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  2. Saya Hideyuki

Saya Hideyuki

  (佐谷 秀行)

Profile Information

Affiliation
Professor (Director), Oncology Innovation Center, Fujita Health University
(Concurrent)Director, Translational Research Center
(Professor Emeritus), Keio University
Researcher number
80264282
J-GLOBAL ID
200901021585172745
researchmap Member ID
1000222498
Hideyuki Saya MD, PhD graduated from Kobe University School of Medicine in 1981 and was Resident in the Neurosurgery until 1983. After which he joined the Graduate School of Medical Sciences granting his PhD in 1987. He studied as a Postdoctoral Fellow in UCSF until 1988 then was appointed Assistant Professor at the Neuro-Oncology, M.D. Anderson Cancer Center. Houston, TX. From 1994 to 2006 he was Professor, Kumamoto University School of Medicine before taking his current position in Keio University School of Medicine in 2007. He is currently a vice president of Keio University Hospital and Director of Clinical and Translational Research Center.

Research Areas

 1

Research History

 1

Awards

 9
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Papers

 628
  • Kenji Zennami, Tetsuya Takimoto, Takuhisa Nukaya, Makoto Sumitomo, Mayu Takeda, Eiji Sugihara, Hideyuki Saya, Ryoichi Shiroki
    Cancer science, Mar 18, 2026  
    The clinical significance of comprehensive genomic profiling (CGP) has been established in metastatic castration-resistant prostate cancer (PC). However, the role of genomic profiling in localized PC remains unclear. In this exploratory study, we evaluated somatic genomic alterations in localized PC using an in-house CGP platform to examine their associations with biochemical recurrence (BCR) and recurrence-free survival (RFS) after radical prostatectomy. DNA extracted from surgical specimens of 314 patients with localized PC was analyzed for alterations in 164 cancer-related genes. Six genes (PTEN, BRCA2, POLD1, ERBB3, MYC, and SETD2) were more frequently altered in patients who developed BCR in exploratory analyses. Patients harboring alterations in any of these genes (n = 96) showed higher pathological T stage, increased BCR rates (27.1% vs. 6.4%), and inferior RFS compared with alteration-negative patients (n = 218; p < 0.001). In multivariate analysis, the presence of these alterations was independently associated with worse RFS. Among individual genes, BRCA2 alteration, and particularly BRCA2-SETD2 co-alteration, were associated with unfavorable outcomes, although the latter finding was based on a limited number of cases. In patients who developed BCR, alterations were associated with shorter PSA doubling time and poorer outcomes after salvage radiotherapy, particularly in margin-negative cases; however, these subgroup analyses were based on small numbers and should be interpreted as hypothesis-generating. These findings suggest that somatic genomic alterations identified at prostatectomy are associated with early recurrence in localized PC. Further validation in independent cohorts is required to determine whether genomic profiling may contribute to future risk stratification and management strategies.
  • Daijiro Kojima, Shigeo Ohba, Yuya Nishiyama, Kazuhide Adachi, Madoka Isomura, Yuka Kondo, Mayu Takeda, Seiji Yamada, Jun Muto, Eiji Sugihra, Sachiko Minamiguchi, Kenji Kawada, Hideyuki Saya, Yuichi Hirose
    Clinical neurology and neurosurgery, 265 109371-109371, Mar 2, 2026  
    OBJECTIVE: Central nervous system (CNS) solitary fibrous tumors (SFTs) are rare mesenchymal neoplasms with a high propensity for local recurrence and extracranial metastasis. Although surgery and radiotherapy are the mainstays of treatment, systemic therapeutic options for recurrent disease remain limited. Pazopanib, a multitargeted tyrosine kinase inhibitor, has demonstrated clinical activity in extracranial SFTs; however, evidence in CNS SFTs is scarce. METHODS: We conducted a retrospective, single-institution study of patients with recurrent CNS SFTs treated with pazopanib. Clinical data, including prior treatments, imaging responses, treatment duration, and adverse events, were collected from medical records. Exploratory next-generation sequencing-based cancer panel testing was performed in two patients. RESULTS: Four patients with recurrent CNS SFTs were included. All had undergone prior surgical resection and radiotherapy. Pazopanib achieved partial response in one patient and stable disease in three patients, with treatment durations ranging from 7 months to over 2 years. One patient experienced disease progression after an initial period of response. Adverse events, including fatigue, gastrointestinal symptoms, and hypertension, were observed in all patients but were generally manageable with supportive care or dose adjustment. Exploratory molecular profiling identified various genomic alterations in two patients. CONCLUSIONS: In this single-institution retrospective series, pazopanib provided durable disease control with acceptable tolerability in selected patients with recurrent CNS SFTs. These findings support considering pazopanib as a systemic treatment option when further local therapies are not feasible, while highlighting the need for larger multicenter studies.
