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781 results on '"Moses, Harold L."'

3. Author Correction: Genotype tunes pancreatic ductal adenocarcinoma tissue tension to induce matricellular fibrosis and tumor progression

Author

Laklai, Hanane, Miroshnikova, Yekaterina A., Pickup, Michael W., Collisson, Eric A., Kim, Grace E., Barrett, Alex S., Hill, Ryan C., Lakins, Johnathon N., Schlaepfer, David D., Mouw, Janna K., LeBleu, Valerie S., Roy, Nilotpal, Novitskiy, Sergey V., Johansen, Julia S., Poli, Valeria, Kalluri, Raghu, Iacobuzio-Donahue, Christine A., Wood, Laura D., Hebrok, Matthias, Hansen, Kirk, Moses, Harold L., and Weaver, Valerie M.

Published
2024
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4. Challenges and Opportunities to Updating Prescribing Information for Longstanding Oncology Drugs

Author

Balogh, Erin P, Bindman, Andrew B, Eckhardt, S Gail, Halabi, Susan, Harvey, R Donald, Jaiyesimi, Ishmael, Miksad, Rebecca, Moses, Harold L, Nass, Sharyl J, Schilsky, Richard L, Sun, Steven, Torrente, Josephine M, and Warren, Katherine E

Subjects
Biomedical and Clinical Sciences, Oncology and Carcinogenesis, Cancer, Rare Diseases, 6.1 Pharmaceuticals, Evaluation of treatments and therapeutic interventions, Drug Labeling, Drug Prescriptions, Humans, Neoplasms, Pharmaceutical Preparations, Pilot Projects, United States, United States Food and Drug Administration, Drug prescriptions, Drug legislation, Drug approval, Pharmaceutical research, Oncology & Carcinogenesis, Oncology and carcinogenesis
Abstract

A number of important drugs used to treat cancer-many of which serve as the backbone of modern chemotherapy regimens-have outdated prescribing information in their drug labeling. The Food and Drug Administration is undertaking a pilot project to develop a process and criteria for updating prescribing information for longstanding oncology drugs, based on the breadth of knowledge the cancer community has accumulated with the use of these drugs over time. This article highlights a number of considerations for labeling updates, including selecting priorities for updating; data sources and evidentiary criteria; as well as the risks, challenges, and opportunities for iterative review to ensure prescribing information for oncology drugs remains relevant to current clinical practice.

Published
2020

5. Challenges and Opportunities to Updating Prescribing Information for Longstanding Oncology Drugs.

Author

Balogh, Erin P, Bindman, Andrew B, Eckhardt, S Gail, Halabi, Susan, Harvey, R Donald, Jaiyesimi, Ishmael, Miksad, Rebecca, Moses, Harold L, Nass, Sharyl J, Schilsky, Richard L, Sun, Steven, Torrente, Josephine M, and Warren, Katherine E

Subjects
Cancer, Drug approval, Drug legislation, Drug prescriptions, Pharmaceutical research, Rare Diseases, 6.1 Pharmaceuticals, Oncology & Carcinogenesis, Oncology and Carcinogenesis
Abstract

A number of important drugs used to treat cancer-many of which serve as the backbone of modern chemotherapy regimens-have outdated prescribing information in their drug labeling. The Food and Drug Administration is undertaking a pilot project to develop a process and criteria for updating prescribing information for longstanding oncology drugs, based on the breadth of knowledge the cancer community has accumulated with the use of these drugs over time. This article highlights a number of considerations for labeling updates, including selecting priorities for updating; data sources and evidentiary criteria; as well as the risks, challenges, and opportunities for iterative review to ensure prescribing information for oncology drugs remains relevant to current clinical practice.

