Yanokura, Megumi



School of Medicine, Department of Obstetrics and Gynecology (Gynecology) (Shinanomachi)


Project Assistant Professor (Non-tenured)/Project Research Associate (Non-tenured)/Project Instructor (Non-tenured)

External Links

Academic Background 【 Display / hide

  • 2013.04

    筑波大学, 生命環境科学, 生物科学

    Graduate School, Completed, Doctoral course

  • 2006.03

    Keio University, Graduate School, Division of Medicine, 医科学

    Graduate School, Completed, Master's course

Academic Degrees 【 Display / hide

  • 修士(医科学), Keio University, Coursework, 2006.03

  • 博士(理学), 筑波大学大学院, Coursework, 2017.07


Research Areas 【 Display / hide

  • Obstetrics and gynecology (Obstetrics and Gynecology)

Research Keywords 【 Display / hide

  • DNAメチル化

  • 子宮体癌

  • 細胞周期チェックポイント

  • 薬剤感受性


Papers 【 Display / hide

  • Erratum: Aurora kinase inhibitors: Potential molecular-targeted drugs for gynecologic malignant tumors (Review).

    Umene K, Banno K, Kisu I, Yanokura M, Nogami Y, Tsuji K, Masuda K, Ueki A, Kobayashi Y, Yamagami W, Nomura H, Tominaga E, Susumu N, Aoki D

    Biomedical reports 11 ( 6 ) 274 2019.12

    Research paper (scientific journal), Accepted,  ISSN  2049-9434

  • Current status of uterine regenerative medicine for absolute uterine factor infertility (Review)

    Matoba Y., Kisu I., Sera A., Yanokura M., Banno K., Aoki D.

    Biomedical Reports (Biomedical Reports)  10 ( 2 ) 79 - 86 2019

    Research paper (scientific journal), Joint Work, Accepted,  ISSN  20499434

     View Summary

    © 2019, Spandidos Publications. All rights reserved. Though assisted reproduction technology has been developed, a treatment for absolute uterine factor infertility (AUFI), such as defects in the uterus, has not yet been established. Regenerative medicine has been developed and applied clinically over recent years; however, whole solid organs still cannot be produced. Though uterine regeneration has the potential to be a treatment for AUFI, there have been only a few studies on uterine regeneration involving the myome-trium in vivo. In the present report, those relevant articles are reviewed. A literature search was conducted in PubMed with a combination of key words, and 10 articles were found, including nine in rat models and one in a mouse model. Of these studies, eight used scaffolds and two were performed without scaffolds. In four of these studies, scaffolds were re-cellularized with various cells. In the remaining four studies, scaffolds were transplanted alone, or other structures were used. Though the methods differed, the injured uterus recovered well, morphologically and functionally, in every study. Only 10 articles were relevant to our investigation, but the results w

  • Mutations of RAS genes in endometrial polyps

    Takeda T., Banno K., Kobayashi Y., Adachi M., Yanokura M., Tominaga E., Kosaki K., Aoki D.

    Oncology Reports (Oncology Reports)  42 ( 6 ) 2303 - 2308 2019

    Research paper (scientific journal), Accepted,  ISSN  1021335X

     View Summary

    © 2019 Spandidos Publications. All rights reserved. Endometrial polyps are common, yet the molecular mechanisms underlying their formation and progression remain unclear. We examined gene mutations possibly related to the pathogenesis of endometrial polyps, as well as to their clinical features. Four premenopausal patients with endometrial polyps, who were not under drug treatment, were recruited. Whole exomes of endometrial polyps and peripheral blood lymphocytes were analyzed by next-generation sequencing, and somatic mutations were derived by subtraction. Then, 35 samples of endometrial polyps and 12 samples of atypical polypoid adenomyoma were newly recruited to validate the identified mutations by polymerase chain reaction-reverse sequence specific oligonucleotide method. The mutations were also analyzed in separate stromal and glandular components of the polyps after laser-capture microdissection. Whole exome sequencing revealed that KRASmutations were the only type of mutation detectable in multiple cases (2/4). Targeted mutation analysis revealed that 16 of 35 samples (45.7%) of endometrial polyps harbored RAS mutations. Mutation-positive cases exhibited a significantly higher number of endometrial polyps (3.25±2.70 vs. 1.74±0.87, P=0.045). Laser-capture microdissection in NRAS-mutated endometrial polyps revealed that both stromal and glandular components harbored RAS mutations. There was no RAS mutation in 12 samples of atypical polypoid adenomyoma. This is the first report demonstrating that pathogenic RAS mutations are frequent in non-treated endometrial polyps. RAS mutations may have an important role in tumorigenesis and in the formation of multiple endometrial polyps.

