Updated on 2025/04/01

写真a

 
MOTOOKA Yashiro
 
Organization
Graduate School of Medicine Center for Research of Laboratory Animals and Medical Research Engineering Division Designated assistant professor
Title
Designated assistant professor
External link

Degree 1

  1. 学士(医学) ( 2012.3   熊本大学 ) 

Research Interests 16

  1. Ovarian cancer

  2. Carcinogenesis

  3. ナノ・マイクロマテリアルが生体に及ぼす影響

  4. BRCA1/2

  5. フェロトーシス

  6. 男性生殖能

  7. 女性生殖能

  8. 創傷治癒

  9. 触媒性二価鉄

  10. 発がん

  11. 活性酸素種

  12. 卵巣がん

  13. 不妊、男性不妊、女性不妊

  14. タルク

  15. アスベスト

Research Areas 6

  1. Life Science / Obstetrics and gynecology  / gynecological cancer

  2. Life Science / Experimental pathology  / Pathology

  3. Life Science / Pathological biochemistry  / 女性不妊

  4. Life Science / Pathological biochemistry  / 男性不妊

  5. Life Science / Obstetrics and gynecology  / 卵巣発がん

  6. Life Science / Experimental pathology  / 鉄と疾病・発がん

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Current Research Project and SDGs 5

  1. 細胞外微粒子への生体応答と発がん・動脈硬化症との関連の解析

  2. 環境中に存在するタルク、アスベストによる、卵巣がん形成機序の解明

  3. 新規ナノマテリアルの医薬への応用

  4. 新規ナノマテリアルのリスク評価

  5. アスベストおよびタルクが タンパク質を吸着することで惹起する、 卵巣におけるcancer initiating eventsの解明

Professional Memberships 17

  1. 日本DDS学会

    2024

  2. 日本がん予防学会

    2024

  3. 日本婦人科病理学会

    2022.4

  4. 日本鉄バイオサイエンス学会

    2021

  5. 日本がん・生殖医療学会

    2020

  6. 日本がん・生殖医療学会

    2020

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  7. 日本癌学会

    2019

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  8. 日本癌学会

    2018.4

  9. 日本酸化ストレス学会

    2018

  10. 日本酸化ストレス学会

    2018

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  11. 日本病理学会

    2017

  12. 日本婦人科腫瘍学会

    2017

  13. 日本婦人科腫瘍学会

    2017

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  14. 日本病理学会

    2017

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  15. 日本周産期・新生児医学会

    2014

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  16. 日本産科婦人科学会

    2013

  17. 日本産科婦人科学会

    2013

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Awards 10

  1. 若手研究者優秀演題賞

    2024.9   第31回 日本がん予防学会   環境中の微粒子であるアスベストとタルクは 曝露卵巣における発がんに関わる

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    Award type:Award from Japanese society, conference, symposium, etc.  Country:Japan

  2. 若手研究者優秀演題賞

    2024.9   第31回 日本がん予防学会  

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  3. Young Innovator Award

    2024.4   JST CREST「細胞外微粒子」  

  4. Young Innovator Award

    2024.4  

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  5. 学術奨励賞

    2022.5   日本酸化ストレス学会  

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    Award type:Award from Japanese society, conference, symposium, etc.  Country:Japan

  6. Academic Encouragement Award

    2022.5   Society for Free Radical Research Japan  

    Yashiro Motooka

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  7. Young Innovator Award

    2022.4  

  8. CREST "Extracellular Fine Particles" Young Innovator Award

    2022.4   Japan Science and Technology Agency  

    Yashiro Motooka

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  9. Discussant賞

    2021.3   第141回東海産科婦人科学会  

    本岡大社・公立西知多総合病院

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  10. Discussant賞

    2021.2   第141会東海産科婦人科学会  

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Papers 31

  1. Susceptibility of Brca1(L63X/+) rat to ovarian reserve dissipation by chemotherapeutic agents to breast cancer Reviewed International journal Open Access

    Satoshi Kaseki, Reina Sonehara, Yashiro Motooka, Hideaki Tanaka, Tomoko Nakamura, Satoko Osuka, Shinya Akatsuka, Hiroaki Kajiyama, Tomoji Mashimo, Tatsuhiko Imaoka, Shinya Toyokuni

    Cancer Science     2025.2

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    BRCA1 is one of the causative genes for hereditary breast and ovarian cancer syndrome with a high risk of early-onset breast cancer. Whereas olaparib (OLA), an inhibitor of poly-ADP-ribose polymerase, has been applied as adjuvant therapy to those cancer patients, its effect on ovarian reproductive function remains unelucidated. Recently, a rat model (MUT; Brca1(L63X/+) mutation) mimicking a human BRCA1 pathogenic variant has been established. Using this model, we evaluated the effects of OLA on ovarian reproductive function in comparison with the wild-type (WT) rats. MUT showed a significantly reduced number of primordial follicles and subfertility in accordance with aging. Oxidative stress was significantly elevated in the young MUT granulosa cells (GCs) accompanied by increased mTOR but decreased PTEN signals. OLA administration in MUT further decreased primordial follicles, with gene set enrichment analysis, indicating upregulated DNA repair pathways. Furthermore, a combination of OLA and cyclophosphamide (CPA) induced empty primordial follicles, recognized as CPA-induced severe ovarian toxicity. Whereas OLA + CPA caused greater reduction in primordial follicles both in MUT and WT in comparison with CPA alone, MUT ovaries were more susceptible to oxidative stress, potentially depleting primordial follicles via activation of GCs and inducing oocyte death due to accumulated DNA damage by OLA treatment. Our findings in this preclinical model underscore the importance of evaluating ovarian reserve prior to chemotherapy by performing reproductive consultation with female patients with BRCA1 pathogenic variants.

    DOI: 10.1111/cas.16412

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  2. Heterozygous mutation in BRCA2 induces accelerated age-dependent decline in sperm quality with male subfertility in rats. Reviewed International journal Open Access

    Yashiro Motooka, Hideaki Tanaka, Yuki Maeda, Misako Katabuchi, Tomoji Mashimo, Shinya Toyokuni

    Scientific reports   Vol. 15 ( 1 ) page: 447 - 447   2025.1

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    Tumor suppressor BRCA2 executes homologous recombination to repair DNA double-strand breaks in collaboration with RAD51, involving exon 11 and 27. Exon 11 constitutes a region where pathogenic variants (PVs) accumulate, and mutations in this region are known to contribute to carcinogenesis. However, the impact of the heterozygous PVs of BRCA2 exon 11 on the life quality beyond cancer risk, including male fertility, remains unclear. Here, we established a rat model with a frameshift on the seventh BRC repeat in Brca2 exon 11 (Brca2+/p.T1942fs), which is homologous to human BRCA2+/p.T1974fs, using CRISPR/Cas9 system. Our analyses revealed that the heterozygous rats with the PV in the BRCA2 exon 11 showed increased DNA double-strand breaks and apoptosis in spermatogonia and spermatocytes, accelerated testicular germ cell loss, and deterioration in sperm quality according with aging, ultimately resulting in early male reproductive dysfunction. Of note, these alterations in testes and sperm, including DNA fragmentation in spermatozoa, were observed from completion of sexual maturation. The present findings suggest that it is crucial to consider not only cancer risk but also potential declines in reproductive capacity in men carrying BRCA2 exon 11 PVs. Further investigation is warranted to determine whether similar traits appear in humans.

    DOI: 10.1038/s41598-024-84184-8

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  3. Cold plasma irradiation of chitosan: A straight pathway to selective antitumor therapy. Reviewed International journal Open Access

    Camelia Miron, Bianca Andreica, Manuela M Iftime, Adrian Fifere, Taishi Yamakawa, Shinya Toyokuni, Masaaki Mizuno, Liliana M Tartau, Andrei Bejan, Yashiro Motooka, Takashi Kondo, Ion Sava, Valeria Harabagiu, Jun Kumagai, Ayako Tanaka, Hiromasa Tanaka, Luminita Marin, Masaru Hori

    International journal of biological macromolecules   Vol. 281 ( Pt 4 ) page: 136513 - 136513   2024.11

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    Plasma-activated chitosan (PAC) colloids for cancer treatment were obtained by using the cold atmospheric plasma technique. Chitosan solutions were irradiated by plasma ignited in argon gas and in a mixture of argon with nitrogen and oxygen gases in certain ratios. The structural modifications of chitosan and the chemical species generated in plasma were investigated by EPR, LC-MS/MS, XRD, DLS, and TGA methods. The cell viability test showed a selective cytotoxic effect on human breast carcinoma cells (MCF-7), while the human mammary epithelial cells (MCF-10A) were left unharmed. The cytotoxic effect was attributed mainly to chitooligosaccharides, but also to a synergistic effect with other compounds generated in very low concentrations in plasma, such as glyceric acid, ethyl acetate, or tricarballylic acid. The plasma irradiation improved the antioxidant activity and mucoadhesivity, while not affecting the hemocompatibility investigated by a standard hemolysis ex vivo test on mice blood. Moreover, the in vivo biocompatibility investigation at intraperitoneal administration of PAC in mice showed no statistically significant changes in the hematologic, biochemical, and immune system parameters, and no morphologic alterations of the liver and kidney. All these data indicate the cold plasma activation of chitosan as a straight method to produce biocompatible, antitumor systems.