Published
2019

6. Development of Aggressive Pancreatic Ductal Adenocarcinomas Depends on Granulocyte Colony Stimulating Factor Secretion in Carcinoma Cells

Author

Pickup, Michael W, Owens, Philip, Gorska, Agnieszka E, Chytil, Anna, Ye, Fei, Shi, Chanjuan, Weaver, Valerie M, Kalluri, Raghu, Moses, Harold L, and Novitskiy, Sergey V

Subjects
Biomedical and Clinical Sciences, Oncology and Carcinogenesis, Immunology, Rare Diseases, Cancer, Pancreatic Cancer, Digestive Diseases, Stem Cell Research, Aetiology, Development of treatments and therapeutic interventions, 2.1 Biological and endogenous factors, 5.1 Pharmaceuticals, Good Health and Well Being, Adenocarcinoma, Animals, Carcinoma, Pancreatic Ductal, Cell Proliferation, Disease Models, Animal, Disease Progression, Gene Expression Regulation, Neoplastic, Granulocyte Colony-Stimulating Factor, Humans, Interferon-Stimulated Gene Factor 3, gamma Subunit, Mice, Mice, Knockout, Proto-Oncogene Proteins p21(ras), Signal Transduction, T-Lymphocytes, Transforming Growth Factor beta, Pharmacology and Pharmaceutical Sciences, Oncology and carcinogenesis
Abstract

The survival rate for pancreatic ductal adenocarcinoma (PDAC) remains low. More therapeutic options to treat this disease are needed, for the current standard of care is ineffective. Using an animal model of aggressive PDAC (Kras/p48TGFβRIIKO), we discovered an effect of TGFβ signaling in regulation of G-CSF secretion in pancreatic epithelium. Elevated concentrations of G-CSF in PDAC promoted differentiation of Ly6G+ cells from progenitors, stimulated IL10 secretion from myeloid cells, and decreased T-cell proliferation via upregulation of Arg, iNOS, VEGF, IL6, and IL1b from CD11b+ cells. Deletion of csf3 in PDAC cells or use of a G-CSF-blocking antibody decreased tumor growth. Anti-G-CSF treatment in combination with the DNA synthesis inhibitor gemcitabine reduced tumor size, increased the number of infiltrating T cells, and decreased the number of Ly6G+ cells more effectively than gemcitabine alone. Human analysis of human datasets from The Cancer Genome Atlas and tissue microarrays correlated with observations from our mouse model experiments, especially in patients with grade 1, stage II disease. We propose that in aggressive PDAC, elevated G-CSF contributes to tumor progression through promoting increases in infiltration of neutrophil-like cells with high immunosuppressive activity. Such a mechanism provides an avenue for a neoadjuvant therapeutic approach for this devastating disease. Cancer Immunol Res; 5(9); 718-29. ©2017 AACR.

Published
2017

7. Author Correction: Genotype tunes pancreatic ductal adenocarcinoma tissue tension to induce matricellular fibrosis and tumor progression

Author

Laklai, Hanane, primary, Miroshnikova, Yekaterina A., additional, Pickup, Michael W., additional, Collisson, Eric A., additional, Kim, Grace E., additional, Barrett, Alex S., additional, Hill, Ryan C., additional, Lakins, Johnathon N., additional, Schlaepfer, David D., additional, Mouw, Janna K., additional, LeBleu, Valerie S., additional, Roy, Nilotpal, additional, Novitskiy, Sergey V., additional, Johansen, Julia S., additional, Poli, Valeria, additional, Kalluri, Raghu, additional, Iacobuzio-Donahue, Christine A., additional, Wood, Laura D., additional, Hebrok, Matthias, additional, Hansen, Kirk, additional, Moses, Harold L., additional, and Weaver, Valerie M., additional

Published
2023
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8. Age- and Pregnancy-Associated DNA Methylation Changes in Mammary Epithelial Cells

Author

Huh, Sung Jin, Clement, Kendell, Jee, David, Merlini, Alessandra, Choudhury, Sibgat, Maruyama, Reo, Yoo, Ronnie, Chytil, Anna, Boyle, Patrick, Ran, Fei Ann, Moses, Harold L, Barcellos-Hoff, Mary Helen, Jackson-Grusby, Laurie, Meissner, Alexander, and Polyak, Kornelia

