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Mio Tanaka

Section

Graduate School of Medicine

Job title

Assistant Professor

Degree

researchmap

https://researchmap.jp/tanaka-bc8677

J-GLOBAL ID

202301013184305146

ORCID

https://orcid.org/0000-0002-4276-5445

Research History 3

2024/11 - Present

東北大学, 大学院医学系研究科, 病理検査学分野, 助教
2023/04 - Present

東北大学病院　個別化医療センター　助教
2021/04 - 2023/03

日本学術振興会　特別研究員（DC2）

Education 3

東北大学　大学院医学系研究科　保健学専攻博士後期課程

2020/04 - 2023/03
東北大学　大学院医学系研究科　保健学専攻博士前期課程

2018/04 - 2020/03
Tohoku University　Faculty of Medicine

2014/04 - 2018/03

Professional Memberships 2

日本組織細胞化学会
日本癌学会

Research Interests 8

AI
Chemotherapy
Tumor Immunity
Extracellular vesicle
Tumor microenvironment
Androgen
Macrophage
Breast cancer

Research Areas 2

Life sciences / Human pathology /
Life sciences / Tumor biology /

Awards 9

2025 Acta Histochemica et Cytochemica Award

2025/10　Clinicopathological Significance and Prognostic Role of High Mobility Group Box 1 (HMGB1), Toll-Like Receptor (TLR) 2 and TLR4 in Breast Cancer
E-poster Excellence Award

2023/10
国立大学臨床検査学系博士後期課程最優秀賞

2023/05　国立大学臨床検査技師教育協議会
JACLaS Award 2022 優秀演題賞

2022/10　日本医療検査科学会第54回　顕微鏡写真を用いた乳腺病理診断補助AIの開発および有効性の探索
東北大学大学院医学系研究科女子大学院学生奨励賞（七星賞）

2022/04　東北大学大学院医学系研究科
若手奨励研究

2022/01　東北大学大学院医学系研究科付属創生応用医学研究センター AI応用医学部門　病理標本の顕微鏡写真を用いた乳腺病理診断補助AIの開発
若手研究賞最優秀賞

2021/10　第25回日本臨床内分泌病理学会学術総会　アンドロゲンによる乳癌組織随伴マクロファージの悪性形質顕在化メカニズムの解明
学生・初期研修医ポスター発表会長賞

2019/05　第92回日本内分泌学会学術総会　乳癌組織随伴マクロファージにおけるアンドロゲン誘導性液性因子の解析
会長特別賞銀賞

2018/04　第24回特定非営利活動法人東北内分泌研究会・第36回日本内分泌学会東北地方会　乳癌組織浸潤マクロファージにおけるアンドロゲン作用

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Papers 26

T‐Cell Immunoglobulin and Mucin Domain 1 (Tim1) as a Prognostic Factor Associated With Therapeutic Resistance in Human Breast Carcinoma Peer-reviewed

Mio Yamaguchi-Tanaka, Kiyoshi Takagi, Mai Sawafuji, Ai Sato, Kanoko Nakamura, Yasuhiro Miki, Minoru Miyashita, Takashi Suzuki

International Journal of Breast Cancer　2026　(1)　2026/04
Publisher: Wiley
DOI： 10.1155/ijbc/3747828 　

ISSN： 2090-3170

eISSN： 2090-3189

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Background Therapeutic resistance, including resistance to endocrine therapy in ER‐positive tumors and to chemotherapy in aggressive subtypes, remains a major clinical challenge in breast cancer. T‐cell immunoglobulin and mucin domain 1 (Tim1), a Type I transmembrane glycoprotein, has been reported to be aberrantly expressed in various cancer cells and contribute to tumor progression. However, its clinical significance in breast cancer and association with therapy resistance remain largely unclear. Methods We investigated Tim1 expression by immunohistochemistry in 116 breast carcinoma tissues and analyzed its correlation with clinicopathological parameters and clinical outcomes according to chemotherapy and endocrine therapy status. Results Tim1 immunoreactivity was detected in the cytoplasm and cell membranes of breast carcinoma cells but was negligible in the normal breast epithelium. Tim1 expression was significantly associated with pathological T factor, lymph node metastasis, histological grade, and Ki67 labeling index. Tim1 immunoreactivity was significantly correlated with an increased risk of recurrence, and multivariate analyses demonstrated Tim1 as an independent adverse prognostic factor for disease‐free survival. In addition, Tim1 remained correlated with the risk of recurrence in patients who had received chemotherapy or endocrine therapy. Conclusions Tim1 might be an important therapeutic target for improving therapy in breast cancer patients and could be a strong adverse prognostic factor associated with therapeutic resistance.
Infiltration of TIM4-positive intratumoral macrophages serves as an adverse prognostic factor in breast cancer Peer-reviewed

Mio Yamaguchi-Tanaka, Kiyoshi Takagi, Miyu Takahashi, Ai Sato, Yuto Yamazaki, Minoru Miyashita, Takashi Suzuki

Breast Cancer　2026/01/21
Publisher: Springer Science and Business Media LLC
DOI： 10.1007/s12282-026-01825-8 　

ISSN： 1340-6868

eISSN： 1880-4233

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Abstract Background T-cell immunoglobulin and mucin domain containing protein 4 (TIM4), a phosphatidylserine receptor primarily expressed on antigen-presenting cells, has been implicated in phagocytosis and immune regulation in various diseases, including malignancies. However, the significance of TIM4 in the breast cancer microenvironment remains unclear. In this study, we investigated the localization and clinical significance of TIM4 in breast cancer. Methods We immunolocalized TIM4 in human breast carcinoma tissues using immunohistochemistry (IHC) and multiplex fluorescence-immunohistochemistry (F-IHC) and examined its correlation with clinicopathological parameters and clinical outcomes. Results TIM4 was highly expressed in both carcinoma cells and stromal cells in human breast carcinoma tissues. Multiplex F-IHC revealed that TIM4 was co-localized with CD68, a macrophage marker, whereas no co-localization was observed between TIM4 and CD80 (an M1 macrophage marker) or CD163 (an M2 macrophage marker). Prognostic analysis of 171 breast carcinoma tissues by IHC revealed that infiltration of TIM4-positive stromal cells was associated with an aggressive tumor phenotype, including increased proliferative and invasive potential, as well as poorer clinical outcomes. In contrast, TIM4 immunoreactivity in carcinoma cells showed no significant correlation with clinical outcomes. Conclusions These findings suggest that infiltration of TIM4-positive macrophages serves as a strong prognostic indicator in breast cancer and that TIM4 may represent a novel marker for tumor-promoting macrophages.
Establishment and Operation of a New Style Clinical Biobank: The Tohoku University Clinical Biobank Peer-reviewed

