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  1. Article ; Online: The development of integrative biology: bridging the gap--a view from the Scientific Editors. [An interview with David Beebe and Mary Helen Barcellos-Hoff by Kathleen Too].

    Beebe, David / Barcellos-Hoff, Mary Helen

    Integrative biology : quantitative biosciences from nano to macro

    2009  Volume 1, Issue 2, Page(s) 145–147

    MeSH term(s) Biology ; Natural Science Disciplines ; Serial Publications
    Language English
    Publishing date 2009-02
    Publishing country England
    Document type Interview
    ZDB-ID 2480063-6
    ISSN 1757-9708 ; 1757-9694
    ISSN (online) 1757-9708
    ISSN 1757-9694
    DOI 10.1039/b822329g
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  2. Article ; Online: The radiobiology of TGFβ.

    Barcellos-Hoff, Mary Helen

    Seminars in cancer biology

    2022  Volume 86, Issue Pt 3, Page(s) 857–867

    Abstract: Ionizing radiation is a pillar of cancer therapy that is deployed in more than half of all malignancies. The therapeutic effect of radiation is attributed to induction of DNA damage that kills cancers cells, but radiation also affects signaling that ... ...

    Abstract Ionizing radiation is a pillar of cancer therapy that is deployed in more than half of all malignancies. The therapeutic effect of radiation is attributed to induction of DNA damage that kills cancers cells, but radiation also affects signaling that alters the composition of the tumor microenvironment by activating transforming growth factor β (TGFβ). TGFβ is a ubiquitously expressed cytokine that acts as biological lynchpin to orchestrate phenotypes, the stroma, and immunity in normal tissue; these activities are subverted in cancer to promote malignancy, a permissive tumor microenvironment and immune evasion. The radiobiology of TGFβ unites targets at the forefront of oncology-the DNA damage response and immunotherapy. The cancer cell intrinsic and extrinsic network of TGFβ responses in the irradiated tumor form a barrier to both genotoxic treatments and immunotherapy response. Here, we focus on the mechanisms by which radiation induces TGFβ activation, how TGFβ regulates DNA repair, and the dynamic regulation of the tumor immune microenvironment that together oppose effective cancer therapy. Strategies to inhibit TGFβ exploit fundamental radiobiology that may be the missing link to deploying TGFβ inhibitors for optimal patient benefit from cancer treatment.
    MeSH term(s) Humans ; Transforming Growth Factor beta/metabolism ; Radiobiology ; DNA Damage ; Signal Transduction ; Neoplasms/radiotherapy ; Tumor Microenvironment
    Chemical Substances Transforming Growth Factor beta
    Language English
    Publishing date 2022-02-03
    Publishing country England
    Document type Journal Article ; Review ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural
    ZDB-ID 1033980-2
    ISSN 1096-3650 ; 1044-579X
    ISSN (online) 1096-3650
    ISSN 1044-579X
    DOI 10.1016/j.semcancer.2022.02.001
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    In stock of ZB MED Cologne/Königswinter

    Zs.A 2922: Show issues Location:
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  3. Article ; Online: Molecular Pathways and Mechanisms of TGFβ in Cancer Therapy.

    Barcellos-Hoff, Mary Helen / Gulley, James L

    Clinical cancer research : an official journal of the American Association for Cancer Research

    2023  Volume 29, Issue 11, Page(s) 2025–2033

    Abstract: Even though the number of agents that inhibit TGFβ being tested in patients with cancer has grown substantially, clinical benefit from TGFβ inhibition has not yet been achieved. The myriad mechanisms in which TGFβ is protumorigenic may be a key obstacle ... ...

