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413 results on '"Balyasnikova, Irina V."'

3. Metixene is an incomplete autophagy inducer in preclinical models of metastatic cancer and brain metastases

Author

Fares, Jawad, Petrosyan, Edgar, Kanojia, Deepak, Dmello, Crismita, Cordero, Alex, Duffy, Joseph T., Yeeravalli, Ragini, Sahani, Mayurbhai H., Zhang, Peng, Rashidi, Aida, Arrieta, Victor A., Ulasov, Ilya, Ahmed, Atique U., Miska, Jason, Balyasnikova, Irina V., James, C. David, Sonabend, Adam M., Heimberger, Amy B., and Lesniak, Maciej S.

Subjects
Thermo Fisher Scientific Inc., Cell death -- Analysis, Scientific equipment and supplies industry -- Analysis, Temsirolimus -- Analysis, Metastasis -- Analysis, Phenothiazine -- Analysis, Drug approval -- Analysis, Cancer -- Analysis, Antiparkinsonian agents -- Analysis, Health care industry
Abstract

A paucity of chemotherapeutic options for metastatic brain cancer limits patient survival and portends poor clinical outcomes. Using a CNS small-molecule inhibitor library of 320 agents known to be blood-brain barrier permeable and approved by the FDA, we interrogated breast cancer brain metastasis vulnerabilities to identify an effective agent. Metixene, an antiparkinsonian drug, was identified as a top therapeutic agent that was capable of decreasing cellular viability and inducing cell death across different metastatic breast cancer subtypes. This agent significantly reduced mammary tumor size in orthotopic xenograft assays and improved survival in an intracardiac model of multiorgan site metastases. Metixene further extended survival in mice bearing intracranial xenografts and in an intracarotid mouse model of multiple brain metastases. Functional analysis revealed that metixene induced incomplete autophagy through N-Myc downstream regulated 1 (NDRG1) phosphorylation, thereby leading to caspase-mediated apoptosis in both primary and brain-metastatic cells, regardless of cancer subtype or origin. CRISPR/Cas9 KO of NDRG1 led to autophagy completion and reversal of the metixene apoptotic effect. Metixene is a promising therapeutic agent against metastatic brain cancer, with minimal reported side effects in humans, which merits consideration for clinical translation., Introduction Metastasis is a hallmark of cancer that remains a primary cause of cancer-related deaths (1). Brain metastases are the most common type of CNS malignancies. They often manifest with [...]

Published
2023
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4. Ribosomal protein S11 influences glioma response to TOP2 poisons

Author

Awah, Chidiebere U, Chen, Li, Bansal, Mukesh, Mahajan, Aayushi, Winter, Jan, Lad, Meeki, Warnke, Louisa, Gonzalez-Buendia, Edgar, Park, Cheol, Zhang, Daniel, Feldstein, Eric, Yu, Dou, Zannikou, Markella, Balyasnikova, Irina V, Martuscello, Regina, Konerman, Silvana, Győrffy, Balázs, Burdett, Kirsten B, Scholtens, Denise M, Stupp, Roger, Ahmed, Atique, Hsu, Patrick, and Sonabend, Adam M

Subjects
Brain Disorders, Biotechnology, Brain Cancer, Neurosciences, Cancer, Rare Diseases, Genetics, Apoptotic Protease-Activating Factor 1, Brain Neoplasms, CRISPR-Cas Systems, Cell Line, Tumor, DNA Breaks, Double-Stranded, DNA Repair, DNA Topoisomerases, Type II, Doxorubicin, Etoposide, Gene Knockout Techniques, Glioblastoma, Humans, Ribosomal Proteins, Topoisomerase II Inhibitors, Clinical Sciences, Oncology and Carcinogenesis, Oncology & Carcinogenesis
Abstract

