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  1. AU="Ogiwara, Yamato"
  2. AU="Jardim, M."
  3. AU=Round J A
  4. AU=Zhang Huan AU=Zhang Huan
  5. AU="Khalilzad, Mohammad"
  6. AU="Safrida Safrida"
  7. AU="Sheridan, Krystal"
  8. AU="Spencer, Sandra"
  9. AU="Ikhapoh, Izuagie"
  10. AU="Jabeen, Nyla"
  11. AU="Elaine Mary Cowan"
  12. AU="Marcos Federico Pascuali"
  13. AU="Shi, Zhuqing"
  14. AU="Bernard Rosner"
  15. AU="van de Schoor, F."
  16. AU="Strzelecki, Antoine"
  17. AU=Cheung P Y
  18. AU="Arima, Tetsuhiko"
  19. AU="José Del Castillo Diego, Julio"
  20. AU="Han, Shujie"
  21. AU="Hernandez-Garcia, Elena"
  22. AU="Mansfield, Sara A"
  23. AU="Igarashi, Miyako"
  24. AU="Eloisa Romano"

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  1. Artikel ; Online: Blocking FSTL1 boosts NK immunity in treatment of osteosarcoma.

    Ogiwara, Yamato / Nakagawa, Makoto / Nakatani, Fumihiko / Uemura, Yasushi / Zhang, Rong / Kudo-Saito, Chie

    Cancer letters

    2022  Band 537, Seite(n) 215690

    Abstract: Osteosarcoma (OS) is the most common primary bone malignancy. Many patients develop relapse and metastasis after treatments, and more effective treatments are needed for improving the clinical outcome. FSTL1 overexpression has been reported in murine and ...

    Abstract Osteosarcoma (OS) is the most common primary bone malignancy. Many patients develop relapse and metastasis after treatments, and more effective treatments are needed for improving the clinical outcome. FSTL1 overexpression has been reported in murine and human OS, while the functional roles of FSTL1 remain unclear. Here, we elucidated tumor biological and immunological mechanisms underlying the refractory OS using mouse and human OS cell lines, mouse OS models, and clinical specimens. FSTL1 knockout in OS cells significantly suppressed cellular functions, including proliferation, invasion, sphere colony formation, and ALCAM expression. The FSTL1-ablated tumor cells were completely rejected due to generation of potent NK cells in the in vivo setting. Indeed, FSTL1 stimulation suppressed NK activity partly via apoptosis induction, but blocking FSTL1 or CD6, a receptor for ALCAM, significantly restored NK activity. Anti-FSTL1 therapy significantly suppressed tumor growth and metastasis in mouse OS models, and synergized with anti-CD6 therapy in providing significantly better prognosis. These suggest that blocking FSTL1 is a promising strategy for successfully treating OS. This study demonstrates a rationale of targeting the FSTL1-ALCAM axis in the treatment of OS in clinical settings.
    Mesh-Begriff(e) Activated-Leukocyte Cell Adhesion Molecule/metabolism ; Animals ; Apoptosis ; Bone Neoplasms/drug therapy ; Bone Neoplasms/genetics ; Cell Line, Tumor ; Cell Proliferation ; Follistatin-Related Proteins/genetics ; Follistatin-Related Proteins/metabolism ; Humans ; Mice ; Neoplasm Recurrence, Local ; Osteosarcoma/drug therapy ; Osteosarcoma/genetics
    Chemische Substanzen Activated-Leukocyte Cell Adhesion Molecule ; Follistatin-Related Proteins ; Fstl1 protein, mouse ; FSTL1 protein, human (158709-61-6)
    Sprache Englisch
    Erscheinungsdatum 2022-04-16
    Erscheinungsland Ireland
    Dokumenttyp Journal Article
    ZDB-ID 195674-7
    ISSN 1872-7980 ; 0304-3835
    ISSN (online) 1872-7980
    ISSN 0304-3835
    DOI 10.1016/j.canlet.2022.215690
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  2. Artikel ; Online: CD11b

    Imazeki, Hiroshi / Ogiwara, Yamato / Kawamura, Mami / Boku, Narikazu / Kudo-Saito, Chie

    Journal for immunotherapy of cancer

    2021  Band 9, Heft 7

    Abstract: Background: Tumor metastasis is the major cause of death of colorectal cancer (CRC), and metastatic CRC remains incurable in many cases despite great advances in genetic and molecular profiling, and clinical development of numerous drugs, including ... ...