Bin Li, Kazuki Kumada, Muneaki Shimada, Hidekazu Shirota, Hideki Tokunaga, Mio Yamaguchi-Tanaka, Chihiro Inoue, Yuto Yamazaki, Akihiro Yamamura, Toru Furukawa, Keigo Komine, Soichi Ogishima, Toru Tamahara, Sakae Saito, Ritsuko Shimizu, Masahiro Iikubo, Kensuke Yamauchi, Tomo Saito, Shin-ichi Fujimaki, Yuko Abe, Naoki Nakamura, Hideki Ota, Fuji Nagami, Kengo Kinoshita, Toru Nakazawa, Hozumi Motohashi, Naoto Ishii, Chikashi Ishioka, Hideo Harigae, Teiji Tominaga, Nobuo Yaegashi, Masayuki Yamamoto

The Tohoku Journal of Experimental Medicine　2026/01
Publisher: Tohoku University Medical Press
DOI： 10.1620/tjem.2025.j152 　

ISSN： 0040-8727

eISSN： 1349-3329
Artificial Intelligence for Breast Carcinoma Detection in Histopathological Images Based on Single Shot Multibox Detector in Intraoperative Rapid Diagnosis. Peer-reviewed

Mio Yamaguchi-Tanaka, Tomoaki Sasaki, Kodai Uemura, Yuichiro Tajima, Sho Kato, Takayoshi Asakura, Kiyoshi Takagi, Yuto Yamazaki, Atsushi Masamune, Toshio Miyata, Takashi Suzuki

The Tohoku journal of experimental medicine　2025/12/04

DOI： 10.1620/tjem.2025.J120 　
C-type lectin-like domain family 2 (CLEC2D) promotes proliferation and migration of breast cancer and serves as a poor prognostic factor Peer-reviewed

Mio Yamaguchi-Tanaka*, Yui Kurihara*, Kiyoshi Takagi, Ai Sato, Iori Yasuda, Yuto Yamazaki, Minoru Miyashita, Takashi Suzuki

Breast Cancer　2025/09/12
Publisher: Springer Science and Business Media LLC
DOI： 10.1007/s12282-025-01777-5 　

ISSN： 1340-6868

eISSN： 1880-4233

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Abstract Background C-type lectin-like domain family 2 (CLEC2D), a transmembrane protein, is a ligand for the inhibitory receptor CD161, which is expressed in several types of immune cells. CLEC2D expressed on cancer cells suppresses antitumor effect of these cells by interacting with CD161 in human malignancies. However, its clinical significance in breast cancer and its direct biological role in cancer cells remain largely unclear. Methods In this study, we immunolocalized CLEC2D in 174 breast cancer tissues and correlated its immunoreactivity with clinicopathological parameters and clinical outcomes. Additionally, we conducted in vitro assays to examine the effects of CLEC2D on the proliferation and migration of breast cancer cell lines. Results CLEC2D immunoreactivity was predominantly detected in the cytoplasm of breast cancer cells and was associated with increased proliferation and invasion, as well as poor clinical outcomes especially in those who had received chemotherapy. In vitro experiments demonstrated that the knockdown of CLEC2D significantly suppressed the proliferation and migration of MCF-7, MDA-MB-231, T-47D breast cancer cells. Conclusion We therefore concluded that CLED2D directly promoted breast cancer cell proliferation and migration independently of immune cells and served as a poor prognostic factor in breast cancer.
Discoidin Domain Receptor 2 (DDR2) Promotes Prostate Cancer Progression in Cooperation with Collagen Remodeling Peer-reviewed

Mikoto Sagehashi, Kiyoshi Takagi, Ai Sato, Mio Yamaguchi-Tanaka, Yasuhiro Miki, Akihiro Ito, Takashi Suzuki

ACTA HISTOCHEMICA ET CYTOCHEMICA　58　(4)　143-152　2025/08/28
Publisher: Japan Society of Histochemistry & Cytochemistry
DOI： 10.1267/ahc.25-00009 　

ISSN： 0044-5991

eISSN： 1347-5800
5α-reductase type 3 is a predictive marker for chemotherapy efficacy in breast cancer in an androgen-independent manner Peer-reviewed

Kanoko Nakamura, Kiyoshi Takagi, Mio Yamaguchi-Tanaka, Ai Sato, Naoki Inoue, Akiko Ebata, Yasuhiro Miki, Minoru Miyashita, Takashi Suzuki

The Journal of Steroid Biochemistry and Molecular Biology　106818-106818　2025/06
Publisher: Elsevier BV
DOI： 10.1016/j.jsbmb.2025.106818 　

ISSN： 0960-0760
Matrix metalloproteinase-3 is a potent prognostic factor associated with cell proliferation and migration in prostate cancer. International-journal Peer-reviewed

Ai Sato, Kiyoshi Takagi, Mio Yamaguchi-Tanaka, Jotaro Okushima, Yuto Yamazaki, Akihiro Ito, Takashi Suzuki

Experimental and molecular pathology　141　104954-104954　2025/03

DOI： 10.1016/j.yexmp.2025.104954 　

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Prostate cancer is a common malignancy in men around the world, and it is crucial to explore novel biomarkers to improve its treatment. Prostate cancer cells typically invade the surrounding stroma, and remodeling of the extracellular matrix (ECM) is a crucial step in the progress of prostate cancer. Matrix metalloproteinase-3 (MMP3) is an enzyme that degrades several ECM components and is implicated in human malignancies. However, the clinical and biological significance of MMP3 has not been well elucidated. We therefore immunolocalized MMP3 in prostate cancer tissues (n = 117) and demonstrated that MMP3 immunoreactivity was correlated with aggressive phenotype of prostate cancer, including higher proliferation/invasion ability, and shorter disease-free survival. In addition, subsequent in vitro analysis revealed that overexpression of MMP3 significantly increased the proliferative and migratory abilities of PC-3 and DU-145 prostate cancer cell lines, depending on conditioned media from WMPY-1 prostate stromal cells. It was concluded that MMP3 might contribute to prostate cancer progression by modifying the ECM surrounding prostate cancer cells and could serve as a potent prognostic factor in prostate cancer.
Discoidin Domain Receptor 2 Contributes to Breast Cancer Progression and Chemoresistance by Interacting with Collagen Type I Peer-reviewed

