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183 results on '"Hodgson, J. Graeme"'

2. Expression of miR-124 inhibits growth of medulloblastoma cells.

Author

Silber, Joachim, Hashizume, Rintaro, Felix, Tristan, Hariono, Sujatmi, Yu, Mamie, Berger, Mitchel S, Huse, Jason T, VandenBerg, Scott R, James, C David, Hodgson, J Graeme, and Gupta, Nalin

Subjects
Cell Line, Tumor, Animals, Mice, Inbred BALB C, Humans, Mice, Mice, Nude, Medulloblastoma, Cerebellar Neoplasms, MicroRNAs, RNA, Messenger, Blotting, Western, Immunoenzyme Techniques, Flow Cytometry, Reverse Transcriptase Polymerase Chain Reaction, Cell Cycle, Apoptosis, Cell Proliferation, Gene Expression Regulation, Neoplastic, Female, Real-Time Polymerase Chain Reaction, CDK6, D425, medulloblastoma, microRNA, miR-124, Cell Line, Tumor, Inbred BALB C, Nude, RNA, Messenger, Blotting, Western, Gene Expression Regulation, Neoplastic, Oncology & Carcinogenesis, Neurosciences, Oncology and Carcinogenesis
Abstract

Medulloblastoma is the most common malignant brain tumor in children, and a substantial number of patients die as a result of tumor progression. Overexpression of CDK6 is present in approximately one-third of medulloblastomas and is an independent poor prognostic marker for this disease. MicroRNA (miR)-124 inhibits expression of CDK6 and prevents proliferation of glioblastoma and medulloblastoma cells in vitro. We examined the effects of miR-124 overexpression on medulloblastoma cells both in vitro and in vivo and compared cell lines that have low and high CDK6 expression. MiR-124 overexpression inhibits the proliferation of medulloblastoma cells, and this effect is mediated mostly through the action of miR-124 upon CDK6. We further show that induced expression of miR-124 potently inhibits growth of medulloblastoma xenograft tumors in rodents. Further testing of miR-124 will help define the ultimate therapeutic potential of preclinical models of medulloblastoma in conjunction with various delivery strategies for treatment.

Published
2013

3. Increased Microglia/Macrophage Gene Expression in a Subset of Adult and Pediatric Astrocytomas

Author

Engler, Jane R, Robinson, Aaron E, Smirnov, Ivan, Hodgson, J Graeme, Berger, Mitchel S, Gupta, Nalin, James, C David, Molinaro, Annette, and Phillips, Joanna J

Subjects
Biomedical and Clinical Sciences, Oncology and Carcinogenesis, Immunology, Cancer, Brain Cancer, Cancer Genomics, Human Genome, Brain Disorders, Genetics, Neurosciences, Rare Diseases, 2.1 Biological and endogenous factors, Adolescent, Astrocytoma, Female, Glioblastoma, Humans, In Vitro Techniques, Macrophages, Male, Microglia, General Science & Technology
Abstract

Glioblastoma (GBM) is a highly malignant brain tumor with a dismal prognosis. Gene expression profiling of GBM has revealed clinically relevant tumor subtypes, and this provides exciting opportunities to better understand disease pathogenesis. Results from an increasing number of studies demonstrate a role for the immune response in cancer progression, yet it is unclear how the immune response differs across tumor subtypes and how it affects outcome. Utilizing gene expression data from The Cancer Genome Atlas Project and the Gene Expression Omnibus database, we demonstrate an enrichment of immune response-related gene expression in the mesenchymal subtype of adult GBM (n = 173) and pediatric high-grade gliomas (n = 53). In an independent cohort of pediatric astrocytomas (n = 24) from UCSF, we stratified tumors into subtypes and confirmed these findings. Using novel immune cell-specific gene signatures we demonstrate selective enrichment of microglia/macrophage-related genes in adult and pediatric GBM tumors of the mesenchymal subtype. Furthermore, immunostaining of adult GBM tumors showed significantly higher cell numbers of microglia/macrophages in mesenchymal versus non-mesenchymal tumors (p = 0.04). Interestingly, adult GBM tumors with the shortest survival had significant enrichment of microglia/macrophage-related genes but this was not true for pediatric GBMs. Consistent with an association with poor outcome, immune response-related genes were highly represented in an adult poor prognosis gene signature, with the expression of genes related to macrophage recruitment and activation being most strongly associated with survival (p

Published
2012

6. miR-124 and miR-137 inhibit proliferation of glioblastoma multiforme cells and induce differentiation of brain tumor stem cells

