KANAI Yae

写真a

Affiliation

School of Medicine, Department of Pathology Kanai Laboratory (Shinanomachi)

Position

Professor （Keio University）

Related Websites

External Links
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Career 【 Display / hide 】

  • 1993.04
    -
    1998.06

    National Cancer Center, Pathology Division, Research member

  • 1998.07
    -
    2002.06

    National Cancer Center, Pathology Division, Head of Section

  • 2002.07
    -
    2010.03

    National Cancer Center, Pathology Division, Chief

  • 2010.04
    -
    2017.03

    National Cancer Center Research Institute, Division of Molecular Pathology, Chief

  • 2010.11
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    2014.03

    National Cancer Center Research Institute, Deputy Director

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Academic Background 【 Display / hide 】

  • 1983.04
    -
    1989.03

    Keio University, Medical School

    University, Graduated

  • 1989.04
    -
    1993.03

    Keio University, Postgraduate School, Keio University School of Medicine, Pathology Course

    Graduate School, Completed

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Academic Degrees 【 Display / hide 】

  • 博士 (医学), Keio University, Coursework, 1993.03

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Licenses and Qualifications 【 Display / hide 】

  • 医師免許, 1989.05

  • 死体解剖資格, 1992.02

  • 日本病理学会病理専門医, 1994.08

  • 日本臨床細胞学会細胞診専門医, 1998.12

  • 日本病理学会病理専門医研修指導医, 2006.04

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Research Areas 【 Display / hide 】

  • Life Science / Human pathology (Cancer epigenomics)

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Research Keywords 【 Display / hide 】

  • Molecular pathology

  • Tumor pathology

  • DNA methylation

  • Multilayer/integrative comics analysis

  • Genitourinary Pathology

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Books 【 Display / hide 】

  • CPC形式でわかる身につく病理所見の見かた、病態の考えかた

    藏本 純子, 金井 弥栄, 鈴木 秀和, 羊土社, 2023

  • 解明病理学 : 病気のメカニズムを解く

    加藤 光保, 金井 弥栄, 菅野 祐幸, 青笹 克之, 医歯薬出版, 2021

  • DNA and Histone Methylation as Cancer Targets

    Arai E, Yotani T, Kanai Y., Elsevier, 2017

    Scope: Liver Cancer

  • DNA and Histone Methylation in Liver Cancer

    Arai E., Yotani T., Kanai Y., Cancer Drug Discovery and Development, 2017

    　View Summary

    Epigenetic alterations, such as alterations of histone modification and DNA methylation, occur in a genome-wide manner under precancerous conditions resulting from hepatitis B virus (HBV) or hepatitis C virus (HCV) infection followed by chronic hepatitis and cirrhosis, or aberrant lipogenesis and abnormal metabolism of reactive oxygen species that characterize the pathophysiology of non-alcoholic steatohepatitis (NASH). Once DNA methylation alterations occur at the precancerous stage, they are stably preserved on DNA double strands through methylation maintenance by DNA methyltransferase 1 (DNMT1). DNA methylation alterations associated with abnormalities of DNA methyltransferase, such as overexpression of DNMT1 and splicing alterations of DNMT3B, participate in multistage hepatocarcinogenesis from the precancerous stage to the malignant progression stage and are correlated with aggressiveness of hepatocellular carcinomas (HCCs) and poorer outcome of affected patients. A number of tumor-related genes, such as ATK3, APC, BMP4, CCL20, CDH1, CDKN2A, CDKN2B, CSPG2, DAB2IP, DCC, DLC1, DPT, DPYSL3, EMILIN2, FZD7, GRASP, GSTP1, HIST1H4F, IGFALS, MGMT, MZB1, NAT2, NEFH, NFATC1, PAX4, PDSS2, PER3, PROZ, PYCARD, RASSF1A, SPDY1, RUNX3, SCGB1D1, SFN, SMPD3, SOCS1, TIMP3, TLX3, TM6SF1, TRIM33, TRIM58, WFDC6, WNK2 and ZFP41, are known to be silenced by DNA hypermethylation in human HCCs. It is believed that DNA methylation alterations could be excellent biomarkers for carcinogenetic risk estimation and prognostication. To facilitate clinical application of DNA methylation diagnosis, a scaled-down device that allows quick and accurate analysis, even in small hospitals and clinics, is now being developed. One therapeutic strategy against HCC proliferation could involve a combination of epigenetic modifiers, such as a DNA methylation inhibitor, a histone deacetylase inhibitor and an S-adenosylhomocysteine hydrolase inhibitor, to sensitize cancer cells to conventional chemotherapies, in addition to eradication of hepatitis viruses for personalized and/or pre-emptive medical care.