Topoisomerase II poisons are one of the most common class of chemotherapeutics used in cancer. We and others had shown that a subset of glioblastomas, the most malignant of all primary brain tumors in adults, is responsive to TOP2 poisons. To identify genes that confer susceptibility to this drug in gliomas, we performed a genome-scale CRISPR knockout screen with etoposide. Genes involved in protein synthesis and DNA damage were implicated in etoposide susceptibility. To define potential biomarkers for TOP2 poisons, CRISPR hits were overlapped with genes whose expression correlates with susceptibility to this drug across glioma cell lines, revealing ribosomal protein subunit RPS11, 16, and 18 as putative biomarkers for response to TOP2 poisons. Loss of RPS11 led to resistance to etoposide and doxorubicin and impaired the induction of proapoptotic gene APAF1 following treatment. The expression of these ribosomal subunits was also associated with susceptibility to TOP2 poisons across cell lines from gliomas and multiple other cancers.

Published
2020

6. Pharmacologic modulation of nasal epithelium augments neural stem cell targeting of glioblastoma

Author

Spencer, Drew, Yu, Dou, Morshed, Ramin A, Li, Gina, Pituch, Katarzyna C, Gao, David X, Bertolino, Nicola, Procissi, Daniele, Lesniak, Maciej S, and Balyasnikova, Irina V

Subjects
Medical Biotechnology, Biomedical and Clinical Sciences, Oncology and Carcinogenesis, Cancer, Rare Diseases, Brain Cancer, Brain Disorders, Neurosciences, Bioengineering, Orphan Drug, Nanotechnology, Stem Cell Research, Biomedical Imaging, Genetics, Gene Therapy, Biotechnology, Development of treatments and therapeutic interventions, 5.1 Pharmaceuticals, 5.2 Cellular and gene therapies, Adenoviridae, Animals, Antineoplastic Agents, Brain Neoplasms, Cell Line, Cell Line, Tumor, Disease Models, Animal, Glioblastoma, Glioma, Humans, Magnetic Resonance Imaging, Male, Mice, Mice, Nude, Nasal Mucosa, Neural Stem Cells, Oncolytic Virotherapy, Oncolytic Viruses, Xenograft Model Antitumor Assays, neural stem cells, intranasal delivery, glioblastoma, clearance, barrier, Oncology and carcinogenesis
Abstract

Glioblastoma (GBM) remains the most lethal and untreatable central nervous system malignancy. The challenges to devise novel and effective anti-tumor therapies include difficulty in locating the precise tumor border for complete surgical resection, and rapid regrowth of residual tumor tissue after standard treatment. Repeatable and non-invasive intranasal application of neural stem cells (NSCs) was recently shown to enable clinically relevant delivery of therapy to tumors. Treatment with chemotactic NSCs demonstrated significant survival benefits when coupled with radiation and oncolytic virotherapy in preclinical models of GBM. In order to further augment the clinical applicability of this novel therapeutic platform, we postulate that the FDA-approved compound, methimazole (MT), can be safely utilized to delay the nasal clearance and improve the ability of NSCs to penetrate the olfactory epithelium for robust in vivo brain tumor targeting and therapeutic actions.MethodsTo examine the role of reversible reduction of the olfactory epithelial barrier in non-invasive intranasal delivery, we explored the unique pharmacologic effect of MT at a single dosage regimen. In our proof-of-concept studies, quantitative magnetic resonance imaging (MRI), immunocytochemistry, and survival analysis were performed on glioma-bearing mice treated with a single dose of MT prior to intranasal anti-GBM therapy using an oncolytic virus (OV)-loaded NSCs.ResultsBased on histology and in vivo imaging, we found that disrupting the olfactory epithelium with MT effectively delays clearance and allows NSCs to persist in the nasal cavity for at least 24 h. MT pretreatment amplified the migration of NSCs to the tumor. The therapeutic advantage of this enhancement was quantitatively validated by tissue analysis and MRI tracking of NSCs loaded with superparamagnetic iron oxide nanoparticles (SPIOs) in live animals. Moreover, we observed significant survival benefits in GBM-bearing mice treated with intranasal delivery of oncolytic virus-loaded NSCs following MT injection.ConclusionOur work identified a novel pharmacologic strategy to accelerate the clinical application of the non-invasive NSCs-based therapeutic platform to tackle aggressive brain tumors.