Ai Sato, Kiyoshi Takagi, Momoka Yoshida, Mio Yamaguchi-Tanaka, Mikoto Sagehashi, Yasuhiro Miki, Minoru Miyashita, Takashi Suzuki

Cancers　16　(24)　4285-4285　2024/12/23
Publisher: MDPI AG
DOI： 10.3390/cancers16244285 　

eISSN： 2072-6694

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Background: Chemoresistance is an important issue to be solved in breast cancer. It is well known that the content and morphology of collagens in tumor tissues are drastically altered following chemotherapy, and discoidin domain receptor 2 (DDR2) is a unique type of receptor tyrosine kinase (RTK). This RTK is activated by collagens, playing important roles in human malignancies. However, the contribution to the chemoresistance of DDR2 in terms of the association with collagens remains largely unclear in breast cancer. Methods: We immunolocalized DDR2 and collagen type I in 224 breast cancer tissues and subsequently conducted in vitro studies to confirm the role of DDR2 in breast cancer chemoresistance using chemosensitive and chemoresistant cell lines. Results: DDR2 immunoreactivity was positively correlated with aggressive behaviors of breast cancer and was significantly associated with an increased risk of recurrence, especially in those who received chemotherapy. Moreover, in vitro experiments demonstrated that DDR2 promoted the proliferative activity of breast cancer cells, and cell viability after epirubicin treatment was significantly maintained by DDR2 in a collagen I-dependent manner. Conclusions: These data suggested that DDR2 could be a poor prognostic factor associated with cell proliferation and chemotherapy resistance in human breast cancer.
Regulation of Stromal Cells by Sex Steroid Hormones in the Breast Cancer Microenvironment Peer-reviewed

Mio Yamaguchi-Tanaka, Kiyoshi Takagi, Ai Sato, Yuto Yamazaki, Minoru Miyashita, Atsushi Masamune, Takashi Suzuki

Cancers　16　(23)　4043-4043　2024/12/02
Publisher: MDPI AG
DOI： 10.3390/cancers16234043 　

eISSN： 2072-6694

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Breast cancer is a prevalent hormone-dependent malignancy, and estrogens/estrogen receptor (ER) signaling are pivotal therapeutic targets in ER-positive breast cancers, where endocrine therapy has significantly improved treatment efficacy. However, the emergence of both de novo and acquired resistance to these therapies continues to pose challenges. Additionally, androgens are produced locally in breast carcinoma tissues by androgen-producing enzymes, and the androgen receptor (AR) is commonly expressed in breast cancer cells. Intratumoral androgens play a significant role in breast cancer progression and are closely linked to resistance to endocrine treatments. The tumor microenvironment, consisting of tumor cells, immune cells, fibroblasts, extracellular matrix, and blood vessels, is crucial for tumor progression. Stromal cells influence tumor progression through direct interactions with cancer cells, the secretion of soluble factors, and modulation of tumor immunity. Estrogen and androgen signaling in breast cancer cells affects the tumor microenvironment, and the expression of hormone receptors correlates with the diversity of the stromal cell profile. Notably, various stromal cells also express ER or AR, which impacts breast cancer development. This review describes how sex steroid hormones, particularly estrogens and androgens, affect stromal cells in the breast cancer microenvironment. We summarize recent findings focusing on the effects of ER/AR signaling in breast cancer cells on stromal cells, as well as the direct effects of ER/AR signaling in stromal cells.
Receptor for Hyaluronan Mediated Motility (RHAMM)/Hyaluronan Axis in Breast Cancer Chemoresistance Peer-reviewed

Shiori Fujisawa, Kiyoshi Takagi, Mio Yamaguchi-Tanaka, Ai Sato, Yasuhiro Miki, Minoru Miyashita, Hiroshi Tada, Takanori Ishida, Takashi Suzuki

Cancers　16　(21)　3600-3600　2024/10/25
Publisher: MDPI AG
DOI： 10.3390/cancers16213600 　

eISSN： 2072-6694

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Background/Objectives: Receptor for hyaluronan-mediated motility (RHAMM) is a hyaluronan (HA) receptor, which exerts diverse biological functions in not only physiological but also pathological conditions in human malignancies, including breast cancer. Although chemoresistance is a significant clinical challenge in breast cancer, a possible contribution of RHAMM and hyaluronan to breast cancer chemoresistance has remained unclear. Methods: We immunolocalized RHAMM and HA in breast carcinoma tissues. Also, we utilized epirubicin-sensitive (parental) and rpirubicin-resistant (EPIR) breast cancer cell lines to explore the role of RHAMMM in breast cancer progression. Results: We found out that RHAMM and HA were cooperatively correlated with breast cancer aggressiveness and recurrence after chemotherapy. In vitro studies demonstrated that RHAMM was overexpressed in EPIR cells compared to parental cells. In addition, the knockdown of RHAMM significantly suppressed proliferation and migration of both parental and EPIR cells. On the other hand, the expression level of cancer stem cell marker CD44, which was overexpressed in M-EPIR (epirubicin-resistant MCF-7 subline) compared to MCF-7, was significantly suppressed by knockdown of RHAMM. In addition, the knockdown of RHAMM significantly altered the expression of N-cadherin and E-cadherin, leading to an epithelial phenotype. Conclusions: Aberrant RHAMM signaling were considered to cause chemoresistance related to cancer stemness and epithelial to mesenchymal transition, and increased cell proliferation and migration of both chemo-sensitive and chemo-resistant breast cancer cells.
Clinicopathological significance of hyaluronan and hyaluronidase 2 (HYAL2) in breast cancer Peer-reviewed

Shiori Fujisawa, Kiyoshi Takagi, Mio Yamaguchi-Tanaka, Ai Sato, Yasuhiro Miki, Minoru Miyashita, Hiroshi Tada, Takanori Ishida, Takashi Suzuki

Pathology - Research and Practice　155434-155434　2024/06
Publisher: Elsevier BV
DOI： 10.1016/j.prp.2024.155434 　

ISSN： 0344-0338
Toll-like receptor (TLR) 4 is a potent prognostic factor in prostate cancer associated with proliferation and invasion. International-journal Peer-reviewed

