Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1158838 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR30616400_1.fastq.gz | Fastqsanger.gz | |||
| SRR30616400_2.fastq.gz | Fastqsanger.gz | |||
| SRR30628100_1.fastq.gz | Fastqsanger.gz | |||
| SRR30628100_2.fastq.gz | Fastqsanger.gz | |||
| SRR30628200_1.fastq.gz | Fastqsanger.gz |
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Project description:In cancer patients, an elemental diet (ED) reduces adverse effects of chemotherapy, including oral mucositis. However, the detailed mechanism(s) of the healing effects of an ED remains unclear. In this study, the protective effects of the ED, Elental®, were examined against 5-fluorouracil (5-FU)-induced oral mucositis and salivary gland atrophy in mice. Mucositis was induced in female ICR mice by injection of 5-FU. The mice were orally administered Elental® (ED group) or saline (control group). After treatment, whole transcriptome analysis and network analysis were conducted to understand the mechanism(s) of action of Elental® against oral mucositis. Whole transcriptome analysis and Ingenuity Pathways Analysis (IPA) data suggested that Elental® contributed to the recovery of mitochondrial function in 5-FU-damaged salivary glands.
2022-05-05 | GSE196407 | GEO
Project description:To reveal the molecular mechanisms underlying oral ulcerative mucositis-induced pain, we investigated putative pain-associated mediators, pain-related behaviors and gene modulation in a rat oral mucositis model. On day 1 after acetic acid treatment, the mucosal area showed slight redness and swelling but no evidence of ulceration or pain induction. On day 2, oral ulcers were obvious, as was the induction of spontaneous and mechanical pain. In the treated mucosal area, bacterial loading and prostaglandin E2 increased beginning on day 2; no significant changes were observed on day 1. DNA microarray analysis of trigeminal ganglion tissue collected on day 2 identified 32 significantly regulated genes (>1.5-fold change in expression). The up-regulation of the top 3 genes, Hamp (hepcidin antimicrobial peptide), Reg3b (regenerating islet-derived 3β) and Serpina3n (serine peptidase inhibitor A3N), was validated through quantitative RT-PCR. Systemic antibiotic pre-treatment did not increase the mRNA levels. Therefore, we conclude that the oral ulcerative mucositis-induced pain is caused by infectious inflammation of the ulcerative area and stimulates anti-bacterial and anti-peptidase gene expressions in sensory neurons. Oral ulcerative mucositis-induced gene expression in trigeminal ganglion tissue was measured. Ten Wistar rats were divided into the following two groups, control, oral ulcerative mucositis (stomatitis). Five rats were anesthetized with sodium pentobarbital. A piece of filter paper was soaked in 50% acetic acid diluted with water and placed in the labial fornix region of the inferior incisors of rats for 30 sec. Other five rats received only anesthesia without any treatment were used as a control. On day 2 after acetic acid treatment, oral ulcerative mucositis was obvious and trigeminal ganglion tissues in two groups were collected for DNA microarray analysis.
2016-06-15 | E-GEOD-83349 | biostudies-arrayexpress
Project description:Chemotherapy may cause DNA damage within the oral mucosa of cancer patients leading to mucositis, a dose-limiting side effect for effective cancer treatment. We used whole genome gene expression analysis to identify cellular damage to the mucosal tissue occuring two days post induction chemotherapy and identified gene expression patterns that may or may not be predictive of oral mucositis. Keywords: Treatment effect
2009-01-01 | GSE10746 | GEO
Project description:To reveal the molecular mechanisms underlying oral ulcerative mucositis-induced pain, we investigated putative pain-associated mediators, pain-related behaviors and gene modulation in a rat oral mucositis model. On day 1 after acetic acid treatment, the mucosal area showed slight redness and swelling but no evidence of ulceration or pain induction. On day 2, oral ulcers were obvious, as was the induction of spontaneous and mechanical pain. In the treated mucosal area, bacterial loading and prostaglandin E2 increased beginning on day 2; no significant changes were observed on day 1. DNA microarray analysis of trigeminal ganglion tissue collected on day 2 identified 32 significantly regulated genes (>1.5-fold change in expression). The up-regulation of the top 3 genes, Hamp (hepcidin antimicrobial peptide), Reg3b (regenerating islet-derived 3β) and Serpina3n (serine peptidase inhibitor A3N), was validated through quantitative RT-PCR. Systemic antibiotic pre-treatment did not increase the mRNA levels. Therefore, we conclude that the oral ulcerative mucositis-induced pain is caused by infectious inflammation of the ulcerative area and stimulates anti-bacterial and anti-peptidase gene expressions in sensory neurons.
