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Search Results: 1 - 10 of 504 matches for " Wataru Yamagami "
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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.
Atypical Polypoid Adenomyoma (APAM) of the Uterine: Relationship with Endometrial Cancer  [PDF]
Iori Kisu, Kouji Banno, Megumi Yanokura, Yusuke Kobayashi, Arisa Ueki, Asuka Ono, Kennta Masuda, Wataru Yamagami, Hiroyuki Nomura, Akira Hirasawa, Nobuyuki Susumu, Daisuke Aoki
Journal of Cancer Therapy (JCT) , 2011, DOI: 10.4236/jct.2011.24061
Abstract: Atypical polypoid adenomyoma (APAM) is a rare polypoid tumor that generally occurs in women of reproductive age who have abnormal genital bleeding. The tumor was reported as a new disease concept by Mazur in 1981. Pathologically, APAM consist of irregularly proliferated endometrial gland cells and interlacing bundles of smooth muscle cells within the stroma, and have a similar form to adenocarcinoma, adenofibroma, adenosarcoma, and carcinosarcoma. Therefore, differential diagnosis is required in many cases. APAM is pathologically classified as a benign lesion and clinically has a comparatively favorable outcome. However, treatment and follow-up observation should be performed carefully because recurrence and residual lesions occur in many patients after conservative treatment. Concomitant development of endometrial adenocarcinoma also occurs in many cases and it is difficult to differentiate this disease from APAM. Thus, diagnosis of APAM should be made carefully, particularly since the number of cases of endometrial adenocarcinoma has increased in recent years. Furthermore, APAM tends to develop during a woman’s reproductive years, and fertility sparing treatment should be considered. Here, we review the clinicopathological characteristics of APAM, including the difficulty of diagnosis as a benign or malignant uterine tumor, and we examine the relationship between APAM and 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.
A unique case of collagenous colitis presenting as protein-losing enteropathy successfully treated with prednisolone
Soichi Sano, Keiko Yamagami, Ayako Tanaka, Minako Nishio, Tomoyuki Nakamura, Yuki Kubo, Takeshi Inoue, Wataru Ueda, Kiyotaka Okawa, Katsunobu Yoshioka
World Journal of Gastroenterology , 2008,
Abstract: A 76-year-old woman with a 5-mo history of recurrent diarrhea and generalized edema was admitted to our hospital. Colonoscopy revealed edematous mucosa, and histopathological examination was compatible with collagenous colitis. Protein leakage from the colon, particularly in the ascending portion, was identified on 99mTc-human serum albumin scintigraphy. Collagenous colitis associated with protein-losing enteropathy (PLE) without small bowel disease was diagnosed. Prednisolone treatment ameliorated diarrhea and hypoproteinemia. Collagenous colitis should be included in the differential diagnosis of chronic diarrhea with hypoproteinemia for appropriate management.
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.
The Home Market Effect under Constant Returns and Monopolistic Competition  [PDF]
Wataru Johdo
Theoretical Economics Letters (TEL) , 2012, DOI: 10.4236/tel.2012.25082
Abstract: Most existing theoretical studies on home market effects depend crucially on the assumption of increasing returns to scale technology. This paper studies the consequences of the absence of increasing returns to scale on home market effects by employing a constant returns monopolistic competition model. This paper demonstrates that home market effects can emerge or disappear depending on the magnitude of the elasticity of substitution and transport costs even in the constant returns model with firm mobility. In particular, a reverse home market effect can result when the elasticity of substitution is low and transport costs are high.
Asymmetric Transportation Costs and the Home Market Effect  [PDF]
Wataru Johdo
Theoretical Economics Letters (TEL) , 2013, DOI: 10.4236/tel.2013.32013
Abstract:

Most existing theoretical studies on home market effects depend crucially on assumptions of symmetric transportation costs and increasing returns to scale technology. In our model, we remove the home market effect assumptions from the main model used in the literature. Instead, this paper employs a constant returns monopolistic competition model with asymmetric transportation costs. We show that 1) when the home country’s transportation cost is large enough for a given level of the foreign country’s transportation cost, the HME appears in the home country, and 2) the opposite of the HME is observed in the home country as long as the foreign country’s transportation cost is large enough for a given level of the home country’s transportation cost.

Consumption Tax, Nontraded Goods and Welfare  [PDF]
Wataru Johdo
Theoretical Economics Letters (TEL) , 2013, DOI: 10.4236/tel.2013.35044
Abstract: This paper studies the welfare effects of a consumption tax rise based on the two-sector small open economy model of Obstfeld and Rogoff (1995) and Lane (1997). The main findings of our analysis are that 1) in the case of free trade, the consumption tax rise has no effect on welfare, 2) when there is the nontraded goods sector, the consumption tax rise has a negative effect on welfare, and 3) the larger the share of nontraded goods in consumption is, the larger the negative welfare effect of consumption tax will be.
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.
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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