    DOI: 10.1016/j.ijbiomac.2024.136513

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  4. Elaborate cooperation of poly(rC)-binding proteins 1/2 and glutathione in ferroptosis induced by plasma-activated Ringer's lactate. Reviewed International journal Open Access

    Li Jiang, Hao Zheng, Moe Ishida, Qinying Lyu, Shinya Akatsuka, Yashiro Motooka, Kotaro Sato, Yoshitaka Sekido, Kae Nakamura, Hiromasa Tanaka, Kenji Ishikawa, Hiroaki Kajiyama, Masaaki Mizuno, Masaru Hori, Shinya Toyokuni

    Free radical biology & medicine   Vol. 214   page: 28 - 41   2024.3

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    Reactive species are involved in various aspects of neoplastic diseases, including carcinogenesis, cancer-specific metabolism and therapeutics. Non-thermal plasma (NTP) can directly provide reactive species, by integrating atmospheric and interjacent molecules as substrates, to represent a handy strategy to load oxidative stress in situ. NTP causes apoptosis and/or ferroptosis specifically in cancer cells of various types. Plasma-activated Ringer's lactate (PAL) is another modality at the preclinical stage as cancer therapeutics, based on more stable reactive species. PAL specifically kills malignant mesothelioma (MM) cells, employing lysosomal ·NO as a switch from autophagy to ferroptosis. However, the entire molecular mechanisms have not been elucidated yet. Here we studied cytosolic iron regulations in MM and other cancer cells in response to PAL exposure. We discovered that cells with higher catalytic Fe(II) are more susceptible to PAL-induced ferroptosis. PAL caused a cytosolic catalytic Fe(II)-associated pathology through iron chaperones, poly (rC)-binding proteins (PCBP)1/2, inducing a disturbance in glutathione-regulated iron homeostasis. PCBP1/NCOA4-mediated ferritinophagy started at a later phase, further increasing cytosolic catalytic Fe(II), ending in ferroptosis. In contrast, PCBP2 after PAL exposure contributed to iron loading to mitochondria, leading to mitochondrial dysfunction. Therapeutic effect of PAL was successfully applied to an orthotopic MM xenograft model in mice. In conclusion, PAL can selectively sensitize MM cells to ferroptosis by remodeling cytoplasmic iron homeostasis, where glutathione and PCBPs play distinct roles, resulting in lethal ferritinophagy and mitochondrial dysfunction. Our findings indicate the clinical application of PAL as a ferroptosis-inducer and the potential of PCBPs as novel targets in cancer therapeutics.

    DOI: 10.1016/j.freeradbiomed.2024.02.001

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  5. Role of iron, oxygen and ferroptosis in tumor evolutionary biology

    Toyokuni, S; Kong, YY; Luo, YG; Zheng, H; Motooka, Y; Imaoka, T; Akatsuka, S

    CANCER SCIENCE   Vol. 115   page: 907 - 907   2024.3

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  6. Brca2 (p.T1942fs/+) dissipates ovarian reserve in rats through oxidative stress in follicular granulosa cells Reviewed International journal Open Access

    Hideaki Tanaka, Yashiro Motooka, Yuki Maeda, Reina Sonehara, Tomoko Nakamura, Hiroaki Kajiyama, Tomoji Mashimo, Shinya Toyokuni

    Free Radical Research   Vol. 58 ( 2 ) page: 130 - 143   2024.2

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    Pathogenic variants of BRCA1/2 constitute hereditary breast and ovarian cancer (HBOC) syndrome, and BRCA1/2 mutant is a risk for various cancers. Whereas the clinical guideline for HBOC patients has been organized for the therapy and prevention of cancer, there is no recommendation on the female reproductive discipline. Indeed, the role of BRCA1/2 pathogenic variants in ovarian reserve has not been established due to the deficiency of appropriate animal models. Here, we used a rat model of Brca2(p.T1942fs/+) mutant of Sprague-Dawley strain with CRISPR-Cas9 editing to evaluate ovarian reserve in females. Fertility and ovarian follicles were evaluated and anti-Müllerian hormone (AMH) was measured at 8-32 weeks of age with a comparison between the wild-type and the mutant rats (MUT). MUT revealed a significantly smaller number of deliveries with fewer total pups. Furthermore, MUT showed a significant decrease in primordial follicles at 20 weeks and a low AMH level at 28 weeks. RNA-sequencing of the ovary at 10 weeks detected acceleration of the DNA damage repair pathway, which was accompanied by oxidative stress-induced DNA double-strand breaks, a decrease in PTEN, and an increase in mTOR in follicular granulosa cells. In conclusion, Brca2(p.T1942fs/+) dissipates primordial follicles via early activation of granulosa cells through oxidative stress, leading to earlier termination of fertility.

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  7. Epstein-Barr virus lytic gene BNRF1 promotes B-cell lymphomagenesis via IFI27 upregulation. Reviewed International journal Open Access

    Ken Sagou, Yoshitaka Sato, Yusuke Okuno, Takahiro Watanabe, Tomoki Inagaki, Yashiro Motooka, Shinya Toyokuni, Takayuki Murata, Hitoshi Kiyoi, Hiroshi Kimura

    PLoS pathogens   Vol. 20 ( 2 ) page: e1011954   2024.2

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    Epstein-Barr virus (EBV) is a ubiquitous human lymphotropic herpesvirus that is causally associated with several malignancies. In addition to latent factors, lytic replication contributes to cancer development. In this study, we examined whether the lytic gene BNRF1, which is conserved among gamma-herpesviruses, has an important role in lymphomagenesis. We found that lymphoblastoid cell lines (LCLs) established by BNRF1-knockout EBV exhibited remarkably lower pathogenicity in a mice xenograft model than LCLs produced by wild-type EBV (LCLs-WT). RNA-seq analyses revealed that BNRF1 elicited the expression of interferon-inducible protein 27 (IFI27), which promotes cell proliferation. IFI27 knockdown in LCLs-WT resulted in excessive production of reactive oxygen species, leading to cell death and significantly decreased their pathogenicity in vivo. We also confirmed that IFI27 was upregulated during primary infection in B-cells. Our findings revealed that BNRF1 promoted robust proliferation of the B-cells that were transformed by EBV latent infection via IFI27 upregulation both in vitro and in vivo.

    DOI: 10.1371/journal.ppat.1011954

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  8. Role of Iron, Oxygen and Ferroptosis in Tumor Evolutionary Biology Reviewed International journal

    Toyokuni, S; Kong, Y; Luo, Y; Zheng, H; Motooka, Y; Akatsuka, S

    FREE RADICAL BIOLOGY AND MEDICINE   Vol. 208   page: S112 - S112   2023.11

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    DOI: 10.1016/j.freeradbiomed.2023.10.254

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  9. Three-dimensional regulation of ferroptosis at the intersection of iron, sulfur and oxygen executing scrap and build toward evolution. Invited Reviewed International journal

    Shinya Toyokuni, Yingyi Kong, Hao Zheng, Yuki Maeda, Misako Katabuchi, Yashiro Motooka

    Antioxidants & redox signaling   Vol. 39 ( 10-12 ) page: 807 - 815   2023.10

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    Iron is an essential element for every life on earth as a primary media for electron flow. Sulfur compounds as sulfhydryls counteract catalytic activity of iron whereas sulfur overdose is also toxic. In aerobic organisms, oxygen is the major media for electron transfer with higher intracellular mobility, which cooperates with the iron system. Based on the importance of iron, there is no active pathway to excrete iron outside the body in higher species. Whereas bacterial infection causes a scramble for iron in situ, cancer can be the outcome of the side effects of long use of iron and oxygen. Ferroptosis is a recently coined cell death, defined as catalytic Fe(II)-dependent regulated necrosis accompanied by lipid peroxidation. Researchers recently recognized that ferroptosis is involved in a variety of physiological and pathological contexts, including embryonic erythropoiesis, aging, neurodegeneration and cancer cell death. Alternatively, carcinogenesis is a process to obtain iron addiction with ferroptosis-resistance, based on rodent animal studies. Here we propose that ferroptosis is three-dimensionally regulated by iron, sulfur and oxygen, which correspond to oxidants, antioxidants and membrane fluidity with susceptibility to lipid peroxidation, respectively. Whereas life attempts to prevent ferroptosis, ferroptotic cells eventually emit iron-loaded ferritin as extracellular vesicles to maintain monopoly of iron.

    DOI: 10.1089/ars.2022.0142

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  10. Iron links endogenous and exogenous nanoparticles. Reviewed International journal Open Access

    Shinya Toyokuni, Yingyi Kong, Misako Katabuchi, Yuki Maeda, Yashiro Motooka, Fumiya Ito, Izumi Yanatori

    Archives of biochemistry and biophysics   Vol. 745   page: 109718 - 109718   2023.9

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    Current progress in biology and medical science is based on the observation at the level of nanometers via electron microscopy and computation. Of note, the size of most cells in higher species exists in a limited range from 5 to 50 μm. Recently, it was demonstrated that endogenous extracellular nanoparticles play a role in communication among various cellular types in a variety of contexts. Among them, exosomes in serum have been established as biomarkers for human diseases by analyzing the cargo molecules. No life on the earth can survive without iron. However, excess iron can be a risk for carcinogenesis in rodents and humans. Nano-sized molecules may cause unexpected bioeffects, including carcinogenesis, which is a process to establish cellular iron addiction with ferroptosis-resistance. Asbestos and carbon nanotubes are the typical examples, leading to carcinogenesis by the alteration of iron metabolism. Recently, we found that CD63, one of the representative markers of exosomes, is under the regulation of iron-responsive element/iron-regulatory protein system. This is a safe strategy to share excess iron in the form of holo-ferritin between iron-sufficient and -deficient cells. On the other hand, damaged cells may secrete holo-ferritin-loaded exosomes as in the case of macrophages in ferroptosis after asbestos exposure. These holo-ferritin-loaded exosomes can cause mutagenic DNA damage in the recipient mesothelial cells. Thus, there is an iron link between exogenous and endogenous nanoparticles, which requires further investigation for better understanding and the future applications.

