Takaishi, Hiromasa

写真a

Affiliation

School of Medicine, Center for Preventive Medicine (Shinanomachi)

Position

Professor

External Links
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Career 【 Display / hide 】

  • 2002.10
    -
    2007.03

    慶應義塾大学医学部, 包括先進医療センター, 助手

  • 2007.04
    -
    2008.03

    慶應義塾大学医学部, 包括医療先進センター, 助教

  • 2008.04
    -
    2009.03

    慶應義塾大学医学部, 包括医療先進センター, 学部内講師

  • 2009.07
    -
    2013.05

    慶應義塾大学医学部, 腫瘍センター, 専任講師

  • 2009.10
    -
    2017.09

    慶應義塾大学医学部, 腫瘍センター, 副センター長

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Academic Background 【 Display / hide 】

  • 1990.03

    慶應義塾大学, 医学部, 医学科

    University, Graduated

  • 1996.03

    慶應義塾大学, 医学研究科, 内科学

    Withdrawal after completion of doctoral course requirements, Doctoral course

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Academic Degrees 【 Display / hide 】

  • 博士（医学）, 慶應義塾大学, 2000.02

    潰瘍性大腸炎における大腸杯細胞内ムチンに対する自己抗体とその病的意義の検討

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Licenses and Qualifications 【 Display / hide 】

  • 医師免許証, 1990.06

  • 日本内科学会 認定内科医, 1995.09

  • 日本消化器病学会 専門医, 1995.12

  • 日本臨床腫瘍学会がん薬物療法 専門医, 2007.04

  • 日本がん治療認定医機構がん治療 認定医, 2008.04

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Research Areas 【 Display / hide 】

  • Life Science / Gastroenterology

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Research Keywords 【 Display / hide 】

  • Cancer Genome Medicine

  • Medical Oncology

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Books 【 Display / hide 】

  • オンコロジークリニカルガイド　消化器癌化学療法

    高石官均, 南山堂, 2014

    Scope: 83-87

  • 潰瘍性大腸炎・クローン病

    日比紀文、高石官均, プロバイオティクス・プレバイオティクス・バイオジェニックス, 2006

    Scope: 244-247

  • Crohn 病治療の進歩

    日比紀文、高石官均, 最新内科学大系 プログレス, 1997

    Scope: 8: 310-319

  • Magnifying endoscopic and immunohistochemical study of the colonic minute lesions in inflammatory bowel disease. Current topics on mucosal immunology 1993.

    Inoue N, Hibi T, Takaishi H, Ueno Y, Hayashi A, Hosoda Y, Iwao Y, Watanabe N, Watanabe M, Aiso S, Tsuchiya M, Excerpta Medica, 1994

    Scope: 219-222

  • Autoantibodies in ulcerative colitis and Crohn's disease. Current Topics in Mucosal Immunology

    Hibi T, Ohara H, Takaishi H, Inoue N, Ueno Y, Iwao Y, Watanabe M, Kobayashi K, Aiso S, Tsuchiya M, Excerpta Medica, 1994

    Scope: 155-160

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Papers 【 Display / hide 】

  • Predicting exacerbation of renal function by DNA methylation clock and DNA damage of urinary shedding cells: a pilot study

    Hishikawa A., Nishimura E.S., Yoshimoto N., Nakamichi R., Hama E.Y., Ito W., Maruki T., Nagashima K., Shimizu-Hirota R., Takaishi H., Itoh H., Hayashi K.

    Scientific Reports 14 ( 1 )  2024.12

    　View Summary

    Recent reports have shown the feasibility of measuring biological age from DNA methylation levels in blood cells from specific regions identified by machine learning, collectively known as the epigenetic clock or DNA methylation clock. While extensive research has explored the association of the DNA methylation clock with cardiovascular diseases, cancer, and Alzheimer's disease, its relationship with kidney diseases remains largely unexplored. In particular, it is unclear whether the DNA methylation clock could serve as a predictor of worsening kidney function. In this pilot study involving 20 subjects, we investigated the association between the DNA methylation clock and subsequent deterioration of renal function. Additionally, we noninvasively evaluated DNA damage in urinary shedding cells using a previously reported method to examine the correlation with the DNA methylation clock and worsening kidney function. Our findings revealed that patients with an accelerated DNA methylation clock exhibited increased DNA damage in urinary shedding cells, along with a higher rate of eGFR decline. Moreover, in cases of advanced CKD (G4-5), the DNA damage in urinary shedding cells was significantly increased, highlighting the interplay between elevated DNA damage and eGFR decline. This study suggests the potential role of the DNA methylation clock and urinary DNA damage as predictive markers for the progression of chronic kidney disease.

