Updated on 2026/08/27

Information

 

写真a

 
ANDO YUKI
 
Organization
Beppu Hospital Department of Surgery Assistant Professor
Title
Assistant Professor
External link

Degree

  • MD.PhD （ 2025.7 Kyushu University ）

Papers

  • Identification of the novel therapeutic target gene SLC12A9, which determines the prognosis of patients with colorectal cancer Reviewed

    Yonemura Y., Ofuchi T., Nakano T., Higuchi S., Kawata K., Ikehara T., Omachi K., Tsujimoto A., Hirose K., Shibuta S., Ando Y., Hu Q., Otsu H., Yoshizumi T., Mimori K.

    Surgery Today   56 ( 7 )   1412 - 1422   2026.7   （ ISSN:09411291 ）

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    Language：English   Publisher：Surgery Today  

    Background: Feasible therapeutic targets need to be identified to overcome tumor heterogeneity and ameliorate therapeutic resistance. We explored the identification of oncogenes on Ch.7q, which is amplified ubiquitously in colorectal cancer (CRC). In this study, we focused on SLC12A9, which encodes a channel protein that regulates ion concentration inside and outside of the cell. Materials and methods: Expression and survival analyses of SLC12A9 were performed using reverse transcription quantitative polymerase chain reaction, The Cancer Genome Atlas dataset, and immunohistochemistry. A gene set enrichment analysis (GSEA) was performed to elucidate the correlation between SLC12A9 and gene sets associated with tumor progression. Subsequently, an in vitro proliferation assay was performed using SLC12A9-knockdown CRC cells. Results: SLC12A9 was highly expressed in tumor cells, and its high expression was associated with a poor prognosis. The GSEA revealed an association with mTORC1 signaling. In the colony formation assay, SLC12A9 knockdown by siRNA suppressed the proliferative capacity of CRC cells. Public single-cell RNA sequencing data have revealed that SLC12A9 is derived from malignant epithelial cells in CRC tissues. Conclusion: Our results suggest that abundant SLC12A9 expression is associated with a poor prognosis due to the devastating growth of CRC cells, in part via the mTORC1 signaling pathway.

    DOI： 10.1007/s00595-025-03214-8

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  • Identification of the Inflammatory Cytokine Tumor Necrosis Factor Superfamily 4 as an Oncogenic Driver and Potential Druggable Target in Hepatocellular Carcinoma(タイトル和訳中) Reviewed

    Hosoda Kiyotaka, Masuda Takaaki, Saito Hideyuki, Koike Kensuke, Ando Yuki, Abe Tadashi, Hashimoto Masahiro, Nakano Yusuke, Dairaku Katsushi, Hirose Kosuke, Matsumoto Chihiro, Ikehara Tomohiko, Ofuchi Takashi, Kawata Koto, Omachi Kazuki, Tobo Taro, Tsuda Yasuo, Otsu Hajime, Yonemura Yusuke, Shimizu Akira, Soejima Yuji, Mimori Koshi

    Hepatology Research   56 ( 5 )   806 - 819   2026.5   （ ISSN:1386-6346 ）

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    Language：English   Publisher：John Wiley & Sons Australia, Ltd  

  • B4GALT3(Beta-1,4-Galactosyltransferase 3) Promotes Breast Cancer Cell Invasion via Integrin β1-Targeted Glycosylation. Reviewed

    Shibuta, S; Otsu, H; Higuchi, S; Ofuchi, T; Ando, Y; Ikehara, T; Hirose, K; Tsujimoto, A; Kawata, K; Omachi, K; Itoyama, S; Ono, Y; Takahashi, Y; Masuda, T; Mimori, K

    CANCER SCIENCE   117   958 - 958   2026.1   （ ISSN:1347-9032 eISSN:1349-7006 ）

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  • MiR-155-targeted IcosL controls tumor rejection Reviewed

    Otsu, H; Tili, E; Hu, QJ; Ando, Y; Yonemura, Y; Croce, CM; Mimori, K

    CANCER SCIENCE   117   58 - 58   2026.1   （ ISSN:1347-9032 eISSN:1349-7006 ）

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  • Mechanisms of hepatocellular carcinoma recurrence after liver transplantation in the immunosuppressed state Reviewed

    Ikehara, T; Onishi, M; Hosoda, K; Hirose, K; Shibuta, S; Ofuchi, T; Kawata, K; Ando, Y; Hu, Q; Otsu, H; Yonemura, Y; Toshima, T; Masuda, T; Yoshizumi, T; Soejima, Y; Mimori, K

    CANCER SCIENCE   117   1033 - 1033   2026.1   （ ISSN:1347-9032 eISSN:1349-7006 ）

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  • Identification of a Novel Therapeutic Target Gene TONSL in Hepatocellular Carcinoma Reviewed

    Tsujimoto, A; Otsu, H; Ofuchi, T; Ikehara, T; Tatsumi, T; Kawata, K; Shibuta, S; Ando, Y; Hirose, K; Masuda, T; Hu, QJ; Yonemura, Y; Sho, M; Mimori, K

    CANCER SCIENCE   117   542 - 542   2026.1   （ ISSN:1347-9032 eISSN:1349-7006 ）

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  • COX19, a gene identified by chromosome copy number analysis, is a novel driver gene for colorectal cancer Reviewed

    Kawat, K; Masuda, T; Otsu, H; Tsujimoto, A; Omachi, K; Itoyama, S; Ofuchi, T; Ikehara, T; Shibuta, S; Hirose, K; Ando, Y; Hu, Q; Yonemura, Y; Yoshizumi, T; Mimori, K

    CANCER SCIENCE   117   95 - 95   2026.1   （ ISSN:1347-9032 eISSN:1349-7006 ）

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  • Epidermoid Cysts in an Intrapancreatic Accessory Spleen Mimicking Pancreatic Neoplasms: Two Case Reports and a Literature Review of Japanese Cases

    Li Xiufeng, Hu Qingjiang, Takashi Yu, Kawata Koto, Shibuta Shohei, Ando Yuki, Otsu Hajime, Yonemura Yusuke, Tobo Taro, Mimori Koshi

    Surgical Case Reports   12 ( 1 )   n/a   2026   （ ISSN:2198-7793 eISSN:21987793 ）

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    Language：English   Publisher：Japan Surgical Society  

