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  1. Article ; Online: TGF-β signaling in health and disease.

    Massagué, Joan / Sheppard, Dean

    Cell

    2023  Volume 186, Issue 19, Page(s) 4007–4037

    Abstract: The TGF-β regulatory system plays crucial roles in the preservation of organismal integrity. TGF-β signaling controls metazoan embryo development, tissue homeostasis, and injury repair through coordinated effects on cell proliferation, phenotypic ... ...

    Abstract The TGF-β regulatory system plays crucial roles in the preservation of organismal integrity. TGF-β signaling controls metazoan embryo development, tissue homeostasis, and injury repair through coordinated effects on cell proliferation, phenotypic plasticity, migration, metabolic adaptation, and immune surveillance of multiple cell types in shared ecosystems. Defects of TGF-β signaling, particularly in epithelial cells, tissue fibroblasts, and immune cells, disrupt immune tolerance, promote inflammation, underlie the pathogenesis of fibrosis and cancer, and contribute to the resistance of these diseases to treatment. Here, we review how TGF-β coordinates multicellular response programs in health and disease and how this knowledge can be leveraged to develop treatments for diseases of the TGF-β system.
    MeSH term(s) Animals ; Adaptation, Physiological ; Cell Proliferation ; Embryonic Development ; Transforming Growth Factor beta ; Signal Transduction
    Chemical Substances Transforming Growth Factor beta
    Language English
    Publishing date 2023-09-15
    Publishing country United States
    Document type Journal Article ; Review ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 187009-9
    ISSN 1097-4172 ; 0092-8674
    ISSN (online) 1097-4172
    ISSN 0092-8674
    DOI 10.1016/j.cell.2023.07.036
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: TGF-β in developmental and fibrogenic EMTs.

    Lee, Jun Ho / Massagué, Joan

    Seminars in cancer biology

    2022  Volume 86, Issue Pt 2, Page(s) 136–145

    Abstract: TGF-β plays a prominent role as an inducer of epithelial-mesenchymal transitions (EMTs) during development and wound healing and in disease conditions such as fibrosis and cancer. During these processes EMT occurs together with changes in cell ... ...

    Abstract TGF-β plays a prominent role as an inducer of epithelial-mesenchymal transitions (EMTs) during development and wound healing and in disease conditions such as fibrosis and cancer. During these processes EMT occurs together with changes in cell proliferation, differentiation, communication, and extracellular matrix remodeling that are orchestrated by multiple signaling inputs besides TGF-β. Chief among these inputs is RAS-MAPK signaling, which is frequently required for EMT induction by TGF-β. Recent work elucidated the molecular basis for the cooperation between the TGF-β-SMAD and RAS-MAPK pathways in the induction of EMT in embryonic, adult and carcinoma epithelial cells. These studies also provided direct mechanistic links between EMT and progenitor cell differentiation during gastrulation or intra-tumoral fibrosis during cancer metastasis. These insights illuminate the nature of TGF-β driven EMTs as part of broader processes during development, fibrogenesis and metastasis.
    MeSH term(s) Humans ; Epithelial-Mesenchymal Transition/genetics ; Fibrosis ; Neoplasms/metabolism ; Neoplasms/pathology ; Transforming Growth Factor beta/metabolism ; Neoplasm Metastasis
    Chemical Substances Transforming Growth Factor beta
    Language English
    Publishing date 2022-09-29
    Publishing country England
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 1033980-2
    ISSN 1096-3650 ; 1044-579X
    ISSN (online) 1096-3650
    ISSN 1044-579X
    DOI 10.1016/j.semcancer.2022.09.004
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  3. Article ; Online: Kathryn Anderson, grand dame of developmental biology.

    Neill, Ushma S / Massagué, Joan

    Proceedings of the National Academy of Sciences of the United States of America

    2021  Volume 118, Issue 10

    MeSH term(s) Embryology/history ; History, 20th Century ; History, 21st Century ; Portraits as Topic
    Language English
    Publishing date 2021-02-16
    Publishing country United States
    Document type Biography ; Historical Article ; Journal Article
    ZDB-ID 209104-5
    ISSN 1091-6490 ; 0027-8424
    ISSN (online) 1091-6490
    ISSN 0027-8424
    DOI 10.1073/pnas.2101148118
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  4. Article ; Online: Targeting metastatic cancer.

    Ganesh, Karuna / Massagué, Joan

    Nature medicine

    2021  Volume 27, Issue 1, Page(s) 34–44

    Abstract: Despite recent therapeutic advances in cancer treatment, metastasis remains the principal cause of cancer death. Recent work has uncovered the unique biology of metastasis-initiating cells that results in tumor growth in distant organs, evasion of immune ...

