SASAKI Yasushi

写真a

Affiliation

Medical Development Center Dean, Department of Liberal Arts and Sciences, Biology

Job title

Professor

Education 【 display / non-display

  •  
    -
    1988

    Sapporo Medical University   School of Medicine   医学科  

Degree 【 display / non-display

  • 札幌医科大学   Ph.D.(Medical Science)

Research Experience 【 display / non-display

  • 2018.01
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    Now

    Sapporo Medical University   Center for Medical Education   教授

  • 2018.01
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    Now

    Sapporo Medical University   Graduate School of Medicine   教授

  • 2008.06
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    2017.12

    Sapporo Medical University   School of Medicine   准教授

  • 2004.04
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    2008.05

    Sapporo Medical University   School of Medicine   講師

  • 1999.10
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    2004.03

    Sapporo Medical University   School of Medicine   助手

Professional Memberships 【 display / non-display

  • 2021.04
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    Now

    Japan Association for Medical Informatics

  • 2018.04
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    Now

    日本医学教育学会

  • 2010.01
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    Now

    International Society of Oncology & BioMarkers (ISOBM)

  • 2009.01
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    Now

    THE JAPAN SOCIETY OF DRUG DELIVERY SYSTEM

  • 2005.01
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    Now

    Japanese Society of Molecular Medicine

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Research Areas 【 display / non-display

  • Life sciences   Genomics  

  • Life sciences   Tumor biology  

  • Life sciences   Gastroenterology  

Affiliation 【 display / non-display

  • 札幌医科大学   医療人育成センター 教養教育研究部門・生物学   教授  

 

Research Interests 【 display / non-display

  • 癌抑制遺伝子

  • 次世代シーケンサー

  • p53関連遺伝子

  • 消化器癌

  • p53

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Papers 【 display / non-display

  • Targeted dynamic phospho-proteogenomic analysis of gastric cancer cells suggests host immunity provides survival benefit.

    Kohei Kume, Midori Iida, Takeshi Iwaya, Akiko Yashima-Abo, Yuka Koizumi, Akari Endo, Kaitlin Wade, Hayato Hiraki, Valerie Calvert, Julia Wulfkuhle, Virginia Espina, Doris R Siwak, Yiling Lu, Kazuhiro Takemoto, Yutaka Suzuki, Yasushi Sasaki, Takashi Tokino, Emanuel Petricoin 3rd, Lance A Liotta, Gordon B Mills, Satoshi S Nishizuka

    Molecular & cellular proteomics : MCP     100870 - 100870  2024.10  [International journal]

     View Summary

    Despite of massive emergence of molecular targeting drugs, the mainstay of advanced gastric cancer (GC) therapy is DNA-damaging drugs. Using a reverse-phase protein array-based proteogenomic analysis of a panel of eight GC cell lines, we identified genetic alterations and signaling pathways, potentially associated with resistance to DNA-damaging drugs, including 5-fluorouracil (5FU), cisplatin, and etoposide. Resistance to cisplatin and etoposide, but not 5FU, was negatively associated with global copy number loss, vimentin expression, and caspase activity, which are considered hallmarks of previously established EMT subtype. The segregation of 19,392 protein expression time courses by sensitive and resistant cell lines for the drugs tested revealed that 5FU-resistant cell lines had lower changes in global protein dynamics, suggesting their robust protein level regulation, compared to their sensitive counterparts, whereas the cell lines that are resistant to other drugs showed increased protein dynamics in response to each drug. Despite faint global protein dynamics, 5FU-resistant cell lines showed increased STAT1 phosphorylation and PD-L1 expression in response to 5FU. In publicly available cohort data, expression of STAT1 and NFκB target genes induced by proinflammatory cytokines was associated with prolonged survival in GC. In our validation cohort, total lymphocyte count (TLC), rather than PD-L1 positivity, predicted a better relapse-free survival rate in GC patients with 5FU-based adjuvant chemotherapy than those with surgery alone. Moreover, TLC+ patients who had no survival benefit from adjuvant chemotherapy were discriminated by expression of IκBα, a potent negative regulator of NFκB. Collectively, our results suggest that 5FU resistance observed in cell lines may be overcome by host immunity or by combination therapy with immune checkpoint blockade.

    DOI PubMed

  • Synchronous cancers of the stomach and esophagus in a patient with autoimmune gastritis and pernicious anemia: a case report and review of the literature.