2016-06-15 | GSE83349 | GEO
Project description:Background Toxicity of the oral and gastrointestinal mucosa induced by high-dose melphalan is a clinical challenge with no documented prophylactic interventions or predictive tests. The aim of this study was to describe molecular changes in human oral mucosa and to identify biomarkers correlated with the grade of clinical mucositis. Methods and Findings Ten patients with multiple myeloma (MM) were included. For each patient, we acquired three buccal biopsies, one before, one at 2 days, and one at 20 days after high-dose melphalan administration. We also acquired buccal biopsies from 10 healthy individuals that served as controls. We analyzed the biopsies for global gene expression and performed an immunohistochemical analysis to determine HLA-DRB5 expression. We evaluated associations between clinical mucositis and gene expression profiles. Compared to gene expression levels before and 20 days after therapy, at two days after melphalan treatment, we found gene regulation in the p53 and TNF pathways (MDM2, INPPD5, TIGAR), which favored anti-apoptotic defense, and upregulation of immunoregulatory genes (TREM2, LAMP3) in mucosal dendritic cells. This upregulation was independent of clinical mucositis. HLA-DRB1 and HLA-DRB5 (surface receptors on dendritic cells) were expressed at low levels in all patients with MM, in the subgroup of patients with ulcerative mucositis (UM), and in controls; in contrast, the subgroup with low-grade mucositis (NM) displayed 5–6 fold increases in HLA-DRB1 and HLA-DRB5 expression in the first two biopsies, independent of melphalan treatment. Moreover, different splice variants of HLA-DRB1 were expressed in the UM and NM subgroups. Conclusions Our results revealed that, among patients with MM, immunoregulatory genes and genes involved in defense against apoptosis were affected immediately after melphalan administration, independent of the presence of clinical mucositis. Furthermore, our results suggested that the expression levels of HLA-DRB1 and HLA-DRB5 may serve as potential predictive biomarkers for mucositis severity
2016-12-19 | GSE81979 | GEO
Project description:Objectives: In patients with tonsil squamous cell cancer (TSCC), radiation-therapy (RT) induce mucositis, which is clinically challenging with limited prophylactic interventions and no predictive tests. In a pilot study set-up, we performed global gene-expression analysis on human oral mucosa tissue and blood cells to identify differential expressed genes involved in mucositis pathogenesis. Materials and Methods: Eight patients with TSCC had consecutive buccal biopsies and blood samples taken before, after 7 days of RT, and 20 days following RT. We monitored clinical mucositis and applied gene-expression analysis to the tissues. Single biopsies and blood tests from 9 healthy individuals served as controls (CON). Results: In response to RT, we did not register changes in the blood cells, but we found upregulation of both apoptosis inducers and inhibitors in the mucosa: EDA2R and MDM2; and POLH, encoding a polymerase that replicates UV-damaged DNA. Six members of the histone cluster family, e.g., HIST1H3B, involved in nucleosome structure, were downregulated. Genes related to proliferation were also altered: MKI67 (downregulated), encoding Ki-67-proliferation; and KRT16 (upregulated), encoding keratin16, characteristic in early differentiated epithelial cells. None of these alterations were associated to mucositis severity. However, before treatment, LY6G6C, which encodes a surface immunoregulatory protein, was upregulated in NM compared to UM, although not significantly. Conclusion: RT caused divergent changes in genes expression related to DNA damage and proliferation, all independently altered of mucositis severity. LY6G6C may be a potential predictive biomarker for UM following RT. Based on these result, we will design a prospective clinical validation trial, including more patients.
2017-12-22 | GSE103412 | GEO
Project description:Chemotherapy may cause DNA damage within the oral mucosa of cancer patients leading to mucositis, a dose-limiting side effect for effective cancer treatment. We used whole genome gene expression analysis to identify cellular damage to the mucosal tissue occuring two days post induction chemotherapy and identified gene expression patterns that may or may not be predictive of oral mucositis. Experiment Overall Design: Punch buccal biopsies from healthy controls (HC, samples BRENC1, BRENC2, BRENC3, n=3) and five AML patients pre-chemotherapy (Pre-C, samples BREN11, BREN21, BREN41, BREN51, n=4) and (Post-C, samples BREN22, BREN32, BREN42, BREN52, n=4)(Ntotal=11) gave suitable RNA integrity to perform microarray analysis. Samples Pre-C:BREN31 and post-C:BREN12 were not suitable for microarray analysis. Human Genome U133 Plus 2.0 Array (Affymetrix, Santa Clara, CA) was used to conduct gene expression profiling.
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Project description:Pancreatic cancer is the 3rd most prevalent cause of cancer related deaths in United states alone, with over 55000 patients being diagnosed in 2019 alone and nearly as many succumbing to it. Late detection, lack of effective therapy and poor understanding of pancreatic cancer systemically contributes to its poor survival statistics. Obesity and high caloric intake linked co-morbidities like type 2 diabetes (T2D) have been attributed as being risk factors for a number of cancers including pancreatic cancer. Studies on gut microbiome has shown that lifestyle factors as well as diet has a huge effect on the microbial flora of the gut. Further, modulation of gut microbiome has been seen to contribute to effects of intensive insulin therapy in mice on high fat diet. In another study, abnormal gut microbiota was reported to contribute to development of diabetes in Db/Db mice. Recent studies indicate that microbiome and microbial dysbiosis plays a role in not only the onset of disease but also in its outcome. In colorectal cancer, Fusobacterium has been reported to promote therapy resistance. Certain intra-tumoral bacteria have also been shown to elicit chemo-resistance by metabolizing anti-cancerous agents. In pancreatic cancer, studies on altered gut microbiome have been relatively recent. Microbial dysbiosis has been observed to be associated with pancreatic tumor progression. Modulation of microbiome has been shown to affect response to anti-PD1 therapy in this disease as well. However, most of the studies in pancreatic cancer and microbiome have remained focused om immune modulation. In the current study, we observed that in a T2D mouse model, the microbiome changed significantly as the hyperglycemia developed in these animals. Our results further showed that, tumors implanted in the T2D mice responded poorly to Gemcitabine/Paclitaxel (Gem/Pac) standard of care compared to those in the control group. A metabolomic reconstruction of the WGS of the gut microbiota further revealed that an enrichment of bacterial population involved in drug metabolism in the T2D group.
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