Iku Takahashi, Kiyoshi Takagi, Mio Yamaguchi-Tanaka, Ai Sato, Masahiko Sato, Yasuhiro Miki, Akihiro Ito, Takashi Suzuki

Pathology, research and practice　260　155379-155379　2024/05/29

DOI： 10.1016/j.prp.2024.155379 　

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Prostate cancer is one of the most common malignancies in men, and there is a need to explore novel biomarkers or therapeutic targets. Toll-like receptor 4 (TLR4) is expressed not only in antigen-presenting cells but also types of human malignancies, contributing to disease progression, although its clinical significance or functional role in prostate cancer remains unclear. Therefore, we immunolocalized TLR4 in 117 prostate cancer tissues to address its clinicopathological significance. Additionally, we performed in vitro assays to examine the effects of TLR4 on proliferation and migration of prostate cancer cell lines (LNCaP, DU-145 and PC-3). TLR4 immunoreactivity was predominantly detected in the cytoplasm of prostate cancer cells, and it was positively associated with proliferation and invasion abilities, as well as Gleason score. Subsequent in vitro experiments revealed that the inhibition of TLR4 by Sparstolonin B (SsnB) significantly suppressed the proliferation and migration of LNCaP, DU-145 and PC-3 cells. Therefore, we concluded that TLR4 was a potent prognostic factor associated with proliferation and invasion, and it might serve as a therapeutic target in prostate cancer.
Clinicopathological Significance and Prognostic Role of High Mobility Group Box 1 (HMGB1), Toll-Like Receptor (TLR) 2 and TLR4 in Breast Cancer Peer-reviewed

Reina Taguchi*, Mio Yamaguchi-Tanaka*, Kiyoshi Takagi, Ai Sato, Yasuhiro Miki, Minoru Miyashita, Takashi Suzuki

ACTA HISTOCHEMICA ET CYTOCHEMICA　57　(2)　75-83　2024/04/25
Publisher: Japan Society of Histochemistry & Cytochemistry
DOI： 10.1267/ahc.24-00006 　

ISSN： 0044-5991

eISSN： 1347-5800
Interleukin (IL)-17A in triple-negative breast cancer: a potent prognostic factor associated with intratumoral neutrophil infiltration Peer-reviewed

Freeha Khalid, Kiyoshi Takagi, Ai Sato, Mio Yamaguchi, Fouzia Guestini, Yasuhiro Miki, Minoru Miyashita, Hisashi Hirakawa, Yasuyo Ohi, Yoshiaki Rai, Yasuaki Sagara, Hironobu Sasano, Takashi Suzuki

Breast Cancer　30　(5)　748-757　2023/05/13
Publisher: Springer Science and Business Media LLC
DOI： 10.1007/s12282-023-01467-0 　

ISSN： 1340-6868

eISSN： 1880-4233
Kallikrein-Related Peptidase 12 (KLK12) in Breast Cancer as a Favorable Prognostic Marker Peer-reviewed

Ai Sato, Kiyoshi Takagi, Ayano Yoshimura, Wakana Tsukamoto, Mio Yamaguchi-Tanaka, Yasuhiro Miki, Akiko Ebata, Minoru Miyashita, Takashi Suzuki

International Journal of Molecular Sciences　24　(9)　8419-8419　2023/05/08
Publisher: MDPI AG
DOI： 10.3390/ijms24098419 　

eISSN： 1422-0067

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Kallikrein-related peptides (KLKs) form an evolutionally conserved subgroup of secreted serine proteases that consists of 15 members (KLK1-15). Previous studies have shown that KLKs regulate diverse biological processes, but the clinical significance of KLKs remains largely unclear in human breast cancers. We examined the expression profile of 15 KLK genes in breast carcinomas using microarray data. Next, we immunolocalized KLK12 in 140 breast carcinomas and evaluated its clinical significance. Subsequently, we examined the effects of KLK12 on proliferation and migration in breast cancer cell lines. From microarray analyses, it turned out that KLK12 was the most strongly associated with low-grade malignancy in breast carcinomas among the 15 KLK members. Immunohistochemical KLK12 status was positively associated with ER and PR status, while it was inversely associated with stage, pathological T factor, lymph node metastasis, and distant metastasis. Prognostic analyses demonstrated that KLK12 was a favorable prognostic factor for both disease-free and breast cancer-specific survival of the patients. Furthermore, the knockdown of KLK12 significantly increased cell proliferation activity and cell migration of breast cancer cells. These results suggest that KLK12 has antitumorigenic effects associated with proliferation and migration and immunohistochemical KLK12 status as a potent favorable prognostic factor in breast carcinoma patients.
The Pro-Tumorigenic Role of Chemotherapy-Induced Extracellular HSP70 from Breast Cancer Cells via Intratumoral Macrophages Peer-reviewed

Mio Yamaguchi-Tanaka, Kiyoshi Takagi, Yasuhiro Miki, Ai Sato, Erina Iwabuchi, Minoru Miyashita, Takashi Suzuki

Cancers　15　(6)　1903-1903　2023/03/22
Publisher: MDPI AG
DOI： 10.3390/cancers15061903 　

eISSN： 2072-6694

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Tumor-associated macrophages (TAMs) contribute to tumor progression and chemoresistance; it is therefore important to clarify the altered functions of macrophages following chemotherapy. While extracellular heat shock protein (HSP) 70 is associated with therapeutic resistance, the effects of HSP70 on TAMs remain largely unknown. Here, we conducted in vitro experiments and immunohistochemistry in 116 breast carcinoma specimens to determine whether the secretion of HSP70 from breast cancer cells following chemotherapy affects macrophage function. It was revealed that the interaction of epirubicin (EPI)-exposed breast cancer cells with macrophages enhanced tumor progression, and EPI promoted the secretion of extracellular HSP70 from breast cancer cells. The expression of pro-tumorigenic macrophage marker CD163 was decreased in macrophages treated with a conditioned medium (CM) from HSP70-silenced breast cancer cells. Breast cancer cells treated with CM from HSP70-silenced breast cancer cells showed decreased expression of transforming growth factor (TGF)-β, and the pro-tumorigenic effects of macrophages were impaired when TGF-β signaling was inhibited. Immunohistochemistry demonstrated that HSP70 served as a poor prognostic factor in conjunction with macrophage infiltration. It was therefore concluded that extracellular HSP70 levels increased following chemotherapy and enhanced the pro-tumorigenic effects of TAMs, either directly or indirectly, by regulating TGF-β expression in breast cancer cells.
Diverse role of androgen action in human breast cancer Peer-reviewed