    Abstract Background: Tumor metastasis is the major cause of death of colorectal cancer (CRC), and metastatic CRC remains incurable in many cases despite great advances in genetic and molecular profiling, and clinical development of numerous drugs, including immune checkpoint inhibitors. Thus, more effective treatments are urgently needed for the patients in clinical settings.
    Methods: We used mouse CRC metastasis models that murine Colon26 cells were subcutaneously and intravenously implanted and attempted to elucidate the tumor biological and immunological mechanisms underlying cancer metastasis. Then, we evaluated in vivo antitumor efficacy induced by agents targeting the identified molecular mechanisms using the mouse models. We validated the clinical relevancy of the findings using peripheral blood mononuclear cells obtained from stage IV metastatic CRC patients.
    Results: CD11b
    Conclusions: The CD11b
    Mesh-Begriff(e) Aged ; Animals ; CD11 Antigens/metabolism ; CTLA-4 Antigen/metabolism ; Colorectal Neoplasms/genetics ; Colorectal Neoplasms/pathology ; Female ; Humans ; Mice ; Mice, Nude ; Middle Aged ; Myeloid Cells
    Chemische Substanzen CD11 Antigens ; CTLA-4 Antigen ; Ctla4 protein, mouse
    Sprache Englisch
    Erscheinungsdatum 2021-07-11
    Erscheinungsland England
    Dokumenttyp Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2719863-7
    ISSN 2051-1426 ; 2051-1426
    ISSN (online) 2051-1426
    ISSN 2051-1426
    DOI 10.1136/jitc-2021-002841
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  3. Artikel: CD11b

    Kudo-Saito, Chie / Ogiwara, Yamato / Imazeki, Hiroshi / Boku, Narikazu / Uemura, Yasushi / Zhang, Rong / Kawano-Nagatsuma, Akiko / Kojima, Motohiro / Ochiai, Atsushi

    American journal of cancer research

    2021  Band 11, Heft 11, Seite(n) 5428–5439

    Abstract: Colorectal cancer (CRC) is one of the most common malignant tumors worldwide, and tumor metastasis is the leading cause of death. Targeting immune inhibitory checkpoint inhibitory pathways has attracted great attention, since the therapeutic efficacy ... ...

    Abstract Colorectal cancer (CRC) is one of the most common malignant tumors worldwide, and tumor metastasis is the leading cause of death. Targeting immune inhibitory checkpoint inhibitory pathways has attracted great attention, since the therapeutic efficacy induced by the specific blocking antibodies has been demonstrated even in metastatic CRC patients. However, the clinical outcome is low in many cases, and thus more effective treatments are needed in the clinical settings. A SPARC family member follistatin-like 1 (FSTL1) is known as a key driver of tumor metastasis in various types of cancer. However, the immunological roles of the FSTL1 in the CRC pathogenesis remain to be elucidated. In this study, we investigated the molecular mechanisms underlying the refractory FSTL1
    Sprache Englisch
    Erscheinungsdatum 2021-11-15
    Erscheinungsland United States
    Dokumenttyp Journal Article
    ZDB-ID 2589522-9
    ISSN 2156-6976
    ISSN 2156-6976
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  4. Artikel: Targeting AURKA in treatment of peritoneal tumor dissemination in gastrointestinal cancer.

    Ozawa, Hiroki / Imazeki, Hiroshi / Ogiwara, Yamato / Kawakubo, Hirofumi / Fukuda, Kazumasa / Kitagawa, Yuko / Kudo-Saito, Chie

    Translational oncology

    2021  Band 16, Seite(n) 101307

    Abstract: Intraperitoneal (i.p.) tumor dissemination and the consequent malignant ascites remain unpredictable and incurable in patients with gastrointestinal (GI) cancer, and practical advances in diagnosis and treatment are urgently needed in the clinical ... ...

    Abstract Intraperitoneal (i.p.) tumor dissemination and the consequent malignant ascites remain unpredictable and incurable in patients with gastrointestinal (GI) cancer, and practical advances in diagnosis and treatment are urgently needed in the clinical settings. Here, we explored tumor biological and immunological mechanisms underlying the i.p. tumor progression for establishing more effective treatments. We established mouse tumor ascites models that murine and human colorectal cancer cells were both i.p. and subcutaneously (s.c.) implanted in mice, and analyzed peritoneal exudate cells (PECs) obtained from the mice. We then evaluated anti-tumor efficacy of agents targeting the identified molecular mechanisms using the ascites models. Furthermore, we validated the clinical relevancy of the findings using peritoneal lavage fluids obtained from gastric cancer patients. I.p. tumor cells were giant with large nuclei, and highly express AURKA, but less phosphorylated TP53, as compared to s.c. tumor cells, suggesting polyploidy-like cells. The i.p. tumors impaired phagocytic activity and the consequent T-cell stimulatory activity of CD11b
    Sprache Englisch
    Erscheinungsdatum 2021-12-10
    Erscheinungsland United States
    Dokumenttyp Journal Article
    ZDB-ID 2443840-6
    ISSN 1936-5233
    ISSN 1936-5233
    DOI 10.1016/j.tranon.2021.101307
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  5. Artikel: Targeting Oncoimmune Drivers of Cancer Metastasis.

    Kudo-Saito, Chie / Ozaki, Yukinori / Imazeki, Hiroshi / Hayashi, Hideyuki / Masuda, Jun / Ozawa, Hiroki / Ogiwara, Yamato

    Cancers

    2021  Band 13, Heft 3

    Abstract: Residual metastasis is a major cause of cancer-associated death. Recent advances in understanding the molecular basis of the epithelial-mesenchymal transition (EMT) and the related cancer stem cells (CSCs) have revealed the landscapes of cancer ... ...