    Toshiyuki Kubo, Yasushi Adachi, Yasushi Sasaki, Yasuyo Adachi, Yukinari Yoshida, Takao Endo, Yoshifumi Ishii, Hiroaki Takahashi, Akira Goto

    International cancer conference journal   13 ( 4 ) 367 - 373  2024.10  [Refereed]  [International journal]

     View Summary

    Type-A gastritis/autoimmune gastritis (AIG) has gained renewed attention due to declining Helicobacter pylori infection rates and increasing eradication. AIG is associated with pernicious anemia (PA) and is prone to complicate various tumors, such as gastric cancer and neuroendocrine tumors. This report describes a case of AIG with PA in which gastric and esophageal cancers arose simultaneously. An 86-year-old woman had been diagnosed with PA and AIG 9 years earlier. As routine blood tests revealed high levels of carcinoembryonic antigen, she underwent esophagogastroduodenoscopy, which revealed a type 0-IIa lesion in the middle part of the stomach and a type 0-IIa + IIb lesion in the lower esophagus. Endoscopic submucosal dissection was performed on both lesions, since neither distant nor lymph node metastases were identified. Histological examination showed gastric tubular adenocarcinoma and esophageal squamous cell carcinoma. Immunohistology revealed that cells from neither cancer expressed gastrin, gastrin receptor, or p53. Whole-exome sequencing showed 8 gene mutations in the esophageal cancer and 6 mutations in 5 genes in the gastric cancer. The reason for the lack of p53 immunostaining was that TP53 was mutated in these cancers, although TP53 mutations differed. Thus, TP53 mutations may not be detected by immunostaining alone. When treating patients with AIG/PA, clinicians must be aware of the possibility of esophageal cancer coexisting with gastric cancer.

    DOI PubMed

  • Association of serum superoxide dismutase activity and the incidence of colorectal cancer in a nested case-control study.

    Yasushi Adachi, Masanori Nojima, Mitsuru Mori, Hiro-O Yamano, Yasushi Sasaki, Hiroshi Nakase, Yingsong Lin, Kenji Wakai, Akiko Tamakoshi

    Cancer epidemiology   87   102455 - 102455  2023.09  [Refereed]  [International journal]

     View Summary

    BACKGROUND: Superoxide dismutase (SOD) is an antioxidant enzyme that degrades superoxide, a major causative factor in carcinogenesis. We assessed associations between serum SOD activities and incidence of colorectal carcinoma (CRC) in a case-control study nested in the Japan Collaborative Cohort (JACC) study. METHODS: At baseline, 39,242 subjects donated serum samples. Participants diagnosed with CRC during follow-up were regarded as cases. Odds ratios (ORs) for CRC incidence associated with SOD were evaluated with conditional logistic regression models. In the current study, 176 cases and 524 controls were analyzed. RESULTS: For the overall cohort, a decreasing trend in risk of CRC with increasing SOD was observed (P for trend=0.054) and the fourth quartile of SOD level showed the lowest risk compared to the first (OR=0.52, 95% confidence interval [CI]=0.29-0.93). This was significant in men (P for trend=0.001), with the fourth quartile of SOD level showing the lowest risk compared to the first (OR, 0.23; 95%CI, 0.09-0.60). It was also exclusively observed for rectal cancer and left-sided CRC (P for trend, 0.037 and 0.020, respectively), with the fourth quartile again showing the lowest risk compared to the first (OR, 0.28 and 0.38; 95%CI, 0.09-0.84 and 0.16-0.91, respectively). Limiting subjects to those followed-up over 2 years, all trends remained unchanged. CONCLUSIONS: Our findings suggest that serum SOD activity correlates inversely with risk of CRC, particularly in men and individuals with rectal cancer/left-sided CRC.

    DOI PubMed J-GLOBAL

  • Esophageal intraepithelial squamous cell neoplasia with epidermalization-A case with molecular analysis.

    Takao Endo, Toshiyuki Kubo, Yasushi Sasaki, Hiroaki Takahoshi, Yoshifumi Ishii, Yasushi Adachi

    Pathology international    2023.06  [Refereed]  [International journal]

    DOI PubMed

  • Serum soluble Fas levels and incidence of liver cancer in nested case-control study.