    Abstract Despite recent therapeutic advances in cancer treatment, metastasis remains the principal cause of cancer death. Recent work has uncovered the unique biology of metastasis-initiating cells that results in tumor growth in distant organs, evasion of immune surveillance and co-option of metastatic microenvironments. Here we review recent progress that is enabling therapeutic advances in treating both micro- and macrometastases. Such insights were gained from cancer sequencing, mechanistic studies and clinical trials, including of immunotherapy. These studies reveal both the origins and nature of metastases and identify new opportunities for developing more effective strategies to target metastatic relapse and improve patient outcomes.
    MeSH term(s) Humans ; Mutation ; Neoplasm Metastasis/genetics ; Neoplasm Metastasis/therapy ; Neoplasms/pathology ; Neoplasms/therapy ; Neoplastic Cells, Circulating ; Neoplastic Stem Cells/pathology ; Survival Analysis ; Treatment Outcome ; Tumor Microenvironment
    Language English
    Publishing date 2021-01-13
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 1220066-9
    ISSN 1546-170X ; 1078-8956
    ISSN (online) 1546-170X
    ISSN 1078-8956
    DOI 10.1038/s41591-020-01195-4
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  5. Article ; Online: Metastasis-Initiating Cells and Ecosystems.

    Massagué, Joan / Ganesh, Karuna

    Cancer discovery

    2021  Volume 11, Issue 4, Page(s) 971–994

    Abstract: Metastasis is initiated and sustained through therapy by cancer cells with stem-like and immune-evasive properties, termed metastasis-initiating cells (MIC). Recent progress suggests that MICs result from the adoption of a normal regenerative progenitor ... ...

    Abstract Metastasis is initiated and sustained through therapy by cancer cells with stem-like and immune-evasive properties, termed metastasis-initiating cells (MIC). Recent progress suggests that MICs result from the adoption of a normal regenerative progenitor phenotype by malignant cells, a phenotype with intrinsic programs to survive the stresses of the metastatic process, undergo epithelial-mesenchymal transitions, enter slow-cycling states for dormancy, evade immune surveillance, establish supportive interactions with organ-specific niches, and co-opt systemic factors for growth and recurrence after therapy. Mechanistic understanding of the molecular mediators of MIC phenotypes and host tissue ecosystems could yield cancer therapeutics to improve patient outcomes. SIGNIFICANCE: Understanding the origins, traits, and vulnerabilities of progenitor cancer cells with the capacity to initiate metastasis in distant organs, and the host microenvironments that support the ability of these cells to evade immune surveillance and regenerate the tumor, is critical for developing strategies to improve the prevention and treatment of advanced cancer. Leveraging recent progress in our understanding of the metastatic process, here we review the nature of MICs and their ecosystems and offer a perspective on how this knowledge is informing innovative treatments of metastatic cancers.
    MeSH term(s) Cell Transformation, Neoplastic/pathology ; Ecosystem ; Humans ; Neoplasm Metastasis/pathology ; Neoplasms/pathology ; Neoplastic Stem Cells/pathology ; Tumor Microenvironment
    Language English
    Publishing date 2021-04-02
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 2625242-9
    ISSN 2159-8290 ; 2159-8274
    ISSN (online) 2159-8290
    ISSN 2159-8274
    DOI 10.1158/2159-8290.CD-21-0010
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  6. Article ; Online: Filippo Giancotti (1958-2023).

    DePinho, Ronald / Massagué, Joan / Manji, Gulam / Rustgi, Anil K / Izar, Benjamin

    Nature cancer

    2023  Volume 4, Issue 10, Page(s) 1401–1402

    Language English
    Publishing date 2023-09-28
    Publishing country England
    Document type Editorial
    ISSN 2662-1347
    ISSN (online) 2662-1347
    DOI 10.1038/s43018-023-00639-3
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  7. Article ; Online: Transforming Growth Factor-β Signaling in Immunity and Cancer.

    Batlle, Eduard / Massagué, Joan

    Immunity

    2019  Volume 50, Issue 4, Page(s) 924–940

    Abstract: Transforming growth factor (TGF)-β is a crucial enforcer of immune homeostasis and tolerance, inhibiting the expansion and function of many components of the immune system. Perturbations in TGF-β signaling underlie inflammatory diseases and promote tumor ...

