IN8bio Completes Treatment of First Cohort in Phase I Clinical Trial with Gamma Delta T-Cell Therapy in Patients with Newly Diagnosed Glioblastoma Multiforme

IN8bio, Inc. announced an update from the ongoing Phase I clinical trial of INB-200, its DeltEx drug resistant immunotherapy , MGMT-gene modified gamma delta T-cells in patients with newly diagnosed GBM.
[IN8bio, Inc.]
Press Release
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Effects of the DRD2/3 Antagonist ONC201 and Radiation in Glioblastoma

Investigators suggested that combined treatment with the DRD2/3 antagonist ONC201 and radiation improves the efficacy of radiation against glioblastoma (GBM) in vitro and in vivo through suppression of glioma-initiating cells without increasing toxicity in mouse models of GBM.
[Radiotherapy and Oncology]
AbstractGraphical Abstract
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Elevated GIGYF2 Expression Suppresses Tumor Migration and Enhances Sensitivity to Temozolomide in Malignant Glioma

Investigators found that elevation of GIGYF2 expression impaired cell migration and enhanced temozolomide sensitivity of human glioma cells.
[Cancer Gene Therapy]
Abstract
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Novel Dopamine Receptor 3 Antagonists Inhibit the Growth of Primary and Temozolomide Resistant Glioblastoma Cells

To improve treatment of glioblastoma, including those resistant to temozolomide , we explored the potential of targeting dopamine receptor signaling.
[PLoS One]
Williford, S. E., Libby, C. J., Ayokanmbi, A., Otamias, A., Gordillo, J. J., Gordon, E. R., Cooper, S. J., Redmann, M., Li, Y., Griguer, C., Zhang, J., Napierala, M., Ananthan, S., & Hjelmeland, A. B. (2021). Novel dopamine receptor 3 antagonists inhibit the growth of primary and temozolomide resistant glioblastoma cells. PLOS ONE, 16(5), e0250649. https://doi.org/10.1371/journal.pone.0250649 Cite
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FOXO3a Protects Glioma Cells against Temozolomide-Induced DNA Double Strand Breaks via Promotion of BNIP3-Mediated Mitophagy

Scientists investigated the role of forkhead box transcription factor 3a (FOXO3a) in regulating the sensitivity of glioma cells to temozolomide and its relationship with Bcl-2/adenovirus E1B 19-kDa-interacting protein 3 (BNIP3)-mediated mitophagy.
[Acta Pharmacologica Sinica]
FOXO3a protects glioma cells against temozolomide-induced DNA double strand breaks via promotion of BNIP3-mediated mitophagy | Acta Pharmacologica Sinica. (n.d.). Retrieved April 20, 2021, from https://www.nature.com/articles/s41401-021-00663-y Cite
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PI3Kγ Inhibition Suppresses Microglia/TAM Accumulation in Glioblastoma Microenvironment to Promote Exceptional Temozolomide Response

Glioblastoma-associated microglia/macrophages secreted interleukin 11 activated STAT3-MYC signaling in glioblastoma cells. This signaling induced stem cell states that conferred enhanced tumorigenicity and resistance to the standard-of-care chemotherapy, temozolomide.
[Proceedings of the National Academy of Sciences of the United States of America]
Li, J., Kaneda, M. M., Ma, J., Li, M., Shepard, R. M., Patel, K., Koga, T., Sarver, A., Furnari, F., Xu, B., Dhawan, S., Ning, J., Zhu, H., Wu, A., You, G., Jiang, T., Venteicher, A. S., Rich, J. N., Glass, C. K., … Chen, C. C. (2021). PI3Kγ inhibition suppresses microglia/TAM accumulation in glioblastoma microenvironment to promote exceptional temozolomide response. Proceedings of the National Academy of Sciences, 118(16). https://doi.org/10.1073/pnas.2009290118 Cite
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HIF1α/HIF2α–Sox2/Klf4 Promotes the Malignant Progression of Glioblastoma via the EGFR–PI3K/AKT Signaling Pathway with Positive Feedback under Hypoxia