    <p><b>INTRODUCTION:</b> Epidermoid cyst(s) arising in an intrapancreatic accessory spleen (ECIPAS) are rare benign lesions that often mimic pancreatic cystic neoplasms on imaging studies. Owing to their rarity and nonspecific radiological features, ECIPAS are frequently misdiagnosed preoperatively, leading to unnecessary pancreatic resections.</p><p><b>CASE PRESENTATION:</b> We report 2 asymptomatic middle-aged women who were incidentally found to have cystic lesions in the tail of the pancreas during routine imaging examinations. Contrast-enhanced CT and MRI demonstrated well-demarcated cystic lesions with low signal intensity on T1-weighted images and high signal intensity on T2-weighted images. In both cases, mucinous cystic neoplasms or intraductal papillary mucinous neoplasms were suspected, prompting distal pancreatectomies, with a concomitant splenectomy in 1 patient. Histopathological examination revealed cysts lined predominantly by stratified squamous epithelium and surrounded by normal splenic tissue, confirming the diagnosis of ECIPAS. In addition, a review of the Japanese literature identified 52 reported cases of ECIPAS; most patients were asymptomatic, with lesions predominantly located in the pancreatic tail and frequently associated with elevated serum carbohydrate antigen 19-9 levels, although normal levels are also common.</p><p><b>CONCLUSIONS:</b> Recognizing ECIPAS may support more cautious clinical decision-making and help surgeons consider less invasive management strategies, including spleen-preserving distal pancreatectomy when appropriate.</p>

    DOI： 10.70352/scrj.cr.26-0039

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  • DCISに対してBp、術後9年目の断端再発に対してBt+SN、その1年後に対側乳がん発症しBp+SN受けた症例 Reviewed

    田中 文明, 安東 由貴, 三森 功士

    日本乳癌学会総会プログラム抄録集   33回   775 - 775   2025.7

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    Language：Japanese   Publisher：(一社)日本乳癌学会  

  • SET-binding protein 1 (SETBP1) suppresses cell proliferation in estrogen receptor-positive breast cancer

    Ando, Y; Masuda, T; Hayashi, N; Kosai, K; Shibuta, S; Ono, Y; Taro, T; Otsu, H; Hisamatsu, Y; Yoshizumi, T; Mimori, K

    BREAST CANCER   32 ( 3 )   457 - 469   2025.5   （ ISSN:1340-6868 eISSN:1880-4233 ）

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    Language：English   Publisher：Breast Cancer  

    Background: The single-nucleotide polymorphism rs6507583 at the promoter of SET-binding protein 1 (SETBP1) was implicated in estrogen receptor (ER)-positive breast carcinogenesis. Here, we evaluated the clinical and biological relevance of SETBP1 expression in ER-positive breast cancer (BC). Methods: The associations between SETBP1 expression and clinical outcomes in BC patients were analyzed in independent cohorts. The localizations of SETBP1 expression in BC tissues were observed by immunohistochemical staining. Pathway analyses were conducted using TCGA dataset. In vitro proliferation assay, protein phosphatase 2A (PP2A) activity assay, and gene expression analysis were performed in SETBP1-knockdown ER-positive BC cells. We investigated the factors influencing SETBP1 mRNA expression using TCGA dataset. rs6507583 presence and SETBP1 mRNA expression in 11 mammary cell lines and 56 BC tissue samples were examined by target sequencing and RT-qPCR, respectively. Results: SETBP1 was downregulated in BC cells compared with normal ductal epithelial cells. Low SETBP1 mRNA expression was an independent prognostic factor for poor recurrence-free survival. Pathway analyses revealed an inverse relationship between decreased SETBP1 expression and the expression of E2F, MYC, and G2M checkpoint target genes in BC tissues. SETBP1 knockdown promoted proliferation, inhibition of PP2A activity, and phosphorylation of MAPK in ER-positive BC. Low SETBP1 expression was influenced by high SETBP1 promoter methylation and DNA copy number SETBP1 deletion. SETBP1 expression with rs6507583 was lower than without rs6507583 in BC. Conclusions: We demonstrated that low SETBP1 expression could be a poor prognostic biomarker that promotes ER-positive BC proliferation, possibly via phosphorylation of MAPK.

    DOI： 10.1007/s12282-025-01667-w

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  • Validation of molecular prognostic score (mPS) for predicting prognosis in ER-positive Japanese breast cancer patients

    Masuda, T; Igami, K; Kai, Y; Tokieda, K; Gamachi, A; Tobo, T; Shibuta, S; Ando, Y; Ueo, H; Shimizu, H; Nakayama, K; Mimori, K

    CANCER SCIENCE   116   549 - 549   2025.1   （ ISSN:1347-9032 eISSN:1349-7006 ）

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  • Propagermanium treatment increased CD8 positive T cell in breast cancer

    Ando, Y; Masuda, T; Yoshiga, R; Kawata, K; Hirose, K; Ikehara, T; Tatsumi, T; Matsumoto, C; Shibuta, S; Ono, Y; Hosoda, K; Dairaku, K; Tsuda, Y; Ohtsu, H; Yonemura, Y; Mimori, K

    CANCER SCIENCE   116   349 - 349   2025.1   （ ISSN:1347-9032 eISSN:1349-7006 ）

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  • Polarity gene PARD6B promotes tumor growth via MYC expression in colorectal cancer

    Hirose, K; Masuda, T; Matsumoto, C; Ikehara, T; Tatsumi, T; Hosoda, K; Ando, Y; Tsuda, Y; Otsu, H; Yonemura, Y; Mimori, K

    CANCER SCIENCE   116   730 - 730   2025.1   （ ISSN:1347-9032 eISSN:1349-7006 ）

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  • Mechanisms of hepatocellular carcinoma recurrence after liver transplantation in the immunosuppressed state

    Ikehara, T; Onishi, M; Hosoda, K; Motomoura, Y; Ando, Y; Hirose, K; Dairaku, K; Hiraki, Y; Tsuda, Y; Nagao, Y; Yonemura, Y; Masuda, T; Toshima, T; Yoshizumi, T; Soejima, Y; Mimori, K

    CANCER SCIENCE   116   388 - 388   2025.1   （ ISSN:1347-9032 eISSN:1349-7006 ）

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  • Liquid biopsy for breast cancer and other solid tumors: a review of recent advances

    Ohmura, H; Hanamura, F; Okumura, Y; Ando, Y; Masuda, T; Mimori, K; Akashi, K; Baba, E

    BREAST CANCER   32 ( 1 )   33 - 42   2025.1   （ ISSN:1340-6868 eISSN:1880-4233 ）

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    Language：English   Publisher：Breast Cancer  

    Liquid biopsy using circulating tumor DNA (ctDNA) has been reported to be less invasive and effective for comprehensive genetic analysis of heterogeneous solid tumors, including decision-making for therapeutic strategies, predicting recurrence, and detecting genetic factors related to treatment resistance in various types of cancers. Breast cancer, colorectal cancer, and lung cancer are among the most prevalent malignancies worldwide, and clinical studies of liquid biopsy for these cancers are ongoing. Liquid biopsy has been used as a companion diagnostic tool in clinical settings, and research findings have accumulated, especially in cases of colorectal cancer after curative resection and non-small cell lung cancer (NSCLC) after curative chemoradiotherapy, in which ctDNA detection helps predict eligibility for adjuvant chemotherapy. Liquid biopsy using ctDNA shows promise across a wide range of cancer types, including breast cancer, and its clinical applications are expected to expand further through ongoing research. In this article, studies on liquid biopsy in breast cancer, colorectal cancer, and NSCLC are compared focusing on ctDNA.

