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  1. Article ; Online: ONC201 and ONC206: Metabolically ClipPing the wings of diffuse midline glioma.

    Purow, Benjamin

    Neuro-oncology

    2023  Volume 24, Issue 9, Page(s) 1452–1453

    MeSH term(s) Cell Lineage ; Energy Metabolism ; Glioma/genetics ; Glioma/pathology ; Glioma/surgery ; Humans ; Imidazoles ; Pyridines ; Pyrimidines
    Chemical Substances Imidazoles ; Pyridines ; Pyrimidines ; TIC10 compound (9U35A31JAI)
    Language English
    Publishing date 2023-04-21
    Publishing country England
    Document type Editorial ; Comment
    ZDB-ID 2028601-6
    ISSN 1523-5866 ; 1522-8517
    ISSN (online) 1523-5866
    ISSN 1522-8517
    DOI 10.1093/neuonc/noac103
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    Zs.A 5307: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
    Jg. 1995 - 2021: Lesesall (2.OG)
    ab Jg. 2022: Lesesaal (EG)

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  2. Article: Delivering Glioblastoma a Kick-DGKα Inhibition as a Promising Therapeutic Strategy for GBM.

    Purow, Benjamin

    Cancers

    2022  Volume 14, Issue 5

    Abstract: Diacylglycerol kinase α (DGKα) inhibition may be particularly relevant for the treatment of glioblastoma (GBM), a relatively common brain malignancy incurable with current therapies. Prior reports have shown that DGKα inhibition has multiple direct ... ...

    Abstract Diacylglycerol kinase α (DGKα) inhibition may be particularly relevant for the treatment of glioblastoma (GBM), a relatively common brain malignancy incurable with current therapies. Prior reports have shown that DGKα inhibition has multiple direct activities against GBM cells, including suppressing the oncogenic pathways mTOR and HIF-1α. It also inhibits pathways associated with the normally treatment-resistant mesenchymal phenotype, yielding preferential activity against mesenchymal GBM; this suggests possible utility in combining DGKα inhibition with radiation and other therapies for which the mesenchymal phenotype promotes resistance. The potential for DGKα inhibition to block or reverse T cell anergy also suggests the potential of DGKα inhibition to boost immunotherapy against GBM, which is generally considered an immunologically "cold" tumor. A recent report indicates that DGKα deficiency increases responsiveness of macrophages, indicating that DGKα inhibition could also have the potential to boost macrophage and microglia activity against GBM-which could be a particularly promising approach given the heavy infiltration of these cells in GBM. DGKα inhibition may therefore offer a promising multi-pronged attack on GBM, with multiple direct anti-GBM activities and also the ability to boost both adaptive and innate immune responses against GBM. However, both the direct and indirect benefits of DGKα inhibition for GBM will likely require combinations with other therapies to achieve meaningful efficacy. Furthermore, GBM offers other challenges for the application of DGKα inhibitors, including decreased accessibility from the blood-brain barrier (BBB). The ideal DGKα inhibitor for GBM will combine potency, specificity, and BBB penetrability. No existing inhibitor is known to meet all these criteria, but the strong potential of DGKα inhibition against this lethal brain cancer should help drive development and testing of agents to bring this promising strategy to the clinic for patients with GBM.
    Language English
    Publishing date 2022-03-01
    Publishing country Switzerland
    Document type Journal Article ; Review
    ZDB-ID 2527080-1
    ISSN 2072-6694
    ISSN 2072-6694
    DOI 10.3390/cancers14051269
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article ; Online: Cannabinoids and NF-κB: Hijacking a pro-cancer signal Can Be Done.

    Purow, Benjamin

    Neuro-oncology

    2021  Volume 23, Issue 11, Page(s) 1810–1811

    MeSH term(s) Cannabinoids ; Humans ; NF-kappa B ; Neoplasms/drug therapy
    Chemical Substances Cannabinoids ; NF-kappa B
    Language English
    Publishing date 2021-08-02
    Publishing country England
    Document type Editorial ; Comment
    ZDB-ID 2028601-6
    ISSN 1523-5866 ; 1522-8517
    ISSN (online) 1523-5866
    ISSN 1522-8517
    DOI 10.1093/neuonc/noab187
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    In stock of ZB MED Cologne/Königswinter

    Zs.A 5307: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
    Jg. 1995 - 2021: Lesesall (2.OG)
    ab Jg. 2022: Lesesaal (EG)

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  4. Article ; Online: Understanding current experimental models of glioblastoma-brain microenvironment interactions.