  • DNA Methylation Alterations in Human Cancers

    Yae Kanai, Eri Arai, Elsevier Inc., 2012.12

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Papers 【 Display / hide 】

  • Molecular subtypes of lung adenocarcinoma present distinct immune tumor microenvironments

    Fukuda H., Arai K., Mizuno H., Nishito Y., Motoi N., Arai Y., Hiraoka N., Shibata T., Sonobe Y., Kayukawa Y., Hashimoto E., Takahashi M., Fujii E., Maruyama T., Kuwabara K., Nishizawa T., Mizoguchi Y., Yoshida Y., Watanabe S.i., Yamashita M., Kitano S., Sakamoto H., Nagata Y., Mitsumori R., Ozaki K., Niida S., Kanai Y., Hirayama A., Soga T., Tsukada K., Yabuki N., Shimada M., Kitazawa T., Natori O., Sawada N., Kato A., Yoshida T., Yasuda K., Ochiai A., Tsunoda H., Aoki K.

    Cancer Science (Cancer Science)  115 ( 6 ) 1763 - 1777 2024.06

    ISSN  13479032

    　View Summary

    Overcoming resistance to immune checkpoint inhibitors is an important issue in patients with non-small-cell lung cancer (NSCLC). Transcriptome analysis shows that adenocarcinoma can be divided into three molecular subtypes: terminal respiratory unit (TRU), proximal proliferative (PP), and proximal inflammatory (PI), and squamous cell carcinoma (LUSQ) into four. However, the immunological characteristics of these subtypes are not fully understood. In this study, we investigated the immune landscape of NSCLC tissues in molecular subtypes using a multi-omics dataset, including tumor-infiltrating leukocytes (TILs) analyzed using flow cytometry, RNA sequences, whole exome sequences, metabolomic analysis, and clinicopathologic findings. In the PI subtype, the number of TILs increased and the immune response in the tumor microenvironment (TME) was activated, as indicated by high levels of tertiary lymphoid structures, and high cytotoxic marker levels. Patient prognosis was worse in the PP subtype than in other adenocarcinoma subtypes. Glucose transporter 1 (GLUT1) expression levels were upregulated and lactate accumulated in the TME of the PP subtype. This could lead to the formation of an immunosuppressive TME, including the inactivation of antigen-presenting cells. The TRU subtype had low biological malignancy and “cold” tumor-immune phenotypes. Squamous cell carcinoma (LUSQ) did not show distinct immunological characteristics in its respective subtypes. Elucidation of the immune characteristics of molecular subtypes could lead to the development of personalized immune therapy for lung cancer. Immune checkpoint inhibitors could be an effective treatment for the PI subtype. Glycolysis is a potential target for converting an immunosuppressive TME into an antitumorigenic TME in the PP subtype.

  • Aberrant cell adhesiveness due to DNA hypermethylation of KLF11 in papillary urothelial carcinomas

    Tsumura K., Fujimoto M., Tian Y., Kawahara T., Fujimoto H., Maeshima A.M., Nakagawa T., Kume H., Yoshida T., Kanai Y., Arai E.