    DOI： 10.1007/s12282-024-01556-8

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  • <i>SHARPIN</i> is a novel gene of colorectal cancer that promotes tumor growth potentially via inhibition of p53 expression

    Nakano, Y; Masuda, T; Sakamoto, T; Tanaka, N; Tobo, T; Hashimoto, M; Tatsumi, T; Saito, H; Takahashi, J; Koike, K; Abe, T; Ando, Y; Ozato, Y; Hosoda, K; Hirose, K; Higuchi, S; Ikehara, T; Hisamatsu, Y; Toshima, T; Yonemura, Y; Ogino, T; Uemura, M; Eguchi, H; Doki, Y; Mimori, K

    INTERNATIONAL JOURNAL OF ONCOLOGY   65 ( 6 )   2024.12   （ ISSN:1019-6439 eISSN:1791-2423 ）

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    Language：English   Publisher：International Journal of Oncology  

    Colorectal cancer (CRC) is widely prevalent and represents a significant contributor to global cancer‑related mortality. There remains a pressing demand for advance‑ ments in CRC treatment modalities. The E3 ubiquitin ligase is a critical enzyme involved in modulating protein expression levels via posttranslational ubiquitin‑mediated proteolysis, and it is reportedly involved in the progression of various cancers, making it a target of recent interest in anticancer therapy. In the present study, using comprehensive expression analysis involving spatial transcriptomic analysis with single‑cell RNA sequencing in clinical CRC datasets, the ubiquitin‑associated protein Shank‑associated RH domain interactor (SHARPIN) was identified, located on amplified chromosome 8q, which could promote CRC progression. SHARPIN was found to be upregulated in tumor cells, with elevated expression observed in tumor tissues. This heightened expression of SHARPIN was positively associated with lymphatic invasion and served as an independent predictor of a poor prognosis in patients with CRC. In vitro and in vivo analyses using SHARPIN‑overexpressing or ‑knockout CRC cells revealed that SHARPIN overexpression upregulated MDM2, resulting in the downregulation of p53, while SHARPIN silencing or knockout downregulated MDM2, leading to p53 upregulation, which affects cell cycle progression, tumor cell apoptosis and tumor growth in CRC. Furthermore, SHARPIN was found to be overexpressed in several cancer types, exerting significant effects on survival outcomes. In conclusion, SHARPIN represents a newly identified novel gene with the potential to promote tumor growth following apoptosis inhibition and cell cycle progression in part by inhibiting p53 expression via MDM2 upregulation; therefore, SHARPIN represents a potential therapeutic target for CRC.

    DOI： 10.3892/ijo.2024.5701

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  • Acute Dapagliflozin Administration Ameliorates Cardiac Surgery-Associated Acute Kidney Injury in a Rabbit Model Reviewed

    Matsuda, K; Mitsuo, H; Nishijima, T; Uchiyama, H; Nita, T; Matsunaga, S; Fujimoto, N; Ushijima, T; Ando, Y; Kan-o, M; Shinohara, G; Kimura, S; Sonoda, H; Shiose, A

    CIRCULATION JOURNAL   88 ( 9 )   1488 - 1498   2024.9   （ ISSN:1346-9843 eISSN:1347-4820 ）

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    Language：English   Publisher：Circulation Journal  

    Background: Several studies have shown that sodium-glucose cotransporter-2 inhibitors have a renoprotective effect on acute kidney injury (AKI), but their effect on cardiac surgery-associated AKI is unknown. Methods and Results: AKI was induced in 25 rabbits without diabetes mellitus by cardiopulmonary bypass (CPB) for 2 h and they were divided into 5 groups: sham; dapagliflozin-treated sham; CPB; dapagliflozin-treated CPB; and furosemide-treated CPB (n=5 in each group). Dapagliflozin was administered via the femoral vein before initiating CPB. Kidney tissue and urine and blood samples were collected after the surgical procedure. There were no differences in the hemodynamic variables of each group. Dapagliflozin reduced serum creatinine and blood urea nitrogen concentrations, and increased overall urine output (all P<0.05). Hematoxylin and eosin staining showed that the tubular injury score was improved after dapagliflozin administration (P<0.01). Dapagliflozin administration mitigated reactive oxygen species and kidney injury molecule-1 as assessed by immunohistochemistry (both P<0.0001). Protein expression analysis showed improvement of inflammatory cytokines and apoptosis, and antioxidant enzyme expression was elevated (all P<0.05) through activation of the nuclear factor erythroid 2-related factor 2 pathway (P<0.01) by dapagliflozin. Conclusions: Acute intravenous administration of dapagliflozin protects against CPB-induced AKI. Dapagliflozin may have direct renoprotective effects in renal tubular cells.

    DOI： 10.1253/circj.CJ-23-0864

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  • Tumor suppressive role of the epigenetic master regulator BRD3 in colorectal cancer

    Hashimoto, M; Masuda, T; Nakano, Y; Tobo, T; Saito, H; Koike, K; Takahashi, J; Abe, T; Ando, Y; Ozato, Y; Hosoda, K; Higuchi, S; Hisamatsu, Y; Toshima, T; Yonemura, Y; Hata, T; Uemura, M; Eguchi, H; Doki, Y; Mori, M; Mimori, K

    CANCER SCIENCE   115 ( 6 )   1866 - 1880   2024.6   （ ISSN:1347-9032 eISSN:1349-7006 ）

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    Language：English   Publisher：Cancer Science  

    Bromodomain and extraterminal domain (BET) family proteins are epigenetic master regulators of gene expression via recognition of acetylated histones and recruitment of transcription factors and co-activators to chromatin. Hence, BET family proteins have emerged as promising therapeutic targets in cancer. In this study, we examined the functional role of bromodomain containing 3 (BRD3), a BET family protein, in colorectal cancer (CRC). In vitro and vivo analyses using BRD3-knockdown or BRD3-overexpressing CRC cells showed that BRD3 suppressed tumor growth and cell cycle G1/S transition and induced p21 expression. Clinical analysis of CRC datasets from our hospital or The Cancer Genome Atlas revealed that BET family genes, including BRD3, were overexpressed in tumor tissues. In immunohistochemical analyses, BRD3 was observed mainly in the nucleus of CRC cells. According to single-cell RNA sequencing in untreated CRC tissues, BRD3 was highly expressed in malignant epithelial cells, and cell cycle checkpoint-related pathways were enriched in the epithelial cells with high BRD3 expression. Spatial transcriptomic and single-cell RNA sequencing analyses of CRC tissues showed that BRD3 expression was positively associated with high p21 expression. Furthermore, overexpression of BRD3 combined with knockdown of, a driver gene in the BRD family, showed strong inhibition of CRC cells in vitro. In conclusion, we demonstrated a novel tumor suppressive role of BRD3 that inhibits tumor growth by cell cycle inhibition in part via induction of p21 expression. BRD3 activation might be a novel therapeutic approach for CRC.