Subjects
Biological Sciences, Genetics, Human Genome, 1.1 Normal biological development and functioning, Underpinning research, Reproductive health and childbirth, Age Factors, Animals, Antigens, Surface, Cell Differentiation, Cluster Analysis, DNA (Cytosine-5-)-Methyltransferase 1, DNA (Cytosine-5-)-Methyltransferases, DNA Methylation, Enhancer Elements, Genetic, Enzyme Activation, Epigenesis, Genetic, Epithelial Cells, Female, Gene Expression Profiling, Gene Expression Regulation, Histones, Immunophenotyping, Mammary Glands, Animal, Mice, Mice, Knockout, Organ Specificity, Phenotype, Pregnancy, Promoter Regions, Genetic, Sexual Maturation, Signal Transduction, Biochemistry and Cell Biology, Clinical Sciences, Biochemistry and cell biology
Abstract

Postnatal mammary gland development and differentiation occur during puberty and pregnancy. To explore the role of DNA methylation in these processes, we determined the genome-wide DNA methylation and gene expression profiles of CD24(+)CD61(+)CD29(hi), CD24(+)CD61(+)CD29(lo), and CD24(+)CD61(-)CD29(lo) cell populations that were previously associated with distinct biological properties at different ages and reproductive stages. We found that pregnancy had the most significant effects on CD24(+)CD61(+)CD29(hi) and CD24(+)CD61(+)CD29(lo) cells, inducing distinct epigenetic states that were maintained through life. Integrated analysis of gene expression, DNA methylation, and histone modification profiles revealed cell-type- and reproductive-stage-specific changes. We identified p27 and TGFβ signaling as key regulators of CD24(+)CD61(+)CD29(lo) cell proliferation, based on their expression patterns and results from mammary gland explant cultures. Our results suggest that relatively minor changes in DNA methylation occur during luminal differentiation compared with the effects of pregnancy on CD24(+)CD61(+)CD29(hi) and CD24(+)CD61(+)CD29(lo) cells.

Published
2015

9. Depletion of Carcinoma-Associated Fibroblasts and Fibrosis Induces Immunosuppression and Accelerates Pancreas Cancer with Reduced Survival

Author

Özdemir, Berna C, Pentcheva-Hoang, Tsvetelina, Carstens, Julienne L, Zheng, Xiaofeng, Wu, Chia-Chin, Simpson, Tyler R, Laklai, Hanane, Sugimoto, Hikaru, Kahlert, Christoph, Novitskiy, Sergey V, De Jesus-Acosta, Ana, Sharma, Padmanee, Heidari, Pedram, Mahmood, Umar, Chin, Lynda, Moses, Harold L, Weaver, Valerie M, Maitra, Anirban, Allison, James P, LeBleu, Valerie S, and Kalluri, Raghu

Subjects
Biomedical and Clinical Sciences, Oncology and Carcinogenesis, Immunology, Rare Diseases, Digestive Diseases, Pancreatic Cancer, Cancer, 2.1 Biological and endogenous factors, Aetiology, Animals, Carcinoma, Pancreatic Ductal, Disease Models, Animal, Fibroblasts, Fibrosis, Humans, Immune Tolerance, Mice, Mice, Transgenic, Pancreatic Neoplasms, Survival Analysis, Neurosciences, Oncology & Carcinogenesis, Biochemistry and cell biology, Oncology and carcinogenesis
Abstract

Pancreatic ductal adenocarcinoma (PDAC) is associated with marked fibrosis and stromal myofibroblasts, but their functional contribution remains unknown. Transgenic mice with the ability to delete αSMA(+) myofibroblasts in pancreatic cancer were generated. Depletion starting at either noninvasive precursor (pancreatic intraepithelial neoplasia) or the PDAC stage led to invasive, undifferentiated tumors with enhanced hypoxia, epithelial-to-mesenchymal transition, and cancer stem cells, with diminished animal survival. In PDAC patients, fewer myofibroblasts in their tumors also correlated with reduced survival. Suppressed immune surveillance with increased CD4(+)Foxp3(+) Tregs was observed in myofibroblast-depleted mouse tumors. Although myofibroblast-depleted tumors did not respond to gemcitabine, anti-CTLA4 immunotherapy reversed disease acceleration and prolonged animal survival. This study underscores the need for caution in targeting carcinoma-associated fibroblasts in PDAC.