Published
2019

9. Neural stem cell delivery of an oncolytic adenovirus in newly diagnosed malignant glioma: a first-in-human, phase 1, dose-escalation trial

Author

Fares, Jawad, Ahmed, Atique U, Ulasov, Ilya V, Sonabend, Adam M, Miska, Jason, Lee-Chang, Catalina, Balyasnikova, Irina V, Chandler, James P, Portnow, Jana, Tate, Matthew C, Kumthekar, Priya, Lukas, Rimas V, Grimm, Sean A, Adams, Ann K, Hébert, Charles D, Strong, Theresa V, Amidei, Christina, Arrieta, Victor A, Zannikou, Markella, Horbinski, Craig, Zhang, Hui, Burdett, Kirsten Bell, Curiel, David T, Sachdev, Sean, Aboody, Karen S, Stupp, Roger, and Lesniak, Maciej S

Published
2021
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11. Mechanisms and Barriers in Nanomedicine: Progress in the Field and Future Directions.

Author

Anchordoquy, Thomas, Artzi, Natalie, Balyasnikova, Irina V., Barenholz, Yechezkel, La-Beck, Ninh M., Brenner, Jacob S., Chan, Warren C. W., Decuzzi, Paolo, Exner, Agata A., Gabizon, Alberto, Godin, Biana, Lai, Samuel K., Lammers, Twan, Mitchell, Michael J., Moghimi, S. Moein, Muzykantov, Vladimir R., Peer, Dan, Nguyen, Juliane, Popovtzer, Rachela, and Ricco, Madison

Published
2024
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13. In vitro vascular differentiation system efficiently produces natural killer cells for cancer immunotherapies

Author

Galat, Yekaterina, primary, Du, Yuchen, additional, Perepitchka, Mariana, additional, Li, Xiao-Nan, additional, Balyasnikova, Irina V, additional, Tse, William T, additional, Dambaeva, Svetlana, additional, Schneiderman, Sylvia, additional, Iannaccone, Philip M, additional, Becher, Oren, additional, Graham, Douglas K, additional, and Galat, Vasiliy, additional

Published
2023
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17. Cytokine Modification of Adoptive Chimeric Antigen Receptor Immunotherapy for Glioblastoma.

Author

Pawlowski, Kristen D., Duffy, Joseph T., Gottschalk, Stephen, and Balyasnikova, Irina V.

Subjects
CYTOKINES, DRUG efficacy, GENOME editing, CHIMERISM, GLIOMAS, CELL receptors, DRUG design, CELLULAR signal transduction, TUMOR antigens, T cells, IMMUNOTHERAPY, ONCOLYTIC virotherapy
Abstract

