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Search Results: 1 - 10 of 1110 matches for " Kenta Masuda "
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Epigenetic Aberrant Hypermethylation of DNA in Endometrial Cancer: Application as a Biomarker  [PDF]
Asuka Ono, Iori Kisu, Kouji Banno, Megumi Yanokura, Kenta Masuda, Yusuke Kobayashi, Kosuke Tsuji, Arisa Ueki, Wataru Yamagami, Hiroyuki Nomura, Nobuyuki Susumu, Daisuke Aoki
Journal of Cancer Therapy (JCT) , 2011, DOI: 10.4236/jct.2011.25082
Abstract: Endometrial cancer is the seventh most common cancer worldwide among females and accounts for about 40% of cancers of the uterus in Japan. An increase in incidence and a reduction in onset age of this disease are also likely, which makes it important to define the pathogenesis and develop effective treatment. However, the mechanism of canceration in the endometrium is unclear and development of endometrial cancer cannot be explained only by mutations of cancer-related genes. In contrast, epigenetic analyses have shown the importance of aberrant DNA hypermethylation in the canceration mechanism. In development of type 1 endometrial cancer, breakdown of the DNA mismatch repair system plays a large role, with changes in the human mutL homologue 1 (hMLH1) gene being of most importance. Studies to detect aberrant DNA hypermethylation of cancer cells present in microscopic amounts in vivo and to apply these data to diagnosis of cancer have been started. Epigenetic changes have also been examined as a marker of sensitivity to anticancer drugs. Aberrant hypermethylation of checkpoint with forkhead-associated and ring finger (CHFR), a mitotic phase checkpoint gene, is correlated with sensitivity to treatment with microtubule inhibitors and may be a marker for the response of endometrial cancer to anticancer drugs. Epigenetic aberrant DNA methylation of other genes may also be useful as clinical biomarkers for diagnosis and treatment of endometrial cancer.
Metformin: A possible drug for treatment of endometrial cancer  [PDF]
Kosuke Tsuji, Iori Kisu, Kouji Banno, Megumi Yanokura, Arisa Ueki, Yusuke Kobayashi, Wataru Yamagami, Hiroyuki Nomura, Nobuyuki Susumu, Daisuke Aoki, Kenta Masuda
Open Journal of Obstetrics and Gynecology (OJOG) , 2012, DOI: 10.4236/ojog.2012.21001
Abstract: Metformin is a widely used first-line drug for treatment of type 2 diabetes mellitus. In recent years, it has been reported that administration of metformin can reduce carcinogenic risk and inhibit proliferation of cancer cells including those from glioma and breast cancer. The underlying mechanism is thought to involve increased LKB-1 phosphorylation induced by metformin, followed by LKB-1 phosphorylation and activation of AMP-activated protein kinase (AMPK), which then inhibits the mammalian target of rapamycin (mTOR) pathway and results in inhibition of cell proliferation. In endometrial cancer, metformin causes cell cycle arrest in vitro, reduces hTERT mRNA, inhibits the mTOR pathway via AMPK, and is involved in inhibition of phosphorylation of S6 ribosomal protein (S6RP). Metformin promotes expression of progesterone receptor by an action opposite to that of insulin-like growth factor-2 (IGF-2) when used in combination with medroxyprogesterone acetate. This enhances the antitumor effect and this approach may be applicable in a clinical setting.
The Impact of Bank Health on Coordination among Creditors  [PDF]
Kenta Toyofuku
Theoretical Economics Letters (TEL) , 2013, DOI: 10.4236/tel.2013.32018
Abstract:

We investigate how the health of a relationship bank impacts upon coordination among creditors and how it affects the firms behavior. We show that if the relationship bank is healthy, creditors coordinate each other and the firm takes an efficient action but if it becomes financially distressed, a coordination problem arises ex post and the inefficient liquidation of the firms projects may occur. This coordination failure, in turn, increases the interest payments ex ante so that the firm is more likely to choose an inefficient action.