    DOI: 10.1016/j.abb.2023.109718

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  11. Ferroptosis as ultimate target of cancer therapy. Invited Reviewed International journal

    Yashiro Motooka, Shinya Toyokuni

    Antioxidants & redox signaling   Vol. 39 ( 1-3 ) page: 206 - 223   2023.7

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    Ferroptosis is a new form of regulated non-apoptotic cell death, which is characterized by iron-dependent lipid peroxidation, leading eventually to plasma membrane rupture. Its core mechanisms have been elucidated consisting of a driving force as catalytic Fe(II)-dependent Fenton reaction and an incorporation of polyunsaturated fatty acids to membrane phospholipids via peroxisome-dependent and -independent pathways, whereas suppressing factors are the prevention of lipid peroxidation by glutathione peroxidase 4 to protect lipid peroxidation and direct membrane repair via coenzyme Q10 and ESCRT-III pathways. The significance of ferroptosis in cancer therapeutics has now been unveiled. Specific ferroptosis inducers are expected as a promising strategy for cancer treatment, especially in cancers with epithelial mesenchymal transition and possibly in cancers with activated Hippo signaling pathways, both of which cause resistance to traditional chemotherapy but tend to show ferroptosis susceptibility. Developments of ferroptosis inducers are in progress by nanotechnology-based drugs or by innovative engineering devices. Especially, low-temperature (non-thermal) plasma is a novel technology at the preclinical stage. The exposure can induce ferroptosis selectively in cancer cells which are generally rich in catalytic Fe(II). Here we summarize and discuss the recently uncovered responsible molecular mechanisms in association with iron metabolism, ferroptosis and cancer therapeutics. Finally, we also highlight the current classification of ferroptosis inducers.

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  12. BRCA1 haploinsufficiency impairs iron metabolism to promote chrysotile‐induced mesothelioma via ferroptosis‐resistance Reviewed International journal Open Access

    Yaguang Luo, Shinya Akatsuka, Yashiro Motooka, Yingyi Kong, Hao Zheng, Tomoji Mashimo, Tatsuhiko Imaoka, Shinya Toyokuni

    Cancer Science   Vol. 114 ( 4 ) page: 1423 - 1436   2023.4

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    Malignant mesothelioma (MM) is still a social burden associated with asbestos exposure. Local iron accumulation thereby represents the major pathogenesis, followed by oxidative DNA strand breaks and genomic alterations in the mesothelium. BRCA1 is a critical component of homologous recombination repair directed to DNA double-strand breaks. Whereas BRCA1 germline mutation is an established risk for breast/ovarian cancer, its role in MM development remains to be elucidated. Murine Brca1 mutant models thus far have not reproduced human phenotypes. However, a rat Brca1 mutant model (Mut; L63X/+) recently reproduced them at least partially. Here we describe the differential induction of MM in Brca1 mutant rats by intraperitoneal injection of chrysotile or crocidolite. Only Mut males injected with chrysotile revealed a promotional effect on mesothelial carcinogenesis in comparison to wild-type and/or females, with all the MMs Brca1-haploinsufficient. Array-based comparative genomic hybridization of MMs disclosed a greater extent of chromosomal deletions in Brca1 mutants, including Cdkn2a/2b accompanied by Tfr2 amplification, in comparison to wild-type tumors. Mutant MMs indicated iron metabolism dysregulation, such as increase in catalytic Fe(II) and Ki67-index as well as decrease in Fe(III) and ferritin expression. Simultaneously, mutant MMs revealed ferroptosis-resistance by upregulation of Slc7A11 and Gpx4. At an early carcinogenic stage of 4 weeks, induced Brca1 expression in mesothelial cells was significantly suppressed in chrysotile/Mut in comparison to crocidolite/Mut whereas significant preference to iron with decrease in Fe(III) has been already established. In conclusion, chrysotile exposure can be a higher risk for MM in BRCA1 mutant males, considering the rat results.

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  13. Field-effect transistor antigen/antibody-TMDs sensors for the detection of COVID-19 samples. Reviewed International journal Open Access

    Ruben Canton-Vitoria, Kotaro Sato, Yashiro Motooka, Shinya Toyokuni, Zheng Liu, Ryo Kitaura

    Nanoscale   Vol. 15 ( 9 ) page: 4570 - 4580   2023.3

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    We fabricated sensors by modifying the surface of MoS2 and WS2 with COVID-19 antibodies and investigated their characteristics, including stability, reusability, sensitivity, and selectivity. Thiols and disulfanes in antibodies strongly interact with vacant Mo or W sites of MoS2 or WS2, yielding durable devices that are stable for several days in the air or water. More importantly, detachment of the antibodies is suppressed even during the aggressive cleaning process of the devices at pH 3, which allows reusing the same device in several experiments without appreciable loss of sensitivity. Therefore, the nanodevice may be employed in samples of different patients. Further, we found a limit of detection (LOD) of 1 fg ml-1 at room temperature, time responses of 1 second, and selectivity against interferences such as KLH protein or Albumin.

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  14. DNA oxidative damage caused by the aromatic amine MOCA —Examination of 8-hydroxy-2’-deoxyguanosine levels in rat liver—

    KOBAYASHI Saho, MOTOOKA Yashiro, KASHIWAGI Hiroki, TOYOKUNI Shinya

    Journal of Occupational Safety and Health   Vol. 16 ( 1 ) page: 45 - 49   2023.2

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    <p>MOCA (4,4’-methylenebis (2-chloroaniline)) , an aromatic amine, is industrially used as a curing agent for urethane resins; however, it is classified as a Group 1 compound (carcinogenic to humans) by the International Agency for Research on Cancer, and there is concern regarding its health effects on workers. The mechanism underlying MOCA-mediated carcinogenesis is thought to be related to DNA damage caused by reactive oxygen species (ROS) and DNA adducts, which are mainly generated during metabolism in the liver. 8-Oxoguanine (8-OHdG), a product of ROS-induced oxidation, occurs at high frequency and can induce G→T transversion mutations during DNA replication. However, to the best of our knowledge, no study has examined whether MOCA induces the formation of highly mutagenic 8-OHdG in experimental animals. Here, F344 rats were orally exposed to 0, 0.4, 2, 10, or 50 mg/kg/day MOCA three times a week for 2 weeks; this is expected to exert toxicity through the hepatic metabolism of MOCA. Livers obtained from these animals were examined for pathology and 8-OHdG levels. In pathological sections, vacuolar degeneration was observed with 50 mg/kg/day MOCA. Further, MOCA-induced 8-OHdG levels showed a slight increasing trend, except at 0.4 mg/kg/day. However, none of these differences were significant. Thus, 8-OHdG is unlikely the main cause of carcinogenesis.</p>

    DOI: 10.2486/josh.josh-2022-0022-ta

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  15. Environmental impact on carcinogenesis under BRCA1 haploinsufficiency. Reviewed International journal Open Access

    Shinya Toyokuni, Yingyi Kong, Yashiro Motooka, Shinya Akatsuka

    Genes and environment : the official journal of the Japanese Environmental Mutagen Society   Vol. 45 ( 1 ) page: 2 - 2   2023.1

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    Cancer is the primary cause of human mortality in Japan since 1981. Although numerous novel therapies have been developed and applied in clinics, the number of deaths from cancer is still increasing worldwide. It is time to consider the strategy of cancer prevention more seriously. Here we propose a hypothesis that cancer can be side effects of long time-use of iron and oxygen and that carcinogenesis is an evolution-like cellular events to obtain "iron addiction with ferroptosis-resistance" where genes and environment interact each other. Among the recognized genetic risk factors for carcinogenesis, we here focus on BRCA1 tumor suppressor gene and how environmental factors, including daily life exposure and diets, may impact toward carcinogenesis under BRCA1 haploinsufficiency. Although mice models of BRCA1 mutants have not been successful for decades in generating phenotype mimicking the human counterparts, a rat model of BRCA1 mutant was recently established that reasonably mimics the human phenotype. Two distinct categories of oxidative stress, one by radiation and one by iron-catalyzed Fenton reaction, promoted carcinogenesis in Brca1 rat mutants. Furthermore, mitochondrial damage followed by alteration of iron metabolism finally resulted in ferroptosis-resistance of target cells in carcinogenesis. These suggest a possibility that cancer prevention by active pharmacological intervention may be possible for BRCA1 mutants to increase the quality of their life rather than preventive mastectomy and/or oophorectomy.

    DOI: 10.1186/s41021-023-00258-5

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  16. Iron as spirit of life to share under monopoly. Reviewed Open Access

    Shinya Toyokuni, Yingyi Kong, Hao Zheng, Yuki Maeda, Yashiro Motooka, Shinya Akatsuka

    Journal of clinical biochemistry and nutrition   Vol. 71 ( 2 ) page: 78 - 88   2022.9

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    Any independent life requires iron to survive. Whereas iron deficiency causes oxygen insufficiency, excess iron is a risk for cancer, generating a double-edged sword. Iron metabolism is strictly regulated via specific systems, including iron-responsive element (IRE)/iron regulatory proteins (IRPs) and the corresponding ubiquitin ligase FBXL5. Here we briefly reflect the history of bioiron research and describe major recent advancements. Ferroptosis, a newly coined Fe(II)-dependent regulated necrosis, is providing huge impact on science. Carcinogenesis is a process to acquire ferroptosis-resistance and ferroptosis is preferred in cancer therapy due to immunogenicity. Poly(rC)-binding proteins 1/2 (PCBP1/2) were identified as major cytosolic Fe(II) chaperone proteins. The mechanism how cells retrieve stored iron in ferritin cores was unraveled as ferritinophagy, a form of autophagy. Of note, ferroptosis may exploit ferritinophagy during the progression. Recently, we discovered that cellular ferritin secretion is through extracellular vesicles (EVs) escorted by CD63 under the regulation of IRE/IRP system. Furthermore, this process was abused in asbestos-induced mesothelial carcinogenesis. In summary, cellular iron metabolism is tightly regulated by multi-system organizations as surplus iron is shared through ferritin in EVs among neighbor and distant cells in need. However, various noxious stimuli dramatically promote cellular iron uptake/storage, which may result in ferroptosis.