    DOI： 10.1111/cas.16129

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  • 大腸癌におけるエピジェネティックマスターレギュレーターBRD3の腫瘍抑制的役割(Tumor suppressive role of the epigenetic master regulator BRD3 in colorectal cancer)

    Hashimoto Masahiro, Masuda Takaaki, Nakano Yusuke, Tobo Taro, Saito Hideyuki, Koike Kensuke, Takahashi Junichi, Abe Tadashi, Ando Yuki, Ozato Yuki, Hosoda Kiyotaka, Higuchi Satoshi, Hisamatsu Yuichi, Toshima Takeo, Yonemura Yusuke, Hata Tsuyoshi, Uemura Mamoru, Eguchi Hidetoshi, Doki Yuichiro, Mori Masaki, Mimori Koshi

    Cancer Science   115 ( 6 )   1866 - 1880   2024.6   （ ISSN:1347-9032 ）

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    Language：English   Publisher：John Wiley & Sons Australia, Ltd  

    ブロモドメインとエクストラターミナル(BET)蛋白質ファミリーに属するブロモドメイン含有蛋白質3(BRD3)の大腸癌における臨床的および生物学的役割を検討した。その結果、BRD3ノックダウンまたはBRD3過剰発現大腸癌細胞を用いたin vitroおよびin vivo解析により、BRD3が腫瘍増殖と細胞周期G1/S相転移を抑制し、p21発現を誘導することが示された。当院およびThe Cancer Genome Atlasの大腸癌データセットの臨床解析から、BRD3を含むBETファミリー遺伝子が腫瘍組織で過剰発現していることが明らかになった。免疫組織化学的解析では、BRD3は主に大腸癌細胞の核で観察された。未治療の大腸癌組織におけるシングルセルRNAシーケンス解析では、BRD3は悪性上皮細胞で高発現しており、BRD3が高発現している上皮細胞では細胞周期チェックポイント関連経路が濃縮されていた。大腸癌組織の空間トランスクリプトーム解析とシングルセルRNAシーケンス解析から、BRD3の発現はp21の高発現と正の相関があった。さらに、BRD3の過剰発現とBRDファミリーのドライバー遺伝子のノックダウンの組み合わせにより大腸癌細胞に対する強い抑制が認められた。以上より、BRD3が部分的なp21の発現誘導を介して細胞周期を阻害することにより腫瘍増殖を阻害するというBRD3の新たな腫瘍抑制的役割が示唆された。

  • Clinical significance and functional analysis of a novel driver gene SETBP1 in breast cancer

    Ando, Y; Masuda, T; Hayashi, N; Shibuta, S; Ono, Y; Ikehara, T; Tatsumi, T; Matsumoto, C; Dairaku, K; Hosoda, K; Abe, T; Hirose, K; Tsuda, Y; Nagao, Y; Yonemura, Y; Mimori, K

    CANCER SCIENCE   115   1604 - 1604   2024.3   （ ISSN:1347-9032 eISSN:1349-7006 ）

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  • Tumor necrosis factor superfamily member 4 is a candidate driver gene for hepatocellular carcinoma

    Hosoda, K; Masuda, T; Saito, H; Motomura, Y; Ando, Y; Abe, T; Dairaku, K; Nakano, Y; Hiraki, Y; Ikehara, T; Yonemura, Y; Nagao, Y; Tsuda, Y; Hirose, K; Soejima, Y; Mimori, K

    CANCER SCIENCE   115   1281 - 1281   2024.3   （ ISSN:1347-9032 eISSN:1349-7006 ）

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  • Identifying Effective Subtypes of ERb Inhibitors in Breast Cancer

    Shibuta, S; Masuda, T; Ando, Y; Ono, Y; Miyata, Y; Nakano, Y; Dairaku, K; Abe, T; Hosoda, K; Matsumoto, C; Hirose, K; Ikehara, T; Tatsumi, T; Yonemura, Y; Kouji, H; Mimori, K

    CANCER SCIENCE   115   1933 - 1933   2024.3   （ ISSN:1347-9032 eISSN:1349-7006 ）

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  • Identification of KBTBD2, a candidate driver gene of gastric cancer, and its clinical significance

    Kawata, K; Tatsumi, T; Masuda, T; Ando, Y; Hirose, K; Tsuda, Y; Nagao, Y; Yonemura, Y; Yoshizumi, T; Mimori, K

    CANCER SCIENCE   115   923 - 923   2024.3   （ ISSN:1347-9032 eISSN:1349-7006 ）

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  • Identification of IMPAD1, a candidate driver gene of gastric cancer, and its clinical significance.

    Tatsumi, T; Masuda, T; Matsumoto, C; Ono, Y; Shibuta, S; Hosoda, K; Nakano, Y; Dairaku, K; Abe, T; Ando, Y; Hirose, K; Tsuda, Y; Nagao, Y; Yonemura, Y; Sho, M; Mimori, K

    CANCER SCIENCE   115   584 - 584   2024.3   （ ISSN:1347-9032 eISSN:1349-7006 ）

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  • Identification of candidate driver gene PDCD10 and selection of therapeutic drug candidates in ESCC

    Hiraki, Y; Masuda, T; Motomura, Y; Dairaku, K; Abe, T; Ando, Y; Nakano, Y; Hosoda, K; Tatsumi, T; Kai, S; Tsuda, Y; Nagao, Y; Yonemura, Y; Hirakawa, M; Mimori, K

    CANCER SCIENCE   115   1291 - 1291   2024.3   （ ISSN:1347-9032 eISSN:1349-7006 ）

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  • Detection of PARD6B gene as a candidate of driver gene in colorectal cancer

    Hirose, K; Masuda, T; Ono, Y; Shibuta, S; Ando, Y; Tsuda, Y; Nagao, Y; Yonemura, Y; Mimori, K

    CANCER SCIENCE   115   1280 - 1280   2024.3   （ ISSN:1347-9032 eISSN:1349-7006 ）

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  • Clinical significance of SLC12A9, a novel candidate driver gene for colorectal cancer

    Dairaku, K; Masuda, T; Hosoda, K; Hiraki, Y; Nakano, Y; Abe, T; Ando, Y; Motomura, Y; Hirose, K; Yoshiga, R; Tsuda, Y; Nagao, Y; Yonemura, Y; Ikegami, T; Eto, K; Mimori, K

    CANCER SCIENCE   115   612 - 612   2024.3   （ ISSN:1347-9032 eISSN:1349-7006 ）

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  • Case report: A rare case of triple negative breast cancer with development of acute pancreatitis due to dexamethasone during adjuvant chemotherapy