Kiyoshi Takagi, Mio Yamaguchi, Minoru Miyashita, Hironobu Sasano, Takashi Suzuki

Endocrine Oncology　2　(1)　R102-R111　2022/09/01
Publisher: Bioscientifica
DOI： 10.1530/eo-22-0048 　

eISSN： 2634-4793

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Breast cancer is a hormone-dependent cancer, and sex steroids play a pivotal role in breast cancer progression. Estrogens are strongly associated with breast cancers, and the estrogen receptor (estrogen receptor α; ERα) is expressed in 70–80% of human breast carcinoma tissues. Although antiestrogen therapies (endocrine therapies) have significantly improved clinical outcomes in ERα-positive breast cancer patients, some patients experience recurrence after treatment. In addition, patients with breast carcinoma lacking ERα expression do not benefit from endocrine therapy. The androgen receptor (AR) is also expressed in >70% of breast carcinoma tissues. Growing evidence supports this novel therapeutic target for the treatment of triple-negative breast cancers that lack ERα, progesterone receptor, and human EGF receptor 2, and ERα-positive breast cancers, which are resistant to conventional endocrine therapy. However, the clinical significance of AR expression is still controversial and the biological function of androgens in breast cancers is unclear. In this review, we focus on the recent findings concerning androgen action in breast cancers and the contributions of androgens to improved breast cancer therapy.
Automatic breast carcinoma detection in histopathological micrographs based on Single Shot Multibox Detector Peer-reviewed

Mio Yamaguchi, Tomoaki Sasaki, Kodai Uemura, Yuichiro Tajima, Sho Kato, Kiyoshi Takagi, Yuto Yamazaki, Ryoko Saito-Koyama, Chihiro Inoue, Kurara Kawaguchi, Tomoya Soma, Toshio Miyata, Takashi Suzuki

Journal of Pathology Informatics　13　100147-100147　2022
Publisher: Elsevier BV
DOI： 10.1016/j.jpi.2022.100147 　

ISSN： 2153-3539
D-2-hydroxyglutarate dehydrogenase in breast carcinoma as a potent prognostic marker associated with proliferation. International-journal Peer-reviewed

Chiaki Hayashi, Kiyoshi Takagi, Ai Sato, Mio Yamaguchi, Hiroyuki Minemura, Yasuhiro Miki, Narumi Harada-Shoji, Minoru Miyashita, Hironobu Sasano, Takashi Suzuki

Histology and histopathology　36　(10)　1053-1062　2021/10

DOI： 10.14670/HH-18-362 　

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BACKGROUND: D-2-hydroxyglutarate dehydrogenase (D2HGDH) catalyzes D-2-hydroxyglutarate to α-ketoglutarate and is involved in the regulation of cellular energy and biosynthetic intermediates. Previously, D2HGDH was reported to decrease 2-hydroxyglutarate level in breast carcinoma cells, but no other report has examined D2HGDH in breast carcinoma, and its significance remains unknown. METHODS: We first immunolocalized D2HGDH in 224 invasive breast carcinomas and evaluated its clinicopathological significance. We next examined associations between gene expression of D2HGDH and α-ketoglutarate-dependent dioxygenases in 23 breast carcinoma tissues using the gene expression profile data. Finally, we examined the effects of D2HGDH on the proliferation in three breast carcinoma cells. RESULTS: D2HGDH immunoreactivity was detected in 49% of invasive breast carcinomas, and the immunohistochemical D2HGDH status was positively associated with histological grade, HER2 and Ki-67, while it was inversely associated with estrogen receptor. Moreover, it was significantly associated with worse prognosis of the breast cancer patients, and it turned out to be an independent prognostic factor for both the disease-free and breast cancer-specific survival in these patients. Gene expression profile data revealed that D2HGDH expression was positively associated with the expression of 6 α-ketoglutarate-dependent dioxygenases (KDM3A, PLOD1, EGLN2, ALKBH1, ASPH and ALKBH7). Consequent in vitro experiments demonstrated that D2HGDH overexpression significantly increased the cell proliferation activity of MCF-7, T47D and MDA-MB-231 cells. CONCLUSION: These results suggest that D2HGDH plays an important role in the growth of breast carcinoma, possibly through regulating functions of α-ketoglutarate-dependent dioxygenases, and that D2HGDH status is a potent worse prognostic factor in breast cancer patients.
Forkhead Box I1 in Breast Carcinoma as a Potent Prognostic Factor Peer-reviewed

Yoshiaki Onodera, Kiyoshi Takagi, Yoshimi Neoi, Ai Sato, Mio Yamaguchi, Yasuhiro Miki, Akiko Ebata, Minoru Miyashita, Hironobu Sasano, Takashi Suzuki

ACTA HISTOCHEMICA ET CYTOCHEMICA　54　(4)　123-130　2021/08/25
Publisher: Japan Society of Histochemistry & Cytochemistry
DOI： 10.1267/ahc.21-00034 　

ISSN： 0044-5991

eISSN： 1347-5800
癌細胞および間質細胞から見た乳癌のアンドロゲン環境

高木清司, 山口美桜, 鈴木貴

日本生殖内分泌学会雑誌　26　14-17　2021/08
Publisher: 日本生殖内分泌学会
ISSN： 1348-8031

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乳癌は代表的なエストロゲン依存性腫瘍であるが、乳癌細胞にはエストロゲン受容体と同等以上の頻度でアンドロゲン受容体も発現している。乳癌におけるアンドロゲン作用を規定する因子として、アンドロゲン受容体、アンドロゲン合成酵素、アンドロゲン応答遺伝子について概説した。また、乳癌間質細胞におけるアンドロゲン作用という新たな観点から、乳癌におけるアンドロゲンの役割を述べた。
Androgens enhance the ability of intratumoral macrophages to promote breast cancer progression Peer-reviewed

Mio Yamaguchi, Kiyoshi Takagi, Masayasu Sato, Ai Sato, Yasuhiro Miki, Yoshiaki Onodera, Minoru Miyashita, Hironobu Sasano, Takashi Suzuki

Oncology Reports　46　(3)　2021/07/12
Publisher: Spandidos Publications
DOI： 10.3892/or.2021.8139 　