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  17. BRCA1 haploinsufficiency promotes chromosomal amplification under Fenton reaction-based carcinogenesis through ferroptosis-resistance. Reviewed International journal Open Access

    Yingyi Kong, Shinya Akatsuka, Yashiro Motooka, Hao Zheng, Zhen Cheng, Yukihiro Shiraki, Tomoji Mashimo, Tatsuhiko Imaoka, Shinya Toyokuni

    Redox biology   Vol. 54   page: 102356 - 102356   2022.8

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    Germline-mutation in BRCA1 tumor suppressor gene is an established risk for carcinogenesis not only in females but also in males. Deficiency in the repair of DNA double-strand breaks is hypothesized as a responsible mechanism for carcinogenesis. However, supporting data is insufficient both in the mutation spectra of cancers in the patients with BRCA1 germline-mutation and in murine knockout/knock-in models of Brca1 haploinsufficiency. Furthermore, information on the driving force toward carcinogenesis in BRCA1 mutation carriers is lacking. Here we applied Fenton reaction-based renal carcinogenesis to a rat heterozygously knockout model of BRCA1 haploinsufficiency (mutant [MUT] model; L63X/+). Rat MUT model revealed significant promotion of renal cell carcinoma (RCC) induced by ferric nitrilotriacetate (Fe-NTA). Array-based comparative genome hybridization of the RCCs identified significant increase in chromosomal amplification, syntenic to those in breast cancers of BRCA1 mutation carriers, including c-Myc, in comparison to those in the wild-type. Subacute-phase analysis of the kidney after repeated Fe-NTA treatment in the MUT model revealed dysregulated iron metabolism with mitochondrial malfunction assessed by expression microarray and electron microscopy, leading to renal tubular proliferation with iron overload. In conclusion, we for the first time demonstrate that biallelic wild-type BRCA1 provides more robust protection for mitochondrial metabolism under iron-catalyzed oxidative stress, preventing the emergence of neoplastic cells with chromosomal amplification. Our results suggest that oxidative stress via excess iron is a major driving force for carcinogenesis in BRCA1 haploinsufficiency, which can be a target for cancer prevention and therapeutics.

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  18. Pathologic findings toward the concept of cancer as ferroptosis-resistance

    Toyokuni, S; Zheng, H; Kong, YY; Luo, YG; Motooka, Y

    CANCER SCIENCE   Vol. 113   page: 661 - 661   2022.2

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  19. BRCA1 deficiency regulates the metabolism of iron and oxidative stress-induced carcinogenesis in the kidney

    Kong, YY; Motooka, Y; Akatsuka, S; Mashimo, T; Imaoka, T; Toyokuni, S

    CANCER SCIENCE   Vol. 113   page: 336 - 336   2022.2

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  20. Iron overload led by genital talc exposure contributes to ovarian carcinogenesis

    Motooka, Y; Ito, F; Tashiro, H; Katabuchi, H; Toyokuni, S

    CANCER SCIENCE   Vol. 113   page: 725 - 725   2022.2

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  21. Double-edged Sword Role of Iron-loaded Ferritin in Extracellular Vesicles Reviewed International journal

    Shinya Toyokuni, Yingyi Kong, Hao Zheng, Danyang Mi, Misako Katabuchi, Yashiro Motooka, Fumiya Ito

    Journal of Cancer Prevention   Vol. 26 ( 4 ) page: 244 - 249   2021.12

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    Human epidemiological and animal studies have demonstrated that excess iron is a risk for cancer. The responsible mechanisms are: 1) increased intracellular iron catalyzes the Fenton reaction to generate hydroxyl radicals, leading to mutagenic oxidative DNA lesions; 2) iron is necessary for cellular proliferation as cofactors of many enzymes. Thus, iron-excess milieu promotes selecting cellular evolution to ferroptosis-resistance, a major basis for carcinogenesis. Ferritin is a 24-subunit nanocage protein required for iron storage under the regulation of the iron-regulatory protein (IRP)/iron-responsive element (IRE) system. Ferritin is a serum marker, representing total body iron storage. However, how ferritin is secreted extracellularly has been unelucidated. We recently discovered that an exosomal marker CD63 is regulated by the IRP/IRE system and that iron-loaded ferritin is secreted as extracellular vesicles under the guidance of nuclear receptor coactivator 4 (NCOA4). On the other hand, we found that macrophages under asbestos-induced ferroptosis emit ferroptosis-dependent extracellular vesicles (FedEVs), which are received by nearby mesothelial cells, resulting in significant mutagenic DNA damage. Therefore, cells, including macrophages, can share excess iron with other cells, via iron-loaded ferritin packaged in extracellular vesicles as safe non-catalytic iron. However, similar process, such as one involving FedEVs, may cause accumulation of excess iron in other specific cells, which may eventually promote carcinogenesis.

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  22. Role of ferroptosis in nanofiber-induced carcinogenesis Reviewed International journal

    Toyokuni Shinya, Ito Fumiya, Motooka Yashiro

    Metallomics Research   Vol. 1 ( 1 ) page: rev-14 - rev-21   2021.10

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    <p>Biopersistent nanofibers with specified physical dimension are unexpected human carcinogens whether they are natural or synthetic. Asbestos, a natural fibrous mineral, is classified as a definite human carcinogen (IARC Group 1) to cause malignant mesothelioma (MM) and lung cancer. Multi-walled carbon nanotube of 50 nm-diameter was defined in 2014 as a possible carcinogen (IARC Group 2B) toward MM, fortunately with no authorized patients thus far. Carcinogenic mechanism of asbestos has been a mystery for a long time. It is now recognized that asbestos goes through lung parenchyma by collecting hemoglobin-derived iron to reach pleural cavity, which takes several decades. Iron-loaded asbestos can induce oxidative damage directly to mesothelial cells, carcinogenesis-target cells lining somatic cavities. Recently, it was clarified that surrounding stromal environment are as important for mesothelial carcinogenesis. The novel concept here is ceaseless ferroptosis of macrophages, which forms a Fe(II)-dependent stromal mutagenic milieu indirectly for mesothelial cells and indeed is a revised understanding of frustrated phagocytosis. Deposition of foreign materials eventually causes iron accumulation <i>in situ</i> due to the innate characteristic of preserving iron inside cells. Nanofiber-induced carcinogenesis may be involved in other human carcinogenesis, including ovarian cancer. Alternatively, iron excess can be an optimal target of cancer prevention and cancer treatment. </p>

    DOI: 10.11299/metallomicsresearch.mr202102

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  23. Plasma-activated Ringer's lactate solution inhibits the cellular respiratory system in HeLa cells Reviewed International journal

    Hiromasa Tanaka, Shogo Maeda, Kae Nakamura, Hiroshi Hashizume, Kenji Ishikawa, Mikako Ito, Kinji Ohno, Masaaki Mizuno, Yashiro Motooka, Yasumasa Okazaki, Shinya Toyokuni, Hiroaki Kajiyama, Fumitaka Kikkawa, Masaru Hori

    PLASMA PROCESSES AND POLYMERS   Vol. 18 ( 10 )   2021.10

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    Nonequilibrium atmospheric pressure plasma has enabled a variety of new applications in medicine, agriculture, and other industries. It is particularly noteworthy that plasma itself and/or plasma-activated culture medium have been shown to preferentially kill various cancer cells. We have previously developed a plasma-activated Ringer's lactate solution (PAL) for use as a new cancer treatment. In this study, behaviors of extracellular and intracellular reactive oxygen and nitrogen species in the cellular respiratory system of PAL-treated HeLa cells were investigated using an extracellular flux analyzer and a probe to measure mitochondrial membrane potential. In PAL-treated HeLa cells, extracellular hydrogen peroxide in PAL was found to be responsible for the induction of intracellular hydrogen peroxide and apoptosis, while other components in PAL are responsible for the induction of non-H2O2 intracellular ROS and non-apoptotic cell death, which should be clarified by further experiments. We believe that these are long-lived species derived from plasma-activated lactates. Furthermore, we found that the plasma-activated lactates inhibited glycolysis and the tricarboxylic acid (TCA) cycle, but not the electron transport chain in HeLa cells. These results suggest that PAL induces multiple modes of cell death, including apoptosis through hydrogen peroxide, and non-apoptotic cell death associated with the impairment of mitochondrial functions (glycolysis and TCA cycle). These findings shed light on the novel mechanism underlying plasma-activated lactate-induced cell death.

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  24. Role of ferroptosis in nanofiber-induced carcinogenesis Invited Reviewed

    Shinya Toyokuni, Fumiya Ito, Yashiro Motooka

    Metallomics Research   Vol. 1   page: 14 - 21   2021

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  25. Novel ovarian endometriosis model causes infertility via iron-mediated oxidative stress in mice Reviewed International journal Open Access

    Shotaro Hayashi, Tomoko Nakamura, Yashiro Motooka, Fumiya Ito, Li Jiang, Shinya Akatsuka, Akira Iwase, Hiroaki Kajiyama, Fumitaka Kikkawa, Shinya Toyokuni

    Redox Biology   Vol. 37   page: 101726 - 101726   2020.10

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    Ovarian endometriosis (OE) provides women of reproductive age with not only severe menstrual pain but also infertility and an increased risk for ovarian carcinogenesis. Whereas peritoneal endometriosis models have been developed with syngeneic implantation of minced uterine tissue and oncogenic K-ras allele with conditional Pten deletion within ovarian surface epithelium generated preneoplastic endometrial glandular morphology, followed by endometrioid adenocarcinoma, there has been no mouse model of OE similar to human counterparts, applicable to preclinical studies. Here we for the first time established a murine OE model that reveals infertility, and evaluated the involvement of iron catalyzed oxidative stress in the pathogenesis. Minced uterine tissue from female mice was implanted on ovarian surface of syngeneic mice after bursectomy to induce OE. Ectopic growth of endometrium was observed in association with ovary 4 weeks after implantation in 85.7% (12/14) of the operated mice with our protocol. Endometriotic lesions involved intestine, pancreas and peritoneal wall. Fibrosis around the ovary was prominent and increased time-dependently in the OE group. Iron accumulation was significantly increased in the OE group, leading to oxidative stress in each stage of the follicles as evaluated by 4-hydroxy-2-nonenal-modified proteins and 8-hydroxy-2'-deoxyguanosine. Expression of follicle stimulating hormone receptor in the follicles revealed a significant decrease during pre-antral, antral and pre-ovulatory phases in the OE group. Finally, the number of pups was significantly reduced in the OE group in comparison to the controls. This model affords an opportunity to evaluate agents or procedures to counteract ovarian endometriosis in the preclinical settings.

