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  1. Article: CRIPTO promotes extracellular vesicle uptake and activation of cancer associated fibroblasts.

    Freeman, David W / Gates, Brooke L / Spendlove, Mauri D / Gulbahce, H Evin / Spike, Benjamin T

    bioRxiv : the preprint server for biology

    2024  

    Abstract: Expression of CRIPTO, a factor involved in embryonic stem cells, fetal development, and wound healing, is tied to poor prognosis in multiple cancers. Prior studies in triple negative breast cancer (TNBC) models showed CRIPTO blockade inhibits tumor ... ...

    Abstract Expression of CRIPTO, a factor involved in embryonic stem cells, fetal development, and wound healing, is tied to poor prognosis in multiple cancers. Prior studies in triple negative breast cancer (TNBC) models showed CRIPTO blockade inhibits tumor growth and dissemination. Here, we uncover a previously unidentified role for CRIPTO in orchestrating tumor-derived extracellular vesicle (TEV) uptake and fibroblast activation through discrete mechanisms. We found a novel mechanism by which CRIPTO drives aggressive TNBC phenotypes, involving CRIPTO-laden TEVs that program stromal fibroblasts, toward cancer associated fibroblast cell states, which in turn prompt tumor cell invasion. CRIPTO-bearing TEVs exhibited markedly elevated uptake in target fibroblasts and activated SMAD2/3 through NODAL-independent and - dependent mechanisms, respectively. Engineered expression of CRIPTO on EVs enhanced the delivery of bioactive molecules.
    Language English
    Publishing date 2024-04-02
    Publishing country United States
    Document type Preprint
    DOI 10.1101/2024.03.01.583059
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article: Editorial: Mechanisms of microenvironment governed plasticity and progression in solid tumors.

    Kelber, Jonathan A / Iwanicki, Marcin / Kruithof-de Julio, Marianna / Spike, Benjamin T / Martínez-Montemayor, Michelle M

    Frontiers in cell and developmental biology

    2024  Volume 12, Page(s) 1373496

    Language English
    Publishing date 2024-03-25
    Publishing country Switzerland
    Document type Editorial
    ZDB-ID 2737824-X
    ISSN 2296-634X
    ISSN 2296-634X
    DOI 10.3389/fcell.2024.1373496
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article: OCA-B promotes autoimmune demyelination through control of stem-like CD4

    Hughes, Erik P / Syage, Amber R / Mehrabad, Elnaz Mirzaei / Lane, Thomas E / Spike, Benjamin T / Tantin, Dean

    bioRxiv : the preprint server for biology

    2024  

    Abstract: Stem-like T cell populations can selectively contribute to autoimmunity, but the activities ... that promote and sustain these populations are incompletely understood. Here, we show that T cell-intrinsic ...

    Abstract Stem-like T cell populations can selectively contribute to autoimmunity, but the activities that promote and sustain these populations are incompletely understood. Here, we show that T cell-intrinsic loss of the transcription cofactor OCA-B protects mice from experimental autoimmune encephalomyelitis (EAE) while preserving responses to CNS infection. In adoptive transfer EAE models driven by multiple antigen encounters, OCA-B deletion nearly eliminates CNS infiltration, proinflammatory cytokine production and clinical disease. OCA-B-expressing CD4
    Language English
    Publishing date 2024-04-17
    Publishing country United States
    Document type Preprint
    DOI 10.1101/2023.11.29.569210
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article: Mcam stabilizes luminal progenitor breast cancer phenotypes via Ck2 control and Src/Akt/Stat3 attenuation.

    Balcioglu, Ozlen / Gates, Brooke L / Freeman, David W / Hagos, Berhane M / Mehrabad, Elnaz Mirzaei / Ayala-Talavera, David / Spike, Benjamin T

    bioRxiv : the preprint server for biology

    2024  

    Abstract: Breast cancers are categorized into subtypes with distinctive therapeutic vulnerabilities and prognoses based on their expression of clinically targetable receptors and gene expression patterns mimicking different cell types of the normal gland. Here, we ...