Time-Frequency and Nonlinear Analysis of Tidal Data Observed on the Kuroshio Path  [PDF]
Kenta Kirimoto
International Journal of Modern Nonlinear Theory and Application (IJMNTA) , 2016, DOI: 10.4236/ijmnta.2016.54015
Abstract: The tidal data of Kushimoto and Uragami on flow path of Kuroshio from 2004 to 2005 are investigated and discussed by time-frequency methods and nonlinear methods in this paper. These analyzing methods based on mathematical science show us new findings about the tidal motion observed on Kuroshio flow path. On the time-frequency analysis, 12 hours component and 24 hours component swing during the period of 350 hours and 320 hours respectively. However, any remarkable differences or changes depending on Kuroshio flow path weren’t seen on the result of time-frequency analysis. On the nonlinear analysis, a periodical structure has seen on the mutual information of tidal difference data, while Kuroshio flow is stable. In addition, the mutual information showed a characteristic of randomness and irregularity, while Kuroshio flow is unstable. The important results brought us a new finding such as classification of tidal motion regardless of the flow path of Kuroshio.
Effects of Emotional Valence (Positive or Negative Visual Images) and Arousal Levels (High or Low Arousal Levels) on the Useful Field of View  [PDF]
Naoko Masuda
Psychology (PSYCH) , 2015, DOI: 10.4236/psych.2015.64045
Abstract: One of two emotional valence (positive or negative) images and two arousal (high or low) images was presented for 500 ms to participants. After the image vanished from the screen, a letter was presented in the central visual field, while a number was also presented in one of the peripheral visual fields (upper right, upper left, bottom right, and bottom left). There were four conditions of degree of eccentricity of the presented number. The participants identified both the letter and number simultaneously. By calculating the correct performance rate of the peripheral identification task, the range of the useful field of view (UFOV) was speculated. Results showed that performance rates of the central and peripheral tasks were worse for the high arousal, negative emotion stimuli compared with the other three conditions. Moreover, performance rates of the peripheral task were better for the positive emotion conditions than those for the negative emotion conditions when the stimulus eccentricities were 3 or 12 degrees. We concluded that the range of the UFOV could be affected by the interaction between the emotional valence and arousal level of visual stimuli. This study was the first report that emotional valence and arousal level interacted each other and did affect our human visual cognition.
Candidate Biomarkers for Genetic and Clinicopathological Diagnosis of Endometrial Cancer
Kouji Banno,Yuya Nogami,Iori Kisu,Megumi Yanokura,Kiyoko Umene,Kenta Masuda,Yusuke Kobayashi,Wataru Yamagami,Nobuyuki Susumu,Daisuke Aoki
International Journal of Molecular Sciences , 2013, DOI: 10.3390/ijms140612123
Abstract: The recent increase in the frequency of endometrial cancer has emphasized the need for accurate diagnosis and improved treatment. The current diagnosis is still based on conventional pathological indicators, such as clinical stage, tumor differentiation, invasion depth and vascular invasion. However, the genetic mechanisms underlying endometrial cancer have gradually been determined, due to developments in molecular biology, leading to the possibility of new methods of diagnosis and treatment planning. New candidate biomarkers for endometrial cancer include those for molecular epigenetic mutations, such as microRNAs. These biomarkers may permit earlier detection of endometrial cancer and prediction of outcomes and are likely to contribute to future personalized therapy for endometrial cancer.