ISSN： 1021-335X

eISSN： 1791-2431
Isoforms of IDH in breast carcinoma: IDH2 as a potent prognostic factor associated with proliferation in estrogen-receptor positive cases Peer-reviewed

Hiroyuki Minemura, Kiyoshi Takagi, Ai Sato, Mio Yamaguchi, Chiaki Hayashi, Yasuhiro Miki, Narumi Harada-Shoji, Minoru Miyashita, Hironobu Sasano, Takashi Suzuki

Breast Cancer　28　(4)　915-926　2021/03/12
Publisher: Springer Science and Business Media LLC
DOI： 10.1007/s12282-021-01228-x 　

ISSN： 1340-6868

eISSN： 1880-4233
Stromal CCL5 Promotes Breast Cancer Progression by Interacting with CCR3 in Tumor Cells Peer-reviewed

Mio Yamaguchi, Kiyoshi Takagi, Koki Narita, Yasuhiro Miki, Yoshiaki Onodera, Minoru Miyashita, Hironobu Sasano, Takashi Suzuki

International Journal of Molecular Sciences　22　(4)　1918-1918　2021/02/15
Publisher: MDPI AG
DOI： 10.3390/ijms22041918 　

eISSN： 1422-0067

More details Close

Chemokines secreted from stromal cells have important roles for interactions with carcinoma cells and regulating tumor progression. C-C motif chemokine ligand (CCL) 5 is expressed in various types of stromal cells and associated with tumor progression, interacting with C-C chemokine receptor (CCR) 1, 3 and 5 expressed in tumor cells. However, the expression on CCL5 and its receptors have so far not been well-examined in human breast carcinoma tissues. We therefore immunolocalized CCL5, as well as CCR1, 3 and 5, in 111 human breast carcinoma tissues and correlated them with clinicopathological characteristics. Stromal CCL5 immunoreactivity was significantly correlated with the aggressive phenotype of breast carcinomas. Importantly, this tendency was observed especially in the CCR3-positive group. Furthermore, the risk of recurrence was significantly higher in the patients with breast carcinomas positive for CCL5 and CCR3 but negative for CCR1 and CCR5, as compared with other patients. In summary, the CCL5-CCR3 axis might contribute to a worse prognosis in breast cancer patients, and these findings will contribute to a better understanding of the significance of the CCL5/CCRs axis in breast carcinoma microenvironment.
Rac1 activation in human breast carcinoma as a prognostic factor associated with therapeutic resistance Peer-reviewed

Mio Yamaguchi, Kiyoshi Takagi, Ai Sato, Yasuhiro Miki, Minoru Miyashita, Hironobu Sasano, Takashi Suzuki

Breast Cancer　27　(5)　919-928　2020/04/20
Publisher: Springer Science and Business Media LLC
DOI： 10.1007/s12282-020-01091-2 　

ISSN： 1340-6868

eISSN： 1880-4233

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Misc. 30

乳癌組織における5α-reductase type 3の発現意義

中村佳乃子, 高木清司, 井上直紀, 佐藤和, 田中美桜, 宮下穣, 鈴木貴

日本内分泌学会雑誌　100　(5)　1488-1488　2025/02
Publisher: (一社)日本内分泌学会
ISSN： 0029-0661

eISSN： 2186-506X
乳癌におけるヒアルロン酸関連分子の発現意義(Significance of Hyaluronan-related Molecules Expression in Breast Cance)

藤沢詩織, 高木清司, 田中美桜[山口], 佐藤和, 三木康宏, 宮下穣, 多田寛, 鈴木貴, 石田孝宣, 鈴木貴

日本癌学会総会記事　83回　P-1255　2024/09
Publisher: (一社)日本癌学会
ISSN： 0546-0476
乳癌の進展におけるTim1の役割(The pro-tumorigenic role of Tim1 in human breast cancer)

澤藤真衣, 田中美桜[山口], 高木清司, 佐藤和, 三木康宏, 宮下穣, 鈴木貴, 鈴木貴

日本癌学会総会記事　83回　P-1263　2024/09
Publisher: (一社)日本癌学会
ISSN： 0546-0476
TIM4陽性抗原提示細胞の浸潤は乳癌の予後不良に寄与する(Infiltration of TIM4 expressing antigen-presenting cells is associated with worse prognosis in breast cancer)

田中美桜[山口], 高木清司, 高橋美佑, 佐藤和, 三木康宏, 宮下穣, 鈴木貴, 鈴木貴

日本癌学会総会記事　83回　P-1261　2024/09
Publisher: (一社)日本癌学会
ISSN： 0546-0476
前立腺癌においてMatrix Metalloproteinase-3は予後不良因子となりうる(Matrix metalloproteinase-3 as a potent prognostic factor in human prostate cancer)

佐藤和, 高木清司, 田中美桜[山口], 奥島丈太郎, 伊藤明宏, 鈴木貴, 鈴木貴

日本癌学会総会記事　83回　P-3239　2024/09
Publisher: (一社)日本癌学会
ISSN： 0546-0476
前立腺癌の悪性化におけるI型コラーゲンとdiscoidin domain receptor 2の役割(Collagen I/discoidin domain receptor 2 axis contribute to prostate cancer progression)

提橋美思, 高木清司, 佐藤和, 田中美桜[山口], 伊藤明宏, 鈴木貴, 鈴木貴

日本癌学会総会記事　83回　P-3240　2024/09
Publisher: (一社)日本癌学会
ISSN： 0546-0476
乳腺診療における技術革新デジタルパソロジー遠隔病理診断とAI(人工知能)

鈴木貴, 藤島史喜, 田中美桜, 片岡正子, 戸井雅和

日本外科学会定期学術集会抄録集　124回　SY-2　2024/04
Publisher: (一社)日本外科学会
癌におけるVersicanおよびADAMTS-1の発現意義

高木清司, 田中美桜[山口], 佐藤和, 古川和樹, 藤田愛海, 海谷沙綾香, 小野寺好明, 三木康宏, 宮下穣, 鈴木貴

日本組織細胞化学会総会・学術集会講演プログラム・予稿集　64回　48-48　2023/10
Publisher: 日本組織細胞化学会
乳癌随伴マクロファージにおける膜貫通型受容体TIM4は腫瘍免疫制御を介して乳癌の進展に寄与する