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  26. Connective tissue growth factor produced by cancer‑associated fibroblasts correlates with poor prognosis in epithelioid malignant pleural mesothelioma. Reviewed International journal Open Access

    Yuuki Ohara, Atsushi Enomoto, Yuta Tsuyuki, Kotaro Sato, Tadashi Iida, Hiroki Kobayashi, Yasuyuki Mizutani, Yuki Miyai, Akitoshi Hara, Shinji Mii, Jun Suzuki, Kyoko Yamashita, Fumiya Ito, Yashiro Motooka, Nobuaki Misawa, Takayuki Fukui, Koji Kawaguchi, Kohei Yokoi, Shinya Toyokuni

    Oncology reports   Vol. 44 ( 3 ) page: 838 - 848   2020.9

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    Malignant mesothelioma is an aggressive neoplasm for which effective treatments are lacking. We often encounter mesothelioma cases with a profound desmoplastic reaction, suggesting the involvement of cancer‑associated fibroblasts (CAFs) in mesothelioma progression. While the roles of CAFs have been extensively studied in other tumors and have led to the view that the cancer stroma contains heterogeneous populations of CAFs, their roles in mesothelioma remain unknown. We previously showed that connective tissue growth factor (CTGF), a secreted protein, is produced by both mesothelioma cells and fibroblasts and promotes the invasion of mesothelioma cells in vitro. In this study, we examined the clinical relevance of CAFs in mesothelioma. Using surgical specimens of epithelioid malignant pleural mesothelioma, we evaluated the clinicopathological significance of the expression of α‑smooth muscle actin (αSMA), the most widely used marker of CAFs, the expression of CTGF, and the extent of fibrosis by immunohistochemistry and Elastica‑Masson staining. We also analyzed the expression of mesenchymal stromal cell‑ and fibroblast‑expressing Linx paralogue (Meflin; ISLR), a recently reported CAF marker that labels cancer‑restraining CAFs and differ from αSMA‑positive CAFs, by in situ hybridization. The extent of fibrosis and CTGF expression in mesothelioma cells did not correlate with patient prognosis. However, the expression of αSMA and CTGF, but not Meflin, in CAFs correlated with poor prognosis. The data suggest that CTGF+ CAFs are involved in mesothelioma progression and represent a potential molecular target for mesothelioma therapy.

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  27. Ferroptosis at the crossroads of infection, aging and cancer. Reviewed International journal Open Access

    Shinya Toyokuni, Izumi Yanatori, Yingyi Kong, Hao Zheng, Yashiro Motooka, Li Jiang

    Cancer science   Vol. 111 ( 8 ) page: 2665 - 2671   2020.8

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    Despite significant developments and persistent efforts by scientists, cancer is one of the primary causes of human death worldwide. No form of life on Earth can survive without iron, although some species can live without oxygen. Iron presents a double-edged sword. Excess iron is a risk for carcinogenesis, while its deficiency causes anemia, leading to oxygen shortage. Every cell is eventually destined to death, either through apoptosis or necrosis. Regulated necrosis is recognized in distinct forms. Ferroptosis is defined as catalytic Fe(II)-dependent regulated necrosis accompanied by lipid peroxidation. The main observation was necrosis of fibrosarcoma cells through inhibition of cystine/glutamate antiporter with erastin, which reduced intracellular cysteine and, thus, glutathione levels. Our current understanding of ferroptosis is relative abundance of iron (catalytic Fe[II]) in comparison with sulfur (sulfhydryls). Thus, either excess iron or sulfur deficiency causes ferroptosis. Cell proliferation inevitably requires iron for DNA synthesis and energy production. Carcinogenesis is a process toward iron addiction with ferroptosis resistance. Conversely, ferroptosis is associated with aging and neurodegeneration. Ferroptosis of immune cells during infection is advantageous for infectious agents, whereas ferroptosis resistance incubates carcinogenic soil as excess iron. Cancer cells are rich in catalytic Fe(II). Directing established cancer cells to ferroptosis is a novel strategy for discovering cancer therapies. Appropriate iron regulation could be a tactic to reduce and delay carcinogenesis.

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  28. Connective tissue growth factor produced by cancer-associated fibroblasts correlates with poor prognosis in epithelioid malignant pleural mesothelioma. Reviewed

    Yuuki Ohara, Atsushi Enomoto, Yuta Tsuyuki, Kotaro Sato, Tadashi Iida, Hiroki Kobayashi, Yasuyuki Mizutani, Yuki Miyai, Akitoshi Hara, Shinji Mii, Jun Suzuki, Kyoko Yamashita, Fumiya Ito, Yashiro Motooka, Nobuaki Misawa, Takayuki Fukui, Koji Kawaguchi, Kohei Yokoi, Shinya Toyokuni

    Oncology Report   Vol. 44 ( 3 ) page: 838 - 848   2020

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  29. Novel ovarian endometriosis model causes infertility via iron-mediated oxidative stress in mice. Invited Reviewed

    Shotaro Hayashi, Tomoko Nakamura, Yashiro Motooka, Fumiya Ito, Li Jiang, Shinya Akatsuka, Akira Iwase, Hiroaki Kajiyama, Fumitaka Kikkawa, Shinya Toyokuni.

    Redox Biology   Vol. 37   page: 101726   2020

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  30. Ferroptosis at the crossroads of infection, aging and cancer Reviewed

    Shinya Toyokuni, Izumi Yanatori, Yingyi Kong, Hao Zheng, Yashiro Motooka, Li Jiang

    Cancer science   Vol. 111 ( 8 ) page: 2665 - 2671   2020

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  31. Non-thermal plasma specifically kills oral squamous cell carcinoma cells in a catalytic Fe(II)-dependent manner. Reviewed

    Kotaro Sato, Lei Shi, Fumiya Ito, Yuuki Ohara, Yashiro Motooka, Hiromasa Tanaka, Masaaki Mizuno, Masaru Hori, Tasuku Hirayama, Hideharu Hibi, Shinya Toyokuni

    Journal of Clinical Biochemistry and Nutrition   Vol. 65 ( 1 ) page: 8 - 15   2019

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Books 6

  1. 酸化ストレスの医学

    内藤, 裕二, 豐國, 伸哉, 赤池, 孝章, 半田, 修, 日本酸化ストレス学会

    診断と治療社  2024.6  ( ISBN:9784787826206

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  2. 第3版 酸化ストレスの医学

    一般社団法人 日本酸化ストレス学会( Role: Contributor ,  第2章 20節 婦人科疾患と酸化ストレス)

    診断と治療社  2024  ( ISBN:978-4-7878-2620-6

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    Total pages:520   Responsible for pages:446-452   Language:Japanese

    DOI: https://doi.org/10.34433/9784787881571

  3. マウス・ラット モデル作成・解析プロフェッショナル

    豊國伸哉, 伊藤文哉, 本岡 大社, 蒋麗( Role: Contributor ,  第2章7節 使いたくなる病理解析新技術)

    羊土社  2021.4 

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    Total pages:317   Responsible for pages:147-160   Language:Japanese

  4. マウス・ラットモデル作製・解析プロフェッショナル 編集:先端モデル動物支援プラットフォーム(AdAMS)

    豊國伸哉, 伊藤文哉, 本岡大社, 蒋 麗( Role: Contributor ,  使いたくなる病理解析新技術 第2章 病理形態の解析)

    羊土社  2021.3 

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  5. 図解腫瘍薬学

    川西, 正祐, 賀川, 義之, 大井, 一弥

    南山堂  2020.8  ( ISBN:9784525721619

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  6. 図解腫瘍薬学

    本原剛志、本岡大社、三宅俊介、片渕秀隆、城野博史( Role: Contributor ,  13章臓器別がん薬物療法 7)生殖器がん①(卵巣がん、子宮頸がん、子宮体がん))

    南山堂  2020.7 

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MISC 51

  1. 細胞外微粒子が鉄代謝と酸化ストレスに及ぼす影響と発がんへの関与

    本岡 大社, 豊國 伸哉

    大気環境学会誌   Vol. 60 ( 1 ) page: A32 - A38   2025.1

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  2. 実臨床向き新概念 「抗癌剤の貢献期間」による再発漿液性卵巣癌に対する抗癌剤の有効性の評価

    前田 修, 本岡 大社, 伊藤 真文, 宮本 絵美里, 伊吉 祥平, 吉原 雅人, 池田 芳紀, 芳川 修久, 梶山 広明

    日本婦人科腫瘍学会学術講演会プログラム・抄録集   Vol. 66回   page: 326 - 326   2024.7

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  3. Ovarian vein thrombosis induced by septic infection of group A streptococcus in a woman under oral contraceptives

    永坂万友子, 本岡大社, 太田肇, 川地史高, 齋藤理

    東海産科婦人科学会雑誌   Vol. 60   page: 341 - 346   2024.3

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  4. BRCA2の生殖細胞変異は卵胞発育を促進し卵巣予備能の低下を惹起する(BRCA2 germline mutation accelerates follicle maturation, leading to reduced ovarian reserve)

    田中 秀明, 本岡 大社, 前田 勇貴, 真下 知士, 梶山 広明, 豊國 伸哉

    日本病理学会会誌   Vol. 113 ( 1 ) page: 428 - 429   2024.2

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  5. BRCA2変異はラットモデルにおいて精子の質の低下と精巣の退行性変化をきたし男性不妊を惹起する

    界外 誠, 本岡 大社, 豊國 伸哉

    日本病理学会会誌   Vol. 113 ( 1 ) page: 479 - 479   2024.2

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  6. シクロホスファミドとオラパリブによる卵巣毒性はBRCA1変異で増強される(Ovarian follicle toxicity of Cyclophosphamide and Olaparib in BRCA1 mutant rats)

    可世木 聡, 本岡 大社, 中村 智子, 梶山 広明, 豊國 伸哉

    日本病理学会会誌   Vol. 113 ( 1 ) page: 428 - 428   2024.2

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  7. 病理形態学から発がんメカニズムの本質に迫る 環境中の微粒子であるアスベストやタルクによる卵巣発がん(Mechanisms of carcinogenesis revealed by pathomorphology Ovarian carcinogenesis induced by environmental particulates: asbestos and talc)

