The effect of honey and chamomile mouth washes in the prevention of head and neck radiotherapy –induced stomatitis
Ontology highlight
ABSTRACT:
DISEASE(S): Stomatitis,Oral And Gastrointestinal-inflammatory Bowel Disease,Head And Neck Cancer,Cancer-head And Neck
PROVIDER: 2456220 | ecrin-mdr-crc |
REPOSITORIES: ECRIN MDR
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Project description:Purpose: Decitabine is a deoxycytidine nucleoside derivative inhibitor of DNA-methyltransferases indicated for treatment of myelodysplastic syndrome (MDS). Laboratory evidence shows that pretreatment of AML cell lines can sensitize leukemia cells to chemotherapy and inhibit clonogenic potential. We conducted a randomized study of decitabine when used as priming before standard induction therapy in children with newly diagnosed acute myelogenous leukemia (AML) to evaluate the safety, pharmacokinetics, and any potential early efficacy signal. Exploratory analyses of genomic methylation and RNA expression patterns and minimal residual disease (MRD) were included to elucidate possible biological mechanisms. Methods: This multicenter, randomized, two-arm, open-label study enrolled children ages 1-16 with newly diagnosed de novo AML to either Arm A: daunorubicin, cytarabine, etoposide preceded by a 5-day course of decitabine (experimental arm) or Arm B: daunorubicin, cytarabine, etoposide (control). Following completion of induction therapy, subsequent post-induction treatment was given at the treating physician’s discretion. Patients were monitored for adverse events and samples were collected for PK/PD and biologic analyses. Results: Twenty patients, ages 1-16 years (median 9.4 yrs in both Arms) were treated (10 per Arm). Eighteen of 20 enrolled subjects completed the prescribed treatment. All subjects experienced neutropenia and thrombocytopenia as is expected during AML induction chemotherapy. The most common grade 3 and 4 non-hematologic adverse events observed were caecitis, 2 (20%) subjects in Arm A and 0 (0%) subjects in Arm B; decreased appetite, 3 (30%) subjects in Arm A and 0 (0%) subjects in Arm B; and hypophosphatemia, 2 (20%) subjects in Arm A and 0 (0%) subjects in arm B. One subject in Arm A had appendicitis and colon perforation on Day 6 that led to study discontinuation; the cause was later determined to have been leukemic infiltrate of the bowel wall. Two subjects died (both in Arm A), one of necrotic bowel, pseudomonas sepsis and multisystem organ failure 6 months after study participation and one patient 5 months following study treatment from multisystem organ failure as a complication of stem cell transplant. Plasma concentrations of decitabine showed PK values (mean+SD) of Cmax, 281+113 ng/mL, AUC0-∞, 198+65.3 ng*h/mL, CL, 156+94.6 L/h, Vdss 109+70 L, t1/2 0.48+0.060 h, and median tmax 0.93 h. Overall CR/CRi by morphology was similar between the two treatment arms (92% for the control arm and 100% for the experimental arm). MRD at Day 30 post induction therapy was lower in the control group compared to the decitabine group (67% vs 85% MRD-negative). Changes in DNA epigenetic and RNA expression patterns demonstrated distinct differences involving selective cellular pathways between the two groups of patients comparing diagnostic to day 30 bone marrow samples. Conclusions: This first-in-pediatric trial of epigenetic priming in patients with newly diagnosed AML demonstrates that decitabine pre-treatment followed by standard combination chemotherapy is well tolerated in children with newly diagnosed AML. Morphologic complete responses were similar in both treatment arms. MRD at Day 30 following induction therapy suggests a deeper remission in patients receiving decitabine. No differences were observed between treatment arms in hematologic toxicities although decitabine-treated patients were noted to have more gastrointestinal toxicities, anorexia and hypophosphatemia. Decitabine PK parameters in children were consistent with known adult PK profiles. Molecular changes associated with decitabine pretreatment may be important in the sensitization of clonogenic AML cells. Pre-treatment with decitabine may represent a therapeutic option for use in pediatric AML, when epigenetic modification is a desired focus for treatment.