    Abstract Even though the number of agents that inhibit TGFβ being tested in patients with cancer has grown substantially, clinical benefit from TGFβ inhibition has not yet been achieved. The myriad mechanisms in which TGFβ is protumorigenic may be a key obstacle to its effective deployment; cancer cells frequently employ TGFβ-regulated programs that engender plasticity, enable a permissive tumor microenvironment, and profoundly suppress immune recognition, which is the target of most current early-phase trials of TGFβ inhibitors. Here we discuss the implications of a less well-recognized aspect of TGFβ biology regulating DNA repair that mediates responses to radiation and chemotherapy. In cancers that are TGFβ signaling competent, TGFβ promotes effective DNA repair and suppresses error-prone repair, thus conferring resistance to genotoxic therapies and limiting tumor control. Cancers in which TGFβ signaling is intrinsically compromised are more responsive to standard genotoxic therapy. Recognition that TGFβ is a key moderator of both DNA repair and immunosuppression might be used to synergize combinations of genotoxic therapy and immunotherapy to benefit patients with cancer.
    MeSH term(s) Humans ; Transforming Growth Factor beta/metabolism ; Neoplasms/drug therapy ; Neoplasms/genetics ; Signal Transduction ; DNA Repair ; DNA Damage ; Tumor Microenvironment/genetics
    Chemical Substances Transforming Growth Factor beta
    Language English
    Publishing date 2023-02-08
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Intramural
    ZDB-ID 1225457-5
    ISSN 1557-3265 ; 1078-0432
    ISSN (online) 1557-3265
    ISSN 1078-0432
    DOI 10.1158/1078-0432.CCR-21-3750
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    Zs.A 4223: Show issues Location:
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  4. Article: Editorial: Cell Signaling Mediating Critical Radiation Responses.

    Herskind, Carsten / Barcellos-Hoff, Mary Helen

    Frontiers in oncology

    2021  Volume 11, Page(s) 695355

    Language English
    Publishing date 2021-05-10
    Publishing country Switzerland
    Document type Editorial
    ZDB-ID 2649216-7
    ISSN 2234-943X
    ISSN 2234-943X
    DOI 10.3389/fonc.2021.695355
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  5. Article: Monitoring TGFβ signaling in irradiated tumors.

    Ma, Lin / Gonzalez-Junca, Alba / Chou, William / Barcellos-Hoff, Mary Helen

    Methods in cell biology

    2023  Volume 180, Page(s) 49–67

    Abstract: Transforming growth factor β (TGFβ) is exquisitely regulated under physiological conditions but its activity is highly dysregulated in cancer. All cells make TGFβ and have receptors for the ligand, which is sequestered in the extracellular matrix in a ... ...

    Abstract Transforming growth factor β (TGFβ) is exquisitely regulated under physiological conditions but its activity is highly dysregulated in cancer. All cells make TGFβ and have receptors for the ligand, which is sequestered in the extracellular matrix in a latent form. Ionizing radiation elicits rapid release of TGFβ from these stores, so-called activation, over a wide range of doses and exposures, including low dose (<1Gy) whole-body irradiation, creating an extraordinarily potent signal in the irradiated tissue or tumor. Hence, accurate evaluation of TGFβ activity is complicated because of its ubiquitous distribution as a latent complex. Here we describe conditions for assays that reveal TGFβ activity in situ using either tissue preparations or functional imaging.
    MeSH term(s) Humans ; Transforming Growth Factor beta ; Signal Transduction ; Neoplasms/radiotherapy ; Extracellular Matrix
    Chemical Substances Transforming Growth Factor beta
    Language English
    Publishing date 2023-06-09
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ISSN 0091-679X
    ISSN 0091-679X
    DOI 10.1016/bs.mcb.2023.02.009
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  6. Article ; Online: In Memoriam - Zena Werb 1945-2020.