    本岡 大社, 豊國 伸哉

    日本病理学会会誌   Vol. 113 ( 1 ) page: 194 - 194   2024.2

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  8. マイクロプラスチック曝露によるラット子宮内膜症の増悪(Growth of rat endometriosis is accelerated by microplastics exposure)

    片渕 充沙子, 本岡 大社, 田代 浩徳, 近藤 英治, 豊國 伸哉

    日本病理学会会誌   Vol. 113 ( 1 ) page: 429 - 429   2024.2

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  9. 環境中の微粒子であるアスベストとタルクは曝露卵巣における発がんに関わる

    本岡大社, 豊國伸哉

    がん予防学術大会プログラム・抄録集     2024

  10. BRCA2の生殖細胞変異は卵胞発育を促進し卵巣予備能の低下を惹起する(BRCA2 germline mutation promotes follicle development and induces diminished ovarian reserve)

    田中 秀明, 本岡 大社, 前田 勇貴, 真下 知士, 梶山 広明, 豊國 伸哉

    日本癌学会総会記事   Vol. 82回   page: 172 - 172   2023.9

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  11. BRCA1変異モデルラットの卵巣機能に対する加齢とPARP阻害剤オラパリブの影響(Effect of aging and PARP inhibitor, olaparib on ovarian function with BRCA1 mutant model rats)

    曽根原 玲菜, 本岡 大社, 真下 知士, 今岡 達彦, 梶山 広明, 豊國 伸哉

    日本癌学会総会記事   Vol. 82回   page: 170 - 170   2023.9

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  12. 腫瘍進化生物学における鉄、酸素、フェロトーシスの役割(Role of iron, oxygen and ferroptosis in tumor evolutionary biology)

    豊國 伸哉, 孔 穎怡, 羅 亜光, 鄭 好, 本岡 大社, 今岡 達彦, 赤塚 慎也

    日本癌学会総会記事   Vol. 82回   page: 907 - 907   2023.9

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  13. BRCA2 germline mutation model rat represents decreased ovarian reserve

    田中秀明, 田中秀明, 本岡大社, 前田勇貴, 真下知士, 梶山広明, 豊國伸哉

    日本病理学会会誌   Vol. 112 ( 1 ) page: 370 - 370   2023.3

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  14. Disturbance of EVs-mediated ovarian iron metabolism by talc to increase carcinogenicity

    本岡大社, 加藤大暉, 豊國伸哉

    日本病理学会会誌   Vol. 112 ( 1 ) page: 256 - 256   2023.3

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  15. Primary ovarian squamous cell carcinoma arising in Brenner tumor: a case report

    太田幸希, 永坂万友子, 本岡大社, 東真規子, 足立学, 川地史高, 斎藤理

    東海産科婦人科学会雑誌   Vol. 59   page: 275 - 279   2023.3

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  16. 卵巣における細胞外小胞を介した鉄代謝と酸化ストレス応答の解析

    加藤 大暉, 本岡 大社, 豊國 伸哉

    日本病理学会会誌   Vol. 112 ( 1 ) page: 382 - 382   2023.3

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  17. DNA oxidative damage caused by the aromatic amine MOCA -Examination of 8-hydroxy-2’-deoxyguanosine levels in rat liver-

    小林沙穂, 本岡大社, 柏木裕呂樹, 豊國伸哉, 小林健一

    労働安全衛生研究   Vol. 16 ( 1 ) page: 45 - 49   2023.2

  18. 細胞外小胞吸着によるレドックス撹乱によってタルクは卵巣発がんに関与する

    本岡大社, 豊國伸哉

    日本酸化ストレス学会学術集会プログラム・抄録集   Vol. 76th   2023

  19. 遺伝性腫瘍予防へのアプローチ

    豊國伸哉, 孔頴怡, 羅亜光, 今岡龍彦, 本岡大社, 赤塚慎也

    がん予防学術大会プログラム・抄録集   Vol. 2023   2023

  20. Clinical significance and development of novel therapies for advanced ovarian cancer with loss of tumor suppressor gene CYLD expression

    松山果穂, 三宅俊介, 三宅俊介, 下村祐美, 金丸歩美, 西郷智香, 成田勇樹, 成田勇樹, 本岡大社, 岩越裕, 本原剛志, 片渕秀隆, 齋藤秀之, 齋藤秀之, 城野博史, 城野博史

    日本薬学会年会要旨集(Web)   Vol. 143rd   2023

  21. BRCA1のハプロ不全は発がん過程において、フェロトーシス抵抗性を獲得することにより染色体増幅を促進する(BRCA1 haploinsufficiency promotes carcinogenic chromosomal amplification by ferroptosis-resistance)

    孔 穎怡, 赤塚 慎也, 本岡 大社, 鄭 好, 白木 之浩, 真下 知士, 今岡 達彦, 豊國 伸哉

    Biomedical Research on Trace Elements   Vol. 33 ( 1 ) page: 130 - 130   2022.9

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  22. BRCA1遺伝子ハプロ不全モデルラットを用いた卵巣予備能低下の検証(Validation of reduced ovarian reserve in BRCA1 haploinsufficient rats.)

    曽根原 玲菜, 本岡 大社, 梶山 広明, 真下 知士, 今岡 達彦, 豊國 伸哉

    日本癌学会総会記事   Vol. 81回   page: P - 3012   2022.9

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  23. BRCA1遺伝子ハプロ不全モデルラットを用いた卵巣予備能低下の検証(Validation of reduced ovarian reserve in BRCA1 haploinsufficient rats.)

    曽根原 玲菜, 本岡 大社, 梶山 広明, 真下 知士, 今岡 達彦, 豊國 伸哉

    日本癌学会総会記事   Vol. 81回   page: P - 3012   2022.9

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  24. BRCA1欠損はフェロトーシス抵抗性を誘導することによりアスベスト誘発性腹膜中皮腫を促進する(Ferroptosis resistance is induced by BRCA1 deficiency in asbestos-induced mesothelioma)

    羅 亜光, 本岡 大社, 赤塚 慎也, 真下 知士, 今岡 達彦, 豊國 伸哉

    日本癌学会総会記事   Vol. 81回   page: P - 2003   2022.9

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  25. BRCA1欠損はフェロトーシス抵抗性を誘導することによりアスベスト誘発性腹膜中皮腫を促進する(Ferroptosis resistance is induced by BRCA1 deficiency in asbestos-induced mesothelioma)

    羅 亜光, 本岡 大社, 赤塚 慎也, 真下 知士, 今岡 達彦, 豊國 伸哉

    日本癌学会総会記事   Vol. 81回   page: P - 2003   2022.9

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  26. BRCA1のハプロ不全は発がん過程において、フェロトーシス抵抗性を獲得することにより染色体増幅を促進する(BRCA1 haploinsufficiency promotes carcinogenic chromosomal amplification by ferroptosis-resistance)

    孔 穎怡, 赤塚 慎也, 本岡 大社, 鄭 好, 白木 之浩, 真下 知士, 今岡 達彦, 豊國 伸哉

    Biomedical Research on Trace Elements   Vol. 33 ( 1 ) page: 130 - 130   2022.9

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  27. プラズマ活性化された乳酸リンゲルに誘導されたフェロトーシスにおけるpcbp1/2とグルタチオンとの協同作用(Cooperation of Poly(rC)-binding Proteins 1/2 and Glutathione in Ferroptosis Induced by Plasma-activated Ringer's Lactate)

    鄭 好, 蒋 麗, 呂 沁穎, 赤塚 慎也, 本岡 大社, 関戸 好孝, 中村 香江, 田中 宏昌, 石川 健治, 梶山 広明, 水野 正明, 堀 勝, 豊國 伸哉

    日本癌学会総会記事   Vol. 81回   page: E - 2004   2022.9

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  28. 環境因子であるタルクおよびアスベストの卵巣発がん性とゲノム毒性の検討(Carcinogenic genome toxicity of environmental factors, asbestos and talc in ovary)

    本岡 大社, 鬼丸 洸, 鈴木 洋, 片渕 充沙子, 近藤 英治, 田代 浩徳, 片渕 秀隆, 豊國 伸哉

    日本癌学会総会記事   Vol. 81回   page: P - 2007   2022.9

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  29. 個別化予防医療・先制医療 BRCA1のハプロ不全は、腎臓発がん過程において、フェロトーシス抵抗性を獲得することにより染色体増幅を促進する(BRCA1 haploinsufficiency promotes chromosomal amplification under renal carcinogenesis through ferroptosis-resistance)

    孔 穎怡, 赤塚 慎也, 本岡 大社, 鄭 好, 白木 之浩, 真下 知士, 今岡 達彦, 豊國 伸哉

    日本癌学会総会記事   Vol. 81回   page: S20 - 7   2022.9

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  30. 個別化予防医療・先制医療 BRCA1のハプロ不全は、腎臓発がん過程において、フェロトーシス抵抗性を獲得することにより染色体増幅を促進する(BRCA1 haploinsufficiency promotes chromosomal amplification under renal carcinogenesis through ferroptosis-resistance)

    孔 穎怡, 赤塚 慎也, 本岡 大社, 鄭 好, 白木 之浩, 真下 知士, 今岡 達彦, 豊國 伸哉

    日本癌学会総会記事   Vol. 81回   page: S20 - 7   2022.9

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  31. プラズマ活性化された乳酸リンゲルに誘導されたフェロトーシスにおけるpcbp1/2とグルタチオンとの協同作用(Cooperation of Poly(rC)-binding Proteins 1/2 and Glutathione in Ferroptosis Induced by Plasma-activated Ringer's Lactate)

    鄭 好, 蒋 麗, 呂 沁穎, 赤塚 慎也, 本岡 大社, 関戸 好孝, 中村 香江, 田中 宏昌, 石川 健治, 梶山 広明, 水野 正明, 堀 勝, 豊國 伸哉