    Ohmura, H; Tobo, T; Ando, Y; Masuda, T; Mimori, K; Akashi, K; Baba, E

    FRONTIERS IN ONCOLOGY   14   1340419   2024.2   （ ISSN:2234-943X ）

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    Language：English   Publisher：Frontiers in Oncology  

    Here, we present the case of a 42-year-old female who developed acute pancreatitis due to dexamethasone during adjuvant chemotherapy for early triple negative breast cancer (TNBC). The patient received partial mastectomy and sentinel lymph node biopsy for early TNBC (cT1N0M0, cStage I) of the left breast. Dose-dense doxorubicin plus cyclophosphamide (ddAC) was administered as the adjuvant-chemotherapy; however, epigastralgia appeared on the fifth day of the first administration. A blood test showed a remarkable increase of serum pancreatic enzyme levels and computed tomography (CT) showed the swelling of pancreas and surrounding effusion, and she was diagnosed with moderate acute pancreatitis. As she had no history of excessive alcohol consumption or complication of cholelithiasis, dyslipidemia, or pancreatic neoplasm, drug-induced pancreatitis was suspected. Dexamethasone, which was administered as an antiemetic, was the suspected drug based on the drug administration history and previous report, and dexamethasone was discontinued from the second administration of ddAC. There was subsequently no recurrence of pancreatitis with no increase in serum pancreatic enzyme levels, and it was possible to complete adjuvant-chemotherapy. Alcohol, gallstones, dyslipidemia, and drugs have been reported as causes of pancreatitis; however, steroid-induced acute pancreatitis is extremely rare. We present the first case of acute pancreatitis induced by dexamethasone as the antiemetic.

    DOI： 10.3389/fonc.2024.1340419

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  • ASO Visual Abstract: Transducin Beta-like 2 is a Potential Driver Gene that Adapts to Endoplasmic Reticulum Stress to Promote Tumor Growth of Lung Adenocarcinoma

    Kosai, K; Masuda, T; Kitagawa, A; Tobo, T; Ono, Y; Ando, Y; Takahashi, J; Haratake, N; Kohno, M; Takenaka, T; Yoshizumi, T; Mimori, K

    ANNALS OF SURGICAL ONCOLOGY   30 ( 12 )   7597 - 7598   2023.11   （ ISSN:1068-9265 eISSN:1534-4681 ）

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  • Transducin Beta-Like 2 is a Potential Driver Gene that Adapts to Endoplasmic Reticulum Stress to Promote Tumor Growth of Lung Adenocarcinoma

    Kosai, K; Masuda, T; Kitagawa, A; Tobo, T; Ono, Y; Ando, Y; Takahashi, J; Haratake, N; Kohno, M; Takenaka, T; Yoshizumi, T; Mimori, K

    ANNALS OF SURGICAL ONCOLOGY   30 ( 12 )   7538 - 7548   2023.11   （ ISSN:1068-9265 eISSN:1534-4681 ）

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    Language：English   Publisher：Annals of Surgical Oncology  

    Background: Endoplasmic reticulum (ER) stress has a close relation with cancer progression. Blocking the adaptive pathway of ER stress could be an anticancer strategy. Here, we identified an ER stress-related gene, Transducin beta-like 2 (TBL2), an ER-localized type I transmembrane protein, on increased chromosome 7q as a candidate driver gene of lung adenocarcinoma (LUAD). Methods: The association between TBL2 mRNA expression and prognostic outcomes and clinicopathological factors was analyzed using The Cancer Genome Atlas (TCGA) datasets of LUAD and lung squamous cell carcinoma (LUSC). Localization of TBL2 in tumor tissues was observed by immunohistochemical staining. Gene set enrichment analysis (GSEA) was conducted using TCGA dataset. In vitro cell proliferation assays were performed using TBL2 knockdown LUAD cells, LUSC cells, and LUAD cells overexpressing TBL2. Apoptosis and ATF4 expression (ER stress marker) were evaluated by western blotting. Results: TBL2 was overexpressed in LUAD and LUSC cells. Multivariate analysis indicated high TBL2 mRNA expression was an independent poor prognostic factor of LUAD. GSEA revealed high TBL2 expression was positively correlated to the ER stress response in LUAD. TBL2 knockdown attenuated LUAD cell proliferation under ER stress. TBL2 inhibited apoptosis in LUAD cells under ER stress. TBL2 knockdown reduced ATF4 expression under ER stress. Conclusions: TBL2 may be a novel driver gene that facilitates cell proliferation, possibly by upregulating ATF4 expression followed by adaptation to ER stress, and it is a poor prognostic biomarker of LUAD.

    DOI： 10.1245/s10434-023-13864-y

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  • 集学的治療を行い、アテゾリズマブ+ベバシズマブ併用療法によって完全奏効を達成した90歳の肝細胞癌再発患者の症例(Successful multidisciplinary treatment with complete response to atezolizumab plus bevacizumab in a 90-year-old patient with hepatocellular carcinoma recurrence)

    Hosoda Kiyotaka, Toshima Takeo, Takahashi Junichi, Yonemura Yusuke, Hisamatsu Yuichi, Hirose Kosuke, Masuda Takaaki, Motomura Yushi, Abe Tadashi, Ando Yuki, Dairaku Katsushi, Nakano Yusuke, Hashimoto Masahiro, Hiraki Yoshiki, Soejima Yuji, Yoshizumi Tomoharu, Mimori Koshi

    International Cancer Conference Journal   12 ( 4 )   274 - 278   2023.10

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    Language：English   Publisher：シュプリンガー・ジャパン(株)  

    症例は90歳女性。非B非C型肝炎であり、18ヵ月前に原発性肝細胞癌に対して腹腔鏡下肝切除術が施行された。術後6ヵ月、肝細胞癌再発に対して経カテーテル的肝動脈化学塞栓療法(TACE)が施行されたが、その1年後に2回目の再発が認められた。レンバチニブ(LEN)8mg/日投与を開始したところ、1週間後に極度の疲労や食欲不振などの重篤な有害事象(AE)が出現し、投与量を4mg/日に減量したがAEの管理は困難であった。そこで、LEN導入から1ヵ月後に化学療法をアテゾリズマブ+ベバシズマブ併用療法に変更した。その結果、副作用はほとんど認められず、腫瘍の退縮が認められた。本レジメンを8ヵ月間、10サイクル続け、最終的に完全奏効(CR)を達成した。CR達成後1年経過しても再発はみられていない。

  • Successful multidisciplinary treatment with complete response to atezolizumab plus bevacizumab in a 90-year-old patient with hepatocellular carcinoma recurrence

    Hosoda, K; Toshima, T; Takahashi, J; Yonemura, Y; Hisamatsu, Y; Hirose, K; Masuda, T; Motomura, Y; Abe, T; Ando, Y; Dairaku, K; Nakano, Y; Hashimoto, M; Hiraki, Y; Soejima, Y; Yoshizumi, T; Mimori, K