    Yasushi Adachi, Masanori Nojima, Mitsuru Mori, Toshiyuki Kubo, Noriyuki Akutsu, Yasushi Sasaki, Hiroshi Nakase, Yingsong Lin, Youichi Kurozawa, Kenji Wakai, Akiko Tamakoshi

    Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology   82nd  2022.12  [Refereed]  [International journal]

     View Summary

    BACKGROUND: Soluble Fas (sFas) plays various roles in carcinogenesis and tumor dissemination by preventing apoptosis via binding to Fas ligand. We analyzed associations of serum sFas levels with the incidence of liver cancer in a prospective case-control study nested in the JACC Study. METHODS: A baseline survey was conducted from 1988, with blood samples obtained from 39,242 subjects. Patients diagnosed with liver cancer were regarded as cases. Two or three controls were selected and matched for sex, age, and geographical area. Conditional logistic regression was used to estimate odds ratios (ORs) for cancer incidence associated with sFas. RESULTS: This study contained 86 cases and 249 controls. After controlling for alcohol intake, body mass index, smoking, and hepatitis viral infection, participants with high sFas showed elevated risk of cancer (P-trend = 0.003) and the third tertile of sFas showed a higher risk compared to the first tertile (OR = 3.53, 95% confidence interval (CI) = 1.28-9.69). In hepatocellular carcinoma, high sFas was associated with elevated risk (P-trend < 0.001). In men and the elderly, subjects in the highest tertiles showed higher cancer risk. Limiting subjects to those followed for 3 years, high sFas was related to liver cancer risk (P-trend = 0.033) and the third tertile showed a higher risk compared to the first (OR = 2.94, 95%CI = 0.94-9.14). CONCLUSIONS: High serum sFas may be related to future risk of liver cancer. IMPACT: Our findings highlight this biomarker for further analysis in pooled investigations with different/larger prospective cohorts.

    DOI PubMed J-GLOBAL

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Books and Other Publications 【 display / non-display

  • 分子標的療法の基礎と臨床

    佐々木 泰史, 時野 隆至( Part: Contributor, p53, p63, p73の機能とp53ファミリーを標的としたがん療法への応用)

    篠原出版新社  2005

  • 内科疾患クリニカルガイド 消化器・免疫・血液・代謝疾患

    佐々木 泰史( Part: Contributor, 癌性疼痛治療の実際)

    中山書店  1999

  • 日本臨床別冊巻 肝・胆道系症候群 肝臓編(上巻)

    佐々木泰史, 坂本裕史, 日野田裕治, 矢花剛( Part: Joint author, 肝粘表皮癌、肝内胆管粘表皮癌)

    日本臨床社  1995.04

  • 血液学

    今井浩三, 佐々木泰史, 辻崎正幸( Part: Contributor, 原発性マクログロブリン血症)

    中外医学社  1991

  • Therapeutic plasmapheresis VIII

    Suga M, Tsuchida M, Arimura Y, Matsuno K, Sasaki Y, Miyachi T, Ishida S, Yachi A( Part: Contributor, Basic and clinical evaluation of anion exchange resin column for treatment of jaundice)

    ISAO Press  1989

Misc 【 display / non-display

  • 内視鏡的切除により診断できた皮膚様食道扁平上皮癌

    足立 靖, 菊地 剛史, 後藤 啓, 吉田 幸成, 石井 良文, 高橋 宏明, 佐々木 泰史, 仲瀬 裕志, 遠藤 高夫

    日本消化管学会雑誌 ( (一社)日本消化管学会 )  8 ( Suppl. ) 360 - 360  2024.01

  • 症例報告からPrecision Medicineへ-第1部- 悪性貧血を伴う自己免疫性胃炎における胃癌と食道癌の同時発生(Simultaneous cancers of the stomach and esophagus in autoimmune gastritis with pernicious anemia)

    足立 靖, 久保 俊之, 佐々木 泰史, 安達 靖代, 吉田 幸成, 遠藤 高夫, 石井 良文, 高橋 宏明, 後藤 啓

    日本癌治療学会学術集会抄録集 ( (一社)日本癌治療学会 )  61回   ICCJ1 - 3  2023.10

  • Association of serum superoxide dismutase activity and the incidence of colorectal cancer in a nested case-control study.