    Abstract Residual metastasis is a major cause of cancer-associated death. Recent advances in understanding the molecular basis of the epithelial-mesenchymal transition (EMT) and the related cancer stem cells (CSCs) have revealed the landscapes of cancer metastasis and are promising contributions to clinical treatments. However, this rarely leads to practical advances in the management of cancer in clinical settings, and thus cancer metastasis is still a threat to patients. The reason for this may be the heterogeneity and complexity caused by the evolutional transformation of tumor cells through interactions with the host environment, which is composed of numerous components, including stromal cells, vascular cells, and immune cells. The reciprocal evolution further raises the possibility of successful tumor escape, resulting in a fatal prognosis for patients. To disrupt the vicious spiral of tumor-immunity aggravation, it is important to understand the entire metastatic process and the practical implementations. Here, we provide an overview of the molecular and cellular links between tumors' biological properties and host immunity, mainly focusing on EMT and CSCs, and we also highlight therapeutic agents targeting the oncoimmune determinants driving cancer metastasis toward better practical use in the treatment of cancer patients.
    Sprache Englisch
    Erscheinungsdatum 2021-02-01
    Erscheinungsland Switzerland
    Dokumenttyp Journal Article ; Review
    ZDB-ID 2527080-1
    ISSN 2072-6694
    ISSN 2072-6694
    DOI 10.3390/cancers13030554
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  6. Artikel ; Online: Blocking the FSTL1-DIP2A Axis Improves Anti-tumor Immunity.

    Kudo-Saito, Chie / Ishida, Akiko / Shouya, Yuji / Teramoto, Koji / Igarashi, Tomoyuki / Kon, Ryoko / Saito, Kenji / Awada, Chihiro / Ogiwara, Yamato / Toyoura, Masayoshi

    Cell reports

    2017  Band 24, Heft 7, Seite(n) 1790–1801

    Abstract: Immune dysfunction is a strong factor in the resistance of cancer to treatment. Blocking immune checkpoint pathways is a promising approach to improve anti-tumor immunity, but the clinical efficacies are still limited. We previously identified ... ...

    Abstract Immune dysfunction is a strong factor in the resistance of cancer to treatment. Blocking immune checkpoint pathways is a promising approach to improve anti-tumor immunity, but the clinical efficacies are still limited. We previously identified follistatin-like 1 (FSTL1) as a determinant of immune dysfunction mediated by mesenchymal stromal/stem cells (MSCs) and immunoregulatory cells. Here, we demonstrate that blocking FSTL1 but not immune checkpoint pathways significantly suppresses cancer progression and metastasis in several mouse tumor models with increased MSCs. Expression of DIP2A (the receptor of FSTL1) in tumor cells is critical for FSTL1-induced immunoresistance. FSTL1/DIP2A co-positivity in tumor tissues correlates with poor prognosis in NSCLC patients. Thus, breaking the FSTL1-DIP2A axis may be a useful strategy for successfully inducing anti-tumor immunity.
    Mesh-Begriff(e) Animals ; Carcinoma, Non-Small-Cell Lung/diagnosis ; Carcinoma, Non-Small-Cell Lung/genetics ; Carcinoma, Non-Small-Cell Lung/immunology ; Carcinoma, Non-Small-Cell Lung/mortality ; Carrier Proteins/antagonists & inhibitors ; Carrier Proteins/genetics ; Carrier Proteins/immunology ; Case-Control Studies ; Cell Line, Tumor ; Cell Movement ; Cell Proliferation ; Disease Progression ; Female ; Follistatin-Related Proteins/antagonists & inhibitors ; Follistatin-Related Proteins/genetics ; Follistatin-Related Proteins/immunology ; Gene Expression Regulation, Neoplastic ; Humans ; Immunity, Innate ; Lung Neoplasms/diagnosis ; Lung Neoplasms/genetics ; Lung Neoplasms/immunology ; Lung Neoplasms/mortality ; Male ; Mesenchymal Stem Cells/immunology ; Mesenchymal Stem Cells/pathology ; Mice ; Mice, Inbred BALB C ; Mice, Inbred C57BL ; Nuclear Proteins/antagonists & inhibitors ; Nuclear Proteins/genetics ; Nuclear Proteins/immunology ; Prognosis ; RNA, Small Interfering/genetics ; RNA, Small Interfering/metabolism ; Signal Transduction ; Survival Analysis ; Tumor Burden ; Xenograft Model Antitumor Assays
    Chemische Substanzen Carrier Proteins ; DIP2A protein, human ; Follistatin-Related Proteins ; Nuclear Proteins ; RNA, Small Interfering ; FSTL1 protein, human (158709-61-6)
    Sprache Englisch
    Erscheinungsdatum 2017-10-05
    Erscheinungsland United States
    Dokumenttyp Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2649101-1
    ISSN 2211-1247 ; 2211-1247
    ISSN (online) 2211-1247
    ISSN 2211-1247
    DOI 10.1016/j.celrep.2018.07.043
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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