    INTERNATIONAL CANCER CONFERENCE JOURNAL   12 ( 4 )   274 - 278   2023.10   （ ISSN:2192-3183 ）

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  • Dynamic Changes in Peripheral Systemic Immunity Markers During Chemotherapy in HER2-negative Advanced Breast Cancer

    Masuda, T; Ueo, H; Okumura, Y; Kai, YCR; Ando, Y; Masuguchi, K; Kitagawa, M; Kitagawa, A; Hayashi, N; Tsuruda, Y; Hisamatsu, Y; Suehiro, S; Ohmura, H; Fujiyoshi, K; Tanaka, F; Mimori, K

    CANCER GENOMICS & PROTEOMICS   20 ( 2 )   182 - 194   2023.3   （ ISSN:1109-6535 eISSN:1790-6245 ）

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    Language：English   Publisher：Cancer Genomics and Proteomics  

    Background/Aim: The immune system has a pivotal role in modulating the response to chemotherapy in breast cancer (BC). However, the immune status during chemotherapy remains unclear. We evaluated the sequential changes in peripheral systemic immunity markers in BC patients treated with various chemotherapeutic agents. Materials and Methods: We examined the correlation between the peripheral systemic immunity markers, neutrophil-to-lymphocyte ratio (NLR), absolute lymphocyte count (ALC) and the local cytolytic activity (CYT) score obtained by quantitative reverse-transcription polymerase chain reaction of 84 preoperative BC patients. Next, we observed the sequential changes in the peripheral systemic immunity markers during treatment with four anticancer drugs: oral 5-fluorouracil derivative; S-1, epirubicin plus cyclophosphamide; paclitaxel plus the anti-vascular endothelial growth factor antibody bevacizumab, and eribulin in 172 HER2-negative advanced BC patients. Finally, we examined the correlation between the changes in the peripheral systemic immunity markers, time to treatment failure (TTF) and progression-free survival (PFS). Results: A negative correlation was found between ALC and NLR. ALC-low and NLR-high cases were positively associated with CYT score-low cases. The ratio of ALC-increase and NLR-decrease varies depending on the anticancer drugs used. The responder group (TTF .3 months) had a higher NLR-decrease ratio than the nonresponder group (TTF <3 months). Patients with a high NLR-decrease ratio showed higher PFS. Conclusion: The change in ALC or NLR varies according to the anticancer drugs, suggesting differential immunomodulatory effects of the drugs. Furthermore, the change in NLR reflects the therapeutic efficacy of chemotherapy in advanced BC.

    DOI： 10.21873/cgp.20373

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  • Tumor necrosis factor superfamily member 4 is a candidate driver gene for hepatocellular carcinoma

    Hosoda, K; Masuda, T; Saito, H; Ando, Y; Abe, T; Dairaku, K; Nakano, Y; Hashimoto, M; Hiraki, Y; Yonemura, Y; Toshima, T; Hisamatsu, Y; Takahashi, J; Soejima, Y; Mimori, K

    CANCER SCIENCE   114   2051 - 2051   2023.2   （ ISSN:1347-9032 eISSN:1349-7006 ）

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  • Transducin beta-like 2 (TBL2) on chromosome 7 is a candidate driver gene of lung adenocarcinoma (LUAD)

    Ono, Y; Masuda, T; Kosai, K; Shibuta, S; Miyata, Y; Ando, Y; Motomura, Y; Abe, T; Takahashi, J; Hisamatsu, Y; Toshima, T; Yonemura, Y; Takenaka, T; Yoshizumi, T; Mimori, K

    CANCER SCIENCE   114   1843 - 1843   2023.2   （ ISSN:1347-9032 eISSN:1349-7006 ）

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  • The effect of preoperative chemotherapies for microenvironment in esophageal squamous cell carcinoma

    Hirose, K; Masuda, T; Ando, Y; Toshima, T; Mimori, K

    CANCER SCIENCE   114   504 - 504   2023.2   （ ISSN:1347-9032 eISSN:1349-7006 ）

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  • Identification of candidate driver gene C3orf1 by chromosome copy number analysis in ESCC

    Hiraki, Y; Masuda, T; Motomura, Y; Dairaku, K; Mochizuki, K; Abe, T; Ando, Y; Takahashi, J; Nakano, Y; Hashimoto, M; Hosoda, K; Hisamatsu, Y; Toshima, T; Yonemura, Y; Mimori, K

    CANCER SCIENCE   114   2050 - 2050   2023.2   （ ISSN:1347-9032 eISSN:1349-7006 ）

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  • Genomic characterizations of Japanese breast cancer

    Ando, Y; Masuda, T; Hosoda, K; Hashimoto, M; Nakano, Y; Dairaku, K; Mochizuki, K; Abe, T; Hiraki, Y; Motomura, Y; Takahashi, J; Hisamatsu, Y; Toshima, T; Yonemura, Y; Mimori, K

    CANCER SCIENCE   114   2162 - 2162   2023.2   （ ISSN:1347-9032 eISSN:1349-7006 ）

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  • Dynamic changes in peripheral systemic immunity markers during various chemotherapies in advanced breast cancer

    Masuda, T; Ando, Y; Motomura, Y; Abe, T; Hashimoto, M; Nakano, Y; Dairaku, K; Hiraki, Y; Hosoda, K; Takahashi, J; Hisamatsu, Y; Toshima, T; Yonemura, Y; Mimori, K

    CANCER SCIENCE   114   2151 - 2151   2023.2   （ ISSN:1347-9032 eISSN:1349-7006 ）

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  • A study on tool exchanger for a remote dissection system in the International Space Station

    ANDO Yuki, NOGAMI Hirofumi, Bandara D.S.V., ARATA Jumpei

    The Proceedings of JSME annual Conference on Robotics and Mechatronics (Robomec)   2023 ( 0 )   2P1-C06   2023   （ eISSN:24243124 ）

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    Language：Japanese   Publisher：The Japan Society of Mechanical Engineers  

    <p>We are developing a robotic dissection system remotely operated in the International Space Station. During the dissection process, the tip tool should be replaced when it becomes contaminated with living tissue or body fluids. Therefore, in this study, we developed a tool exchanger that allows the attachment and detachment of the forceps and scissors at the tip of the robotic arm using only the driving force of the robotic arm itself. In this paper, an improved design and prototype, and evaluation test are presented.</p>

    DOI： 10.1299/jsmermd.2023.2p1-c06

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  • A novel murine model of autoimmune dysautonomia by α3 nicotinic acetylcholine receptor immunization Reviewed

    Yamakawa, M; Nakane, S; Ihara, E; Tawara, N; Ikeda, H; Igarashi, Y; Komohara, Y; Takamatsu, K; Ikeda, T; Tomita, Y; Murai, S; Ando, Y; Mukaino, A; Ogawa, Y; Ueda, M