    Yasushi Adachi, Masanori Nojima, Mitsuru Mori, Hiro-O Yamano, Yasushi Sasaki, Hiroshi Nakase, Yingsong Lin, Kenji Wakai, Akiko Tamakoshi

    Cancer epidemiology ( (一社)日本癌学会 )  87   102455 - 102455  2023.09  [International journal]

     View Summary

    BACKGROUND: Superoxide dismutase (SOD) is an antioxidant enzyme that degrades superoxide, a major causative factor in carcinogenesis. We assessed associations between serum SOD activities and incidence of colorectal carcinoma (CRC) in a case-control study nested in the Japan Collaborative Cohort (JACC) study. METHODS: At baseline, 39,242 subjects donated serum samples. Participants diagnosed with CRC during follow-up were regarded as cases. Odds ratios (ORs) for CRC incidence associated with SOD were evaluated with conditional logistic regression models. In the current study, 176 cases and 524 controls were analyzed. RESULTS: For the overall cohort, a decreasing trend in risk of CRC with increasing SOD was observed (P for trend=0.054) and the fourth quartile of SOD level showed the lowest risk compared to the first (OR=0.52, 95% confidence interval [CI]=0.29-0.93). This was significant in men (P for trend=0.001), with the fourth quartile of SOD level showing the lowest risk compared to the first (OR, 0.23; 95%CI, 0.09-0.60). It was also exclusively observed for rectal cancer and left-sided CRC (P for trend, 0.037 and 0.020, respectively), with the fourth quartile again showing the lowest risk compared to the first (OR, 0.28 and 0.38; 95%CI, 0.09-0.84 and 0.16-0.91, respectively). Limiting subjects to those followed-up over 2 years, all trends remained unchanged. CONCLUSIONS: Our findings suggest that serum SOD activity correlates inversely with risk of CRC, particularly in men and individuals with rectal cancer/left-sided CRC.

    DOI PubMed

  • 血清可溶性Fas値と肝臓癌罹患リスク(Serum soluble Fas levels and incidence of liver cancer)

    足立 靖, 野島 正寛, 森 満, 久保 俊之, 阿久津 典之, 佐々木 泰史, 仲瀬 裕志, 遠藤 高夫, 林 櫻松, 若井 建志, 玉腰 暁子

    日本癌学会総会記事 ( (一社)日本癌学会 )  82回   125 - 125  2023.09

  • Prospective observational study of monitoring gene alterations in plasma cell-free DNA using droplet digital PCR system during anti-EGFR antibody treatment in patients with RAS wild-type advanced colorectal cancer.

    Naoki Takahashi, Keishi Nakamura, Yosuke Kito, Eiji Kubota, Masako Asayama, Yosuke Kumekawa, Hiroki Hara, Tomohiro Matsushima, Kunihiro Tsuji, Hiromi Kataoka, Akihiro Tsuyada, Yasushi Sasaki, Masashi Idogawa, Takashi Tokino, Takeshi Sawada

    Journal of Clinical Oncology ( American Society of Clinical Oncology (ASCO) )  41 ( 4_suppl ) 172 - 172  2023.02

    Research paper, summary (international conference)  

     View Summary

    172 Background: Anti-EGFR antibody is recommended as one of the standard treatments in patients with RAS wild-type advanced colorectal cancer (CRC). Few reports have evaluated low-frequency subclones of alterations in EGFR signaling pathway genes in plasma cell-free DNA (cfDNA) during anti-EGFR treatment in prospective cohort of advanced CRC patients. Methods: Key inclusion criteria of this study was as follows: 20 years old and over, performance status 0 to 2, metastatic or recurrent CRC (adenocarcinoma), RAS wild-type CRC diagnosed by PCR-rSSO using tumor tissue, no prior use of anti-EGFR antibody. Plasma samples were prospectively collected at pre-treatment, at 4, 10 weeks, every 10 weeks thereafter, and at the end of the anti-EGFR treatment. With QX200 Droplet Digital PCR platform, we analyzed hotspot mutations of KRAS, NRAS, BRAF, and PIK3CA and copy number (CN) variant of HER2 and MET using plasma samples of pre- and post-treatment as well as during treatment (limited to patients with any gene alterations at pre- and post-treatment). Results: Total 50 patients were registered in this study, but 3 patients were excluded because inclusion criteria were not met. Finally, 47 patients were included in full analysis set. In 15 patients (31.9%), genetic alterations including KRAS (G12G13: 10.1%, A59Q61: 2.2%), NRAS (G12G13: 2.2%, Q61: 2.1%), BRAF (V600: 6.4%) , PIK3CA (E545: 4.3%, H1047: 4.3%) , and HER2 (amplification: 6.5%) were detected in pre-treatment samples. Analysis of pre-treatment samples showed that response rates of patients with any gene alterations (N = 13) and that without any gene alterations (N = 29) were 30.8% and 58.6%, respectively (p = 0.095). When the cut-off of variant allele frequency (VAF) was set as 0.5% in patients with any gene mutations, the response rates for cases with VAF ≥0.5% (N = 6) and those with VAF < 0.5% (N = 7) were 0% and 57.1%, respectively (p = 0.049). Among 41 patients with detectable target lesions by CT scan, there was significant difference in percentage of best tumor shrinkage between patients with gene alterations and those without gene alterations (32.1% vs 10.5%, p = 0.037), when cut-off VAF of any gene mutations was set as 0.5% and cut-off CN of HER2 or MET was set as 4 at pre-treatment. Due to dynamics of each gene alteration in cfDNA during treatment, mutations of KRAS A59Q61, NRAS Q61, and MET amplification were characterized as acquired alterations which were newly detected after the administration of anti-EGFR antibodies. Conclusions: Our study demonstrated the clinical relevance of minor mutant subclones in EGFR signaling pathway genes in plasma for predicting response to anti-EGFR treatment. Although sample size of this study was small, preferable threshold for distinguishing responders from non-responders may be 0.5% as VAF of these gene mutations. Clinical trial information: 000034923 .

