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14 results on '"Hudson, Kadie"'

3. Focused ultrasound delivery of miR-142-3p for glioblastoma therapy

Author

Zhang, Ying, primary, Saha, Shekhar, additional, Dube, Collin, additional, Sun, Yunan, additional, Hudson, Kadie, additional, Klibanov, Alexander L, additional, Hanes, Justin, additional, Suk, Jung Soo, additional, Kwak, Gijung, additional, Mata, Jaime F, additional, and Abounader, Roger, additional

Published
2024
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4. CNSC-14. T-TYPE CALCIUM CHANNELS REGULATE NEURON-GLIOBLASTOMA INTERACTIONS AND PROMOTE TUMOR GROWTH

Author

Dube, Collin, primary, Zhang, Ying, additional, Saha, Shekhar, additional, Lai, Michelle, additional, Gibert, Myron, additional, Escalante, Miguel, additional, Hudson, Kadie, additional, Yener, Ulas, additional, Hanif, Farina, additional, Kefas, Benjamin, additional, Xu, Esther, additional, Sorot, Aditya, additional, Sontheimer, Harald, additional, and Abounader, Roger, additional

Published
2023
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5. CSIG-05. A FIRST COMPREHENSIVE ANALYSIS OF TRANSCRIBED ULTRA CONSERVED REGIONS UNCOVERS IMPORTANT REGULATORY FUNCTIONS OF NOVEL NON-CODING TRANSCRIPTS IN GLIOMAS

Author

Gibert, Myron, primary, Saha, Shekhar, additional, Zhang, Ying, additional, Marcinkiewicz, Pawel Pawel, additional, Chagari, Bilhan, additional, Roig-Laboy, Christian, additional, Sarkar, Aditya, additional, Dube, Collin, additional, Hudson, Kadie, additional, Sun, Yunan, additional, Kefas, Benjamin, additional, and Abounader, Roger, additional

Published
2023
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7. A first comprehensive analysis of Transcribed Ultra Conserved Regions uncovers important regulatory functions of novel non-coding transcripts in gliomas.

Author

Gibert, Myron K, primary, Zhang, Ying, additional, Saha, Shekhar, additional, Marcinkiewicz, Pawel, additional, Dube, Collin, additional, Hudson, Kadie, additional, Sun, Yunan, additional, Bednarek, Sylwia, additional, Chagari, Bilhan, additional, Sarkar, Aditya, additional, Roig-Laboy, Christian, additional, Neace, Natalie, additional, Saoud, Karim, additional, Setiady, Initha, additional, Hanif, Farina, additional, Kumar, Pankaj, additional, Kefas, Benjamin, additional, and Abounader, Roger, additional

Published
2023
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9. CNSC-11. T-TYPE CALCIUM CHANNELS DRIVE GLIOBLASTOMA GROWTH BY PROMOTING NEURONAL INTERACTIONS

Author

Dube, Collin, primary, Zhang, Ying, additional, Saha, Shekhar, additional, Lai, Michelle, additional, Gibert, Myron, additional, Escalante, Miguel, additional, Mulcahy, Elizabeth, additional, Ottolini, Matteo, additional, Hudson, Kadie, additional, Yener, Ulas, additional, Bednarek, Sylwia, additional, Hanif, Farina, additional, Xu, Esther, additional, Sorot, Aditya, additional, Sonkusare, Swapnil, additional, Sontheimer, Harald, additional, and Abounader, Roger, additional

Published
2022
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10. Transcribed Ultraconserved Regions in Cancer

Author

Gibert, Myron K., primary, Sarkar, Aditya, additional, Chagari, Bilhan, additional, Roig-Laboy, Christian, additional, Saha, Shekhar, additional, Bednarek, Sylwia, additional, Kefas, Benjamin, additional, Hanif, Farina, additional, Hudson, Kadie, additional, Dube, Collin, additional, Zhang, Ying, additional, and Abounader, Roger, additional

Published
2022
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12. Microenvironment T-Type calcium channels regulate neuronal and glial processes to promote glioblastoma growth.