Published
2014

10. Stromally Derived Lysyl Oxidase Promotes Metastasis of Transforming Growth Factor-β–Deficient Mouse Mammary Carcinomas

Author

Pickup, Michael W, Laklai, Hanane, Acerbi, Irene, Owens, Philip, Gorska, Agnieszka E, Chytil, Anna, Aakre, Mary, Weaver, Valerie M, and Moses, Harold L

Subjects
Breast Cancer, Cancer, 2.1 Biological and endogenous factors, Aetiology, Animals, Carcinogenesis, Collagen, Enzyme Inhibitors, Female, Fibroblasts, Focal Adhesion Kinase 1, Humans, In Situ Hybridization, Keratin-14, Lung Neoplasms, Mammary Neoplasms, Experimental, Mice, Mice, Transgenic, Microscopy, Atomic Force, Myeloid Cells, Phosphorylation, Protein Serine-Threonine Kinases, Protein-Lysine 6-Oxidase, Receptor, Transforming Growth Factor-beta Type II, Receptors, Transforming Growth Factor beta, Signal Transduction, Stromal Cells, Transforming Growth Factor beta, Protein-Serine-Threonine Kinases, Oncology and Carcinogenesis, Oncology & Carcinogenesis
Abstract

The tumor stromal environment can dictate many aspects of tumor progression. A complete understanding of factors driving stromal activation and their role in tumor metastasis is critical to furthering research with the goal of therapeutic intervention. Polyoma middle T-induced mammary carcinomas lacking the type II TGF-β receptor (PyMT(mgko)) are highly metastatic compared with control PyMT-induced carcinomas (PyMT(fl/fl)). We hypothesized that the PyMT(mgko)-activated stroma interacts with carcinoma cells to promote invasion and metastasis. We show that the extracellular matrix associated with PyMT(mgko) tumors is stiffer and has more fibrillar collagen and increased expression of the collagen crosslinking enzyme lysyl oxidase (LOX) compared with PyMT(fl/fl) mammary carcinomas. Inhibition of LOX activity in PyMT(mgko) mice had no effect on tumor latency and size, but significantly decreased tumor metastasis through inhibition of tumor cell intravasation. This phenotype was associated with a decrease in keratin 14-positive myoepithelial cells in PyMT(mgko) tumors following LOX inhibition as well as a decrease in focal adhesion formation. Interestingly, the primary source of LOX was found to be activated fibroblasts. LOX expression in these fibroblasts can be driven by myeloid cell-derived TGF-β, which is significantly linked to human breast cancer. Overall, stromal expansion in PyMT(mgko) tumors is likely caused through the modulation of immune cell infiltrates to promote fibroblast activation. This feeds back to the epithelium to promote metastasis by modulating phenotypic characteristics of basal cells. Our data indicate that epithelial induction of microenvironmental changes can play a significant role in tumorigenesis and attenuating these changes can inhibit metastasis. Cancer Res; 73(17); 5336-46. ©2013 AACR.

Published
2013

11. Soluble VCAM-1 promotes gemcitabine resistance via macrophage infiltration and predicts therapeutic response in pancreatic cancer

Author

Takahashi, Ryota, Ijichi, Hideaki, Sano, Makoto, Miyabayashi, Koji, Mohri, Dai, Kim, Jinsuk, Kimura, Gen, Nakatsuka, Takuma, Fujiwara, Hiroaki, Yamamoto, Keisuke, Kudo, Yotaro, Tanaka, Yasuo, Tateishi, Keisuke, Nakai, Yousuke, Morishita, Yasuyuki, Soma, Katsura, Takeda, Norihiko, Moses, Harold L., Isayama, Hiroyuki, and Koike, Kazuhiko

Published
2020
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24. Data from Pathway Analyses Identify TGFBR2 as Potential Breast Cancer Susceptibility Gene: Results from a Consortium Study among Asians