田中美桜[山口], 高木清司, 高橋美佑, 佐藤和, 三木康宏, 宮下穣, 石岡千加史, 鈴木貴

日本組織細胞化学会総会・学術集会講演プログラム・予稿集　64回　48-48　2023/10
Publisher: 日本組織細胞化学会
乳癌におけるRHAMMとヒアルロン酸の発現意義(The role of RHAMM and Hyaluronan in human breast carcinoma)

藤沢詩織, 高木清司, 田中美桜, 佐藤和, 三木康宏, 宮下穣, 多田寛, 鈴木貴, 石田孝宣

日本癌学会総会記事　82回　1939-1939　2023/09
Publisher: (一社)日本癌学会
ISSN： 0546-0476
乳癌随伴マクロファージにおけるホスファチジルセリン受容体TIM4の役割(The role of the phosphatidylserine receptor TIM4 expressed on macrophages in breast cancers)

田中美桜, 高木清司, 高橋美佑, 佐藤和, 三木康宏, 宮下穣, 石岡千加史, 鈴木貴, 石岡千加史

日本癌学会総会記事　82回　1938-1938　2023/09
Publisher: (一社)日本癌学会
ISSN： 0546-0476
乳癌の化学療法耐性における14-3-3ζの役割(The role of 14-3-3ζ in breast cancer chemoresistance)

高橋郁, 高木清司, 田中美桜, 佐藤和, 三木康宏, 宮下穣, 鈴木貴

日本癌学会総会記事　82回　2121-2121　2023/09
Publisher: (一社)日本癌学会
ISSN： 0546-0476
乳癌におけるコンドロイチン硫酸-Cの発現意義(Prognostic role of chondroitin sulfate-C in breast cancer)

佐藤結名子, 高木清司, 田中美桜, 藤沢詩織, 佐藤和, 三木康宏, 宮下穣, 鈴木貴

日本癌学会総会記事　82回　2122-2122　2023/09
Publisher: (一社)日本癌学会
ISSN： 0546-0476
乳癌の治療抵抗性におけるHMGB1/TLR2,4の役割(HMGB1/TLR2,4 axis is associated with therapeutic resistance of human breast cancer)

高木清司, 田口玲奈, 田中美桜, 佐藤和, 三木康宏, 宮下穣, 鈴木貴

日本癌学会総会記事　82回　2124-2124　2023/09
Publisher: (一社)日本癌学会
ISSN： 0546-0476
乳癌における膜型アンドロゲン受容体ZIP9の発現意義

田中美桜[山口], 橋場克幸, 高木清司, 佐藤和, 江幡明子, 三木康宏, 宮下穣, 鈴木貴

日本内分泌学会雑誌　99　(3)　718-718　2023/07
Publisher: (一社)日本内分泌学会
ISSN： 0029-0661

eISSN： 2186-506X
乳癌におけるRHAMMの発現意義

藤沢詩織, 高木清司, 田中美桜[山口], 佐藤和, 三木康宏, 宮下穣, 多田寛, 石田孝宣, 鈴木貴

日本乳癌学会総会プログラム抄録集　31回　440-440　2023/06
Publisher: (一社)日本乳癌学会
乳癌におけるRHAMM(ヒアルロン酸媒介運動性受容体)の発現意義(The role of RHAMM(receptor for hyaluronan-mediated motility) in human breast carcinoma)

藤沢詩織, 高木清司, 山口美桜, 佐藤和, 三木康宏, 宮下穣, 多田寛, 鈴木貴, 石田孝宣

日本癌学会総会記事　81回　P-3244　2022/09
Publisher: (一社)日本癌学会
ISSN： 0546-0476
化学療法誘導性細胞外HSP70はマクロファージの腫瘍促進作用を介して乳癌の進展を促進する(Chemotherapy-induced extracellular HSP70 enhances the ability of marcophages to promote breast cancer progression.)

山口美桜, 高木清司, 三木康宏, 岩渕英里奈, 宮下穣, 鈴木貴

日本癌学会総会記事　81回　P-3245　2022/09
Publisher: (一社)日本癌学会
ISSN： 0546-0476
顕微鏡写真を用いた乳腺病理診断補助AIの開発および有効性の探索

山口美桜, 佐々木友謙, 上村紘大, 田島裕一郎, 加藤翔, 高木清司, 山崎有人, 小山涼子[齊藤], 井上千裕, 相馬知也, 宮田敏男, 鈴木貴

医療検査と自動化　47　(4)　358-358　2022/08
Publisher: (一社)日本医療検査科学会
ISSN： 2435-7391

eISSN： 2435-2713
化学療法後の乳癌細胞は細胞外HSP70の分泌を介してマクロファージの腫瘍促進作用を誘導する

山口美桜, 高木清司, 三木康宏, 岩渕英里奈, 宮下穣, 笹野公伸, 鈴木貴

日本乳癌学会総会プログラム抄録集　30回　EP1-14　2022/06
Publisher: (一社)日本乳癌学会
アンドロゲンによる乳癌組織随伴マクロファージの悪性形質顕在化メカニズムの解明

山口美桜, 高木清司, 三木康宏, 小野寺好明, 宮下穣, 笹野公伸, 鈴木貴

日本内分泌学会雑誌　97　(5)　1624-1624　2022/03
Publisher: (一社)日本内分泌学会
ISSN： 0029-0661

eISSN： 2186-506X
乳癌細胞における化学療法誘導性エクソソーム内包HSP70はマクロファージの腫瘍促進作用を誘導する

山口美桜, 高木清司, 三木康宏, 岩渕英里奈, 宮下穣, 笹野公伸, 鈴木貴

日本癌学会総会記事　80回　[P14-5]　2021/09
Publisher: (一社)日本癌学会
ISSN： 0546-0476
乳癌の進展および治療耐性における活性型Rac1の意義

高木清司, 山口美桜, 佐藤和, 三木康宏, 宮下穣, 笹野公伸, 鈴木貴

日本乳癌学会総会プログラム抄録集　28回　219-219　2020/10
Publisher: (一社)日本乳癌学会
アンドロゲン作用を受けた腫瘍随伴マクロファージはCCL5-CCR3の相互作用を介し乳癌の進展を促進する

山口美桜, 高木清司, 三木康宏, 小野寺好明, 宮下穣, 笹野公伸, 鈴木貴

日本乳癌学会総会プログラム抄録集　28回　221-221　2020/10
Publisher: (一社)日本乳癌学会
乳癌におけるイソクエン酸脱水素酵素(IDH)アイソフォームの免疫局在 IDH2は増殖に関係し予後不良因子となる