    Abstract Breast cancers are categorized into subtypes with distinctive therapeutic vulnerabilities and prognoses based on their expression of clinically targetable receptors and gene expression patterns mimicking different cell types of the normal gland. Here, we tested the role of Mcam in breast cancer cell state control and tumorigenicity in a luminal progenitor-like murine tumor cell line (Py230) that exhibits lineage and tumor subtype plasticity. Mcam knockdown Py230 cells show augmented Stat3 and Pi3K/Akt activation associated with a lineage state switch away from a hormone-sensing/luminal progenitor state toward alveolar and basal cell related phenotypes that were refractory to growth inhibition by the anti-estrogen therapeutic, tamoxifen. Inhibition of Stat3, or the upstream activator Ck2, reversed these cell state changes. Mcam binds Ck2 and acts as a regulator of Ck2 substrate utilization across multiple mammary tumor cell lines. In Py230 cells this activity manifests as increased mesenchymal morphology, migration, and Src/Fak/Mapk/Paxillin adhesion complex signaling
    Language English
    Publishing date 2024-03-20
    Publishing country United States
    Document type Preprint
    DOI 10.1101/2023.05.10.540211
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  5. Article: Cell state plasticity, stem cells, EMT, and the generation of intra-tumoral heterogeneity.

    Wahl, Geoffrey M / Spike, Benjamin T

    NPJ breast cancer

    2017  Volume 3, Page(s) 14

    Abstract: Cellular heterogeneity in cancer represents a significant challenge. In order to develop effective and lasting therapies, it is essential to understand the source of this heterogeneity, and its role in tumor progression and therapy resistance. Here, we ... ...

    Abstract Cellular heterogeneity in cancer represents a significant challenge. In order to develop effective and lasting therapies, it is essential to understand the source of this heterogeneity, and its role in tumor progression and therapy resistance. Here, we consider not only genetic and epigenetic mechanisms, but also inflammation and cell state reprogramming in creating tumor heterogeneity. We discuss similarities between normal mammary epithelial developmental states and various breast cancer molecular sub-types, and the cells that are thought to propagate them. We emphasize that while stem cell phenotypes and mesenchymal character have often been conflated, existing data suggest that the combination of intrinsic genetic and epigenetic changes, and microenvironmental influences generate multiple types of tumor propagating cells distinguishable by their positions along a continuum of epithelial to mesenchymal, stem to differentiated and embryonic to mature cell states. Consequently, in addition to the prospect of stem cell-directed tumor therapies, there is a need to understand interrelationships between stem cell, epithelial-mesenchymal, and tumor-associated reprogramming events to develop new therapies that mitigate cell state plasticity and minimize the evolution of tumor heterogeneity.
    Language English
    Publishing date 2017-04-19
    Publishing country United States
    Document type Journal Article
    ISSN 2374-4677
    ISSN 2374-4677
    DOI 10.1038/s41523-017-0012-z
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  6. Article ; Online: Multiparametric quantitative phase imaging for real-time, single cell, drug screening in breast cancer.

    Polanco, Edward R / Moustafa, Tarek E / Butterfield, Andrew / Scherer, Sandra D / Cortes-Sanchez, Emilio / Bodily, Tyler / Spike, Benjamin T / Welm, Bryan E / Bernard, Philip S / Zangle, Thomas A

    Communications biology

    2022  Volume 5, Issue 1, Page(s) 794

    Abstract: Quantitative phase imaging (QPI) measures the growth rate of individual cells by quantifying changes in mass versus time. Here, we use the breast cancer cell lines MCF-7, BT-474, and MDA-MB-231 to validate QPI as a multiparametric approach for ... ...

    Abstract Quantitative phase imaging (QPI) measures the growth rate of individual cells by quantifying changes in mass versus time. Here, we use the breast cancer cell lines MCF-7, BT-474, and MDA-MB-231 to validate QPI as a multiparametric approach for determining response to single-agent therapies. Our method allows for rapid determination of drug sensitivity, cytotoxicity, heterogeneity, and time of response for up to 100,000 individual cells or small clusters in a single experiment. We find that QPI EC
    MeSH term(s) Antineoplastic Agents/pharmacology ; Antineoplastic Agents/therapeutic use ; Breast Neoplasms/drug therapy ; Breast Neoplasms/metabolism ; Cell Proliferation ; Drug Evaluation, Preclinical ; Early Detection of Cancer ; Female ; Humans
    Chemical Substances Antineoplastic Agents
    Language English
    Publishing date 2022-08-08
    Publishing country England
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S.
    ISSN 2399-3642
    ISSN (online) 2399-3642
    DOI 10.1038/s42003-022-03759-1
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  7. Article ; Online: FoxA1 and FoxA2 control growth and cellular identity in NKX2-1-positive lung adenocarcinoma.