    日本癌学会総会記事   Vol. 81回   page: E - 2004   2022.9

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  32. Asbestos contributes to ovarian carcinogenesis via iron overload by hemoglobin adsorption

    本岡大社, 豊國伸哉

    日本病理学会会誌   Vol. 111 ( 1 ) page: 249 - 249   2022.3

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  33. 腹腔内に多発する腹膜原発肝様腺癌(hepatoid adenocarcinoma)に対し、腫瘍減量術と化学療法により良好な生命予後が得られた一例

    本岡 大社, 永坂 万友子, 川地 史高, 齋藤 理

    東海産科婦人科学会雑誌   Vol. 58   page: 313 - 313   2022.3

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  34. Contralateral vertebral artery dissection after laparoscopic surgery in a patient treated unilateral vertebral artery dissection after spinal manipulative therapy

    齋藤理, 本岡大社, 太田肇, 永坂真友子, 川地史高

    東海産科婦人科学会雑誌   Vol. 58   page: 263 - 267   2022.3

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  35. 子宮内腔に類内膜腺癌から進展したと思われる癌肉腫を認めた1例

    齋藤 理, 川地 史高, 永坂 万由子, 本岡 大社

    東海産科婦人科学会雑誌   Vol. 58   page: 315 - 315   2022.3

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  36. タルクは曝露卵巣に鉄過剰状態とフェロトーシス抵抗性を誘導し発がんに関わる

    井上 陽太, 本岡 大社, 豊國 伸哉

    日本病理学会会誌   Vol. 111 ( 1 ) page: 353 - 353   2022.3

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  37. BRCA1 haploinsufficiency promotes chromosomal amplification under renal carcinogenesis through ferroptosis-resistance Introduction

    孔穎怡, 赤塚慎也, 本岡大社, 鄭好, 白木之浩, 真下知士, 今岡達彦, 豊國伸哉

    日本癌学会学術総会抄録集(Web)   Vol. 81st   2022

  38. BRCA1のハプロ欠損はフェントン反応に基づく発がんにおいて,フェロトーシス抵抗性を介して染色体増幅を促進する

    孔穎怡, 赤塚慎也, 本岡大社, 真下知士, 今岡達彦, 豊國伸哉

    がん予防学術大会プログラム・抄録集   Vol. 2022   2022

  39. タルクはヘモグロビンを吸着し鉄過剰状態を卵巣表層上皮に形成することで卵巣がん形成に関わる

    本岡大社, 片渕充沙子, 片渕充沙子, 豊國伸哉

    日本酸化ストレス学会学術集会プログラム・抄録集   Vol. 75th (CD-ROM)   2022

  40. Ferroptosis-resistance in rodent cancer models

    豊國伸哉, 孔穎怡, 赤塚慎也, 本岡大社, 鄭好, 真下知士, 今岡達彦

    日本癌学会学術総会抄録集(Web)   Vol. 81st   2022

  41. BRCA1欠損は腎臓における鉄代謝の変化と酸化ストレスによる腎発がんに関わる

    孔 穎怡, 本岡 大社, 赤塚 慎也, 真下 知士, 今岡 達彦, 豊國 伸哉

    日本癌学会総会記事   Vol. 80回   page: [P2 - 1]   2021.9

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  42. 乳癌術後ホルモン療法中に発生した子宮体部腺線維腫に対して子宮鏡手術を施行した2例

    永坂 万友子, 齋藤 理, 川地 史高, 本岡 大社, 小川 明男

    日本産科婦人科内視鏡学会雑誌   Vol. 37 ( Suppl.I ) page: 254 - 254   2021.9

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  43. 女性器へのタルクの曝露は鉄過剰環境を形成し卵巣がんの発がんに関わる

    本岡 大社, 伊藤 文哉, 田代 浩徳, 片渕 秀隆, 豊國 伸哉

    日本癌学会総会記事   Vol. 80回   page: [E1 - 6]   2021.9

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  44. 変革する病理学:形態診断から普遍的研究プラットフォームへ 実験病理学に起源を持つがんのフェロトーシス抵抗性

    豊國 伸哉, Zheng Hao, Kong Yingyi, Yaguang Luo, 本岡 大社

    日本癌学会総会記事   Vol. 80回   page: [S10 - 6]   2021.9

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  45. 術前に組織型の予想が困難であった卵巣腫瘍の一例

    岸本 かおり, 大竹 秀幸, 本岡 大社, 三好 潤也, 本田 律生

    熊本産科婦人科学会雑誌   ( 65 ) page: 147 - 147   2021.3

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  46. 卵巣癌における腫瘍抑制遺伝子CYLD発現低下の臨床的・生物学的意義の解明

    三宅俊介, 三宅俊介, 松山果穂, 下村祐美, 金丸歩美, 西郷智香, 本岡大社, 岩越裕, 本原剛志, 片渕秀隆, 齋藤秀之, 齋藤秀之, 城野博史, 城野博史

    日本薬学会九州支部大会講演要旨集   Vol. 38th (CD-ROM) ( Suppl.1 ) page: 209 - 209   2021

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  47. 異時性発生の卵巣成熟奇形腫の手術中に微小腹膜インプラントを認めた1例

    齋藤 理, 川地 史高, 永坂 万友子, 本岡 大社

    日本産科婦人科内視鏡学会雑誌   Vol. 36 ( Suppl.I ) page: [O - 356]   2020.11

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  48. 異時性発生の卵巣成熟奇形腫の手術中に微小腹膜インプラントを認めた1例

    齋藤 理, 川地 史高, 永坂 万友子, 本岡 大社

    日本産科婦人科内視鏡学会雑誌   Vol. 36 ( Suppl.I ) page: [O - 356]   2020.11

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  49. アスベストとタルクは鉄過剰環境を形成し卵巣がんの発がんに関わる

    本岡 大社, 伊藤 文哉, 田代 浩徳, 片渕 秀隆, 豊國 伸哉

    日本癌学会総会記事   Vol. 79回   page: OJ1 - 1   2020.10

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  50. Asbestos contribute to ovarian carcinogenesis via iron overload in ovarian surface epithelia

    本岡大社, 伊藤文哉, 豊國伸哉

    日本病理学会会誌   Vol. 109 ( 1 ) page: 314 - 314   2020.3

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  51. Clinical significance of CYLD down-regulation in ovarian cancer as a novel prognosis biomarker

    西郷智香, 三宅俊介, 三宅俊介, 下村祐美, 金丸歩美, 本岡大社, 本原剛志, 片渕秀隆, 齋藤秀之, 齋藤秀之, 城野博史, 城野博史

    日本薬学会年会要旨集(CD-ROM)   Vol. 140年会   page: 28P - am045S   2020.3

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Presentations 25

  1. 新規二次元ナノマテリアルが 皮膚創傷治癒とレドックスに及ぼす影響の検討 

    本岡 大社、加藤 勝洋、佐藤 好隆、大町 遼、豊國 伸哉

    日本酸化ストレス学会東海支部 第13回学術集会  2025.2.8  田中 宏昌

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    Event date: 2025.2

    Language:Japanese   Presentation type:Oral presentation (general)  

    Venue:名古屋大学野依記念学術交流館   Country:Japan  

  2. アスベストおよびタルクのタンパク質吸着性と卵巣発がん Invited

    本岡 大社、田代浩徳、片渕秀隆、豊國 伸哉

    第56回日本臨床分子形態学会総会・学術集会  2024.9.28  森谷 卓也

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    Event date: 2024.9

    Language:Japanese   Presentation type:Symposium, workshop panel (nominated)  

    Venue:川崎医科大学   Country:Japan  

  3. 細胞外微粒子が鉄代謝と酸化ストレスに及ぼす影響と発がんへの関与 Invited

    本岡大社,豊國伸哉

    第65回大気環境学会年会  2024.9.11  奥田 知明

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    Event date: 2024.9

    Language:Japanese   Presentation type:Oral presentation (invited, special)  

    Venue:慶應義塾大学日吉キャンパス  

  4. 環境中の微粒子であるアスベストとタルクは曝露卵巣における発がんに関わる

    本岡 大社、豊國伸哉

    第31回日本がん予防学会総会  2024.9.12  高山 哲治

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    Event date: 2024.9

    Language:Japanese   Presentation type:Oral presentation (general)  

    Venue:徳島県医師会館   Country:Japan  

  5. アスベストとタルクは曝露卵巣における鉄代謝を撹乱し発がんを惹起する

    本岡大社、豊國伸哉

    第48回日本鉄バイオサイエンス学会  2024.8.30  岩井 一宏

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    Event date: 2024.8

    Language:Japanese   Presentation type:Oral presentation (general)  

    Venue:京都大学医学部 芝蘭会館   Country:Japan  

  6. BRCA2 germline mutation promotes follicle development and induces diminished ovarian reserve

    Tanaka, H; Motooka, Y; Maeda, Y; Mashimo, T; Kajiyama, H; Toyokuni, S

    CANCER SCIENCE  2024.3 

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    Event date: 2024.3

  7. Effect of aging and PARP inhibitor, olaparib on ovarian function with <i>BRCA1</i> mutant model rats

    Sonehara, R; Motooka, Y; Mashimo, T; Imaoka, T; Kajiyama, H; Toyokuni, S

    CANCER SCIENCE  2024.3 

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    Event date: 2024.3

  8. Validation of reduced ovarian reserve in BRCA1 haploinsufficient rats

    Sonehara, R; Motooka, Y; Kajiyama, H; Mashimo, T; Imaoka, T; Toyokuni, S

    CANCER SCIENCE  2023.2 

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    Event date: 2023.2

    Language:English   Presentation type:Poster presentation  

  9. Cooperation of Poly(rC)-binding Proteins 1/2 and Glutathione in Ferroptosis Induced by Plasmaactivated Ringer's Lactate

    Zheng, H; Jiang, L; Lyu, QY; Akatsuka, S; Motooka, Y; Sekido, Y; Nakamura, K; Tanaka, H; Ishikawa, K; Kajiyama, H; Mizuno, M; Hori, M; Toyokuni, S