Simple Summary: Chimeric antigen receptor (CAR) cell-based therapy is a promising treatment approach for glioblastoma, a fatal brain cancer with limited treatment options. Efforts to improve these therapies are currently underway, with one method being cytokine modification. Cytokines are a type of protein created by cells in the body that can change the function of immune cells. In this review, the authors summarize approaches that employ cytokines to improve CAR cell therapies. These include coadministering CAR T-cells or CAR NK-cells with cytokines, antibodies, or oncolytic viruses or via engineering CAR cell therapies to secrete or express cytokines, express a cytokine receptor, or genetically alter cytokine signaling pathways. We hope that providing cytokine support to CAR cell-based therapies will improve their efficacy for patients with glioblastoma. Chimeric antigen receptor (CAR) cell-based therapies have demonstrated limited success in solid tumors, including glioblastoma (GBM). GBMs exhibit high heterogeneity and create an immunosuppressive tumor microenvironment (TME). In addition, other challenges exist for CAR therapy, including trafficking and infiltration into the tumor site, proliferation, persistence of CARs once in the tumor, and reduced functionality, such as suboptimal cytokine production. Cytokine modification is of interest, as one can enhance therapy efficacy and minimize off-target toxicity by directly combining CAR therapy with cytokines, antibodies, or oncolytic viruses that alter cytokine response pathways. Alternatively, one can genetically modify CAR T-cells or CAR NK-cells to secrete cytokines or express cytokines or cytokine receptors. Finally, CARs can be genetically altered to augment or suppress intracellular cytokine signaling pathways for a more direct approach. Codelivery of cytokines with CARs is the most straightforward method, but it has associated toxicity. Alternatively, combining CAR therapy with antibodies (e.g., anti-IL-6, anti-PD1, and anti-VEGF) or oncolytic viruses has enhanced CAR cell infiltration into GBM tumors and provided proinflammatory signals to the TME. CAR T- or NK-cells secreting cytokines (e.g., IL-12, IL-15, and IL-18) have shown improved efficacy within multiple GBM subtypes. Likewise, expressing cytokine-modulating receptors in CAR cells that promote or inhibit cytokine signaling has enhanced their activity. Finally, gene editing approaches are actively being pursued to directly influence immune signaling pathways in CAR cells. In this review, we summarize these cytokine modification methods and highlight any existing gaps in the hope of catalyzing an improved generation of CAR-based therapies for glioblastoma. [ABSTRACT FROM AUTHOR]

Published
2023
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19. Data from Myeloid-Derived Suppressive Cells Promote B cell–Mediated Immunosuppression via Transfer of PD-L1 in Glioblastoma

Author

Lee-Chang, Catalina, primary, Rashidi, Aida, primary, Miska, Jason, primary, Zhang, Peng, primary, Pituch, Katarzyna C., primary, Hou, David, primary, Xiao, Ting, primary, Fischietti, Mariafausta, primary, Kang, Seong Jae, primary, Appin, Christina L., primary, Horbinski, Craig, primary, Platanias, Leonidas C., primary, Lopez-Rosas, Aurora, primary, Han, Yu, primary, Balyasnikova, Irina V., primary, and Lesniak, Maciej S., primary

Published
2023
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20. Supplementary Figures from Myeloid-Derived Suppressive Cells Promote B cell–Mediated Immunosuppression via Transfer of PD-L1 in Glioblastoma

Author

Lee-Chang, Catalina, primary, Rashidi, Aida, primary, Miska, Jason, primary, Zhang, Peng, primary, Pituch, Katarzyna C., primary, Hou, David, primary, Xiao, Ting, primary, Fischietti, Mariafausta, primary, Kang, Seong Jae, primary, Appin, Christina L., primary, Horbinski, Craig, primary, Platanias, Leonidas C., primary, Lopez-Rosas, Aurora, primary, Han, Yu, primary, Balyasnikova, Irina V., primary, and Lesniak, Maciej S., primary

Published
2023
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21. Supplementary Tables and Figure Legends from Myeloid-Derived Suppressive Cells Promote B cell–Mediated Immunosuppression via Transfer of PD-L1 in Glioblastoma

Author

Lee-Chang, Catalina, primary, Rashidi, Aida, primary, Miska, Jason, primary, Zhang, Peng, primary, Pituch, Katarzyna C., primary, Hou, David, primary, Xiao, Ting, primary, Fischietti, Mariafausta, primary, Kang, Seong Jae, primary, Appin, Christina L., primary, Horbinski, Craig, primary, Platanias, Leonidas C., primary, Lopez-Rosas, Aurora, primary, Han, Yu, primary, Balyasnikova, Irina V., primary, and Lesniak, Maciej S., primary