    DOI

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Industrial Property Rights 【 display / non-display

Other 【 display / non-display

  • 緩和ケア研修会修了(北-4252号)

    2017.05
     
     
  • 日本がん治療認定医機構 がん治療認定医(第09100061号)

    2010.04
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    Now
  • 日本癌治療学会臨床試験登録医 (0985号)

    2004.08
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    Now
  • 日本肝臓学会肝臓専門医(3150号)

    1999.04
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    Now
  • 日本消化器内視鏡学会 専門医(0094005号)

    1994.12
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    Now

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Awards 【 display / non-display

  • 北海道医師会賞

    2021.10  

    Winner: Yasushi Sasaki

  • 北海道知事賞

    2021.10   がん抑制遺伝子p53とそのファミリー (p73、p63)の機能解明

    Winner: Yasushi Sasaki

  • 第14回日本消化器関連学会週間優秀演題賞

    2006.12   日本消化器関連学会週間  

    Winner: Yasushi Sasaki

  • 第44回日本癌治療学会総会優秀演題賞

    2006.10   日本癌治療学会総会  

    Winner: Yasushi Sasaki

  • 札幌医科大学医師会学術賞

    2003.03   札幌医科大学医師会  

    Winner: Yasushi Sasaki

Research Projects 【 display / non-display

  • Development of molecular targeted therapy for primary central nervous system lymphomas based on genome and metabolome data.

    Grant-in-Aid for Scientific Research (B)

    Project Year :

    2024.04
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    2026.03
     

    山中 龍也, 高島 康郎, 川口 淳, 佐々木 泰史, 深井 順也

  • p53の機能獲得変異に関わる小型タンパク質の探索と機能解明

    日本イーライリリー イノベーション研究助成

    Project Year :

    2023.12
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    2025.03
     

    佐々木泰史

    Authorship: Principal investigator

  • p53ネットワークに関わるマイクロプロテインの探索と食道扁平上皮癌新規治療戦略

    科学研究費助成事業 基盤研究(C)

    Project Year :

    2023.04
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    2026.03
     

    佐々木 泰史

    Authorship: Principal investigator

  • 非乳頭部十二指腸腺癌の2つの独立した発癌経路の検証とその分子機構の解明

    金沢大学がん進展制御研究所共同研究(一般研究、新規)

    Project Year :

    2023.04
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    2024.03
     

    佐々木泰史, 澤田 武, 中村 慶史, 源 利成

    Authorship: Principal investigator

  • p53標的小型タンパク質の探索と機能解明

    2023年度 秋山記念生命科学振興財団 研究助成(一般)

    Project Year :

    2023.04
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    2024.03
     

    Yasushi Sasaki

    Authorship: Principal investigator

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Committee Memberships 【 display / non-display

  • 2022.04
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    Now

      日本電気泳動学会 評議員

  • 2012.01
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      日本DDS学会 評議員

  • 2011.01
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      日本臨床分子医学会 評議員

  • 2010.01
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      日本癌学会 評議員

  • 2005.01
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      日本消化器病学会 北海道支部評議員

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Social Activities 【 display / non-display

  • 札幌医科大学ゴルフ部 顧問

    2014.04
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    Now

Academic Activities 【 display / non-display

  • Translational Oncology: International Advisory Review Board

  • Gastroenterology Insights: Editorial Board

  • Molecular Medicine Reports: Editorial Board