    Experimental and Molecular Pathology (Experimental and Molecular Pathology)  137   104908 2024.06

    ISSN  00144800

    　View Summary

    Purpose: The aim of this study was to clarify DNA methylation profiles determining the clinicopathological diversity of urothelial carcinomas. Methods: Genome-wide DNA methylation analysis was performed using the Infinium HumanMethylation450 BeadChip in 46 paired samples of non-cancerous urothelium (N) and corresponding cancerous tissue (T), and 26 samples of normal control urothelium obtained from patients without urothelial carcinomas (C). For genes of interest, correlation between DNA methylation and mRNA expression was examined using the Cancer Genome Atlas database. In addition, the role of a selected target for cancer-relevant endpoints was further examined in urothelial carcinoma cell lines. Results: The genes showing significant differences in DNA methylation levels between papillary carcinomas and more aggressive non-papillary (nodular) carcinomas were accumulated in signaling pathways participating in cell adhesion and cytoskeletal remodeling. Five hundred ninety-six methylation sites showed differences in DNA methylation levels between papillary and nodular carcinomas. Of those sites, that were located in CpG-islands around transcription start site, 5′-untranslated region or 1st exon, 16 genes exhibited inverse correlations between DNA methylation and mRNA expression levels. Among the latter, only the KLF11 gene showed papillary T sample-specific DNA hypermethylation in comparison to C and N samples. The DNA methylation levels of KLF11 were not significantly different between T samples and N samples or T samples and C samples for patients with papillo-nodular or nodular carcinomas. Knockdown experiments using the urothelial carcinoma cell lines HT1376 and 5637, which are considered models for papillary carcinoma, revealed that KLF11 participates in altering the adhesiveness of cells to laminin-coated dishes, although cell growth was not affected. Conclusion: These data indicate that DNA hypermethylation of KLF11 may participate in the generation of papillary urothelial carcinomas through induction of aberrant cancer cell adhesion to the basement membrane.

  • Molecular pathological approach to cancer epigenomics and its clinical application

    Kanai Y.

    Pathology International (Pathology International)  74 ( 4 ) 167 - 186 2024.04

    ISSN  13205463

    　View Summary

    Careful microscopic observation of histopathological specimens, accumulation of large numbers of high-quality tissue specimens, and analysis of molecular pathology in relation to morphological features are considered to yield realistic data on the nature of multistage carcinogenesis. Since the morphological hallmark of cancer is disruption of the normal histological structure maintained through cell−cell adhesiveness and cellular polarity, attempts have been made to investigate abnormalities of the cadherin-catenin cell adhesion system in human cancer cells. It has been shown that the CDH1 tumor suppressor gene encoding E-cadherin is silenced by DNA methylation, suggesting that a “double hit” involving DNA methylation and loss of heterozygosity leads to carcinogenesis. Therefore, in the 1990s, we focused on epigenomic mechanisms, which until then had not received much attention. In chronic hepatitis and liver cirrhosis associated with hepatitis virus infection, DNA methylation abnormalities were found to occur frequently, being one of the earliest indications that such abnormalities are present even in precancerous tissue. Aberrant expression and splicing of DNA methyltransferases, such as DNMT1 and DNMT3B, was found to underlie the mechanism of DNA methylation alterations in various organs. The CpG island methylator phenotype in renal cell carcinoma was identified for the first time, and its therapeutic targets were identified by multilayer omics analysis. Furthermore, the DNA methylation profile of nonalcoholic steatohepatitis (NASH)-related hepatocellular carcinoma was clarified in groundbreaking studies. Since then, we have developed diagnostic markers for carcinogenesis risk in NASH patients and noninvasive diagnostic markers for upper urinary tract cancer, as well as developing a new high-performance liquid chromatography-based diagnostic system for DNA methylation diagnosis. Research on the cancer epigenome has revealed that DNA methylation alterations occur from the precancerous stage as a result of exposure to carcinogenic factors such as inflammation, smoking, and viral infections, and continuously contribute to multistage carcinogenesis through aberrant expression of cancer-related genes and genomic instability. DNA methylation alterations at the precancerous stages are inherited by or strengthened in cancers themselves and determine the clinicopathological aggressiveness of cancers as well as patient outcome. DNA methylation alterations have applications as biomarkers, and are expected to contribute to diagnosis, as well as preventive and preemptive medicine.