峯村洋行, 高木清司, 佐藤和, 山口美桜, 林千陽, 原田成美, 宮下穣, 石田孝宣, 笹野公伸, 鈴木貴

日本癌学会総会記事　79回　PJ14-2　2020/10
Publisher: (一社)日本癌学会
ISSN： 0546-0476
乳癌における活性型Rac1(Rac1-GTP)の発現意義

高木清司, 山口美桜, 佐藤和, 三木康宏, 宮下穣, 笹野公伸, 鈴木貴

日本癌学会総会記事　79回　PJ14-3　2020/10
Publisher: (一社)日本癌学会
ISSN： 0546-0476
アンドロゲン作用を受けた腫瘍随伴マクロファージはCCL5-CCR3相互作用を介して乳癌の進展に寄与する

山口美桜, 高木清司, 三木康宏, 小野寺好明, 宮下穣, 笹野公伸, 鈴木貴

日本癌学会総会記事　79回　PJ14-5　2020/10
Publisher: (一社)日本癌学会
ISSN： 0546-0476
腫瘍随伴マクロファージにおけるアンドロゲン誘導性液性因子CCL5は乳癌の進展に寄与する(Androgen-induced C-C motif chemokine ligand 5 secretion of macrophages regulate breast cancer progression)

山口美桜, 高木清司, 三木康宏, 小野寺好明, 石田孝宣, 笹野公伸, 鈴木貴

日本癌学会総会記事　78回　P-1340　2019/09
Publisher: (一社)日本癌学会
ISSN： 0546-0476
免疫組織化学法による乳癌組織随伴マクロファージにおけるアンドロゲン誘導性液性因子CCL5の発現意義の検討

山口美桜, 高木清司, 佐藤正康, 三木康宏, 石田孝宣, 笹野公伸, 鈴木貴

宮城県臨床検査技師会誌　9　(1)　33-33　2019/06
Publisher: (一社)宮城県臨床検査技師会
ISSN： 2186-6899
乳癌組織随伴マクロファージにおけるアンドロゲン誘導性液性因子の解析

山口美桜, 高木清司, 佐藤正康, 三木康宏, 石田孝宣, 笹野公伸, 鈴木貴

日本内分泌学会雑誌　95　(1)　488-488　2019/04
Publisher: (一社)日本内分泌学会
ISSN： 0029-0661

eISSN： 2186-506X

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Books and Other Publications 1

組織細胞化学2024「包埋、薄切、染色における初学者向けの注意点」

高木清司, 佐藤和, 田中美桜

日本組織細胞化学会　2024/07

Research Projects 6

細胞外基質の特性から乳癌におけるメカノセンサーの制御機構に迫る

田中美桜

Offer Organization: 日本学術振興会

System: 科学研究費助成事業

Category: 若手研究

Institution: 東北大学

2025/04/01 - 2027/03/31
乳癌における性ホルモンによるコンドロイチン硫酸の生理活性調節に関する研究

鈴木貴, 髙木清司, 田中美桜

Offer Organization: 日本学術振興会

System: 科学研究費助成事業

Category: 基盤研究(C)

Institution: 東北大学

2024/04 - 2027/03
細胞外小胞受容体による乳癌微小環境リモデリング機構の解明

田中美桜

Offer Organization: 日本学術振興会

System: 科学研究費助成事業

Category: 研究活動スタート支援

Institution: 東北大学

2023/08/31 - 2025/03/31
細胞外基質が生み出す力学的環境が乳癌細胞にもたらす影響と新規治療標的の探索

田中美桜

Offer Organization: 公益財団法人宮城県対がん協会

System: 黒川利雄がん研究基金

2024/06 - 2025/03
化学療法に伴う乳癌組織随伴マクロファージの悪性形質顕在化メカニズムの解明

山口美桜

Offer Organization: 日本学術振興会

System: 科学研究費助成事業

Category: 特別研究員奨励費

Institution: 東北大学

2021/04 - 2023/03

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①化学療法後の乳癌細胞がマクロファージに与える影響：抗癌剤であるエピルビシン（EPI）に曝露した乳癌細胞と共培養したヒト単球系細胞株由来マクロファージは、乳癌細胞の増殖能および遊走能を促進した。これらより、化学療法後の乳癌細胞がマクロファージの腫瘍促進作用を誘導することを確かめることができた。 ②化学療法誘導性エクソソーム内包因子の探索：EPI曝露後の乳癌細胞と、当分野で樹立したEPI耐性乳癌細胞の培養上清および分泌するエクソソームにおいて、Heat shock protein (HSP) 70の発現が上昇した。また、蛍光免疫組織化学法により、EPI曝露に伴い、乳癌細胞の細胞質におけるHSP70の発現することを見出した。 ③細胞外HSP70がマクロファージに与える影響：siRNAを用いて、乳癌細胞の培養上清および分泌するエクソソームにおけるHSP70の発現を抑制した。HSP70抑制培養上清をマクロファージに添加した結果、腫瘍促進型であるM2マクロファージへの分化が抑制された。しかし、HSP70抑制培養上清を添加したマクロファージが、乳癌細胞に与える顕著な影響は見出すことが出来なかった。そこで、HSP70抑制培養上清を添加した乳癌細胞において、Transforming Growth Factor (TGF)-betaの分泌が低下し、マクロファージのM2分化を抑制することを見出した。 ④乳癌組織におけるHSP70の発現意義：ヒト乳癌組織116例を対象としてHSP70の免疫染色を行い、臨床病理学的因子および予後との関連について解析した。その結果、乳癌細胞の細胞質におけるHSP70陽性症例は悪性度が高く、予後不良であることを確認した。さらに、HSP70陽性症例においてのみ、マクロファージの浸潤は有意に健存期間を短縮し、HSP70陰性症例においてこの傾向は認められなかった。
病理標本の顕微鏡写真を用いた乳腺病理診断補助AIの開発

山口美桜

Offer Organization: 東北大学大学院医学系研究科付属創生応用医学研究センター AI応用医学部門

System: 若手奨励研究

2022/01 -

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Teaching Experience 6

病理学　仙台市医師会看護専門学校
病理検査学実習　東北大学医学部保健学科検査技術科学専攻
病理検査学　東北大学医学部保健学科検査技術科学専攻
病理学　相馬看護専門学校
病理学　東北労災看護専門学校
微生物学　相馬看護専門学校

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