    Abstract Transforming growth factor (TGF)-β is a crucial enforcer of immune homeostasis and tolerance, inhibiting the expansion and function of many components of the immune system. Perturbations in TGF-β signaling underlie inflammatory diseases and promote tumor emergence. TGF-β is also central to immune suppression within the tumor microenvironment, and recent studies have revealed roles in tumor immune evasion and poor responses to cancer immunotherapy. Here, we present an overview of the complex biology of the TGF-β family and its context-dependent nature. Then, focusing on cancer, we discuss the roles of TGF-β signaling in distinct immune cell types and how this knowledge is being leveraged to unleash the immune system against the tumor.
    MeSH term(s) Adaptive Immunity ; Animals ; Dendritic Cells/immunology ; Disease Progression ; Epithelial-Mesenchymal Transition ; Fibroblasts/immunology ; Humans ; Immunity, Innate ; Inflammation ; Macrophages/immunology ; Mice, Knockout ; Neoplasms/immunology ; Neutrophils/immunology ; Receptors, Transforming Growth Factor beta/physiology ; Signal Transduction/immunology ; T-Lymphocyte Subsets/immunology ; Transforming Growth Factor beta/immunology ; Transforming Growth Factor beta/physiology ; Tumor Escape ; Tumor Microenvironment
    Chemical Substances Receptors, Transforming Growth Factor beta ; Transforming Growth Factor beta
    Language English
    Publishing date 2019-04-17
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 1217235-2
    ISSN 1097-4180 ; 1074-7613
    ISSN (online) 1097-4180
    ISSN 1074-7613
    DOI 10.1016/j.immuni.2019.03.024
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  8. Article ; Online: TGF-β signaling in development and disease.

    Massagué, Joan

    FEBS letters

    2012  Volume 586, Issue 14, Page(s) 1833

    MeSH term(s) Animals ; Developmental Biology/methods ; Epithelial-Mesenchymal Transition ; Gene Expression Regulation, Developmental ; Humans ; Models, Biological ; Neoplasms/metabolism ; Receptors, Transforming Growth Factor beta/metabolism ; Signal Transduction ; Transforming Growth Factor beta/metabolism
    Chemical Substances Receptors, Transforming Growth Factor beta ; Transforming Growth Factor beta
    Language English
    Publishing date 2012-05-28
    Publishing country England
    Document type Introductory Journal Article
    ZDB-ID 212746-5
    ISSN 1873-3468 ; 0014-5793
    ISSN (online) 1873-3468
    ISSN 0014-5793
    DOI 10.1016/j.febslet.2012.05.030
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  9. Article ; Online: Publisher Correction: Contextual determinants of TGFβ action in development, immunity and cancer.

    David, Charles J / Massagué, Joan

    Nature reviews. Molecular cell biology

    2018  Volume 19, Issue 7, Page(s) 479

    Abstract: In the section 'Combinatorial ligand perception' of the original article, DMP1 was incorrectly used in place of BMP. This has now been corrected in the HTML and PDF versions of the article. ...

    Abstract In the section 'Combinatorial ligand perception' of the original article, DMP1 was incorrectly used in place of BMP. This has now been corrected in the HTML and PDF versions of the article.
    Language English
    Publishing date 2018-05-08
    Publishing country England
    Document type Published Erratum
    ZDB-ID 2031313-5
    ISSN 1471-0080 ; 1471-0072
    ISSN (online) 1471-0080
    ISSN 1471-0072
    DOI 10.1038/s41580-018-0018-x
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  10. Article ; Online: TGF-β Inhibition and Immunotherapy: Checkmate.

    Ganesh, Karuna / Massagué, Joan

    Immunity

    2018  Volume 48, Issue 4, Page(s) 626–628

    Abstract: Immune checkpoint therapy can induce durable remissions, but many tumors demonstrate resistance. In a recent issue of Nature, Mariathasan et al. (2018) and Tauriello et al. (2018) identify stromal TGF-β signaling as a determinant of immune exclusion. ... ...

    Abstract Immune checkpoint therapy can induce durable remissions, but many tumors demonstrate resistance. In a recent issue of Nature, Mariathasan et al. (2018) and Tauriello et al. (2018) identify stromal TGF-β signaling as a determinant of immune exclusion. Combination TGF-β inhibition and immunotherapy induces complete responses in mouse models.
    MeSH term(s) Animals ; Disease Models, Animal ; Immunotherapy ; Mice ; Neoplasms ; T-Lymphocytes ; Transforming Growth Factor beta
    Chemical Substances Transforming Growth Factor beta
    Language English
    Publishing date 2018-12-15
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Comment
    ZDB-ID 1217235-2
    ISSN 1097-4180 ; 1074-7613
    ISSN (online) 1097-4180
    ISSN 1074-7613
    DOI 10.1016/j.immuni.2018.03.037
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