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Search Results: 1 - 10 of 371 matches for " Megumi Yanokura "
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Gynecological tumors in patients with Peutz-Jeghers syndrome (PJS)  [PDF]
Arisa Ueki, Iori Kisu, Kouji Banno, Megumi Yanokura, Kennta Masuda, Yusuke Kobayashi, Akira Hirasawa, Daisuke Aoki
Open Journal of Genetics (OJGen) , 2011, DOI: 10.4236/ojgen.2011.13012
Abstract: Peutz-Jeghers syndrome (PJS) is an autosomal dominant disorder characterized by the development of hamartomatous polyposis in the gastrointestinal tract and melanin-pigmented macules on the skin mucosa. The responsible gene is a tumor suppressor, STK11/LKB1, on chromosome 19p13.3. PJS complicates with benign and malignant tumors in various organs. In gynecology, there has been a particular focus on complications of PJS with sex cord tumor with annular tubules (SCTAT) and minimal deviation adenocarcinoma (MDA), which are rare diseases. Approximately 36% of patients with SCTAT are complicated with PJS and these patients are characterized by multifocal, bilateral, small and benign lesions that develop into tumors with mucinous to serous ratios of 8:1. In addition, 10% of cases of MDA are complicated with PJS and mutation of STK11, the gene responsible for PJS, has a major effect on onset and prognosis. The disease concept of lobular endocervical glandular hyper-plasia (LEGH) has recently been proposed and LEGH is thought to be a potential premalignant lesion of MDA, however, the relationship between PJS and LEGH remains unclear. Several case reports of PJS patients complicated with gynecological tumors have been published and further studies are needed to determine the underlying causes
Oncofertility in Gynecologic Malignant Tumors  [PDF]
Masataka Adachi, Kouji Banno, Iori Kisu, Megumi Yanokura, Moito Iijima, Takashi Takeda, Kiyoko Umene, Yuya Nogami, Eiichiro Tominaga, Daisuke Aoki
Journal of Cancer Therapy (JCT) , 2015, DOI: 10.4236/jct.2015.614128
Abstract: Long-term survival is the priority in treatment of patients with malignant tumors. In the field of gynecology, fertility preservation has also recently become an important objective due to improved treatment outcomes and different needs of patients. Methods for fertility preservation include cervical conization, ovarian protection against radiation or chemotherapy for ovarian cancer since the ovary is hypersensitive to cancer therapies, treatment of gynecological cancer during pregnancy, and cryopreservation of oocytes, embryos or ovarian tissue before treatment of malignant tumors. Radical trachelectomy for early cervical cancer and treatment with medroxy progesterone acetate for early endometrial carcinoma are also options for fertility preservation, but the efficacy and risk of recurrence have yet to be fully evaluated. The first childbirth following uterine transplantation was also achieved last year and this success has expanded the potential for pregnancy and delivery among cancer survivors.
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.
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.
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
Indocyanine Green Fluorescence Imaging for Evaluation of Uterine Blood Flow in Cynomolgus Macaque
Iori Kisu, Kouji Banno, Makoto Mihara, Li-Yu Lin, Kosuke Tsuji, Megumi Yanokura, Hisako Hara, Jun Araki, Takuya Iida, Takayuki Abe, Keisuke Kouyama, Nobuhiko Suganuma, Daisuke Aoki
PLOS ONE , 2012, DOI: 10.1371/journal.pone.0035124
Abstract: Background Uterine blood flow is an important factor in uterine viability, but the number of blood vessels required to maintain viability is uncertain. In this study, indocyanine green (ICG) fluorescence imaging was used to examine uterine hemodynamics and vessels associated with uterine blood flow in cynomolgus macaque. Methods The uterus of a female cynomolgus macaque was cut from the vaginal canal to mimic a situation during trachelectomy or uterine transplantation surgery in which uterine perfusion is maintained only with uterine and ovarian vessels. Intraoperative uterine hemodynamics was observed using ICG fluorescence imaging under conditions in which various nutrient vessels were selected by clamping of blood vessels. A time-intensity curve was plotted using imaging analysis software to measure the Tmax of uterine perfusion for selected blood vessel patterns. Open surgery was performed with the uterus receiving nutritional support only from uterine vessels on one side. The size of the uterus after surgery was monitored using transabdominal ultrasonography. Results The resulting time-intensity curves displayed the average intensity in the regions of the uterine corpus and uterine cervix, and in the entire uterus. Analyses of the uterine hemodynamics in the cynomolgus macaque showed that uterine vessels were significantly related to uterine perfusion (P = 0.008), whereas ovarian vessels did not have a significant relationship (P = 0.588). When uterine vessels were clamped, ovarian vessels prolonged the time needed to reach perfusion maximum. Postoperative transabdominal ultrasonography showed that the size of the uterus was not changed 2 months after surgery, with recovery of periodic menstruation. The cynomolgus macaque has got pregnant with favorable fetus well-being. Conclusion Uterine vessels may be responsible for uterine blood flow, and even one uterine vessel may be sufficient to maintain uterine viability in cynomolgus macaque. Our results show that ICG fluorescence imaging is useful for evaluation of uterine blood flow since this method allows real-time observation of uterine hemodynamics.
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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