Project description:Genome-wide analysis of boswellic acids-mediated gene regulation. The hypothesis tested in the present study was that boswellic acids up-regulate some subset of genes in part thorough demethylation of those promotor regions. Results provide important information on boswellic acids-mediated anti-cancer effects in human colon cancer. Total RNA obtained from the human colorectal cancer SW48 cells treated with DMSO alone or acetyl-11-keto-?-boswellic acid (AKBA).
Project description:Genome wide DNA methylation profiling of colorectal cancer cell lines treated with acetyl-11-keto-β-boswellic acid (AKBA) or 5-aza-2’-deoxycytidine (DAC). The Illumina Infinium 27k Human DNA methylation Beadchip v1.2 was used to obtain DNA methylation profiles across approximately 27,000 CpGs in the colorectal cancer cell line SW48. Samples included non-treated, AKBA-treated, and DAC-treated SW48 cells.
Project description:Genome wide DNA methylation profiling of colorectal cancer cell lines treated with acetyl-11-keto-β-boswellic acid (AKBA) or 5-aza-2’-deoxycytidine (DAC). The Illumina Infinium 27k Human DNA methylation Beadchip v1.2 was used to obtain DNA methylation profiles across approximately 27,000 CpGs in the colorectal cancer cell line SW48. Samples included non-treated, AKBA-treated, and DAC-treated SW48 cells. Bisulphite converted DNA from the 3 samples were hybridised to the Illumina Infinium 27k Human Methylation Beadchip v1.2
Project description:Genome-wide analysis of boswellic acids-mediated gene regulation. The hypothesis tested in the present study was that boswellic acids up-regulate some subset of genes in part thorough demethylation of those promotor regions. Results provide important information on boswellic acids-mediated anti-cancer effects in human colon cancer.
Project description:Interventions: Nucleic acid from tumor tissues and serum SNPs
Primary outcome(s): 1. Tissue biomarkers including mutation, gene expression, and DNA methylation that correlate with efficacy from trifluridine/tipiracil hydrochloride therapy 2. Serum biomarkers including mutation, gene expression, and DNA methylation that correlate with efficacy from trifluridine/tipiracil hydrochloride therapy 3. SNPs that correlate with toxicities from trifluridine/tipiracil hydrochloride therapy
Study Design: Single arm Non-randomized
Project description:Introduction: Pediatric high-grade gliomas (pedHGG) comprise a very poor prognosis. Thus, parents of affected children are increasingly resorting to complementary and alternative medicine (CAM). Among others, one of the most frequently used CAM are boswellic acids (BA). Methods: The therapeutic effectiveness of the three main BA, alpha-boswellic acid (α-BA), beta-boswellic acid (β-BA) and 3-acetyl-11-keto-beta-boswellic acid (AKBA) was analyzed in a histone 3 (H3)-wildtype and a H3.3K27M-mutant pedHGG cell line, either alone or in combination with radiotherapy and/or temozolomide chemotherapy. Cell viability, stemness properties and apoptosis as well as mRNA sequencing and in ovo tumor growth was investigated upon BA treatment. Results: Whereas α-BA and β-BA exert only mild anti-tumor effects in H3WT and H3.3K27M-mutated pedHGG cells, AKBA treatment reduced cell viability and stemness potential especially in H3.3K27M-mutant pedHGG cells. In addition, slight anti-inflammatory effects were observed after AKBA treatment of H3.3K27M-mutant pedHGG cells. However, no effects on apoptosis and in ovo tumor growth were found. Of note, α-BA and β-BA treatment even resulted in tumor promoting effects in both pedHGG cells.
Project description:Colorectal cancer is the third most common cancer. Obesity is a major risk factor with long-lasting effects on the predisposition to colorectal cancer; however, the mechanistic underpinnings remain poorly understood. To explore epigenetic mechanisms involved, we performed whole-genome bisulfite sequencing and RNA-Seq in colonic epithelium from control mice, obese mice, and formerly obese mice. We found that obesity-induced DNA methylation changes reprogrammed the transcriptome leading to a metabolic switch favoring long chain fatty acid oxidation, which is essential to colonic stem cell functions and colon tumorigenesis. Remarkably, persistent changes were observed after weight loss mainly at metabolic and cancer-related genes, underlying the long-term predisposition to colorectal cancer. In summary, we provide the epigenetic and metabolic basis of the link between obesity and colorectal cancer.
