Murakami Y.,Kyoto University |
Tanaka M.,Tokyo Medical University |
Toyoda H.,Ogaki Municipal Hospital |
Hayashi K.,DNA Chip Research Inc. |
And 3 more authors.
BMC Medical Genomics | Year: 2010
Background. HCV infection frequently induces chronic liver diseases. The current standard treatment for chronic hepatitis (CH) C combines pegylated interferon (IFN) and ribavirin, and is less than ideal due to undesirable effects. MicroRNAs (miRNAs) are endogenous small non-coding RNAs that control gene expression by degrading or suppressing the translation of target mRNAs. In this study we administered the standard combination treatment to CHC patients. We then examined their miRNA expression profiles in order to identify the miRNAs that were associated with each patient's drug response. Methods. 99 CHC patients with no anti-viral therapy history were enrolled. The expression level of 470 mature miRNAs found their biopsy specimen, obtained prior to the combination therapy, were quantified using microarray analysis. The miRNA expression pattern was classified based on the final virological response to the combination therapy. Monte Carlo Cross Validation (MCCV) was used to validate the outcome of the prediction based on the miRNA expression profile. Results. We found that the expression level of 9 miRNAs were significantly different in the sustained virological response (SVR) and non-responder (NR) groups. MCCV revealed an accuracy, sensitivity, and specificity of 70.5%, 76.5% and 63.3% in SVR and non-SVR and 70.0%, 67.5%, and 73.7% in relapse (R) and NR, respectively. Conclusions. The hepatic miRNA expression pattern that exists in CHC patients before combination therapy is associated with their therapeutic outcome. This information can be utilized as a novel biomarker to predict drug response and can also be applied to developing novel anti-viral therapy for CHC patients. © 2010 Murakami et al; licensee BioMed Central Ltd. Source
DNA Chip Research Inc., Saitama University and Keio University | Date: 2011-11-17
The object of the invention is to find a simple biomarker with high reproducibility with regard to a method for evaluating the activity of the condition and progression of rheumatoid arthritis disease and provide an effective evaluation method therefor. The invention is to provide a method for determining the value of a rheumatoid arthritis-linked indicator in a subject, the method being characterized by comprising a step for measuring the amount of expression of the FAM20A gene in blood collected from the subject, a step for analyzing the measured amount of expression using a gene expression profile that is prepared in advance and correlates with the indicator and a step for estimating the value of the indicator in the subject on the basis of the analysis results.
DNA Chip Research Inc. and Osaka Prefectural Hospital Organization | Date: 2012-05-16
The object of the invention is to provide a method for quantitatively assessing the degree of progression of a malignant neoplasm in a patient who has been medicated. Provided is a method for assessing the progression of the clinical state of a malignant neoplasm in a subject who has been administered with a medicine for treating the malignant neoplasm, the method being characterized by comprising: (1) a step of determining the ratio of DNA molecules having an activation mutation that serves as an activation marker for the medicine to DNA molecules having a normal marker gene in DNA in the blood from the subject; (2) a step of determining the ratio of DNA molecules having a resistance mutation that serves as a resistance marker for the medicine to DNA molecules having a normal marker gene in the DNA in the blood from the subject; and (3) a step of comparing a value obtained in the step (2) with a value obtained in the step (1) to thereby assess whether or not the malignant neoplasm in the subject has acquired resistance to the treatment with the medicine.
Yamaoka M.,Osaka University |
Maeda N.,Osaka University |
Nakamura S.,DNA Chip Research Inc. |
Kashine S.,Osaka University |
And 8 more authors.
PLoS ONE | Year: 2012
Evidence suggests that visceral fat accumulation plays a central role in the development of metabolic syndrome. Excess visceral fat causes local chronic low-grade inflammation and dysregulation of adipocytokines, which contribute in the pathogenesis of the metabolic syndrome. These changes may affect the gene expression in peripheral blood cells. This study for the first time examined the association between visceral fat adiposity and gene expression profile in peripheral blood cells. The gene expression profile was analyzed in peripheral blood cells from 28 obese subjects by microarray analysis. Reverse transcription-polymerase chain reaction (RT-PCR) was performed using peripheral blood cells from 57 obese subjects. Obesity was defined as body mass index (BMI) greater than 25 kg/m2 according to the Japanese criteria, and the estimated visceral fat area (eVFA) was measured by abdominal bioelectrical impedance. Analysis of gene expression profile was carried out with Agilent whole human genome 4×44 K oligo-DNA microarray. The expression of several genes related to circadian rhythm, inflammation, and oxidative stress correlated significantly with visceral fat accumulation. Period homolog 1 (PER1) mRNA level in blood cells correlated negatively with visceral fat adiposity. Stepwise multiple regression analysis identified eVFA as a significant determinant of PER1 expression. In conclusion, visceral fat adiposity correlated with the expression of genes related to circadian rhythm and inflammation in peripheral blood cells. © 2012 Yamaoka et al. Source
Itakura H.,Shinagawa East One Medical Clinic |
Kobayashi M.,DNA Chip Research Inc. |
Nakamura S.,DNA Chip Research Inc.
Clinical Nutrition ESPEN | Year: 2015
Background & aims: Type 2 diabetes can lead to arteriosclerosis, renal damage, retinopathy, and several other serious complications. To prevent or delay the progression of this disease, considerable attention has been paid to improve exercise and dietary habits. Chlorella ingestion can reportedly reduce high blood glucose and cholesterol levels in mice and humans, although no studies have critically evaluated the effects of Chlorella on human borderline diabetics. Thus, we conducted a randomized, double-blind placebo-controlled test with volunteer borderline diabetics. Methods: We recruited 57 subjects and randomly divided into a Chlorella ingestion group (n = 28) and a Placebo ingestion group (n = 29). Blood samples were collected every 4 weeks for laboratory tests. Gene expression analyses using peripheral blood cell RNA were performed before and 12 weeks after the trial. Results: A total of 252 genes showed changed expression levels between these two groups. Six of these were type 2 diabetes-associated genes, including resistin, an insulin resistance inducer that exhibited markedly reduced expression with Chlorella ingestion (P = 0.01). Resistin mRNA expression significantly correlated with changes in HbA1c and TNF-α and IL-levels, all of which are strongly associated with glucose metabolism and/or inflammation. Conclusions: Chlorella ingestion may be useful in preventing or ameliorating the course of type 2 diabetes development. In addition, gene expression analysis may be a means to investigate the effects of foods and supplements in humans. © 2015 European Society for Clinical Nutrition and Metabolism. Source