Published
2023
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30. Supplementary Figure 2 from Durable Therapeutic Efficacy Utilizing Combinatorial Blockade against IDO, CTLA-4, and PD-L1 in Mice with Brain Tumors

Author

Wainwright, Derek A., primary, Chang, Alan L., primary, Dey, Mahua, primary, Balyasnikova, Irina V., primary, Kim, Chung Kwon, primary, Tobias, Alex, primary, Cheng, Yu, primary, Kim, Julius W., primary, Qiao, Jian, primary, Zhang, Lingjiao, primary, Han, Yu, primary, and Lesniak, Maciej S., primary

Published
2023
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31. Supplementary Materials and Methods from Durable Therapeutic Efficacy Utilizing Combinatorial Blockade against IDO, CTLA-4, and PD-L1 in Mice with Brain Tumors

Author

Wainwright, Derek A., primary, Chang, Alan L., primary, Dey, Mahua, primary, Balyasnikova, Irina V., primary, Kim, Chung Kwon, primary, Tobias, Alex, primary, Cheng, Yu, primary, Kim, Julius W., primary, Qiao, Jian, primary, Zhang, Lingjiao, primary, Han, Yu, primary, and Lesniak, Maciej S., primary

Published
2023
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37. Supplementary Data from Mesenchymal Stem Cells Successfully Deliver Oncolytic Virotherapy to Diffuse Intrinsic Pontine Glioma

Author

Chastkofsky, Michael I., primary, Pituch, Katarzyna C., primary, Katagi, Hiroaki, primary, Zannikou, Markella, primary, Ilut, Liliana, primary, Xiao, Ting, primary, Han, Yu, primary, Sonabend, Adam M., primary, Curiel, David T., primary, Bonner, Erin R., primary, Nazarian, Javad, primary, Horbinski, Craig M., primary, James, C. David, primary, Saratsis, Amanda M., primary, Hashizume, Rintaro, primary, Lesniak, Maciej S., primary, and Balyasnikova, Irina V., primary

Published
2023
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38. Supplementary Figure Legends from Durable Therapeutic Efficacy Utilizing Combinatorial Blockade against IDO, CTLA-4, and PD-L1 in Mice with Brain Tumors

Author

Wainwright, Derek A., primary, Chang, Alan L., primary, Dey, Mahua, primary, Balyasnikova, Irina V., primary, Kim, Chung Kwon, primary, Tobias, Alex, primary, Cheng, Yu, primary, Kim, Julius W., primary, Qiao, Jian, primary, Zhang, Lingjiao, primary, Han, Yu, primary, and Lesniak, Maciej S., primary

Published
2023
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39. Supplementary Figure 1 from Durable Therapeutic Efficacy Utilizing Combinatorial Blockade against IDO, CTLA-4, and PD-L1 in Mice with Brain Tumors

Author

Wainwright, Derek A., primary, Chang, Alan L., primary, Dey, Mahua, primary, Balyasnikova, Irina V., primary, Kim, Chung Kwon, primary, Tobias, Alex, primary, Cheng, Yu, primary, Kim, Julius W., primary, Qiao, Jian, primary, Zhang, Lingjiao, primary, Han, Yu, primary, and Lesniak, Maciej S., primary

Published
2023
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43. Supplementary figure 4 from Decoy Receptor DcR1 Is Induced in a p50/Bcl3–Dependent Manner and Attenuates the Efficacy of Temozolomide

Author

Mansour, Nassir M., primary, Bernal, Giovanna M., primary, Wu, Longtao, primary, Crawley, Clayton D., primary, Cahill, Kirk E., primary, Voce, David J., primary, Balyasnikova, Irina V., primary, Zhang, Wei, primary, Spretz, Ruben, primary, Nunez, Luis, primary, Larsen, Gustavo F., primary, Weichselbaum, Ralph R., primary, and Yamini, Bakhtiar, primary