2017-10-31 | GSE78963 | GEO
Project description:Intervention 1: ?1st Arm: Short course radiotherapy with 25 Gy in 5 fractions with concurrent chemotherapy regimen including Capecitabine 625mg/m2/bid for 5 days and Oxaliplatin 50mg/m2/day for 1 day then one cycle chemotherapy with XELOX regimen (Capecitabine 1000mg/m2/bid for 14 days and Oxaliplatin 130mg/m2/day for 1 day) 3 - 4 weeks after completion of radiotherapy then surgery at least 8 weeks after the radiotherapy last session. Intervention 2: 2nd Arm (Control): Long course radiotherapy with 50 Gy in 25 fractions with concurrent Capecitabine 825mg/m2/bid for 5 days each week then one cycle chemotherapy with XELOX regimen (Capecitabine 1000mg/m2/bid for 14 days and Oxaliplatin 130mg/m2/day for 1 day) 3 - 4 weeks after completion of radiotherapy then surgery at least 8 weeks after the radiotherapy last session.;Treatment - Drugs;Treatment - Drugs;?1st Arm: Short course radiotherapy with 25 Gy in 5 fractions with concurrent chemotherapy regimen including Capecitabine 625mg/m2/bid for 5 days and Oxaliplatin 50mg/m2/day for 1 day then one cycle chemotherapy with XELOX regimen (Capecitabine 1000mg/m2/bid for 14 days and Oxaliplatin 130mg/m2/day for 1 day) 3 - 4 weeks after completion of radiotherapy then surgery at least 8 weeks after the radiotherapy last session.;2nd Arm (Control): Long course radiotherapy with 50 Gy in 25 fractions with concurrent Capecitabine 825mg/m2/bid for 5 days each week then one cycle chemotherapy with XELOX regimen (Capecitabine 1000mg/m2/bid for 14 days and Oxaliplatin 130mg/m2/day for 1 day) 3 - 4 weeks after completion of radiotherapy then surgery at least 8 weeks after the radiotherapy last session.
Primary outcome(s): Complications. Timepoint: At the Initiation of Radiotherapy up to one month after surgery. Method of measurement: Common terminology criteria for cancer related therapy adverse events.
Study Design: Randomization: Randomized, Blinding: Not blinded, Placebo: Not used, Assignment: Parallel, Purpose: Treatment.
| 2495080 | ecrin-mdr-crc
Project description:Healthy flavivirus-naive volunteers (n=11) were infected with the live attenuated dengue serotype 2 challenge virus (rDEN2delta30) as the control arm of a dengue vaccine challenge trial. Whole blood RNA was collected in Paxgene tubes for expression profiling prior to infection (day 0), and on days 8, and 28 after rDEN2delta30 infection. Whole blood RNA was depleted of globin-and rRNA transcripts and equal amounts of depleted RNAs were used to generate libraries for SE 100 RNA sequencing per sample on by Illumina. To generate technical replicates, each library was run in different flow cells/lanes and aggregated to an average of approximately 26 million reads total per sample with <1% variation in counts across lanes in a given sample. Comparisons of gene expression in count-normalized samples were focused on analysis of grouping data by timepoint as well as by examining consensus intra-subject timepoint-associated gene expression changes after rDEN2delta30 infection, focusing on pairwise comparisons (Day 8 vs Day 0, Day 28 vs Day 8, and Day 28 vs,. Day 0).
2020-06-12 | GSE152255 | GEO
Project description:Genome wide DNA methylation profiling of human blood samples. The Illumina Infinium EPIC DNA methylation Beadchip was used to obtain DNA methylation profiles Survival has increased in early stage breast cancer (BC), and the late effects of cancer treatment can persist for decades. The molecular mechanisms underlying acceleration of age-related diseases after chemotherapy and radiotherapy are poorly understood. We examined epigenetic changes in peripheral blood in early stage BC patients undergoing either adjuvant radiotherapy, or adjuvant chemotherapy and radiotherapy. DNA methylation experiments were performed on peripheral blood samples from women collected prior to and following completion of adjuvant therapy. Methylation profiles were used to estimate three measures of epigenetic age acceleration - intrinsic, extrinsic, and phenotypic - as well as estimated cell counts.