Synthesis and Solvatochromic Behavior of Hexaphenylbenzenes and Indeno[1,2-b]fluorene Derivatives with Hydroxy Groups  [PDF]
Isao Yamaguchi, Kenta Tsuchie
International Journal of Organic Chemistry (IJOC) , 2012, DOI: 10.4236/ijoc.2012.23027
Abstract: Hexakis(4-methoxyphenyl)benzene (HPB-OMe(1)) and hexakis(2,6-dimethyl-4-methoxyphenyl)benzene (HPB-OMe(2)) were synthesized via organometallic complex catalysis. The treatment of HPB-OMe(1) with FeCl3 caused cyclodehydrogenation at two positions to yield an oligophenylene with an indeno[1,2-b]fluorene structure (IF-OMe). Deprotection of the methoxy groups of these compounds was conducted by treatment with BBr3. Deprotonation of the OH groups of HPB-OH(1), HPB-OH(2), and IF-OH through treatment with NaH caused a bathochromic shift in the absorption and photoluminescence (PL) peaks. The bathochromic shift of the deprotonated species increased with the donor number (DN) of the solvents. These observations can be explained as the consequence of intramolecular charge transfer (ICT) from the ONa groups to the inner benzene rings.
Endometrial Cancer and Hypermethylation: Regulation of DNA and MicroRNA by Epigenetics
Kouji Banno,Iori Kisu,Megumi Yanokura,Kenta Masuda,Yusuke Kobayashi,Arisa Ueki,Kosuke Tsuji,Wataru Yamagami,Hiroyuki Nomura,Nobuyuki Susumu,Daisuke Aoki
Biochemistry Research International , 2012, DOI: 10.1155/2012/738274
Abstract: Endometrial cancer is the seventh most common cancer in women worldwide. Therefore elucidation of the pathogenesis and development of effective treatment for endometrial cancer are important. However, several aspects of the mechanism of carcinogenesis in the endometrium remain unclear. Associations with genetic variation and mutations of cancer-related genes have been shown, but these do not provide a complete explanation. Therefore, in recent years, epigenetic mechanisms that do not involve changes in DNA sequences have been examined. Studies aimed at detection of aberrant DNA hypermethylation in cancer cells present in microscopic amounts in vivo and application of the results to cancer diagnosis have also started. Breakdown of the DNA mismatch repair mechanism is thought to play a large role in the development of endometrial cancer, with changes in the expression of the hMLH1 gene being particularly important. Silencing of genes such as APC and CHFR, Sprouty 2, RASSF1A, GPR54, CDH1, and RSK4 by DNA hypermethylation, onset of Lynch syndrome due to hereditary epimutation of hMLH1 and hMSH2 mismatch repair genes, and regulation of gene expression by microRNAs may also underlie the carcinogenic mechanisms of endometrial cancer. Further understanding of these issues may permit development of new therapies.
Relationship between DNA Mismatch Repair Deficiency and Endometrial Cancer
Kenta Masuda,Kouji Banno,Megumi Yanokura,Yusuke Kobayashi,Iori Kisu,Arisa Ueki,Asuka Ono,Nana Asahara,Hiroyuki Nomura,Akira Hirasawa,Nobuyuki Susumu,Daisuke Aoki
Molecular Biology International , 2011, DOI: 10.4061/2011/256063
Abstract: Some cases of endometrial cancer are associated with a familial tumor and are referred to as hereditary nonpolyposis colorectal cancer (HNPCC or Lynch syndrome). Lynch syndrome is thought to be induced by germline mutation of the DNA mismatch repair (MMR) gene. An aberration in the MMR gene prevents accurate repair of base mismatches produced during DNA replication. This phenomenon can lead to an increased frequency of errors in target genes involved in carcinogenesis, resulting in cancerization of the cell. On the other hand, aberrant DNA methylation is thought to play a key role in sporadic endometrial carcinogenesis. Hypermethylation of unmethylated CpG islands in the promoter regions of cancer-related genes associated with DNA repair leads to the cell becoming cancerous. Thus, both genetic and epigenetic changes are intricately involved in the process through which cells become cancerous. In this review, we introduce the latest findings on the DNA mismatch repair pathway in endometrial cancer. 