Scientists discovered that glioblastoma cells exhibited features indicative of malignant progression and were present in a hypoxic environment.
[Cell Death & Disease]
HIF1α/HIF2α–Sox2/Klf4 promotes the malignant progression of glioblastoma via the EGFR–PI3K/AKT signalling pathway with positive feedback under hypoxia | Cell Death & Disease. (n.d.). Retrieved March 24, 2021, from https://www.nature.com/articles/s41419-021-03598-8 Cite
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Cancer-Specific Loss of TERT Activation Sensitizes Glioblastoma to DNA Damage

The authors demonstrated increased binding of a specific GA binding protein B1L (GABPB1L)-isoform–containing complex to the mutant telomerase reverse transcriptase (TERT) promoter. They found that TERT promoter mutant glioblastoma cells, unlike wild-type cells, exhibited a critical near-term dependence on GABPB1L for proliferation.
[Proceedings of the National Academy of Sciences of the United States of America]
Amen, A. M., Fellmann, C., Soczek, K. M., Ren, S. M., Lew, R. J., Knott, G. J., Park, J. E., McKinney, A. M., Mancini, A., Doudna, J. A., & Costello, J. F. (2021). Cancer-specific loss of TERT activation sensitizes glioblastoma to DNA damage. Proceedings of the National Academy of Sciences, 118(13). https://doi.org/10.1073/pnas.2008772118 Cite
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Cyclin-Dependent Kinase Inhibitors Exert Distinct Effects on Patient-Derived 2D and 3D Glioblastoma Cell Culture Models

Investigators describe the antitumoral potential of selective cyclin-dependent kinase inhibitors on low-passage glioblastoma multiforme 2D- and 3D models, cultured as neurospheres or glioma stem-like cells.
[Cell Death Discovery]
Riess, C., Koczan, D., Schneider, B., Linke, C., del Moral, K., Classen, C. F., & Maletzki, C. (2021). Cyclin-dependent kinase inhibitors exert distinct effects on patient-derived 2D and 3D glioblastoma cell culture models. Cell Death Discovery, 7(1), 1–15. https://doi.org/10.1038/s41420-021-00423-1 Cite
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CDK1 Is Up-Regulated by Temozolomide in an NF-κB Dependent Manner in Glioblastoma

While cyclin-dependent kinase 1 (CDK1) phosphorylation is a well-described consequence of temozolomide (TMZ) treatment, researchers found that TMZ also robustly induced CDK1 expression.
[Scientific Reports]
Voce, D. J., Bernal, G. M., Cahill, K. E., Wu, L., Mansour, N., Crawley, C. D., Campbell, P.-A. S., Arina, A., Weichselbaum, R. R., & Yamini, B. (2021). CDK1 is up-regulated by temozolomide in an NF-κB dependent manner in glioblastoma. Scientific Reports, 11(1), 5665. https://doi.org/10.1038/s41598-021-84912-4 Cite
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Hsa_circ_0110757 Upregulates ITGA1 to Facilitate Temozolomide Resistance in Glioma by Suppressing Hsa-miR-1298-5p

The role of hsa_circ_0110757 in temozolomide (TMZ)-resistant glioma was evaluated both in vitro and in vivo. It was found that hsa_circ_0110757 and ITGA1 were more highly expressed in TMZ-resistant glioma than in TMZ-sensitive glioma.
[Cell Death & Disease]
Li, H., Liu, Q., Chen, Z., Wu, M., Zhang, C., Su, J., Li, Y., & Zhang, C. (2021). Hsa_circ_0110757 upregulates ITGA1 to facilitate temozolomide resistance in glioma by suppressing hsa-miR-1298-5p. Cell Death & Disease, 12(3), 1–12. https://doi.org/10.1038/s41419-021-03533-x Cite
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