). Decreased autoantibody reactivity to citrullinated peptides from vimentin and fibromodulin were also observed in sera from mice treated with 30 mg/kg bid GSK199 compared to controls treated with saline (q < 0.1%), but not by GSK199 30 mg/kg qd. There were no differences between treatment with GSK199 or saline alone in the levels of autoantibodies to 38 other citrullinated proteins in the array. These data demonstrated that GSK199 treatment decreases the development of autoantibodies in CIA and impairs epitope spreading to a degree similar to that observed with pan-PAD inhibition.
2015-10-08 | GSE69680 | GEO
Project description:We performed RNA sequencing on tumors harvested from OV5398 (ovarian) PDX treated for 40-50 days with either control vehicle (PEG), 100 mg/kg BID INX-315 or 200 mg/kg QD INX315.
2023-11-22 | GSE243151 | GEO
Project description:Interventions: XELOX Capecitabine:2000mg/m2 d1-14 Oxaliplatin:130mg/m2 d1 Q3w
Primary outcome(s): Completion rate of treatment
Study Design: Single arm Non-randomized
| 2623439 | ecrin-mdr-crc
Project description:Metronidazole (15mg/kg BID PO) was given to horses (n=5) with in-dwelling cecal cannulas. The study was suspended after the fifth dose (day 3) due to adverse gastrointestinal effects. Cecal and fecal samples were obtained before and after (Days days -52, -28, -14, 0, 7, 14, 28 and 52) metronidazole administration. The metabolome was characterized by mass spectrometry-based methods. Fecal, but not cecal metabolites were affected by metronidazole. The fecal metabolites affected represented diverse metabolic pathways such as nucleic acid metabolism, secondary bile metabolism, fatty acid synthesis/degradation/elongation or metabolism and sugar metabolism.
2019-09-04 | ST001248 | MetabolomicsWorkbench
Project description:Interventions: XELOX+BEV Capecitabine:2000mg/m2 d1-14 Oxaliplatin:130mg/m2 d1 Bevacizumab:7.5mg/kg d1 Q3w Discontinuation of oxaliplatin when neurotoxicity develops >=Grade2
Primary outcome(s): Rate of Grade3 neuropathy
Study Design: Single arm Non-randomized
| 2631347 | ecrin-mdr-crc
Project description:Interventions: Combination treatment using cetuximab, cobimetinib and palbociclib.
This is a two part open label study using escalating doses of these drugs.
Phase 1 will enroll 3-6 patients in one of 6 Cohorts, for dose escalation.
The initial dose escalation will start at cetuximab 150mg/m2 intravenously (IV) + cobimetinib 20 mg orally once daily (po qd) + palbociclib 50mg orally once daily (po qd), for Cohort 1.
Cohort 2 = cetuximab 150mg/m2 IV + cobimetinib 20 mg po qd + palbociclib 75mg po qd.
Cohort 3 = cetuximab 150mg/m2 IV + cobimetinib 40 mg po qd + palbociclib 75mg po qd.
Cohort 4 = cetuximab 150mg/m2 IV + cobimetinib 60 mg po qd + palbociclib 75mg po qd.
Cohort 5 = cetuximab 200mg/m2 IV + cobimetinib 60 mg po qd + palbociclib 75mg po qd.
Cohort 6 = cetuximab 250mg/m2 IV + cobimetinib 60 mg po qd + palbociclib 100mg po qd.
Cetuximab will be administered weekly via intravenous infusion.
Cobimetinib will be taken orally once daily for the first 21 consecutive days in a 28 day treatment cycle. Cobimetinib will be taken in tablet form.
Palbociclib will be taken orally once daily for first 21 consecutive days in a 28 day treatment cycle. Palbociclib will be taken in capsule form.
Neither of these two drugs will be given in the last 7 days of this 28 day cycle.
Cohorts of 3 patients will be enrolled at each dose level (with the option of up to six patients for each cohort if necessary) to assess toxicity. Each patient will participate in only one cohort to determine dose limiting toxicities of the combination. Patients at each dose level will be treated and observed through the end of the first cycle before treatment of subjects at the next higher dose level can begin.
Cohorts 1 to 6 will randomly assign consecutive patien
Primary outcome(s): Phase 1: Determination of Dose Limiting Toxicity (DLT). A DLT will be defined using the National Cancer Institute (NCI) Common Toxicity Criteria for Adverse Events (CTCAE) v 5.0
[Phase 1 DLTs will be assessed during the first cycle of treatment (28 days) and are events that are considered possiby related to the study drug combination for each cohort. After the treatment of each cohort, data will be reviewed to assess patient status and study drug related toxicities from the current cohort before deciding the escalation plan and dose level for the next cohort.