    Orstad, Grace / Fort, Gabriela / Parnell, Timothy J / Jones, Alex / Stubben, Chris / Lohman, Brian / Gillis, Katherine L / Orellana, Walter / Tariq, Rushmeen / Klingbeil, Olaf / Kaestner, Klaus / Vakoc, Christopher R / Spike, Benjamin T / Snyder, Eric L

    Developmental cell

    2022  Volume 57, Issue 15, Page(s) 1866–1882.e10

    Abstract: Changes in cellular identity (also known as histologic transformation or lineage plasticity) can drive malignant progression and resistance to therapy in many cancers, including lung adenocarcinoma (LUAD). The lineage-specifying transcription factors ... ...

    Abstract Changes in cellular identity (also known as histologic transformation or lineage plasticity) can drive malignant progression and resistance to therapy in many cancers, including lung adenocarcinoma (LUAD). The lineage-specifying transcription factors FoxA1 and FoxA2 (FoxA1/2) control identity in NKX2-1/TTF1-negative LUAD. However, their role in NKX2-1-positive LUAD has not been systematically investigated. We find that Foxa1/2 knockout severely impairs tumorigenesis in KRAS-driven genetically engineered mouse models and human cell lines. Loss of FoxA1/2 leads to the collapse of a dual-identity state, marked by co-expression of pulmonary and gastrointestinal transcriptional programs, which has been implicated in LUAD progression. Mechanistically, FoxA1/2 loss leads to aberrant NKX2-1 activity and genomic localization, which in turn actively inhibits tumorigenesis and drives alternative cellular identity programs that are associated with non-proliferative states. This work demonstrates that FoxA1/2 expression is a lineage-specific vulnerability in NKX2-1-positive LUAD and identifies mechanisms of response and resistance to targeting FoxA1/2 in this disease.
    MeSH term(s) Adenocarcinoma/genetics ; Adenocarcinoma/metabolism ; Adenocarcinoma of Lung/genetics ; Animals ; Cell Transformation, Neoplastic ; Hepatocyte Nuclear Factor 3-alpha/genetics ; Hepatocyte Nuclear Factor 3-beta/genetics ; Humans ; Lung Neoplasms/metabolism ; Mice ; Thyroid Nuclear Factor 1
    Chemical Substances FOXA1 protein, human ; FOXA2 protein, human ; Foxa1 protein, mouse ; Foxa2 protein, mouse ; Hepatocyte Nuclear Factor 3-alpha ; NKX2-1 protein, human ; Thyroid Nuclear Factor 1 ; Hepatocyte Nuclear Factor 3-beta (135845-92-0)
    Language English
    Publishing date 2022-07-13
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural
    ZDB-ID 2054967-2
    ISSN 1878-1551 ; 1534-5807
    ISSN (online) 1878-1551
    ISSN 1534-5807
    DOI 10.1016/j.devcel.2022.06.017
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  8. Article ; Online: Multiparametric quantitative phase imaging for real-time, single cell, drug screening in breast cancer

    Edward R. Polanco / Tarek E. Moustafa / Andrew Butterfield / Sandra D. Scherer / Emilio Cortes-Sanchez / Tyler Bodily / Benjamin T. Spike / Bryan E. Welm / Philip S. Bernard / Thomas A. Zangle

    Communications Biology, Vol 5, Iss 1, Pp 1-

    2022  Volume 12

    Abstract: The authors developed a real-time and label-free approach based on quantitative phase imaging to determine drug sensitivity with significant advantages over endpoint viability or metabolic assays, and which reveals single cell response heterogeneity. ...