  • Yu Kato, Naoki Yamamoto, Yuichiro Uchida, Noriko Hiramatsu, Takato Ozeki, Yukari Minobe, Yukika Hasegawa, Sho Kawabe, Hikaru Yabuuchi, Seiji Yamada, Yuko Hata, Eiji Sugihara, Tetsuya Takimoto, Kuniaki Saito, Takeshi Takahara, Koichi Suda, Osamu Nagano, Hideyuki Saya
    Cells, 15(4) 313-313, Feb 7, 2026  
    Pancreatic cancer is a highly intractable malignancy that necessitates personalized treatment strategies. Conventional patient-derived models, such as three-dimensional organoids, are often limited by intellectual property constraints and high costs. In this study, we developed an affordable adherent culture system for patient-derived pancreatic cancer cells using a proprietary medium and laminin-coated dishes. Primary cultures were successfully established from 28 patients with pancreatic ductal adenocarcinoma, exceeding a 90% success rate. Validation of eight samples confirmed maintenance of epithelial cell adhesion molecule expression and preservation of oncogenic KRAS mutations. Transcriptomic profiling revealed consistent upregulation of a six-gene signature (FAP, IGFBP5, PRRX1, SPARC, WNT5A, and ADAMTS12), which is associated with malignancy. In vitro drug sensitivity assays revealed interpatient heterogeneity with preliminary clinical associations. In conclusion, this simplified platform provides high-purity cancer cells and serves as a functional precision medicine tool. Beyond conventional chemotherapy, this platform has the potential to support applications ranging from biomarker validation and exploratory preclinical testing of novel therapeutics, including immune checkpoint inhibitors and antibody–drug conjugates. This optimization can lead to personalized therapeutic strategies for pancreatic cancer.
  • Seiji Yamada, Tetsuya Takimoto, Yoshiteru Shimoda, Fumiharu Ohka, Masayuki Kanamori, Kennosuke Karube, Hidenori Endo, Ryuta Saito, Hideyuki Saya, Eiji Sugihara
    Brain tumor pathology, Jan 21, 2026  
  • Shogo Okazaki, Shintaro Nakamura, Tomoya Soma, Momoko Yoshikawa, Seiji Asoda, Yurika Nakajima, Kenji Tsuchihashi, Mitsuyo Ohmura, Ryo Goitsuka, Kenichi Imai, Hideyuki Saya, Osamu Nagano, Hiroyuki Ozawa
    Cancer science, Nov 20, 2025  
    Redox regulation is a key mechanism supporting tumor survival and an attractive therapeutic target. In this study, we screened 1161 FDA-approved compounds to identify agents that induce reactive oxygen species (ROS) accumulation in head and neck squamous cell carcinoma (HNSCC) cells. Pimozide, a dopamine D2 receptor antagonist, emerged as the most potent ROS inducer. It selectively suppresses the growth of HNSCC cells with high oxidative stress resistance while exhibiting only modest effects on less resistant cells and normal keratinocytes. Notably, pimozide exhibited anti-tumor effects as a monotherapy and in combination with paclitaxel at clinically relevant doses. Mechanistic analysis revealed that pimozide rapidly induced ROS accumulation via a mechanism distinct from its known action on dopamine D2 receptors and STAT3/5. To identify markers of ROS-induced responses, we examined ROS-responsive genes and found that early growth response 1 (EGR1) was selectively induced in sensitive cells and correlated with pimozide responsiveness. Functional analysis revealed that EGR1 knockdown suppressed pimozide-induced cytotoxicity, suggesting its role as a functional pharmacodynamic marker of pimozide sensitivity. In a patient-derived xenograft model of HNSCC, pimozide significantly reduced the tumor burden alone and in combination with paclitaxel. While tumor volume reduction in the combination group was not statistically greater than that in the monotherapy group, fluorescence immunohistochemistry revealed a marked decrease in undifferentiated tumor cells, indicating enhanced therapeutic effects of combination treatment. Taken together, these findings indicate that pimozide is a promising candidate for repurposing as a novel therapeutic agent against HNSCC.
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