  • 特集 ゲノム医学を外科診療に活かす! ゲノム医療の最新動向 ゲノム解析に適した手術検体の取り扱い

    金井 弥栄

    臨床外科 (株式会社医学書院)  79 ( 2 ) 138 - 143 2024.02

    ISSN  03869857

  • Clinicopathological significance of androgen receptor expression in extramammary Paget disease: An analysis of 92 patients

    Kuramoto J, Kobayashi K, Hirai I, Nakamura Y, Funakoshi T, Kanai Y

    Pathology Research and Practice (Pathology Research and Practice)  249   154775 2023.09

    ISSN  03440338

    　View Summary

    Extramammary Paget disease (EMPD) is a rare cutaneous malignant neoplasm arising in apocrine gland-rich areas. Although – like normal apocrine glands – EMPD frequently expresses androgen receptor (AR), the clinical significance of AR expression remains unclear. The present study investigated the clinicopathological impact of AR expression in EMPD. Immunohistochemistry for AR was performed in a retrospective cohort of 92 EMPD patients with 108 EMPD lesions, including 102 primary lesions, five lymph node [LN] metastases and one local recurrence. The total AR staining score was calculated as staining intensity score (IS 0–3) × positive-cell percentage score (PS 1–4). Expression levels were graded as Grade 1 (scores 0 and 1), Grade 2 (scores 2–4), and Grade 3 (scores 6–12). Higher expression grade was correlated with tumor thickness (P = 0.011), LN metastasis (P = 0.008), and higher EMPD stage (P = 0.023). Grade 1 EMPDs did not invade into the dermis and did not generate metastatic and/or recurrent lesions, whereas only Grade 2 or 3 EMPDs did so. AR expression in invasive components was significantly higher (P = 0.023) than in non-invasive components remaining within the epidermis. AR expression was further elevated in metastatic and/or recurrent lesions relative to locally invasive lesions (P = 0.014). These results clearly indicate that increased AR expression is associated with malignant progression of EMPD and that androgen blockade might be an effective therapy. Furthermore, AR expression assessed by immunohistochemistry may have potential for prediction of LN metastasis and local recurrence in EMPD.

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

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Reviews, Commentaries, etc. 【 Display / hide 】

  • 【ゲノム医学を外科診療に活かす!】ゲノム医療の最新動向　ゲノム解析に適した手術検体の取り扱い

    金井 弥栄

    臨床外科 ((株)医学書院)  79 ( 2 ) 138 - 143 2024.02

    ISSN  0386-9857

    　View Summary

    ＜文献概要＞ポイント　◆手術標本より研究用組織検体を採取する際には,病理診断に支障をきたさないよう,出血・壊死巣を回避し,がん部・非がん部を採取する.◆臓器摘出後,室温で30分以内あるいは4℃保管3時間以内に研究用組織検体を採取し,2～3mm角に細切して急速凍結し,液体窒素保管容器あるいは超低温槽に保管する.◆ホルマリン固定・パラフィン包埋標本の品質は,固定までの時間・固定時間・ホルマリンの種類と濃度に依存する.

  • 難治性精巣腫瘍に対して化学療法とdesperation surgeryを施行し完全奏効を得た一例

    蛭田 慎之介, 田中 伸之, 小森 貴大, 岩澤 智裕, 小坂 威雄, 水野 隆一, 浅沼 宏, 大家 基嗣, 新井 恵吏, 金井 弥栄

    泌尿器外科 (医学図書出版(株))  36 ( 10 ) 1167 - 1167 2023.10

    ISSN  0914-6180

  • 尿道憩室に存在した腸上皮に発生した腺癌の1例

    星野 佑介, 松本 一宏, 馬場 優人, 秋田 大宇, 新井 恵吏, 安水 洋太, 田中 伸之, 武田 利和, 森田 伸也, 小坂 威雄, 水野 隆一, 浅沼 宏, 陣崎 雅弘, 金井 弥栄, 大家 基嗣

    泌尿器外科 (医学図書出版(株))  36 ( 10 ) 1162 - 1163 2023.10

    ISSN  0914-6180

  • がん免疫研究の基礎と臨床　抗腫瘍免疫を司る2つのTh1-like CD4+T-cell clusters

    各務 博, 山崎 智, 北野 滋久, 金井 弥栄, 柴田 龍弘, 堀本 勝久

    肺癌 ((NPO)日本肺癌学会)  63 ( 5 ) 404 - 404 2023.10

    ISSN  0386-9628

  • 日米の非アルコール性脂肪性肝炎由来肝細胞がんにおけるゲノム網羅的DNAメチル化解析(Genome-wide DNA methylation analysis of non-alcoholic steatohepatitis in Japanese and American cohorts)