    Barcellos-Hoff, Mary Helen / Weaver, Valerie M

    Journal of mammary gland biology and neoplasia

    2020  Volume 25, Issue 3, Page(s) 179–180

    Language English
    Publishing date 2020-09-30
    Publishing country United States
    Document type Editorial
    ZDB-ID 1327345-0
    ISSN 1573-7039 ; 1083-3021
    ISSN (online) 1573-7039
    ISSN 1083-3021
    DOI 10.1007/s10911-020-09459-y
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    In stock of ZB MED Cologne/Königswinter

    Zs.A 4478: Show issues Location:
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  7. Article ; Online: Mammary Tumor-Derived Transplants as Breast Cancer Models to Evaluate Tumor-Immune Interactions and Therapeutic Responses.

    Moore, Jade / Ma, Lin / Lazar, Ann A / Barcellos-Hoff, Mary Helen

    Cancer research

    2021  Volume 82, Issue 3, Page(s) 365–376

    Abstract: In breast cancer, the type and distribution of infiltrating immune cells are associated with clinical outcome. Moreover, cancers with abundant tumor-infiltrating lymphocytes (TIL) are more likely to respond to immunotherapy, whereas those in which ... ...

    Abstract In breast cancer, the type and distribution of infiltrating immune cells are associated with clinical outcome. Moreover, cancers with abundant tumor-infiltrating lymphocytes (TIL) are more likely to respond to immunotherapy, whereas those in which CD8
    MeSH term(s) Animals ; Breast Neoplasms/physiopathology ; Disease Models, Animal ; Female ; Lymphocytes, Tumor-Infiltrating/immunology ; Mammary Neoplasms, Animal/physiopathology ; Mice ; Mice, Nude ; Tumor Microenvironment
    Language English
    Publishing date 2021-12-13
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural
    ZDB-ID 1432-1
    ISSN 1538-7445 ; 0008-5472
    ISSN (online) 1538-7445
    ISSN 0008-5472
    DOI 10.1158/0008-5472.CAN-21-0253
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    In stock of ZB MED Cologne/Königswinter

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  8. Article ; Online: BUB1-bling over with possibilities.

    Barcellos-Hoff, Mary Helen

    Neoplasia (New York, N.Y.)

    2015  Volume 17, Issue 2, Page(s) 153–154

    Abstract: In a new report, Nyati et al. identified a previously undetected participant mediating both canonical signaling, i.e., TGF-β receptor kinase mediated, and non-canonical signaling, budding uninhibited by benzimidazole 1 (BUB1). ...

    Abstract In a new report, Nyati et al. identified a previously undetected participant mediating both canonical signaling, i.e., TGF-β receptor kinase mediated, and non-canonical signaling, budding uninhibited by benzimidazole 1 (BUB1).
    MeSH term(s) Animals ; Humans ; Protein-Serine-Threonine Kinases/metabolism ; Receptors, Transforming Growth Factor beta/metabolism ; Signal Transduction/physiology ; Smad Proteins, Receptor-Regulated/metabolism ; Transforming Growth Factor beta/physiology
    Chemical Substances Receptors, Transforming Growth Factor beta ; Smad Proteins, Receptor-Regulated ; Transforming Growth Factor beta ; Protein-Serine-Threonine Kinases (EC 2.7.11.1)
    Language English
    Publishing date 2015-02
    Publishing country United States
    Document type Comment ; Journal Article
    ZDB-ID 1483840-0
    ISSN 1476-5586 ; 1522-8002
    ISSN (online) 1476-5586
    ISSN 1522-8002
    DOI 10.1016/j.neo.2015.01.002
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    Zs.A 5203: Show issues Location:
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  9. Article: Lack of TGFβ signaling competency predicts conversion of immune poor cancer to immune rich and response to checkpoint blockade.

    Moore, Jade / Gkantalis, Jim / Guix, Ines / Chou, William / Yuen, Kobe / Lazar, Ann A / Spitzer, Mathew / Combes, Alexis J / Barcellos-Hoff, Mary Helen

    bioRxiv : the preprint server for biology

    2024  

    Abstract: Background: Transforming growth factor beta (TGFβ) is well-recognized as an immunosuppressive player in the tumor microenvironment but also has a significant impact on cancer cell phenotypes. Loss of TGFβ signaling impairs DNA repair competency, which ... ...