    FRONTIERS IN NEUROSCIENCE   16   1006923   2022.11   （ ISSN:16624548 eISSN:1662-453X ）

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    Language：English   Publisher：Frontiers in Neuroscience  

    We aimed to establish a novel murine model of autoimmune autonomic ganglionopathy (AAG), which represents autoimmune dysautonomia, associated with MHC class II to understand its pathomechanism and the pathogenicity of nicotinic acetylcholine receptor (nAChR) antibodies. The amino acid sequence of the mouse nAChRα3 protein was analyzed using an epitope prediction tool to predict the possible MHC class II binding mouse nAChRα3 peptides. We focused on two nAChRα3 peptides in the extracellular region, and experimental AAG (EAAG) was induced by immunization of C57BL/6 mice with these two different peptides. EAAG mice were examined both physiologically and histologically. Mice with EAAG generated nAChRα3 antibodies and exhibited autonomic dysfunction, including reduced heart rate, excessive fluctuations in systolic blood pressure, and intestinal transit slowing. Additionally, we observed skin lesions, such as alopecia and skin ulcers, in immunized mice. Neuronal cell density in the sympathetic cervical ganglia in immunized mice was significantly lower than that in control mice at the light microscopic level. We interpreted that active immunization of mice with nAChRα3 peptides causes autonomic dysfunction similar to human AAG induced by an antibody-mediated mechanism. We suggested a mechanism by which different HLA class II molecules might preferentially affect the nAChR-specific immune response, thus controlling diversification of the autoantibody response. Our novel murine model mimics AAG in humans and provides a useful tool to investigate its pathomechanism.

    DOI： 10.3389/fnins.2022.1006923

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  • Luminal A、pStageIA浸潤性乳管癌が術後1年で腹膜播種を来した症例(第2報)　BRCA変異陽性 Reviewed

    田中 文明, 増田 隆明, 安東 由貴, 三森 功士, 奥村 祐太, 東保 太郎

    日本乳癌学会総会プログラム抄録集   30回   EP28 - 208   2022.6

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    Language：Japanese   Publisher：(一社)日本乳癌学会  

  • Clinical significance of SETBP1 expression in breast cancer.

    Ando, Y; Masuda, T; Hayashi, N; Mochizuki, K; Abe, T; Saito, H; Ozato, Y; Nakano, T; Koike, K; Motomura, Y; Takahashi, J; Toshima, T; Hisamatsu, Y; Yonemura, Y; Mimori, K

    CANCER SCIENCE   113   741 - 741   2022.2   （ ISSN:1347-9032 eISSN:1349-7006 ）

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  • Low expression of transmembrane glycoprotein GPA33 is a poor prognostic factor in colorectal cancer.

    Abe, T; Masuda, T; Saito, H; Dairaku, K; Hashimoto, M; Nakano, Y; Hiraki, Y; Mochizuki, K; Ozato, Y; Ando, Y; Nakano, T; Koike, K; Takahashi, J; Motomura, Y; Toshima, T; Mimori, K

    CANCER SCIENCE   113   455 - 455   2022.2   （ ISSN:1347-9032 eISSN:1349-7006 ）

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  • High expression of the glycolytic enzyme gene PGK1 is a prognostic factor in esophageal cancer

    Saito, H; Masuda, T; Mochizuki, K; Abe, T; Ozato, Y; Ando, Y; Nakano, T; Motomura, Y; Koike, K; Takahashi, J; Hisamatsu, Y; Toshima, T; Yonemura, Y; Saeki, H; Mimori, K

    CANCER SCIENCE   113   1196 - 1196   2022.2   （ ISSN:1347-9032 eISSN:1349-7006 ）

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  • GET4 is a novel driver gene regulating the localization of BAG6 in colorectal cancer.

    Koike, K; Masuda, T; Nakano, T; Motomura, Y; Takahashi, J; Ando, Y; Toshima, T; Yonemura, Y; Nakagawa, T; Mimori, K

    CANCER SCIENCE   113   739 - 739   2022.2   （ ISSN:1347-9032 eISSN:1349-7006 ）

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  • Fanconi Anemia Complementation Group E, a DNA Repair-Related Gene, Is a Potential Marker of Poor Prognosis in Hepatocellular Carcinoma

    Takahashi, J; Masuda, T; Kitagawa, A; Tobo, T; Nakano, Y; Abe, T; Ando, Y; Kosai, K; Kobayashi, Y; Matsumoto, Y; Yoshizumi, T; Mori, M; Mimori, K

    ONCOLOGY   100 ( 2 )   101 - 113   2022.2   （ ISSN:0030-2414 eISSN:1423-0232 ）

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    Language：English   Publisher：Oncology United States  

    Introduction: Fanconi anemia complementation group E (FANCE) is a Fanconi anemia (FA) pathway gene that regulates DNA repair. We evaluated the clinical relevance of FANCE expression in hepatocellular carcinoma (HCC). Methods: First, the associations between the expression of FA pathway genes including FANCE and clinical outcomes in HCC patients were analyzed in 2 independent cohorts: The Cancer Genome Atlas (TCGA, n = 373) and our patient cohort (n = 53). Localization of FANCE expression in HCC tissues was observed by immunohistochemical staining. Gene set enrichment analysis (GSEA) and gene network analysis (SiGN_BN) were conducted using the TCGA dataset. Next, an in vitro proliferation assay was performed using FANCE-knockdown HCC cell lines (HuH7 and HepG2). The association between mRNA expression of FANCE and that of DNA damage response genes in HCC was analyzed using TCGA and Cancer Cell Line Encyclopedia datasets. Finally, the association between FANCE mRNA expression and overall survival (OS) in various digestive carcinomas was analyzed using TCGA data. Results: FANCE was highly expressed in HCC cells. Multivariate analysis indicated that high FANCE mRNA expression was an independent factor predicting poor OS. GSEA revealed a positive relationship between enhanced FANCE expression and E2F and MYC target gene expression in HCC tissues. FANCE knockdown attenuated the proliferation of HCC cells, as well as reduced cdc25A expression and elevated histone H3 pSer10 expression. SiGN_BN revealed that FANCE mRNA expression was positively correlated with DNA damage response genes (H2A histone family member X and checkpoint kinase 1) in HCC tissues. Significant effects of high FANCE expression on OS were observed in hepatobiliary pancreatic carcinomas, including HCC. Conclusions: FANCE may provide a potential therapeutic target and biomarker of poor prognosis in HCC, possibly by facilitating tumor proliferation, which is mediated partly by cell cycle signaling activation.

    DOI： 10.1159/000520582

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  • FANCE, one of the Fanconi anemia (FA) pathway genes, could be a potential therapeutic target for HCC.