];Phase 2: Determination of Objective Response Rate as determined by MRI scanning with RECIST criteria reporting[Phase 2: patients will be reviewed for objective response rate after at least 2 treatment cycles]
Study Design: Purpose: Treatment; Allocation: Non-randomised trial; Masking: Open (masking not used);Assignment: Other;Type of endpoint: Safety
| 2473029 | ecrin-mdr-crc
Project description:Background: Clenbuterol, a beta2-adrenergic receptor agonist, is used therapeutically to treat respiratory conditions in the horse. However, by virtue of its mechanism of action it has been suggested that clenbuterol may also have repartitioning affects in horses and as such the potential to affect performance. Clenbuterol decreases the percent fat and increases fat-free mass following high dose administration in combination with intense exercise in horses. In the current study, microarray analysis and real-time PCR were used to study the temporal effects of low and high dose chronic clenbuterol administration on differential gene expression of several skeletal muscle myosin heavy chains, genes involved in lipid metabolism and the β2-adrenergic receptor. The effect of clenbuterol administration on differential gene expression has not been previously reported in the horse, therefore the primary objective of the current study was to describe clenbuterol-induced temporal changes in gene expression following chronic oral administration of clenbuterol at both high and low doses. Steady state clenbuterol concentrations were achieved at approximately 50 hours post administration of the first dose for the low dose regimen and at approximately 18-19 days (10 days post administration of 3.2 μg/kg) for the escalating dosing regimen. Following chronic administration of the low dose (0.8 µg/kg BID) of clenbuterol, a total of 114 genes were differentially expressed, however, none of these changes were found to be significant following FDR adjustment of the p-values. A total of 7,093 genes were differentially expressed with 3,623 genes up regulated and 3,470 genes down regulated following chronic high dose administration. Of the genes selected for further study by real-time PCR, down-regulation of genes encoding myosin heavy chains 2 and 7, steroyl CoA desaturase and the β2-adrenergic receptor were noted. For most genes, expression levels returned towards baseline levels following cessation of drug administration. Conclusion: This study showed no evidence of modified gene expression following chronic low dose administration of clenbuterol to horses. However, following chronic administration of high doses of clenbuterol alterations were noted in transcripts encoding various myosin heavy chains, lipid metabolizing enzymes and the β2-adrenergic receptor. Five healthy horses were studied. Twenty-two of the horses received 0.8 µg/kg clenbuterol PO BID for 30 days and an additional 4 horses received 0.8 µg/kg, BID x 3 days; 1.6 µg/kg, BID x 3 days; 2.4 µg/kg, BID x 3 days; 3.2 µg/kg, BID for 21 days. Muscle biopsy samples were collected one day prior to administration of the first dose of clenbuterol and at a number of times post drug administration. A final sample was collected one-week post administration of the final dose (35 days post administration of the first dose). The tissue was transferred to a cryovial containing RNAlater (Qiagen Inc, Valencia, CA) and stored at -20° C until processed. Total RNA was purified using a miRNeasy Mini kit (RNeasy Mini, Qiagen Inc, Valencia, CA) and following the manufacturerâs instructions. Total RNA integrity was assessed using the Experion Automated Electrophoresis System (Bio-rad, Hercules, CA). Only RNA samples with RIN ⥠8 and 260/280 ratios between 1.7 and 2.1 were used. Equine specific microarrays (EquGene-1.0-st; Affymetrix, Santa Clara, CA), containing expression profiling of 30,559 well-characterized genes using 504,603 probes were utilized. To reduce biological noise as a result of genetic variability, each horse was analyzed separately and served as their own control for comparison of baseline samples to day 14 (low dose administration) or day 28 (escalating dose regimen). Five biological replicates per time point were tested. Purified total RNA (5 µg) was used for cDNA synthesis in accordance with the Ambion® WT Expression assay kit (Affymetrix, Santa Clara, CA) manufacturerâs protocol. In vitro transcription was used to incorporate biotin labels using the GeneChip® WT Terminal Labeling system (Affymetrix, Santa Clara, CA) and samples hybridized to the Equine microarray. Arrays were washed and stained on a Fluidics Station 450 (Affymetrix, Santa Clara, CA) and scanned on a GeneChip Scanner 3000 (Affymetrix, Santa Clara, CA) in accordance with manufacturerâs protocols. The microarrays were evaluated for differential gene expression using Transcriptome Analysis Console (TAC) and for hybridization quality control using Expression Console Software (Affymetrix, Santa Clara, CA). In brief, a total of five Cell Intensity Files were generated per time point, uploaded and normalized under the following conditions: PM (perfect match)-only as a PM intensity adjustment and the Robust Multichip Analysis (RMA) quantification method. For evaluation of the assays performance the number of differentially expressed genes detected between baseline and day 14 (low dose administration) or day 28 (escalating dose regimen) were assessed. Based on the TAC software userâs manual, genes with mean transformed ratios significantly less than -2 and larger than +2 were considered significantly regulated. A number of the significant genes were selected by filtering the genes using an ANOVA (p value < 0.05). A Pearson's correlation coefficient was used to calculate linear dependence between time point and baseline samples to evaluate the correlation coefficient, where 1 was a positive correlation and 0 was no correlation. For each probeset, expression at day 14 (low dose administration) or day 28 (escalating dose regimen) was compared to expression at baseline in the same horse using a paired t-test. Fold changes and their confidence intervals were calculated by exponentiating (base 2) the mean within-horse difference in expression for each gene and the associated t confidence intervals. P-values were adjusted for multiple testing using the False Discovery Rate (FDR) method. Analyses were conducted using the statistical software environment R, version 3.0.2 (R Core Team, 2013).
2016-03-24 | E-GEOD-79559 | biostudies-arrayexpress