    Yadav, Niket / Purow, Benjamin W

    Journal of neuro-oncology

    2024  Volume 166, Issue 2, Page(s) 213–229

    Abstract: Glioblastoma (GBM) is a common and devastating primary brain tumor, with median survival of 16-18 months after diagnosis in the setting of substantial resistance to standard-of-care and inevitable tumor recurrence. Recent work has implicated the brain ... ...

    Abstract Glioblastoma (GBM) is a common and devastating primary brain tumor, with median survival of 16-18 months after diagnosis in the setting of substantial resistance to standard-of-care and inevitable tumor recurrence. Recent work has implicated the brain microenvironment as being critical for GBM proliferation, invasion, and resistance to treatment. GBM does not operate in isolation, with neurons, astrocytes, and multiple immune populations being implicated in GBM tumor progression and invasiveness. The goal of this review article is to provide an overview of the available in vitro, ex vivo, and in vivo experimental models for assessing GBM-brain interactions, as well as discuss each model's relative strengths and limitations. Current in vitro models discussed will include 2D and 3D co-culture platforms with various cells of the brain microenvironment, as well as spheroids, whole organoids, and models of fluid dynamics, such as interstitial flow. An overview of in vitro and ex vivo organotypic GBM brain slices is also provided. Finally, we conclude with a discussion of the various in vivo rodent models of GBM, including xenografts, syngeneic grafts, and genetically-engineered models of GBM.
    MeSH term(s) Humans ; Glioblastoma/pathology ; Brain Neoplasms/pathology ; Neoplasm Recurrence, Local/pathology ; Brain/pathology ; Models, Theoretical ; Tumor Microenvironment/physiology ; Cell Line, Tumor
    Language English
    Publishing date 2024-01-05
    Publishing country United States
    Document type Journal Article ; Review
    ZDB-ID 604875-4
    ISSN 1573-7373 ; 0167-594X
    ISSN (online) 1573-7373
    ISSN 0167-594X
    DOI 10.1007/s11060-023-04536-8
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 1825: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
    Jg. 1995 - 2021: Lesesall (1.OG)
    ab Jg. 2022: Lesesaal (EG)

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  5. Article ; Online: Divergent transcriptomic signatures from putative mesenchymal stimuli in glioblastoma cells.

    Hart, William S / Myers, Paul J / Purow, Benjamin W / Lazzara, Matthew J

    Cancer gene therapy

    2024  

    Abstract: In glioblastoma, a mesenchymal phenotype is associated with especially poor patient outcomes. Various glioblastoma microenvironmental factors and therapeutic interventions are purported drivers of the mesenchymal transition, but the degree to which these ...

    Abstract In glioblastoma, a mesenchymal phenotype is associated with especially poor patient outcomes. Various glioblastoma microenvironmental factors and therapeutic interventions are purported drivers of the mesenchymal transition, but the degree to which these cues promote the same mesenchymal transitions and the uniformity of those transitions, as defined by molecular subtyping systems, is unknown. Here, we investigate this question by analyzing publicly available patient data, surveying commonly measured transcripts for mesenchymal transitions in glioma-initiating cells (GIC), and performing next-generation RNA sequencing of GICs. Analysis of patient tumor data reveals that TGFβ, TNFα, and hypoxia signaling correlate with the mesenchymal subtype more than the proneural subtype. In cultured GICs, the microenvironment-relevant growth factors TGFβ and TNFα and the chemotherapeutic temozolomide promote expression of commonly measured mesenchymal transcripts. However, next-generation RNA sequencing reveals that growth factors and temozolomide broadly promote expression of both mesenchymal and proneural transcripts, in some cases with equal frequency. These results suggest that glioblastoma mesenchymal transitions do not occur as distinctly as in epithelial-derived cancers, at least as determined using common subtyping ontologies and measuring response to growth factors or chemotherapeutics. Further understanding of these issues may identify improved methods for pharmacologically targeting the mesenchymal phenotype in glioblastoma.
    Language English
    Publishing date 2024-02-09
    Publishing country England
    Document type Journal Article
    ZDB-ID 1212513-1
    ISSN 1476-5500 ; 0929-1903
    ISSN (online) 1476-5500
    ISSN 0929-1903
    DOI 10.1038/s41417-023-00724-w
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 4125: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
    Jg. 1995 - 2021: Lesesall (2.OG)
    ab Jg. 2022: Lesesaal (EG)

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  6. Article ; Online: For glioma, a sweet side to diabetes.