  • Synchronous endometrial and ovarian cancer in Lynch syndrome with a MSH2 germline mutation: A case report.

    Takeda T, Banno K, Yanokura M, Anko M, Kobayashi A, Sera A, Takahashi T, Adachi M, Kobayashi Y, Hayashi S, Nomura H, Hirasawa A, Tominaga E, Aoki D

    Molecular and clinical oncology 9 ( 5 ) 479 - 484 2018.11

    Research paper (scientific journal), Joint Work, Accepted,  ISSN  2049-9450

  • Screening for Lynch syndrome using risk assessment criteria in patients with ovarian cancer

    Takeda, Takashi, Tsuji, Kosuke, Banno, Kouji, Yanokura, Megumi, Kobayashi, Yusuke, Tominaga, Eiichiro, Aoki, Daisuke

    JOURNAL OF GYNECOLOGIC ONCOLOGY (Journal of Gynecologic Oncology)  29 ( 3 ) 41 - 48 2018.05

    Research paper (scientific journal), Single Work, Accepted,  ISSN  2005-0380

     View Summary

    © 2018, Korean Society of Gynecologic Oncology and Colposcopy. All rights reserved. Objective: Lynch syndrome is a cancer predisposition syndrome caused by germline mutation of DNA mismatch repair (MMR) genes. Lynch syndrome only causes about 0.4% of cases of ovarian cancer, which suggests that universal screening may not be cost-efficient. However, the frequency of Lynch syndrome in ovarian cancer is unclear in the Asian population. The goal of the study was to investigate a screening strategy using family history. Methods: The subjects were 129 patients with ovarian cancer. Clinical and family history were collected using a self-administered questionnaire, and Society of Gynecologic Oncology (SGO) criteria 2007 and PREMM 5 were used for risk assessment. Microsatellite instability, immunohistochemistry, and methylation of MMR genes were analyzed. Results: Of the 129 cases, 25 (19.4%) met the SGO criteria, and 4 of these 25 had MSI-high and MMR deficiency. Two cases had loss of MSH2 and MSH6, indicating MSH2 mutation, and the other two had loss of MLH1 and PMS2, including one without MLH1 methylation indicating MLH1 mutation. These results show that screening using family history

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Papers, etc., Registered in KOARA 【 Display / hide

Presentations 【 Display / hide

  • ヒト子宮体癌由来培養細胞を用いたReprogrammed-Cancer cellの作成

    矢野倉 恵, 阪埜 浩司, 的場 優介, 辻 浩介, 小林 佑介, 冨永 英一郎, 田中 守, 青木 大輔

    日本産科婦人科学会雑誌, 2019.02, (公社)日本産科婦人科学会

  • 【婦人科がん(第2版)-最新の研究動向-】 子宮体がん 子宮体癌の発生 子宮内膜癌(類内膜癌)のゲノム解析

    阪埜 浩司, 矢野倉 恵, 青木 大輔

    日本臨床, 2018.03, Other, (株)日本臨床社

  • CIMP-H子宮体癌患者の末梢血を利用したTargeted bisulfite sequencing

    矢野倉 恵, 阪埜 浩司, 安達 将隆, 梅根 紀代子, 小林 佑介, 山上 亘, 冨永 英一郎, 進 伸幸, 青木 大輔

    日本癌学会総会記事, 2016.10, Other, 日本癌学会

  • 子宮体部明細胞癌に対するARID1Aタンパクの発現解析 卵巣明細胞癌との比較

    大川 隆一朗, 阪埜 浩司, 矢野倉 恵, 増田 健太, 安達 将隆, 野上 侑哉, 國富 晴子, 冨永 英一郎, 田中 守, 青木 大輔

    日本産科婦人科学会雑誌, 2016.02, Other, (公社)日本産科婦人科学会

  • メトホルミンとジエノゲストの併用はDNAのメチル化を変化させ子宮体癌細胞の増殖を抑制させる

    矢野倉 恵, 阪埜 浩司, 増田 健太, 梅根 紀代子, 野上 侑哉, 入江 晴子, 飯田 美穂, 中村 加奈子, 安達 将隆, 冨永 英一郎, 田中 守, 青木 大輔