2020-06-23 | GSE140038 | GEO
Project description:To gain further insights into a larger number of processes potentially altered by high nickel (Ni), we performed a transcriptional profiling of whole roots of Arabidopsis thaliana accession Columbia-0 (Col-0) exposed to 100 µM nickel, a concentration that induces slight chlorosis and intermediate inhibition of root and shoot growth.
2019-10-16 | GSE138859 | GEO
Project description:<p>The SUCCESS-A Study (<a href="http://www.success-studie.de">http://www.success-studie.de</a>) is a randomized Phase III study of response to treatment of early primary breast cancer with adjuvant therapy after surgical resection. The primary outcome is disease-free survival and secondary outcomes are overall survival and toxicity. The study design includes comparison of two pairs of treatment regimes performed in sequence. The first randomization contrasts treatment with and without Gemcitabine (3 cycles of Epirubicin-Fluorouracil-Cyclophosphamide(FEC)-chemotherapy, followed by 3 cycles of Docetaxel(D)-chemotherapy versus 3 cycles of Epirubicin-Fluorouracil-Cyclophosphamide(FEC), followed by 3 cycles of Gemcitabine-Docetaxel(DG)-chemotherapy). The second randomization contrasts treatment with Zoledronate for two versus five years. Patients were recruited from 2005 to 2007 and a total of 3754 patients were included from 250 study sites across Germany. Genome-wide SNP microarray data and phenotype outcomes for the first phase of the study (treatment with and without Gemcitabine) are included in the GARNET (Genomics and Randomized Trials Network) pharmacogenomic study in this dbGaP submission. (The Zoledronate treatments are still underway).</p> <p>SUCCESS-A is a an open-label, multicenter, 2x2 factorial design, randomized controlled, Phase III study comparing the disease free survival after randomization in patients treated with 3 cycles of Epirubicin-Fluorouracil-Cyclophosphamide(FEC)-chemotherapy, followed by 3 cycles of Docetaxel(D)-chemotherapy versus 3 cycles of Epirubicin-Fluorouracil-Cyclophosphamide(FEC), followed by 3 cycles of Gemcitabine-Docetaxel(DG)-chemotherapy, and to compare the disease free survival after randomization in patients treated with 2 years of Zoledronate versus 5 years of Zoledronate in patients with early primary breast cancer. Patients were required to have histopathological proof of axillary lymph node metastases (pN1-3) or high risk node negative, defined as: pT>2 or histopathological grade 3, or age , ≤ 35 or negative hormone receptor, but were not allowed to have evidence of distant disease. Patients were entered into the study no later than 6 weeks after complete resection of the primary tumor. No antineoplastic treatment other than surgical treatment, the defined cytotoxic and endocrine treatment, and radiotherapy was allowed prior to study entry and during the course of the study. After surgery, leading to complete resection of the invasive and intraductal components of the primary tumor, patients were randomized to one of the following two treatments for the first phase of the project (which is included in this GARNET pharmacogenomics study):</p> <p><b>AA</b>: 3 cycles of 5-Fluorouracil 500 mg/m² i.v. body surface area and Epirubicin 100 mg/m² i.v. and Cyclophosphamide 500 mg/m² i.v., (FEC100), each administered on day 1, repeated on day 22, subsequently followed by 3 cycles of Docetaxel 75 mg/m² body surface area i.v. (D), and Gemcitabine 1000 mg/m² i.v. (30 min infusion) (G), administered on day 1, followed by Gemcitabine 1000 mg/m² i.v. (30 min infusion) on day 8, repeated on day22</p> <p><b>AB</b>: 3 cycles of 5-Fluorouracil 500 mg/m² i.v. body surface area and Epirubicin 100 mg/m² i.v. and Cyclophosphamide 500 mg/m² i.v., (FEC100), each administered on day 1, repeated on day 22, subsequently followed by 3 cycles of Docetaxel 100 mg/m² body surface area i.v. (D), administered on day 1, repeated on day 22</p> <p>A second randomization was made for assigning patients to one of the following two subsequent treatments for the second phase of the project (NOT included in the pharmacogenetic study in this dbGaP submission):</p> <p><b>BA</b>: Zoledronic acid 4 mg i.v., every 