  • Optimal number of images and 2-year interval affect cancer detection in screening esophagogastroduodenoscopy: An observational study

    Ksahiwagi K., Yoshida T., Fukuhara K., Bessho R., Ichikawa H., Inoue N., Takaishi H., Iwao Y., Kanai T.

    Medicine (United States) 103 ( 26 )  2024.06

    ISSN  00257974

    　View Summary

    We aimed to identify quality indicator for esophagogastroduodenoscopy for detecting upper gastrointestinal (UGI) cancer. Data from 43,526 consecutive health checkups from August 2012 to January 2022 were retrospectively collected. The study ultimately analyzed 42,387 examinations by 12 endoscopists who performed more than 1000 examinations, including all cancers detected. These endoscopists were classified either into fast/slow group based on their mean examination time for a normal finding of esophagogastroduodenoscopy during their first year of the examination, or small/large group based on number of endoscopic images, respectively. The association between UGI cancer detection rate and examination time or the number of images was analyzed, using 5 minutes or 50 images as cutoff values. The detection rate of overall (8 pharyngeal, 39 esophageal, 69 gastric) cancers in the fast, slow, small, and large groups were 0.17%, 0.32%, 0.21%, and 0.31%, respectively. On multivariable analysis, endoscopists in the fast group or the small group were less likely to detect overall UGI cancer (OR: 0.596, 95% CI: 0.373-0.952, P = .030; OR: 0.652, 95% CI: 0.434-0.979, P = .039). Additionally, repeated endoscopy within 2 years had a higher overall cancer detection rate, compared with repeated screening after 2 years. In a sub-analysis, a significant negative relationship was found between the detection rate of gastric cancer and the number of gastric images < 35 (OR: 0.305, 95% CI: 0.189-0.492, P = .000). There was also a negative correlation trend between the detection rate of pharyngeal and esophageal cancers and the number of esophageal images < 11 (OR: 0.395, 95% CI: 0.156-1.001, P = .050). The optimal number of images and screening 2-year interval are considered useful quality indicators for detecting UGI cancer. This study also suggests that a total of 50 images, or 35 images of the stomach are suitable for detecting UGI cancer, or gastric cancer, during screening endoscopy.

  • WJOG13219G: The Efficacy and Safety of FOLFOXIRI or Doublet plus Anti-VEGF Therapy in Previously Untreated BRAF<sup>V600E</sup> Mutant Metastatic Colorectal Cancer: A Multi-Institutional Registry-Based Study (BRACELET Study)

    Shimozaki K., Hirata K., Sato T., Nakamura M., Kato K., Hirano H., Kumekawa Y., Hino K., Kawakami K., Kito Y., Matsumoto T., Kawakami T., Komoda M., Nagashima K., Sato Y., Yamazaki K., Hironaka S., Takaishi H., Hamamoto Y., Muro K.

    Clinical Colorectal Cancer 21 ( 4 ) 339 - 346 2022.12

    ISSN  15330028

    　View Summary

    Background: The real-world survival benefit of FOLFOXIRI (fluorouracil, leucovorin, oxaliplatin, and irinotecan) plus anti-VEGF therapy (Triplet) over doublet chemotherapy (Doublet) remains controversial in patients with BRAFV600E mutant metastatic colorectal cancer (mCRC). Patients and Methods: WJOG13219G was a multicenter, retrospective, registry-based study of patients with BRAFV600E mutant mCRC who received first-line triplet or doublet chemotherapy from January 2014 to December 2019 in Japan. Inverse probability of treatment weighting (IPTW) was used to adjust for patient background. Results: The analysis included 79 and 91 patients in the Triplet and Doublet groups, respectively. The Triplet group was significantly younger and had better performance status. No statistical difference was noted in progression-free survival (PFS; HR, 0.82; 95% CI, 0.60–1.13; P = .22) and overall survival (OS; HR, 0.88; 95% CI, 0.62–1.25; P = .48) between both groups. IPTW analysis also showed no difference between the 2 groups in PFS (HR, 0.86; 95% CI, 0.69–1.08; P = .20) and OS (HR, 0.93; 95% CI, 0.73–1.20; P = .59). The Triplet and Doublet groups had an objective response rate of 53% and 41%, respectively (P = .10). At least one grade 3 or 4 adverse event was seen in 51 (65%) and 43 (47%) patients in the Triplet and Doublet groups, respectively, with the incidence of neutropenia being significantly higher in the former. Conclusion: Triplet therapy had no survival benefit versus doublet therapy in the overall and IPTW cohorts or specific subgroups for real-world patients with BRAFV600E mutant mCRC.

  • A significant risk of metabolic dysfunction-associated fatty liver disease plus diabetes on subclinical atherosclerosis

    Bessho R., Kashiwagi K., Ikura A., Yamataka K., Inaishi J., Takaishi H., Kanai T.