    藏本 純子, 新井 恵吏, 藤本 真央, 牧内 里美, 津田 昇, 安田 和基, 平岡 伸介, 吉田 輝彦, Evason Kimberley, 金井 弥栄

    日本癌学会総会記事 ((一社)日本癌学会)  82回   1615 - 1615 2023.09

    ISSN  0546-0476

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Presentations 【 Display / hide 】

  • Quantification of DNA methylation for carcinogenic risk estimation in patients with non-alcoholic steatohepatitis.

    Junko Kuramoto, Eri Arai, Mao Fujimoto, Ying Tian, Yuriko Yamada, Takuya Yotani, Satomi Makiuchi, Noboru Tsuda, Hidenori Ojima, Moto Fukai, Yosuke Seki, Kazunori Kasama, Nobuaki Funahashi, Haruhide Udagawa, Takao Nammo, Kazuki Yasuda, Akinobu Taketomi, Tatsuya Kanto, Yae Kanai.

    America Association for Cancer Research Annual Meeting 2022, 

    2022.04

  • Correlations between genome-wide DNA methylation profiles and genomic driver aberrations during multistage lung adenocarcinogenesis.

    Kenichi Hamada, Ying Tian, Mao Fujimoto, Yoriko Takahashi, Takashi Kohno, Koji Tsuta, Shun-ichi Watanabe, Teruhiko Yoshida, Hisao Asamura, Yae Kanai, Eri Arai.

    America Association for Cancer Research Annual Meeting 2021, 

    2021.04

  • Simple vs. comprehensive prediction models of homologous recombination deficiency based on mutational and clinical features in three independent breast cancer datasets.

    Maki Tanioka, Tomoko Watanabe, Takayuki Honda, Hirohiko Totsuka, Eri Arai, Yae Kanai, Kouya Shiraishi, Kenji Tamura, Takashi Kohno.

    America Association for Cancer Research Annual Meeting 2020, 

    2020.04

  • Establishment of diagnostic criteria for upper urinary tract urothelial carcinoma based on genome-wide DNA methylation analysis.

    Mao Fujimoto, Eri Arai, Koji Tsumura, Takuya Yotani, Yuriko Yamada, Yoriko Takahashi, Akiko Miyagi Maeshima, Hiroyuki Fujimoto, Teruhiko Yoshida, Yae Kanai.

    America Association for Cancer Research Annual Meeting 2020 , 

    2020.04

  • Intratumor DNA methylation heterogeneity reflects differentiation plasticity and malignant progression of human glioblastoma: a methylome analysis using microdissected specimens.

    Kentaro Ohara, Eri Arai, Hikaru Sasaki, Masashi Nakatsukasa, Kazunari Yoshida, Yae Kanai.

    11th AACR-JCA Joint Conference on Breakthroughs in Cancer. (Hawaii) , 

    2019.02
    , 

    Poster presentation

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

  • Multi-omics analysis - particularly epigenomic analysis - to elucidate the nature of NASH-derived hepatocellular carcinoma and identify therapeutic targets

    2024.04
    -
    2027.03

    Grants-in-Aid for Scientific Research, Grant-in-Aid for Scientific Research (B), No Setting

    　View Summary

    病理組織検体のエピゲノム解析結果に基づいて、NASH由来肝細胞がん症例をクラスタリングする。層別化された各症例群ごとに、ゲノム・エピゲノム・トランスクリプトーム・プロテオーム・メタボローム異常を高頻度にきたす分子を同定し、各層のオミックス異常が有意に集積する分子経路を同定する。これら分子経路内に、各症例群の治療標的候補を同定し、治療標的としての妥当性を、生体内の状況をよく反映する正常肝細胞ならびにNASH由来肝がん細胞オルガノイドによりin vitroで証明する。エピゲノムプロファイルによる症例層別化を再現できるCpG部位を同定して、各症例群の標的治療に対するコンパニオン診断マーカーとする。