    Takahashi, J; Masuda, T; Kitagawa, A; Ozato, Y; Nakano, T; Kosai, K; Kobayashi, Y; Koike, K; Motomura, Y; Ando, Y; Toshima, T; Hisamatsu, Y; Yonemura, Y; Yoshizumi, T; Mimori, K

    CANCER SCIENCE   113   950 - 950   2022.2   （ ISSN:1347-9032 eISSN:1349-7006 ）

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  • Search for Glycolytic Genes as Biomarkers

    Saito H, Hosoda K, Dairaku K, Nakano Y, Hashimoto M, Hiraki Y, Abe T, Ando Y, Motomura Y, Hisamatsu Y, Toshima T, Yonemura Y, Masuda T, Saeki H, Mimori K

    Japan Journal of Molecular Tumor Marker Research   38 ( 0 )   24 - 25   2022   （ eISSN:24338575 ）

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    Language：Japanese   Publisher：Japanese Society for Molecular Tumor Marker Research  

    DOI： 10.11241/jsmtmr.38.24

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Books

  • Characteristics of Aggregate-Induced Deteriorated Microstructure in High-Strength Concrete

    Ando Y., Hirono S., Era K., Sagawa Y.

    Rilem Bookseries  2024    （ ISSN:22110844 ）

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    In this study, the causes of degradation of high-strength concrete are determined using a petrological approach that incorporates polarizing microscopy, electron microscopy, and EDS analysis, and the factors that lead to the formation of a DEF-like degradation textures are clarified, taking into account the aggregate structure, constituent minerals, and compressive strength of the concrete. Precast RC box culverts for bridge and pretensioned PC hollow girders were used as observation samples. For the bridge box culverts, ASR was the cause of deterioration in the box culverts where meta-gabbro was used as the coarse aggregate, and drying shrinkage cracking was the cause of deterioration in the box culverts where serpentinite was used as the coarse aggregate. Observations showed that the PC hollow girder was primarily ASR in granite cataclasite of the coarse aggregate and chert in the fine aggregate, which contains late expansive reactive minerals. In both cases, the cracks propagated through the relatively weak aggregate interface and into the cement paste. Inside the cracks, ettringite was formed due to the high cement content, forming a microstructure similar to DEF.

    DOI： 10.1007/978-3-031-59419-9_65

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  • Expansion Properties and Microscopic Features of DEF and ASR Expansive Specimens Subjected to Residual Expansion Tests

    Yoshida N., Ando Y., Kawabata Y., Sagawa Y., Kawakami T., Shibui Y.

    Rilem Bookseries  2024    （ ISSN:22110844 ）

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    It is important to distinguish between DEF (delayed ettringite formation) from ASR (alkali-silica reaction), which show similar macroscopic deterioration phenomena, using microscopic techniques. In addition to the petrographic observation, a residual expansion test of a concrete core has been proposed to distinguish DEF from ASR. In this method, concrete cores are immersed in a solution saturated with Ca(OH)<inf>2</inf> (or water) and a 1 mol/L NaOH solution. The DEF potential is evaluated under the former condition and the ASR potential under the latter. Alkali leaching promotes DEF and alkali supply promotes ASR. However, the use of this type of the test method has been limited, and its validity has not been adequately verified. In this study, relatively large concrete specimens with DEF and ASR expansion potential were prepared under 80 °C pre-curing and using ASR reactive aggregate, and cores were taken for residual expansion testing. The results of the tests conducted by four institutes confirmed that the specimen with only DEF potential expanded in water and gaps filled with ettringite were observed around the aggregates. Specimens with both DEF and ASR potential expanded in both water and NaOH immersion, and the characteristics of DEF and/or ASR were identified by microscopic observation. In addition to the petrographic observation, the water and NaOH immersion tests were useful in distinguishing DEF from ASR.

    DOI： 10.1007/978-3-031-59419-9_26

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Presentations

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MISC

Research Projects

  • Development of a next-generation therapeutic strategy targeting TNBC-specific genomic G-quadruplex structures detected using ultra-short cfDNA.

    Grant number：26K11484  2026.4 - 2029.3

    Grants-in-Aid for Scientific Research  Grant-in-Aid for Scientific Research (C)

    安東 由貴, 清宮 啓之, 三森 功士, 三浦 史仁, 増田 隆明

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    Grant type：Scientific research funding

    乳癌は女性の主要な死亡原因であり、特にトリプルネガティブ乳癌（TNBC）は治療選択肢の限られているため再発・転移の克服が大きな課題である。血中循環DNA（cfDNA）の解析は近年約50ntの超短鎖一本鎖cfDNA（uscfDNA）が血漿中に存在することが発見され、癌臓器特異性を持ち、さらにG4構造に濃縮されることが明らかとなった。本研究では、TNBC患者の術前・術後検体からuscfDNAを検出・解析し、TNBC特異的G4構造領域との対応を明らかにする。また、TNBC株化細胞および動物モデルを用い、G4安定化剤の抗腫瘍効果を検証し、uscfDNA解析と治療応答性との関連を探る。

    CiNii Research

  • VISIUMによる乳がん転移阻害剤プロパゲルマニウムによる免疫能賦活化誘導機構の解明

    Grant number：23K06698  2023.4 - 2026.3

    Grants-in-Aid for Scientific Research  Grant-in-Aid for Scientific Research (C)

    安東 由貴, 鈴木 絢子, 三森 功士, 増田 隆明

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    Grant type：Scientific research funding

    われわれは前臨床試験(J Clin Invest 2015)で再発抑制効果を示したリポジショニング薬、プロパゲルマニウム(PG)に第I相試験を医師主導型治験(UMIN000022494)として実施し安全性を確認した。転移抑制効果の確認についての追加解析を加え論文報告した(Cancer Sci, 2020)。がん組織におけるPGの作用点と機序の解明は不明である。本研究ではPGの作用点を明確にするために、scRNA Seqデータと空間的転写産物(VISIUM)解析とを実施しdeconvolutionにより共局在細胞を特定しクロストーク遺伝子を同定し新しい局所免疫寛容の獲得機構を明らかにする。

    CiNii Research

  • Anti-tumour effects of the hepatitis drug propagermanium on breast cancer via immunostimulation.

    Grant number：20K17556  2020.4 - 2023.3

    Grants-in-Aid for Scientific Research  Grant-in-Aid for Early-Career Scientists

    Ando Yuki

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    Grant type：Scientific research funding

    In this study, blood samples and tumour tissue from the clinical trial were analysed. Multi-cytokine chemokines were measured in blood samples and cytokines that showed changes in the PG-treated group were identified. RNA sequencing analysis of tumour tissue showed increased CD8 expression in the PG-treated group, which was also confirmed by immunohistochemical staining. Breast cancer cells were transplanted into mice and validated in mouse experiments, and similar results were obtained by immunohistochemical staining.
    The mechanism of immunostimulation by PG in tumour tissue is thought to be the activation of CD8-positive T cells under the influence of cytokine chemokines, which were found to change in the PG-treated group, and will be investigated in the future.

    CiNii Research

Year of medical license acquisition

  • 2014