    日本産科婦人科学会雑誌, 2015.02, Other, (公社)日本産科婦人科学会

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Research Projects of Competitive Funds, etc. 【 Display / hide

  • Reprogramming study of endometrial cancer cells for restoring fertility


    MEXT,JSPS, Grant-in-Aid for Scientific Research, 矢野倉 恵, Grant-in-Aid for Scientific Research (C), Principal Investigator

  • Genome-wide DNA methylation analysis in endometrial cancer


    MEXT,JSPS, Grant-in-Aid for Scientific Research, YANOKURA Megumi, 阪埜 浩司, Grant-in-Aid for Scientific Research (C), Principal Investigator

     View Summary

    [Objective] Concurrent DNA methylation of multiple genes occurs in endometrial cancer. However, the features and causes of high-methylation rate endometrial cancer are not well understood. Therefore, the aim of this study was to investigate the DNA methylation status in normal tissue from patients with endometrial cancer.
    [Methods] The study was approved by the Ethics Committee. The subjects were 25 patients with endometrial cancer from whom cancer tissue and peripheral blood cells (PBCs) were obtained. The 25 cancer samples were classified as Methyl-high, and Methyl-negative (Methyl(-)) by methylation-specific PCR (MSP) analysis of three genes. DNA libraries were prepared from peripheral blood DNAs from 2 Methyl-H and 2 Methyl(-) patients, and bisulfite sequencing was performed.
    [Results] PBC DNA in Methyl-H cases had significant hypermethylation in the miR-663a promoter region, compared to Methyl(-) cases.

  • Application to the development and diagnosis of miRNA therapeutic agent in endometrial cancer


    Keio University, YANOKURA MEGUMI, Grant-in-Aid for Young Scientists (B)

     View Summary

    [Objective] microRNAs have key roles in the onset, development and drug resistance of cancer. We identified miR-34b as a tumor suppressor-type microRNA with expression that is epigenetically suppressed in endometrial cancer. In this study, the antitumor effect of combined miR-34b and antitumor drugs on endometrial cancer was examined.
    [Results] There was no change in cell viability after administration of miR-34b following application of cisplatin or adriamycin to HEC-108, HEC-1B and KLE cells. However, after treatment with paclitaxel, cell viability after administration of miR-34b decreased in all three cell lines. Tumor development occurred 14 days after transplantation of HEC-1B cells in nude mice. Drugs were administered on that day and thereafter. The tumor diameter significantly decreased in mice treated with paclitaxel + miR-34b compared with the results for other treatments (P<0.05). The GFP fluorescence signal also markedly decreased after treatment with paclitaxel + miR-34b.

  • endometrial cancer therapy using epigenetically regulated small RNA


    Keio University, BANNO Kouji, YANOKURA Megumi, Grant-in-Aid for Scientific Research (C)

     View Summary

    It is revealed that CHFR gene is epigenetically regulated in endometrial cancer. CHFR gene methylation is correlated with response to Taxane. Micro RNA is also regulated by DNA methylation in endometrial cancer. miR-34b is important for the oncogenesis of

  • Antitumor effect of siRNA on endometrial cancer


    Keio University, YANOKURA Megumi, Grant-in-Aid for Young Scientists (B)

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    Tumor development occurred 3 weeks after transplantation of HEC-1B cells in nude mice. Drugs were administered on that day and thereafter. The tumor diameter significantly decreased in mice treated with paclitaxel+Aurora-A siRNA compared with the results for other treatments(P<0. 05). The GFP fluorescence signal also markedly decreased after treatment with paclitaxel+Aurora-A siRNA.
    Aurora-A siRNA may have the potential to increase the sensitivity of endometrial tumors to treatment with paclitaxel.

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