    Abstract Background: Transforming growth factor beta (TGFβ) is well-recognized as an immunosuppressive player in the tumor microenvironment but also has a significant impact on cancer cell phenotypes. Loss of TGFβ signaling impairs DNA repair competency, which is described by a transcriptomic score, βAlt. Cancers with high βAlt have more genomic damage and are more responsive to genotoxic therapy. The growing appreciation that cancer DNA repair deficits are important determinants of immune response prompted us to investigate βAlt's association with response to immune checkpoint blockade (ICB). We predicted that high βAlt tumors would be infiltrated with lymphocytes because of DNA damage burden and hence responsive to ICB.
    Methods: We analyzed public transcriptomic data from clinical trials and preclinical models using transcriptomic signatures of TGFβ targets, DNA repair genes, tumor educated immune cells and interferon. A high βAlt, immune poor mammary tumor derived transplant model resistant to programmed death ligand 1 (PD-L1) antibodies was studied using multispectral flow cytometry to interrogate the immune system.
    Results: Metastatic bladder patients in IMvigor 210 who responded to ICB had significantly increased βAlt scores and experienced significantly longer overall survival compared to those with low βAlt scores (hazard ratio 0.62,
    Conclusions: Our studies confirm βAlt as a biomarker that predicts response to ICB in immune poor cancers., which has implications for the development of therapeutic strategies to increase the number of cancer patients who will benefit from immunotherapy.
    Language English
    Publishing date 2024-03-08
    Publishing country United States
    Document type Preprint
    DOI 10.1101/2024.03.06.583752
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  10. Article ; Online: Exploiting Canonical TGFβ Signaling in Cancer Treatment.

    Liu, Qi / Chen, Genwen / Moore, Jade / Guix, Ines / Placantonakis, Dimitris / Barcellos-Hoff, Mary Helen

    Molecular cancer therapeutics

    2021  Volume 21, Issue 1, Page(s) 16–24

    Abstract: TGFβ is a pleiotropic cytokine that plays critical roles to define cancer cell phenotypes, construct the tumor microenvironment, and suppress antitumor immune responses. As such, TGFβ is a lynchpin for integrating cancer cell intrinsic pathways and ... ...

    Abstract TGFβ is a pleiotropic cytokine that plays critical roles to define cancer cell phenotypes, construct the tumor microenvironment, and suppress antitumor immune responses. As such, TGFβ is a lynchpin for integrating cancer cell intrinsic pathways and communication among host cells in the tumor and beyond that together affect responses to genotoxic, targeted, and immune therapy. Despite decades of preclinical and clinical studies, evidence of clinical benefit from targeting TGFβ in cancer remains elusive. Here, we review the mechanisms by which TGFβ acts to oppose successful cancer therapy, the reported prognostic and predictive value of TGFβ biomarkers, and the potential impact of inhibiting TGFβ in precision oncology. Paradoxically, the diverse mechanisms by which TGFβ impedes therapeutic response are a principal barrier to implementing TGFβ inhibitors because it is unclear which TGFβ mechanism is functional in which patient. Companion diagnostic tools and specific biomarkers of TGFβ targeted biology will be the key to exploiting TGFβ biology for patient benefit.
    MeSH term(s) Humans ; Neoplasms/drug therapy ; Prognosis ; Signal Transduction ; Transforming Growth Factor beta/pharmacology ; Transforming Growth Factor beta/therapeutic use
    Chemical Substances Transforming Growth Factor beta
    Language English
    Publishing date 2021-10-20
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Review
    ZDB-ID 2063563-1
    ISSN 1538-8514 ; 1535-7163
    ISSN (online) 1538-8514
    ISSN 1535-7163
    DOI 10.1158/1535-7163.MCT-20-0891
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    Zs.A 5750: Show issues Location:
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