Published
2023
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44. Data from Decoy Receptor DcR1 Is Induced in a p50/Bcl3–Dependent Manner and Attenuates the Efficacy of Temozolomide

Author

Mansour, Nassir M., primary, Bernal, Giovanna M., primary, Wu, Longtao, primary, Crawley, Clayton D., primary, Cahill, Kirk E., primary, Voce, David J., primary, Balyasnikova, Irina V., primary, Zhang, Wei, primary, Spretz, Ruben, primary, Nunez, Luis, primary, Larsen, Gustavo F., primary, Weichselbaum, Ralph R., primary, and Yamini, Bakhtiar, primary

Published
2023
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45. Supplementary figure 2 from Decoy Receptor DcR1 Is Induced in a p50/Bcl3–Dependent Manner and Attenuates the Efficacy of Temozolomide

Author

Mansour, Nassir M., primary, Bernal, Giovanna M., primary, Wu, Longtao, primary, Crawley, Clayton D., primary, Cahill, Kirk E., primary, Voce, David J., primary, Balyasnikova, Irina V., primary, Zhang, Wei, primary, Spretz, Ruben, primary, Nunez, Luis, primary, Larsen, Gustavo F., primary, Weichselbaum, Ralph R., primary, and Yamini, Bakhtiar, primary

Published
2023
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47. Supplementary Data Legends from Decoy Receptor DcR1 Is Induced in a p50/Bcl3–Dependent Manner and Attenuates the Efficacy of Temozolomide

Author

Mansour, Nassir M., primary, Bernal, Giovanna M., primary, Wu, Longtao, primary, Crawley, Clayton D., primary, Cahill, Kirk E., primary, Voce, David J., primary, Balyasnikova, Irina V., primary, Zhang, Wei, primary, Spretz, Ruben, primary, Nunez, Luis, primary, Larsen, Gustavo F., primary, Weichselbaum, Ralph R., primary, and Yamini, Bakhtiar, primary

Published
2023
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48. Supplementary figure 1Figure S1 from Decoy Receptor DcR1 Is Induced in a p50/Bcl3–Dependent Manner and Attenuates the Efficacy of Temozolomide

Author

Mansour, Nassir M., primary, Bernal, Giovanna M., primary, Wu, Longtao, primary, Crawley, Clayton D., primary, Cahill, Kirk E., primary, Voce, David J., primary, Balyasnikova, Irina V., primary, Zhang, Wei, primary, Spretz, Ruben, primary, Nunez, Luis, primary, Larsen, Gustavo F., primary, Weichselbaum, Ralph R., primary, and Yamini, Bakhtiar, primary

Published
2023
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49. Supplementary figure 5 from Decoy Receptor DcR1 Is Induced in a p50/Bcl3–Dependent Manner and Attenuates the Efficacy of Temozolomide

Author

Mansour, Nassir M., primary, Bernal, Giovanna M., primary, Wu, Longtao, primary, Crawley, Clayton D., primary, Cahill, Kirk E., primary, Voce, David J., primary, Balyasnikova, Irina V., primary, Zhang, Wei, primary, Spretz, Ruben, primary, Nunez, Luis, primary, Larsen, Gustavo F., primary, Weichselbaum, Ralph R., primary, and Yamini, Bakhtiar, primary

Published
2023
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50. Supplementary figure 3 from Decoy Receptor DcR1 Is Induced in a p50/Bcl3–Dependent Manner and Attenuates the Efficacy of Temozolomide

Author

Mansour, Nassir M., primary, Bernal, Giovanna M., primary, Wu, Longtao, primary, Crawley, Clayton D., primary, Cahill, Kirk E., primary, Voce, David J., primary, Balyasnikova, Irina V., primary, Zhang, Wei, primary, Spretz, Ruben, primary, Nunez, Luis, primary, Larsen, Gustavo F., primary, Weichselbaum, Ralph R., primary, and Yamini, Bakhtiar, primary

Published
2023
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