  • 尿路上皮がんに対する新規エピゲノム解析による治療効果予測バイオマーカー開発

    2023.04
    -
    2028.03

    Grants-in-Aid for Scientific Research, Grant-in-Aid for Scientific Research (C), No Setting

    　View Summary

    本研究の目的は、約500例を目標とする切除不能尿路上皮がんの多施設共同前向き観察研究から得られた組織・血液を用いてエピゲノム解析を行い、1・2次治療に向けた治療効果診断マーカーを開発し、予後不良である切除不能尿路上皮がんの、治療のブレイクスルー創出と治療成績の向上に貢献する。（１）尿路上皮がん手術材料より組織検体を採取し、エピゲノム解析により治療効果予測バイオマーカーを開発すると同時に、その信頼度の前向き検証を行う。新たに開発した診断基準で予後予測し、最適な治療法を目指した医師主導治験等に進むための、基盤となる知見を得る。

  • Pathological diagnosis based on integration of morphological images and multi-layer omics data by artificial intelligence

    2021.04
    -
    2024.03

    Keio University, Grants-in-Aid for Scientific Research, Grant-in-Aid for Scientific Research (B), No Setting

    　View Summary

    本研究は、人工知能 (AI)の支援を受けて病理形態像とゲノム等オミックス情報を融合させ、がんの治療奏効性・有害事象・予後を予測する深層学習モデルを構築することを目的とする。予測時のAIの着眼点を可視化し、形態学的診断基準に翻訳して、病理医が顕微鏡で見るだけでモデルと同等の治療奏効性・有害事象・予後予測を可能にすることを目指す。悪性度が高い腎淡明細胞がんのCpGアイランドメチル化形質 (CIMP)の予測モデルを構築する過程で、病理画像とオミックスデータを統合する至適研究手法を確立し、「病理医とAIの創造的協働による、オミックス情報を統合した新しい病理診断の創出 (病理診断学の革新)」を図る。

  • Elucidation of Aging Mechanisms by Regulation of NAD+ and Epigenome and Development of New Anti-Aging Interventions

    2019.06
    -
    2021.03

    Keio University, Grants-in-Aid for Scientific Research, Saito Yoshimasa, Challenging Research (Exploratory), No Setting

    　View Summary

    To elucidate the molecular mechanism of aging, we established organoids from the intestinal epithelium of aging mice and analyzed gene expression changes and epigenomic changes.
    The organoids from aged mice showed reduced proliferative capacity and tissue building ability. In addition, epigenomic changes led to decreased gene expression of stem cell markers such as Lgr5 and Wnt signaling pathway in organoids from aged mice. In addition, administration of nicotinamide mononucleotide (NMN), an NAD+ precursor, changed the morphology of intestinal epithelial organoids from aged mice to that of young mice and restored the expression of stem cell-related genes, suggesting that NMN increases NAD+ activity and has an anti-aging effect.

  • Established epigenetic treatment for chemotherapy-resistant metastatic bladder cancer

    2019.04
    -
    2022.03

    University of Toyama, Grants-in-Aid for Scientific Research, Nishiyama Naotaka, Grant-in-Aid for Scientific Research (C), No Setting

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    Chromatin accessibility was analyzed by the AcceSssIble assay, revealing that the CDDP / GEM-resistant cell lines differ in histone-modified regions compared to the parental strain. It was clarified that the change in chromatin structure due to histone modification contributed to the drug resistance. Comprehensive DNA methylation analysis revealed that resistance was not contributed by genetic changes at a particular site, but by both genome-wide DNA methylation changes and structural changes due to histone modifications. In an in vivo study, low-dose 5-aza-CdR showed a synergistic effect with CDDP administration, and a growth-suppressing effect was also observed in resistant strains.