    Purow, Benjamin

    Neuro-oncology

    2016  Volume 18, Issue 3, Page(s) 306–307

    MeSH term(s) Diabetes Mellitus ; Glioma ; Humans
    Language English
    Publishing date 2016-02-18
    Publishing country England
    Document type Editorial ; Comment
    ZDB-ID 2028601-6
    ISSN 1523-5866 ; 1522-8517
    ISSN (online) 1523-5866
    ISSN 1522-8517
    DOI 10.1093/neuonc/nov328
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    In stock of ZB MED Cologne/Königswinter

    Zs.A 5307: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
    Jg. 1995 - 2021: Lesesall (2.OG)
    ab Jg. 2022: Lesesaal (EG)

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  7. Article: Repurposing existing agents as adjunct therapies for glioblastoma.

    Purow, Benjamin

    Neuro-oncology practice

    2015  Volume 3, Issue 3, Page(s) 154–163

    Abstract: Numerous non-oncologic medications have been found in the last decade to have anti-cancer properties. While the focus in oncology research should clearly remain on deriving new therapeutic strategies, repurposing these existing medications may offer the ... ...

    Abstract Numerous non-oncologic medications have been found in the last decade to have anti-cancer properties. While the focus in oncology research should clearly remain on deriving new therapeutic strategies, repurposing these existing medications may offer the potential to rapidly enhance the effectiveness of treatment for resistant cancers. Glioblastoma, the most common and lethal brain cancer, is highly resistant to standard therapies and would benefit from even minor improvements in treatment. Numerous agents already in the clinic for non-cancer applications have been found to also possess potential against cancer or specifically against glioblastoma. These include agents with activities affecting oxidative stress, the immune reponse, epigenetic modifiers, cancer cell metabolism, and angiogenesis and invasiveness. This review serves as a guide for potential ways to repurpose individual drugs alongside standard glioblastoma therapies.
    Language English
    Publishing date 2015-09-30
    Publishing country England
    Document type Journal Article
    ZDB-ID 2768945-1
    ISSN 2054-2585 ; 2054-2577
    ISSN (online) 2054-2585
    ISSN 2054-2577
    DOI 10.1093/nop/npv041
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  8. Article: Molecular Pathways: Targeting Diacylglycerol Kinase Alpha in Cancer.

    Purow, Benjamin

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

    2015  Volume 21, Issue 22, Page(s) 5008–5012

    Abstract: Lipid kinases have largely been neglected as targets in cancer, and an increasing number of reports suggest diacylglycerol kinase alpha (DGKα) may be one with promising therapeutic potential. DGKα is one of 10 DGK family members that convert ... ...

    Abstract Lipid kinases have largely been neglected as targets in cancer, and an increasing number of reports suggest diacylglycerol kinase alpha (DGKα) may be one with promising therapeutic potential. DGKα is one of 10 DGK family members that convert diacylglycerol (DAG) to phosphatidic acid (PA), and both DAG and PA are critical lipid second messengers in the plasma membrane. A host of important oncogenic proteins and pathways affect cancer cells in part through DGKα, including the c-Met and VEGF receptors. Others partially mediate the effects of DGKα inhibition in cancer, such as mTOR and HIF-1α. DGKα inhibition can directly impair cancer cell viability, inhibits angiogenesis, and notably may also boost T-cell activation and enhance cancer immunotherapies. Although two structurally similar inhibitors of DGKα were established decades ago, they have seen minimal in vivo usage, and it is unlikely that either of these older DGKα inhibitors will have utility for cancer. An abandoned compound that also inhibits serotonin receptors may have more translational potential as a DGKα inhibitor, but more potent and specific DGKα inhibitors are sorely needed. Other DGK family members may also provide therapeutic targets in cancer, but require further investigation.
    MeSH term(s) Cell Differentiation/genetics ; Cell Survival/genetics ; Diacylglycerol Kinase/antagonists & inhibitors ; Diacylglycerol Kinase/chemistry ; Diacylglycerol Kinase/genetics ; Enzyme Inhibitors/chemistry ; Enzyme Inhibitors/therapeutic use ; Humans ; Hypoxia-Inducible Factor 1, alpha Subunit/genetics ; Immunotherapy ; Lymphocyte Activation/drug effects ; Lymphocyte Activation/immunology ; Neoplasms/genetics ; Neoplasms/pathology ; Neoplasms/therapy ; Phosphatidic Acids/genetics ; Proto-Oncogene Proteins c-met/genetics ; Receptors, Vascular Endothelial Growth Factor/genetics ; Signal Transduction/drug effects ; TOR Serine-Threonine Kinases/genetics
    Chemical Substances Enzyme Inhibitors ; HIF1A protein, human ; Hypoxia-Inducible Factor 1, alpha Subunit ; Phosphatidic Acids ; MTOR protein, human (EC 2.7.1.1) ; TOR Serine-Threonine Kinases (EC 2.7.1.1) ; Diacylglycerol Kinase (EC 2.7.1.107) ; Proto-Oncogene Proteins c-met (EC 2.7.10.1) ; Receptors, Vascular Endothelial Growth Factor (EC 2.7.10.1)
    Language English
    Publishing date 2015-11-15
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural
    ZDB-ID 1225457-5
    ISSN 1557-3265 ; 1078-0432
    ISSN (online) 1557-3265
    ISSN 1078-0432
    DOI 10.1158/1078-0432.CCR-15-0413
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    Zs.A 4223: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
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    ab Jg. 2022: Lesesaal (EG)

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  9. Article ; Online: Open-Top Patterned Hydrogel-Laden 3D Glioma Cell Cultures for Creation of Dynamic Chemotactic Gradients to Direct Cell Migration.