    PLoS ONE 17 ( 5 May )  2022.05

    　View Summary

    Background This cross-sectional study aims to investigate the association between subclinical atherosclerosis and metabolic dysfunction-associated fatty liver disease (MAFLD) or non-alcoholic fatty liver disease (NAFLD), and a synergistic effect of diabetes mellitus (DM) and MAFLD on subclinical atherosclerosis. Methods Of 977 subjects who underwent health checkups with coronary artery calcification (CAC), carotid intima-media thickness, and brachial-ankle pulse wave velocity (ba-PWV), 890 were included in this study. They were classified as MAFLD, NAFLD, or Neither-FLD, and MAFLD was further categorized into three groups by three metabolic disorders (obesity, lean with metabolic dysregulation, DM), according to its new definition: Obesity-MAFLD, Lean-MAFLD and DM-MAFLD. Results In a multivariable analysis, MAFLD and NAFLD were significantly associated with subclinical atherosclerosis, except for an association between ba-PWV and NAFLD. MAFLD had higher odds for CAC than NAFLD (for CAC score > 100, odds ratio (OR) = 2.599, 95% confidence interval (CI) = 1.625–4.157; OR = 1.795, 95%CI = 1.145–2.814, respectively). In a sub-analysis, DM-MAFLD had higher odds for CAC (for CAC score > 100, OR = 5.833, 95% CI = 3.047–11.164) than the other groups of MAFLD, when compared to Neither FLD as a reference. Moreover, DM-MAFLD had a higher level of homeostasis model assessment of insulin resistance and high sensitive C-reactive protein, compared to the other groups of MAFLD. Conclusions MAFLD was significantly associated with subclinical atherosclerosis in the general population. Additionally, DM-MAFLD could be a significant risk factor for cardiovascular disease through insulin resistance and low-grade inflammation and requires careful follow-up or appropriate intervention.

  • Unbiased, comprehensive analysis of Japanese health checkup data reveals a protective effect of light to moderate alcohol consumption on lung function

    Makino K., Shimizu-Hirota R., Goda N., Hashimoto M., Kawada I., Kashiwagi K., Hirota Y., Itoh H., Jinzaki M., Iwao Y., Ko M., Ko S., Takaishi H.

    Scientific Reports 11 ( 1 )  2021.12

    　View Summary

    The overall effect of lifestyle habits, such as alcohol consumption, on general health remains controversial and it is important to clarify how such habits affect aging-related health impairments. To discover novel impacts of lifestyle on general health, we employed a mathematical approach to perform a comprehensive, unbiased, cross-sectional analysis of data from 6036 subjects who participated in a Japanese health checkup. Notably, we found that moderate alcohol consumption was positively correlated with lung function, muscle mass, and strength. Health checkup data were collected periodically from the same subjects. These people were light to moderate drinkers who had high health awareness and were basically free of major underlying diseases. We next analyzed 5 years of data from 1765 of these subjects. We found that higher baseline alcohol consumption, as well as increased alcohol intake over 5 years attenuated time-related deterioration of forced vital capacity without affecting total lung volume. This effect was independent of smoking. Our study suggests a possible protective effect of moderate amounts of alcohol on lung function, due to increased muscle mass/strength and forced vital capacity.

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

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Reviews, Commentaries, etc. 【 Display / hide 】

  • Correction to: Predicting exacerbation of renal function by DNA methylation clock and DNA damage of urinary shedding cells: a pilot study (Scientific Reports, (2024), 14, 1, (11530), 10.1038/s41598-024-62405-4)

    Hishikawa A., Nishimura E.S., Yoshimoto N., Nakamichi R., Hama E.Y., Ito W., Maruki T., Nagashima K., Shimizu‑Hirota R., Takaishi H., Itoh H., Hayashi K.

    Scientific Reports 14 ( 1 )  2024.12

    　View Summary

    Correction to: Scientific Reportshttps://doi.org/10.1038/s41598-024-62405-4, published online 21 May 2024 The Acknowledgements section in the original version of this Article was incomplete. “We acknowledge Dr. Hideaki Nakaya for assistance during the initial stage of this study. This study was supported by the Grants for Scientific Research (22H03091) from the Ministry of Education, Culture, Sports, Science and Technology (MEXT) of Japan and a grant from the Japan Foundation for Applied Enzymology.” now reads: "We acknowledge Dr. Hideaki Nakaya for assistance during the initial stage of this study. This study was supported by the Grants for Scientific Research (22H03091) from the Ministry of Education, Culture, Sports, Science and Technology (MEXT) of Japan, the JST FOREST Program (Grant number JPMJFR210V, Japan) and a grant from the Japan Foundation for Applied Enzymology.” The original Article has been corrected.