3 months for the duration of two years, subsequently followed by zoledronic acid 4 mg i.v., every 6 months for the duration of additional three years</p> <p><b>BB</b>: Zoledronic acid 4 mg i.v., every 3 months for the duration of two years</p> <p>Patients with positive hormone receptor status (≥10% positively stained cells for estrogen and/or progesterone) of the primary tumor were recommended to receive Tamoxifen treatment 20 mg p.o. per day for 2 years, after the end of chemotherapy . Subsequent to chemotherapy, postmenopausal patients with positive hormone receptor status were recommended to be treated with Anastrozole (Arimidex®) 1 mg p.o. for additional 3 years, premenopausal patients will continue Tamoxifen treatment for those additional 3 years. In addition to tamoxifen, all patients with positive hormone receptor status of the primary tumor and under the age of 40 or restart of menstrual bleeding within 6 months after the completion of cytostatic treatment or with premenopausal hormone levels as defined below were recommended to receive Goserelin (Zoladex®) 3.6 mg subcutaneously every 4 weeks over a period of 2 years following chemotherapy. Premenopausal endocrine status will be assumed, if the following serum levels are met: LH < 20 mIE/ml, FSH < 20 mIE/ml and E2 > 20 pg/ml. Endocrine therapy will start after the end of chemotherapy.</p> <p>All patients with breast conserving therapy or more than 3 axillary lymph node metastases or in the following cases after mastectomy will receive adjuvant radiotherapy: T3/T4-carcinoma, T2-carcinoma > 3 cm, multicentric tumor growth, lymphangiosis carcinomatosa or vessel involvement, involvement of the pectoralis fascia or a safety margin < 5 mm. Radiotherapy was usually performed after the chemotherapy and parallel to the beginning of the zoledronic acid therapy.</p> <p>Initially, DNA was extracted for performing SNP microarray assays using blood collected at baseline prior to the first randomization. However, the first set of SNP microarray results indicated a quality problem with approximately 50% of the DNA samples. A majority of the problematic samples were replaced with DNA extracted from redrawn blood. The remaining problematic samples were 'restored' using an Illumina FFPE Restoration procedure. A total of 3322 subjects (1638 from arm AA and 1684 from arm AB) were successfully genotyped. Among those, 1771 were from original blood samples, 1092 from redrawn blood samples and 459 from restored blood samples.</p> <p>The SUCCESS-A study is part of the Genomics and Randomized Trials Network (GARNET, <a href="http://www.garnetstudy.org">http://www.garnetstudy.org</a>) funded by the National Human Genome Research Institute (NHGRI). The overarching goal is to identify novel genetic factors that contribute to disease-free survival for breast cancer patients using different forms of chemotherapy through large-scale genome-wide association studies of treatment response in randomized clinical trials. The study was conducted at the University Hospital Erlangen, Friedrich-Alexander University Erlangen-Nuremberg, Germany. Genotyping was performed at the Johns Hopkins University Center for Inherited Disease Research (CIDR). Data cleaning and harmonization were performed at the GARNET Coordinating Center at the University of Washington.</p>
| phs000547 | dbGaP
Project description:Interventions: Short course radiotherapy with 25 Gy in 5 fractions with concurrent chemotherapy regimen including Capecitabine 850mg/m2/bid for 5 days and Oxaliplatin 85mg/m2/day for 1 day then one cycle chemotherapy with XELOX regimen (Capecitabine 1000mg/m2/bid for 14 days and Oxaliplatin 130mg/m2/day for 1 day) 3 weeks after completion of radiotherapy then surgery 8 weeks after the radiotherapy last session..;Treatment - Other;Short course radiotherapy with 25 Gy in 5 fractions with concurrent chemotherapy regimen including Capecitabine 850mg/m2/bid for 5 days and Oxaliplatin 85mg/m2/day for 1 day then one cycle chemotherapy with XELOX regimen (Capecitabine 1000mg/m2/bid for 14 days and Oxaliplatin 130mg/m2/day for 1 day) 3 weeks after completion of radiotherapy then surgery 8 weeks after the radiotherapy last session.