Author

Ma, Xiangyu, primary, Beeghly-Fadiel, Alicia, primary, Lu, Wei, primary, Shi, Jiajun, primary, Xiang, Yong-Bing, primary, Cai, Qiuyin, primary, Shen, Hongbing, primary, Shen, Chen-Yang, primary, Ren, Zefang, primary, Matsuo, Keitaro, primary, Khoo, Ui Soon, primary, Iwasaki, Motoki, primary, Long, Jirong, primary, Zhang, Ben, primary, Ji, Bu-Tian, primary, Zheng, Ying, primary, Wang, Wenjing, primary, Hu, Zhibin, primary, Liu, Yao, primary, Wu, Pei-Ei, primary, Shieh, Ya-Lan, primary, Wang, Shenming, primary, Xie, Xiaoming, primary, Ito, Hidemi, primary, Kasuga, Yoshio, primary, Chan, Kelvin Y.K., primary, Iwata, Hiroji, primary, Tsugane, Shoichiro, primary, Gao, Yu-Tang, primary, Shu, Xiao Ou, primary, Moses, Harold L., primary, and Zheng, Wei, primary

Published
2023
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27. Supplementary Tables 1 - 3 from Pathway Analyses Identify TGFBR2 as Potential Breast Cancer Susceptibility Gene: Results from a Consortium Study among Asians

Author

Ma, Xiangyu, primary, Beeghly-Fadiel, Alicia, primary, Lu, Wei, primary, Shi, Jiajun, primary, Xiang, Yong-Bing, primary, Cai, Qiuyin, primary, Shen, Hongbing, primary, Shen, Chen-Yang, primary, Ren, Zefang, primary, Matsuo, Keitaro, primary, Khoo, Ui Soon, primary, Iwasaki, Motoki, primary, Long, Jirong, primary, Zhang, Ben, primary, Ji, Bu-Tian, primary, Zheng, Ying, primary, Wang, Wenjing, primary, Hu, Zhibin, primary, Liu, Yao, primary, Wu, Pei-Ei, primary, Shieh, Ya-Lan, primary, Wang, Shenming, primary, Xie, Xiaoming, primary, Ito, Hidemi, primary, Kasuga, Yoshio, primary, Chan, Kelvin Y.K., primary, Iwata, Hiroji, primary, Tsugane, Shoichiro, primary, Gao, Yu-Tang, primary, Shu, Xiao Ou, primary, Moses, Harold L., primary, and Zheng, Wei, primary

Published
2023
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29. Supplementary Figures from PI3K Inhibition Reduces Mammary Tumor Growth and Facilitates Antitumor Immunity and Anti-PD1 Responses

Author

Sai, Jiqing, primary, Owens, Philip, primary, Novitskiy, Sergey V., primary, Hawkins, Oriana E., primary, Vilgelm, Anna E., primary, Yang, Jinming, primary, Sobolik, Tammy, primary, Lavender, Nicole, primary, Johnson, Andrew C., primary, McClain, Colt, primary, Ayers, Gregory D., primary, Kelley, Mark C., primary, Sanders, Melinda, primary, Mayer, Ingrid A., primary, Moses, Harold L., primary, Boothby, Mark, primary, and Richmond, Ann, primary

Published
2023
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30. Supplementary Methods from PI3K Inhibition Reduces Mammary Tumor Growth and Facilitates Antitumor Immunity and Anti-PD1 Responses

Author

Sai, Jiqing, primary, Owens, Philip, primary, Novitskiy, Sergey V., primary, Hawkins, Oriana E., primary, Vilgelm, Anna E., primary, Yang, Jinming, primary, Sobolik, Tammy, primary, Lavender, Nicole, primary, Johnson, Andrew C., primary, McClain, Colt, primary, Ayers, Gregory D., primary, Kelley, Mark C., primary, Sanders, Melinda, primary, Mayer, Ingrid A., primary, Moses, Harold L., primary, Boothby, Mark, primary, and Richmond, Ann, primary

Published
2023
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33. Supplementary Figure 2 from Erlotinib Prolongs Survival in Pancreatic Cancer by Blocking Gemcitabine-Induced MAPK Signals

Author

Miyabayashi, Koji, primary, Ijichi, Hideaki, primary, Mohri, Dai, primary, Tada, Motohisa, primary, Yamamoto, Keisuke, primary, Asaoka, Yoshinari, primary, Ikenoue, Tsuneo, primary, Tateishi, Keisuke, primary, Nakai, Yousuke, primary, Isayama, Hiroyuki, primary, Morishita, Yasuyuki, primary, Omata, Masao, primary, Moses, Harold L., primary, and Koike, Kazuhiko, primary