    Rane, Aditya / Tate, Steven / Sumey, Jenna L / Zhong, Qing / Zong, Hui / Purow, Benjamin / Caliari, Steven R / Swami, Nathan S

    ACS biomaterials science & engineering

    2024  

    Abstract: The laminar flow profiles in microfluidic systems coupled to rapid diffusion at flow streamlines have been widely utilized to create well-controlled chemical gradients in cell cultures for spatially directing cell migration. However, within hydrogel- ... ...

    Abstract The laminar flow profiles in microfluidic systems coupled to rapid diffusion at flow streamlines have been widely utilized to create well-controlled chemical gradients in cell cultures for spatially directing cell migration. However, within hydrogel-based closed microfluidic systems of limited depth (≤0.1 mm), the biomechanical cues for the cell culture are dominated by cell interactions with channel surfaces rather than with the hydrogel microenvironment. Also, leaching of poly(dimethylsiloxane) (PDMS) constituents in closed systems and the adsorption of small molecules to PDMS alter chemotactic profiles. To address these limitations, we present the patterning and integration of a PDMS-free open fluidic system, wherein the cell-laden hydrogel directly adjoins longitudinal channels that are designed to create chemotactic gradients across the 3D culture width, while maintaining uniformity across its ∼1 mm depth to enhance cell-biomaterial interactions. This hydrogel-based open fluidic system is assessed for its ability to direct migration of U87 glioma cells using a hybrid hydrogel that includes hyaluronic acid (HA) to mimic the brain tumor microenvironment and gelatin methacrylate (GelMA) to offer the adhesion motifs for promoting cell migration. Chemotactic gradients to induce cell migration across the hydrogel width are assessed using the chemokine CXCL12, and its inhibition by AMD3100 is validated. This open-top hydrogel-based fluidic system to deliver chemoattractant cues over square-centimeter-scale areas and millimeter-scale depths can potentially serve as a robust screening platform to assess emerging glioma models and chemotherapeutic agents to eradicate them.
    Language English
    Publishing date 2024-04-23
    Publishing country United States
    Document type Journal Article
    ISSN 2373-9878
    ISSN (online) 2373-9878
    DOI 10.1021/acsbiomaterials.4c00041
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  10. Article: Notch inhibition as a promising new approach to cancer therapy.

    Purow, Benjamin

    Advances in experimental medicine and biology

    2012  Volume 727, Page(s) 305–319

    Abstract: The Notch pathway powerfully influences stem cell maintenance, development and cell fate and is increasingly recognized for the key roles it plays in cancer. Notch promotes cell survival, angiogenesis and treatment resistance in numerous cancers, making ... ...

    Abstract The Notch pathway powerfully influences stem cell maintenance, development and cell fate and is increasingly recognized for the key roles it plays in cancer. Notch promotes cell survival, angiogenesis and treatment resistance in numerous cancers, making it a promising target for cancer therapy. It also crosstalks with other critical oncogenes, providing a means to affect numerous signaling pathways with one intervention. While the gamma-secretase inhibitors are the only form of Notch inhibitors in clinical trials, other forms of Notch inhibition have been developed or are theoretically feasible. In this chapter we review the rationales for Notch inhibition in cancer and then discuss in detail the various modalities for Notch inhibition, both current and speculative.
    MeSH term(s) Animals ; Antineoplastic Agents/therapeutic use ; Humans ; Neoplasms/metabolism ; Neoplasms/prevention & control ; Receptors, Notch/antagonists & inhibitors ; Receptors, Notch/metabolism ; Signal Transduction
    Chemical Substances Antineoplastic Agents ; Receptors, Notch
    Language English
    Publishing date 2012-03-08
    Publishing country United States
    Document type Journal Article ; Review
    ISSN 2214-8019 ; 0065-2598
    ISSN (online) 2214-8019
    ISSN 0065-2598
    DOI 10.1007/978-1-4614-0899-4_23
    Database MEDical Literature Analysis and Retrieval System OnLINE

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