Author

Dube CJ, Zhang Y, Saha S, Lai M, Gibert MK, Escalante M, Hudson K, Wong D, Marcinkiewicz P, Yener U, Sun Y, Xu E, Sorot A, Mulcahy E, Kefas B, Hanif F, Guessous F, Vernon A, Patel MK, Schiff D, Zong H, Purow B, Holland E, Sonkusare S, Sontheimer H, and Abounader R

Abstract

Background: Glioblastoma (GBM) is the most common primary malignant brain tumor. The aim of this study was to elucidate the role of microenvironment and intrinsic T-type calcium channels (Cav3) in regulating tumor growth and progression., Methods: We grafted syngeneic GBM cells into Cav3.2 knockout mice to assess the role of microenvironment T-Type calcium channels on GBM tumor growth. We performed single-cell RNA-seq (scRNA-seq) of tumors from WT and Cav3.2 KO mice to elucidate the regulation of tumors by the microenvironment. We used neurons from WT and Cav3.2 KO mice in co-culture with GBM stem cells (GSC) to assess the effects of Cav3.2 on neuron/GSC synaptic connections and tumor cell growth., Results: Cav3.2 KO in the microenvironment led to significant reduction of GBM growth and prolongation of animal survival. scRNA-seq showed that microenvironment Cav3.2 regulates neuronal and glial biological processes. Microenvironment Cav3.2 downregulated numerous genes associated with regulating the OPC cell state in GBM tumors such as SOX10 and Olig2. Neuronal Cav3.2 promoted neuron/GSC synaptic connections and GSC growth. Treatment of GSCs with the Cav3 blocker mibefradil downregulated genes associated with neuronal processes. The Cav3 blocker drug mibefradil synergized with temozolomide (TMZ) and radiation to reduce in vivo tumor growth and prolong animal survival., Conclusions: Together these data reveal a role for microenvironment Cav3 in promoting GBM tumor progression through regulating neuronal and glial processes particularly associated with the OPC-cell state. Targeting both intrinsic and microenvironment Cav3 with the inhibitor mibefradil significantly enhanced the anti-GBM effects of TMZ and radiation., Competing Interests: Conflict of Interest The authors have declared that no conflicts of interest exist

Published
2024
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13. A first comprehensive analysis of Transcribed Ultra Conserved Regions uncovers important regulatory functions of novel non-coding transcripts in gliomas.

Author

Gibert MK Jr, Zhang Y, Saha S, Marcinkiewicz P, Dube C, Hudson K, Sun Y, Bednarek S, Chagari B, Sarkar A, Roig-Laboy C, Neace N, Saoud K, Setiady I, Hanif F, Schiff D, Kumar P, Kefas B, Hafner M, and Abounader R

Abstract

Transcribed Ultra-Conserved Regions (TUCRs) represent a severely understudied class of putative non-coding RNAs (ncRNAs) that are 100% conserved across multiple species. We performed the first-ever analysis of TUCRs in glioblastoma (GBM) and low-grade gliomas (LGG). We leveraged large human datasets to identify the genomic locations, chromatin accessibility, transcription, differential expression, correlation with survival, and predicted functions of all 481 TUCRs, and identified TUCRs that are relevant to glioma biology. Of these, we investigated the expression, function, and mechanism of action of the most highly upregulated intergenic TUCR, uc.110, identifying it as a new oncogene. Uc.110 was highly overexpressed in GBM and LGG, where it promoted malignancy and tumor growth. Uc.110 activated the WNT pathway by upregulating the expression of membrane frizzled-related protein (MFRP), by sponging the tumor suppressor microRNA miR-544. This pioneering study shows important roles for TUCRs in gliomas and provides an extensive database and novel methods for future TUCR research., Competing Interests: Additional Declarations: There is NO Competing Interest.

Published
2024
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14. A first comprehensive analysis of Transcribed Ultra Conserved Regions uncovers important regulatory functions of novel non-coding transcripts in gliomas.

Author

Gibert MK, Zhang Y, Saha S, Marcinkiewicz P, Dube C, Hudson K, Sun Y, Bednarek S, Chagari B, Sarkar A, Roig-Laboy C, Neace N, Saoud K, Setiady I, Hanif F, Schiff D, Kumar P, Kefas B, Hafner M, and Abounader R

Abstract

Transcribed Ultra-Conserved Regions (TUCRs) represent a severely understudied class of putative non-coding RNAs (ncRNAs) that are 100% conserved across multiple species. We performed the first-ever analysis of TUCRs in glioblastoma (GBM) and low-grade gliomas (LGG). We leveraged large human datasets to identify the genomic locations, chromatin accessibility, transcription, differential expression, correlation with survival, and predicted functions of all 481 TUCRs, and identified TUCRs that are relevant to glioma biology. Of these, we investigated the expression, function, and mechanism of action of the most highly upregulated intergenic TUCR, uc.110, identifying it as a new oncogene. Uc.110 was highly overexpressed in GBM and LGG, where it promoted malignancy and tumor growth. Uc.110 activated the WNT pathway by upregulating the expression of membrane frizzled-related protein (MFRP), by sponging the tumor suppressor microRNA miR-544. This pioneering study shows important roles for TUCRs in gliomas and provides an extensive database and novel methods for future TUCR research.

Published
2024
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