Primary outcome(s): Complications. Timepoint: At the Initiation of Radiotherapy up to one month after surgery. Method of measurement: Common terminology criteria for cancer related therapy adverse events.
Study Design: Randomization: N/A, Blinding: Not blinded, Placebo: Not used, Assignment: Single, Purpose: Treatment.
| 2491836 | ecrin-mdr-crc
Project description:The aerobic yeast Yarrowia lipolytica is an established model organism to study mitochondrial protein complexes. Here we performed a complexome analysis of intact mitochondria to study the function of NDUFAF1 in the assembly of respiratory complex I. In the ndufaf1 deletion strain the PD module of the membrane arm accumulated but mature complex I was virtually absent.
2022-12-21 | PXD033522 | Pride
Project description:DP-ribosylation factors (Arfs) are small GTPases regulating membrane traffic in the secretory pathway. They are closely related and appear to have overlapping functions, regulators, and effectors. The functional specificity of individual Arfs and the extent of redundancy are still largely unknown. We addressed these questions by CRISPR/Cas9-mediated genomic deletion of the human class I (Arf1/3) and class II (Arf4/5) Arfs, either individually or in combination. Most knockout cell lines were viable with slight growth defects only when lacking Arf1 or Arf4. However, Arf1+4, and Arf4+5 could not be deleted simultaneously. Class I Arfs are non-essential and Arf4 alone is sufficient for viability. Upon Arf1 deletion, the Golgi was enlarged and recruitment of vesicle coats decreased, confirming a major role of Arf1 in vesicle formation at the Golgi. Knockout of Arf4 caused secretion of ER-resident proteins, indicating specific defects in coatomer-dependent ER protein retrieval by KDEL receptors. The knockout cell lines will be useful tools to study other Arf-dependent processes.
2021-11-02 | PXD028846 | Pride
Project description:Mapping the Drosophila melanogaster centromeric heterochromatin by CGH analysis of embryos lacking specific chromosomes or chromosome arms. Nine chromosome or chromosome arm deletions were tested: embryos lacking the entire second chromosome (2En-), 2L (2L-), 2R (2R-), the entire third chromosome (3En-), 3L (3L-), 3R (3R-), the entire fourth chromosome (4En-), the X chromosome (X-), or both X and Y chromosomes (XY-). Control: Blastoderm stage wild type Oregon R embryos. For each experiment 100-150 embryos of the appropriate genotype were collected. DNA from randomly staged 0-8 hr wild type Oregon R embryos was used as reference for all experiments. Embryos with no X chromosome were obtained by crossing attached-X/Y females (C(1)DX, y f) to X/Y males. Embryos with no X and Y chromosomes were obtained by crossing attached-X/Y females (C(1)RM, y2suwawa) to attached-XY males (YSX YL, In(1)EN, y B). The compound II chromosomes RM(2L); RM(2R)=C(2)v and the compound III chromosomes RM(3L); RM(3R)=C(3)se were used to generate 2L- and 2R-, and 3L- and 3R- embryos, respectively. The compound II C(2)EN and compound III C(3)EN st1 cu1es stocks were used to generate embryos deficient for the entire second and third chromosome, respectively. The compound IV C(4)RM, ci1eyR/0 were used to generate embryos deficient for the fourth chromosome. Embryos deficient for chromosome 4 were identified by their defects in denticle belt patterning during late embryogenesis, whereas embryos deficient for other chromosome/chromosome arm were recognized based on their specific phenotypic defects during early embryonic development. All embryos were collected at room temperature.
2012-03-06 | E-GEOD-36260 | biostudies-arrayexpress