Published
2023
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35. Data from ALCAM/CD166 Is a TGF-β–Responsive Marker and Functional Regulator of Prostate Cancer Metastasis to Bone

Author

Hansen, Amanda G., primary, Arnold, Shanna A., primary, Jiang, Ming, primary, Palmer, Trenis D., primary, Ketova, Tatiana, primary, Merkel, Alyssa, primary, Pickup, Michael, primary, Samaras, Susan, primary, Shyr, Yu, primary, Moses, Harold L., primary, Hayward, Simon W., primary, Sterling, Julie A., primary, and Zijlstra, Andries, primary

Published
2023
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39. Supplementary Materials from Erlotinib Prolongs Survival in Pancreatic Cancer by Blocking Gemcitabine-Induced MAPK Signals

Author

Miyabayashi, Koji, primary, Ijichi, Hideaki, primary, Mohri, Dai, primary, Tada, Motohisa, primary, Yamamoto, Keisuke, primary, Asaoka, Yoshinari, primary, Ikenoue, Tsuneo, primary, Tateishi, Keisuke, primary, Nakai, Yousuke, primary, Isayama, Hiroyuki, primary, Morishita, Yasuyuki, primary, Omata, Masao, primary, Moses, Harold L., primary, and Koike, Kazuhiko, primary

Published
2023
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43. Supplementary Table 1 from Erlotinib Prolongs Survival in Pancreatic Cancer by Blocking Gemcitabine-Induced MAPK Signals

Author

Miyabayashi, Koji, primary, Ijichi, Hideaki, primary, Mohri, Dai, primary, Tada, Motohisa, primary, Yamamoto, Keisuke, primary, Asaoka, Yoshinari, primary, Ikenoue, Tsuneo, primary, Tateishi, Keisuke, primary, Nakai, Yousuke, primary, Isayama, Hiroyuki, primary, Morishita, Yasuyuki, primary, Omata, Masao, primary, Moses, Harold L., primary, and Koike, Kazuhiko, primary

Published
2023
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45. Supplementary Figures 1 through 9 from ALCAM/CD166 Is a TGF-β–Responsive Marker and Functional Regulator of Prostate Cancer Metastasis to Bone

Author

Hansen, Amanda G., primary, Arnold, Shanna A., primary, Jiang, Ming, primary, Palmer, Trenis D., primary, Ketova, Tatiana, primary, Merkel, Alyssa, primary, Pickup, Michael, primary, Samaras, Susan, primary, Shyr, Yu, primary, Moses, Harold L., primary, Hayward, Simon W., primary, Sterling, Julie A., primary, and Zijlstra, Andries, primary

Published
2023
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48. Supplementary Figure 1 from Erlotinib Prolongs Survival in Pancreatic Cancer by Blocking Gemcitabine-Induced MAPK Signals

Author

Miyabayashi, Koji, primary, Ijichi, Hideaki, primary, Mohri, Dai, primary, Tada, Motohisa, primary, Yamamoto, Keisuke, primary, Asaoka, Yoshinari, primary, Ikenoue, Tsuneo, primary, Tateishi, Keisuke, primary, Nakai, Yousuke, primary, Isayama, Hiroyuki, primary, Morishita, Yasuyuki, primary, Omata, Masao, primary, Moses, Harold L., primary, and Koike, Kazuhiko, primary

Published
2023
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50. Supplementary Figure 3-2 from Erlotinib Prolongs Survival in Pancreatic Cancer by Blocking Gemcitabine-Induced MAPK Signals

Author

Miyabayashi, Koji, primary, Ijichi, Hideaki, primary, Mohri, Dai, primary, Tada, Motohisa, primary, Yamamoto, Keisuke, primary, Asaoka, Yoshinari, primary, Ikenoue, Tsuneo, primary, Tateishi, Keisuke, primary, Nakai, Yousuke, primary, Isayama, Hiroyuki, primary, Morishita, Yasuyuki, primary, Omata, Masao, primary, Moses, Harold L., primary, and Koike, Kazuhiko, primary

Published
2023
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