    Abstract The authors developed a real-time and label-free approach based on quantitative phase imaging to determine drug sensitivity with significant advantages over endpoint viability or metabolic assays, and which reveals single cell response heterogeneity.
    Keywords Biology (General) ; QH301-705.5
    Language English
    Publishing date 2022-08-01T00:00:00Z
    Publisher Nature Portfolio
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  9. Article ; Online: Whence CRIPTO: The Reemergence of an Oncofetal Factor in 'Wounds' That Fail to Heal.

    Freeman, David W / Rodrigues Sousa, Elisa / Karkampouna, Sofia / Zoni, Eugenio / Gray, Peter C / Salomon, David S / Kruithof-de Julio, Marianna / Spike, Benjamin T

    International journal of molecular sciences

    2021  Volume 22, Issue 18

    Abstract: There exists a set of factors termed oncofetal proteins that play key roles in ontogeny before they decline or disappear as the organism's tissues achieve homeostasis, only to then re-emerge in cancer. Although the unique therapeutic potential presented ... ...

    Abstract There exists a set of factors termed oncofetal proteins that play key roles in ontogeny before they decline or disappear as the organism's tissues achieve homeostasis, only to then re-emerge in cancer. Although the unique therapeutic potential presented by such factors has been recognized for more than a century, their clinical utility has yet to be fully realized1. This review highlights the small signaling protein CRIPTO encoded by the tumor derived growth factor 1 (
    MeSH term(s) Animals ; Humans ; Signal Transduction/genetics ; Signal Transduction/physiology ; Stem Cells/metabolism ; Stem Cells/physiology ; Transforming Growth Factor beta/metabolism
    Chemical Substances Transforming Growth Factor beta
    Language English
    Publishing date 2021-09-21
    Publishing country Switzerland
    Document type Journal Article ; Review
    ZDB-ID 2019364-6
    ISSN 1422-0067 ; 1422-0067 ; 1661-6596
    ISSN (online) 1422-0067
    ISSN 1422-0067 ; 1661-6596
    DOI 10.3390/ijms221810164
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  10. Article ; Online: p53, Stem Cells, and Reprogramming: Tumor Suppression beyond Guarding the Genome.

    Spike, Benjamin T / Wahl, Geoffrey M

    Genes & cancer

    2011  Volume 2, Issue 4, Page(s) 404–419

    Abstract: p53 is well recognized as a potent tumor suppressor. In its classic role, p53 responds to genotoxic insults by inducing cell cycle exit or programmed cell death to limit the propagation of cells with corrupted genomes. p53 is also implicated in a variety ...

    Abstract p53 is well recognized as a potent tumor suppressor. In its classic role, p53 responds to genotoxic insults by inducing cell cycle exit or programmed cell death to limit the propagation of cells with corrupted genomes. p53 is also implicated in a variety of other cellular processes in which its involvement is less well understood including self-renewal, differentiation, and reprogramming. These activities represent an emerging area of intense interest for cancer biologists, as they provide potential mechanistic links between p53 loss and the stem cell-like cellular plasticity that has been suggested to contribute to tumor cell heterogeneity and to drive tumor progression. Despite accumulating evidence linking p53 loss to stem-like phenotypes in cancer, it is not yet understood how p53 contributes to acquisition of "stemness" at the molecular level. Whether and how stem-like cells confer survival advantages to propagate the tumor also remain to be resolved. Furthermore, although it seems reasonable that the combination of p53 deficiency and the stem-like state could contribute to the genesis of cancers that are refractory to treatment, direct linkages and mechanistic underpinnings remain under investigation. Here, we discuss recent findings supporting the connection between p53 loss and the emergence of tumor cells bearing functional and molecular similarities to stem cells. We address several potential molecular and cellular mechanisms that may contribute to this link, and we discuss implications of these findings for the way we think about cancer progression.
    Language English
    Publishing date 2011-07-14
    Publishing country United States
    Document type Journal Article
    ZDB-ID 2538519-7
    ISSN 1947-6027 ; 1947-6019
    ISSN (online) 1947-6027
    ISSN 1947-6019
    DOI 10.1177/1947601911410224
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