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Intellectual Property Rights, etc. 【 Display / hide 】

  • 尿路上皮癌のリスク判定方法

    Date applied： PCT/JP2019/011442  2019.03 

    Patent, Joint

  • 子宮体癌の予後の判定方法

    Date applied： 特願2018-228276  2018.11 

    Patent, Joint

  • Method for assessing risk of hepatocellular carcinoma

    Date applied： PCT/JP2018/031092  2018.08 

    Patent, Joint

  • 尿路上皮癌のリスク判定方法

    Date applied： 特願2018-051464  2018.03 

    Patent, Single

  • 肝細胞癌のリスク評価方法

    Date applied： 特願2017-160284  2017.08 

    Patent, Joint

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Awards 【 Display / hide 】

  • JCA Women Scientists Award

    Yae Kanai, 2018.09, Japanese Cancer Association, Molecular pathological approach ti epigenome mechanisms of multistage human carcinogenesis

    Type of Award： Award from Japanese society, conference, symposium, etc.

  • Tamiya Prize

    2006.02, Foundation for Promotion of Cancer Research, Cancer development, invasion and metastasis: Epigenetic research based on histopathological approach

    Type of Award： Award from publisher, newspaper, foundation, etc.

  • Incitement Award of the Japanese Cancer Association

    2003.09, Japanese Cancer Association, DNA methylation abnormalities participating in multistage human carcinogenesis

    Type of Award： Award from Japanese society, conference, symposium, etc.

  • Incitement Award of the Japanese Society of Pathology

    Yae Kanai, 2002.03, Japanese Society of Pathology, DNA methylation alterations during multistage human carcinogenesis

    Type of Award： Award from Japanese society, conference, symposium, etc.

  • Baelz Prize

    Setsuo Hirohashi, Atsushi Ochiai, Yae Kanai, 2000.11, ベルツ財団, Inactivation of E-cadherin cell adhesion system in human cancer invasion and metastasis

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Courses Taught 【 Display / hide 】

  • PATHOLOGY: SEMINAR

    2025

  • PATHOLOGY: PRACTICE

    2025

  • PATHOLOGY

    2025

  • GENERAL PATHOLOGY

    2025

  • DISEASES OF ORGAN SYSTEMS

    2025

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Courses Previously Taught 【 Display / hide 】

  • General Pathology

    Keio University

    2018.04
    -
    2019.03
    , 

    Full academic year, Lecture

  • Diseases of organ systems

    Keio University

    2018.04
    -
    2019.03
    , 

    Full academic year, Lecture

  • 症例検討 (基礎臨床統合医学)

    Keio University

    2018.04
    -
    2019.03

  • 医学概論 (大学院医学研究科修士課程)

    Keio University

    2018.04
    -
    2019.03

  • 医学特別講義 (大学院医学研究科博士課程)

    Keio University

    2018.04
    -
    2019.03

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Memberships in Academic Societies 【 Display / hide 】

  • Associate member, Science Council of Japan, 

    2006
    -
    Present

  • 日本病理学会: 拡大常任理事・学術評議員 (病理専門医、病理専門医研修指導医、分子病理専門医、ゲノム病理診断検討委員会委員長・ゲノム研究用病理組織検体取扱い規程策定委員会委員長・ゲノム病理標準化講習会委員会委員長・教育委員会委員長・病理診療ガイドライン作成委員会委員長・固形癌HER2病理診断ガイドライン策定ワーキンググループ委員長・企画委員会委員・学術委員会委員・編集委員会委員・ゲノム診療用病理組織検体取扱い規程策定ワーキンググループ委員・病理専門医制度運営委員会委員等), 

    1989
    -
    Present

  • 日本癌学会: 評議員 (女性科学者委員会委員), 

    1994.08
    -
    Present

  • 日本臨床細胞学会

    　

  • 日本エピジェネティクス研究会 (幹事)

    　

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Committee Experiences 【 Display / hide 】

  • 2021
    -
    Present

    厚生労働省がんゲノム医療中核拠点病院等の指定要件に関するワーキンググループ構成員

  • 2020.04
    -
    Present

    日本学術振興会学術システム研究センタープログラムオフィサー (専門研究員)

  • 2020
    -
    Present

    科学技術振興機構ＮＢＤＣヒトデータベース倫理審査委員会委員

  • 2017
    -
    Present

    日本医療研究開発機構プログラムオフィサー・課題評価委員会委員・アドバイザー

  • 2015
    -
    2016

    文部科学省科学研究費補助金における評価に関する委員会生物系委員会委員

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