1. Introduction The incidence of endometrial cancer among malignant gynecological tumors has increased with lifestyle and environmental changes. In the US, 40,000 patients are diagnosed with endometrial cancer annually, and 7,500 patients die of this disease [1]. The number and prevalence of cases of endometrial cancer have increased worldwide and control of this cancer is urgently required. However, many aspects of the mechanism of carcinogenesis and pattern of advancement are unclear. Environmental factors such as obesity and a high estrogen level are thought to play important carcinogenic roles, but a close association with hereditary disposition has also been suggested, since double cancer and an increased incidence of cancer in relatives are common in patients with endometrial cancer. Lynch syndrome, also known as hereditary nonpolyposis colorectal cancer (HNPCC), is a hereditary disease in which there is frequent development of colorectal, endometrial, and ovarian cancers. The cause is thought to be mutation of the DNA mismatch repair (MMR) gene in germ cells. However, the conventional explanation of the mechanism involving genetic changes—mutations of cancer-related genes—is inadequate and epigenetic changes in endometrial cancer are now being examined. In particular, aberrant DNA methylation is thought to play a key role in endometrial carcinogenesis. Breakdown of the DNA mismatch repair mechanism due to DNA hypermethylation plays a particularly important role in the development of endometrial cancer. 2. Lynch Syndrome Lynch syndrome is a hereditary
Endometrial Cancer and Hypermethylation: Regulation of DNA and MicroRNA by Epigenetics
Kouji Banno,Iori Kisu,Megumi Yanokura,Kenta Masuda,Yusuke Kobayashi,Arisa Ueki,Kosuke Tsuji,Wataru Yamagami,Hiroyuki Nomura,Nobuyuki Susumu,Daisuke Aoki
Biochemistry Research International , 2012, DOI: 10.1155/2012/738274
Abstract: Endometrial cancer is the seventh most common cancer in women worldwide. Therefore elucidation of the pathogenesis and development of effective treatment for endometrial cancer are important. However, several aspects of the mechanism of carcinogenesis in the endometrium remain unclear. Associations with genetic variation and mutations of cancer-related genes have been shown, but these do not provide a complete explanation. Therefore, in recent years, epigenetic mechanisms that do not involve changes in DNA sequences have been examined. Studies aimed at detection of aberrant DNA hypermethylation in cancer cells present in microscopic amounts in vivo and application of the results to cancer diagnosis have also started. Breakdown of the DNA mismatch repair mechanism is thought to play a large role in the development of endometrial cancer, with changes in the expression of the hMLH1 gene being particularly important. Silencing of genes such as APC and CHFR, Sprouty 2, RASSF1A, GPR54, CDH1, and RSK4 by DNA hypermethylation, onset of Lynch syndrome due to hereditary epimutation of hMLH1 and hMSH2 mismatch repair genes, and regulation of gene expression by microRNAs may also underlie the carcinogenic mechanisms of endometrial cancer. Further understanding of these issues may permit development of new therapies. 1. Introduction Endometrial cancer is the seventh most common cancer in women worldwide. In Japan, westernization of lifestyle has increased the number of patients with endometrial cancer, and this disease now accounts for about 40% of cancers of the uterus. A further increase, and a younger onset age are also predicted, and therefore elucidation of the pathogenesis and development of effective treatment are needed. However, the mechanism of carcinogenesis in the endometrium remains unclear. Genetic aberrances such as variations in gene expression and mutation of cancer-related genes have been identified, but these do not fully explain canceration in the endometrium. Therefore, epigenetic changes in gene expression through effects on chromatin without DNA mutation are drawing attention. Breakdown of the DNA mismatch repair mechanism by aberrant DNA hypermethylation is particularly important for development of type 1 endometrial cancer, and changes in expression of genes such as human MutL homolog1 (hMLH1) and human MutS homolog2 (hMSH2) may be involved in this mechanism. The possible epigenetic mechanisms include epimutation, hypermethylation causing epimutation, and regulation of gene expression by small noncoding RNAs, called microRNAs, that bind
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