    CANCER SCIENCE  2023.2 

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    Event date: 2023.2

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  10. Ferroptosis-resistance in rodent cancer models

    Toyokuni, S; Kong, Y; Akatsuka, S; Motooka, Y; Zheng, H; Mashimo, T; Imaoka, T

    CANCER SCIENCE  2023.2 

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    Event date: 2023.2

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  11. Ferroptosis resistance is induced by BRCA1 deficiency in asbestos-induced mesothelioma

    Luo, YG; Motooka, Y; Akatsuka, S; Mashimo, T; Imaoka, T; Toyokuni, S

    CANCER SCIENCE  2023.2 

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    Event date: 2023.2

    Language:English   Presentation type:Poster presentation  

  12. Cooperation of Poly(rC)-binding Proteins 1/2 and Glutathione in Ferroptosis Induced by Plasma-activated Ringer's Lactate

    Zheng, H; Jiang, L; Lyu, QY; Akatsuka, S; Motooka, Y; Sekido, Y; Nakamura, K; Tanaka, H; Ishikawa, K; Kajiyama, H; Mizuno, M; Hori, M; Toyokuni, S

    CANCER SCIENCE  2023.2 

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    Event date: 2023.2

    Language:English   Presentation type:Poster presentation  

  13. Carcinogenic genome toxicity of environmental factors, asbestos and talc in ovary

    Motooka, Y; Onimaru, K; Suzuki, HI; Katabuchi, M; Kondoh, E; Tashiro, H; Katabuchi, H; Toyokuni, S

    CANCER SCIENCE  2023.2 

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    Event date: 2023.2

    Language:English   Presentation type:Poster presentation  

  14. <i>BRCA1</i> haploinsufficiency promotes chromosomal amplification under renal carcinogenesis through ferroptosis-resistance Invited

    Kong, YY; Akatsuka, S; Motooka, Y; Zheng, H; Shiraki, Y; Mashimo, T; Imaoka, T; Toyokuni, S

    CANCER SCIENCE  2023.2 

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    Event date: 2023.2

    Language:English   Presentation type:Symposium, workshop panel (nominated)  

  15. BRCA1 deficiency regulates the metabolism of iron and oxidative stress-induced carcinogenesis in the kidney

    Kong, YY; Motooka, Y; Akatsuka, S; Mashimo, T; Imaoka, T; Toyokuni, S

    CANCER SCIENCE  2022.2 

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    Event date: 2022.2

    Language:English   Presentation type:Poster presentation  

  16. Pathologic findings toward the concept of cancer as ferroptosis-resistance

    Toyokuni, S; Zheng, H; Kong, YY; Luo, YG; Motooka, Y

    CANCER SCIENCE  2022.2 

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    Event date: 2022.2

    Language:English  

  17. Iron overload led by genital talc exposure contributes to ovarian carcinogenesis

    Motooka, Y; Ito, F; Tashiro, H; Katabuchi, H; Toyokuni, S

    CANCER SCIENCE  2022.2 

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    Event date: 2022.2

    Language:English   Presentation type:Oral presentation (general)  

  18. BRCA1 deficiency regulates the metabolism of iron and oxidative stress-induced carcinogenesis in the kidney

    Kong, YY; Motooka, Y; Akatsuka, S; Mashimo, T; Imaoka, T; Toyokuni, S

    CANCER SCIENCE  2022.2 

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    Event date: 2022.2

  19. BRCA1 deficiency regulates the metabolism of iron and oxidative stress-induced carcinogenesis in the kidney

    Kong, YY; Motooka, Y; Akatsuka, S; Mashimo, T; Imaoka, T; Toyokuni, S

    CANCER SCIENCE  2022.2 

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    Event date: 2022.2

  20. アスベストとタルクは鉄代謝異常による 酸化ストレスの増加から卵巣発がんに関与する

    本岡 大社、豊國 伸哉

    レドックスR&D戦略委員会 第1回若手シンポジウム  2021.11.8  熊本大学微生物学講座

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    Event date: 2021.11

    Language:Japanese   Presentation type:Oral presentation (general)  

    Venue:web   Country:Japan  

  21. Iron overload led by genital talc exposure contributes to ovarian carcinogenesis

    Yashiro Motooka, Fumiya Ito, Hironori Tashiro, Hidetaka Katabuchi, Shinya Toyokunii

    2021.10 

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    Event date: 2021.9 - 2021.10

    Language:English   Presentation type:Oral presentation (general)  

    Country:Japan  

  22. Asbestos contributes to ovarian carcinogenesis Invited International conference

    Yashiro Motooka, Hironori Tashiro, Shinya Toyokuni, Hidetaka Katabuchi

    The 60th Annual Congress and The 9th International Symposium of the Taiwan Association of Obstetrics and Gynecology  2021.5.30  Taiwan Association of Obstetrics and Gynecology

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    Event date: 2021.5

    Language:English   Presentation type:Oral presentation (invited, special)  

    Venue:Taiwan   Country:Taiwan, Province of China  

  23. BRCA1 deficiency regulates the metabolism of iron and oxidative stress-induced carcinogenesis in the kidney

    Kong Yingyi, Motooka Yashiro, Akatsuka Shinya, Mashimo Tomoji, Imaoka Tatsuhiko, Toyokuni Shinya

    CANCER SCIENCE  2022.2 

  24. Pathologic findings toward the concept of cancer as ferroptosis-resistance

    Toyokuni Shinya, Zheng Hao, Kong Yingyi, Luo Yaguang, Motooka Yashiro

    CANCER SCIENCE  2022.2 

  25. Iron overload led by genital talc exposure contributes to ovarian carcinogenesis

    Motooka Yashiro, Ito Fumiya, Tashiro Hironori, Katabuchi Hidetaka, Toyokuni Shinya

    CANCER SCIENCE  2022.2 

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Research Project for Joint Research, Competitive Funding, etc. 3

  1. 二次元ナノマテリアルMXene (Ti3C2Tx) の創傷治癒への応用

    2024.4 - 2025.3

    令和6年度 CREST「細胞外微粒子」若手チャレンジ  

    本岡 大社

  2. タルクによるEVs伝達阻害:卵巣における評価と応用

    2022.4 - 2023.3

    令和4年度 CREST「細胞外微粒子」若手チャレンジ  

    本岡 大社

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    Grant type:Competitive

    Grant amount:\500000

  3. アスベストおよびタルクがタンパク質を吸着することで惹起する、卵巣におけるcancer initiating eventsの解明

    2021.4 - 2022.3

    令和3年度 CREST「細胞外微粒子」若手チャレンジ 

    本岡大社

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    Authorship:Principal investigator  Grant type:Competitive

    Grant amount:\1800000 ( Direct Cost: \1800000 )

KAKENHI (Grants-in-Aid for Scientific Research) 1

  1. 環境中微粒子によるタンパク質や細胞外小胞の吸着が鉄代謝と卵巣がん形成に及ぼす影響

    Grant number:23K08883  2023.4 - 2026.3

    日本学術振興会  科学研究費助成事業  基盤研究(C)

    本岡 大社

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    Authorship:Principal investigator  Grant type:Competitive

    Grant amount:\4680000 ( Direct Cost: \3600000 、 Indirect Cost:\1080000 )

    ナノマテリアルを含む微粒子は「吸着性」を示すことが多いが、この性質が生体に及ぼす影響は未だ明らかではない。本研究では、卵巣がんとの関連性が指摘されているアスベストとタルクを具体的な微粒子として選び、「吸着性」が「発がん」にどのように関わるかを解明することを目的とする。また、微粒子の吸着性を調整することで人体に安全なナノマテリアルおよび微粒子の開発と運用を進め、危険な微粒子の環境中への拡散を防ぎ、健康寿命の延伸を図ることを最終的な目標としている。
    本検討では2023年度、2024年度、2025年度それぞれの進捗目標を掲げている。2023年度の目標は、アスベストとタルクが吸着する物質の同定と、そのタンパク質の吸着が発がん性に及ぼす影響を明らかにすることとしていた。
    2023年度の検討では、アスベストとタルクが中性条件のpH下で吸着するタンパク質を質量分析で網羅的に検出した。検出した吸着タンパク質の中に、アスベスト・タルクによる卵巣の発がんリスクが特に大きいとされる生殖年齢女性の骨盤内で周期的に増加する特定のタンパク質(X)が含まれていたため、これに着目した。動物実験および細胞実験の結果、アスベスト・タルク曝露で惹起される曝露卵巣・細胞におけるDNAの二本鎖切断が、X吸着後の曝露でさらに増加することが示された。これは、Xの吸着がアスベストおよびタルクの発がん性を増強する因子である可能性を示唆している。
    このほか、研究を効率的に進めるため卵巣発がんに関わる癌抑制遺伝子であるBRCA2の変異モデルラットを作成・樹立した。このモデルでは雌雄ともにヘテロ接合体変異で生殖能が低下することを見出している。

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Teaching Experience (On-campus) 18

  1. 基礎医学セミナー

    2024

  2. 病理病態学

    2024

  3. 臨床病理学実習

    2024

  4. 基礎セミナー

    2024

  5. ベーシックトレーニング(プラズマ活性化水の作成)

    2024

  6. ベーシックトレーニング(レーザーマイクロダイセクション)

    2024

  7. 臨床病理学実習

    2023

  8. 基礎セミナー

    2023

  9. 病理病態学

    2023

  10. 基礎医学セミナー

    2023

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    10月から3月上旬の学内発表会まで学部3年生の基礎研究、実験、発表にかんする指導をおこなう。

  11. 病理病態学

    2022

  12. 基礎セミナー

    2022

  13. 基礎医学セミナー

    2022

  14. 臨床病理学実習

    2022

  15. 基礎セミナー

    2021

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    医学英語

  16. 病理学実習

    2021

  17. 基礎医学セミナー

    2021

  18. 臨床病理学実習

    2021

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Teaching Experience (Off-campus) 1

  1. 母性

    2015.4 - 2015.3

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    Level:Undergraduate (specialized)