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Presentations 【 Display / hide 】

  • Racl Activation Promotes Invasive Phentype of Side Population in Cancer Cells by Destalizing the E-cadherin-βcatenin Ligation.

    TAKAISHI HIROMASA

    The 8th international symposium on cancer research and therapy., 

    2012.11

  • 切除不能胃癌に対するPaclitaxel、CDDP、S-1併用化学療法の臨床第Ⅰ相試験(KOGC-02)

    TAKAISHI HIROMASA

    第50回日本癌治療学会学術集会, 

    2012.10

  • 外来がん化学療法における副作用マネジメントシステムの構築と実践-カペシタビンによる手足症候群対策-

    TAKAISHI HIROMASA

    第10回日本臨床腫瘍学会学術総会, 

    2012.07

  • HER2陽性胃癌のセカンドライン治療をどう行うか

    TAKAISHI HIROMASA

    第10回日本臨床腫瘍学会学術総会, 

    2012.07

  • PEM+CDDPによる全身化学療法が著効した作成腹膜中皮腫の一例

    TAKAISHI HIROMASA

    第319回日本消化器病学会関東支部例会, 

    2012.05

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

  • 膵胆道癌細胞における抗アポトーシス遺伝子発現調整機構の解析と分子標的治療への応用

    2006
    -
    2007

    基盤研究(C), Grant-in-Aid for Scientific Research, No Setting

  • 膵癌細胞における上皮由来増殖因子シグナルの解析とアポトーシス抵抗性機序の解明

    2006
    -
    2007

    基盤研究(C), Grant-in-Aid for Scientific Research, No Setting

  • 消化器癌における癌幹細胞の同定、分離および生物学的特性の解析

    2008
    -
    2010

    基盤研究(C), Grant-in-Aid for Scientific Research, No Setting

  • プロテオミクス解析およびパスウェイ解析による新規胃癌バイオマーカーの検討

    2014
    -
    2016

    基盤研究(C), Grant-in-Aid for Scientific Research, No Setting

  • リシルオキシダーゼによる血管平滑筋細胞脱分化が大動脈解離発症に与える影響の検討

    2022.04
    -
    2025.03

    MEXT,JSPS, Grant-in-Aid for Scientific Research, 基盤研究(C), Principal investigator

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Awards 【 Display / hide 】

  • 第26回日本消化器病学会奨励賞

    2012

  • 第14回日本消化器病学会奨励賞

    2001

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Courses Taught 【 Display / hide 】

  • LECTURE SERIES, INTERNAL MEDICINE (GASTROENTEROLOGY)

    2022

  • LECTURE SERIES, INTERNAL MEDICINE (GASTROENTEROLOGY)

    2021

  • LECTURE SERIES, INTERNAL MEDICINE (GASTROENTEROLOGY)

    2020

  • LECTURE SERIES, INTERNAL MEDICINE (GASTROENTEROLOGY)

    2019

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Courses Previously Taught 【 Display / hide 】

  • 臨床腫瘍

    Keio University

    2018.04
    -
    2019.03

  • 消化器内科

    Keio University

    2018.04
    -
    2019.03

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Educational Activities and Special Notes 【 Display / hide 】

  • 基礎診断学「消化器」下部消化管の腫瘍性疾患 各論「消化器」消化器悪性腫瘍の化学療法

    2006
    -
    Present

    , Device of Educational Contents

  • 学生症例検討クルズス担当

    2006
    -
    Present

    , Device of Educational Contents

  • 慶應義塾大学病院看護部・がん化学療法講習会

    2006.09

    , Lecture at Education Method and Practice

  • 慶應義塾大学21世紀COEプログラム 研究会報告「がん治療認定医制度をめぐって」

    2007.04

    , Device of Educational Contents

  • 慶應義塾大学病院看護部・がん看護研修　第1回総論

    2008
    -
    2011

    , Device of Educational Contents

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Memberships in Academic Societies 【 Display / hide 】

  • 日本内科学会

    　

  • 日本消化器病学会

    　

  • 日本消化器内視鏡学会

    　

  • 日本癌学会

    　

  • 日本癌治療学会

    　

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Committee Experiences 【 Display / hide 】

  • 2002.04

    リサーチレジメント, 厚生労働省

  • 2008
    -
    Present

    がん登録部会委員, 東京都がん診療連携協議会

  • 2008
    -
    Present

    研修部会委員, 東京都がん診療連携協議会

  • 2008
    -
    Present

    クリティカルパス部会委員, 東京都がん診療連携協議会

  • 2008
    -
    Present

    相談・情報部会委員, 東京都がん診療連携協議会

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