Author

Silber, Joachim, Lim, Daniel A, Petritsch, Claudia, Persson, Anders I, Maunakea, Alika K, Yu, Mamie, Vandenberg, Scott R, Ginzinger, David G, James, C David, Costello, Joseph F, Bergers, Gabriele, Weiss, William A, Alvarez-Buylla, Arturo, and Hodgson, J Graeme

Subjects
Biomedical and Clinical Sciences, Oncology and Carcinogenesis, Biotechnology, Stem Cell Research - Nonembryonic - Non-Human, Cancer, Genetics, Brain Disorders, Rare Diseases, Stem Cell Research - Nonembryonic - Human, Orphan Drug, Stem Cell Research, Neurosciences, Brain Cancer, 1.1 Normal biological development and functioning, 2.1 Biological and endogenous factors, Animals, Brain Neoplasms, Cell Cycle, Cell Differentiation, Down-Regulation, Gene Expression, Glioblastoma, Humans, Mice, MicroRNAs, Neoplastic Stem Cells, Neurons, Oligodendroglioma, Transfection, Tumor Cells, Cultured, Up-Regulation, Medical and Health Sciences, General & Internal Medicine, Biomedical and clinical sciences, Health sciences
Abstract

BackgroundGlioblastoma multiforme (GBM) is an invariably fatal central nervous system tumor despite treatment with surgery, radiation, and chemotherapy. Further insights into the molecular and cellular mechanisms that drive GBM formation are required to improve patient outcome. MicroRNAs are emerging as important regulators of cellular differentiation and proliferation, and have been implicated in the etiology of a variety of cancers, yet the role of microRNAs in GBM remains poorly understood. In this study, we investigated the role of microRNAs in regulating the differentiation and proliferation of neural stem cells and glioblastoma-multiforme tumor cells.MethodsWe used quantitative RT-PCR to assess microRNA expression in high-grade astrocytomas and adult mouse neural stem cells. To assess the function of candidate microRNAs in high-grade astrocytomas, we transfected miR mimics to cultured-mouse neural stem cells, -mouse oligodendroglioma-derived stem cells, -human glioblastoma multiforme-derived stem cells and -glioblastoma multiforme cell lines. Cellular differentiation was assessed by immunostaining, and cellular proliferation was determined using fluorescence-activated cell sorting.ResultsOur studies revealed that expression levels of microRNA-124 and microRNA-137 were significantly decreased in anaplastic astrocytomas (World Health Organization grade III) and glioblastoma multiforme (World Health Organization grade IV) relative to non-neoplastic brain tissue (P < 0.01), and were increased 8- to 20-fold during differentiation of cultured mouse neural stem cells following growth factor withdrawal. Expression of microRNA-137 was increased 3- to 12-fold in glioblastoma multiforme cell lines U87 and U251 following inhibition of DNA methylation with 5-aza-2'-deoxycytidine (5-aza-dC). Transfection of microRNA-124 or microRNA-137 induced morphological changes and marker expressions consistent with neuronal differentiation in mouse neural stem cells, mouse oligodendroglioma-derived stem cells derived from S100 beta-v-erbB tumors and cluster of differentiation 133+ human glioblastoma multiforme-derived stem cells (SF6969). Transfection of microRNA-124 or microRNA-137 also induced G1 cell cycle arrest in U251 and SF6969 glioblastoma multiforme cells, which was associated with decreased expression of cyclin-dependent kinase 6 and phosphorylated retinoblastoma (pSer 807/811) proteins.ConclusionmicroRNA-124 and microRNA-137 induce differentiation of adult mouse neural stem cells, mouse oligodendroglioma-derived stem cells and human glioblastoma multiforme-derived stem cells and induce glioblastoma multiforme cell cycle arrest. These results suggest that targeted delivery of microRNA-124 and/or microRNA-137 to glioblastoma multiforme tumor cells may be therapeutically efficacious for the treatment of this disease.

Published
2008

7. Mammary carcinoma behavior is programmed in the precancer stem cell

Author

Damonte, Patrizia, Hodgson, J Graeme, Chen, Jane Qian, Young, Lawrence JT, Cardiff, Robert D, and Borowsky, Alexander D

Subjects
Biomedical and Clinical Sciences, Oncology and Carcinogenesis, Breast Cancer, Human Genome, Cancer, Biotechnology, Cancer Genomics, Women's Health, Stem Cell Research, Genetics, Animals, Cell Line, Tumor, Disease Progression, Lung Neoplasms, Mammary Neoplasms, Animal, Mice, Microsatellite Repeats, Neoplasm Metastasis, Neoplasm Transplantation, Neoplastic Stem Cells, Nucleic Acid Hybridization, Phenotype, Polymerase Chain Reaction, Precancerous Conditions, Telomerase, Oncology & Carcinogenesis, Oncology and carcinogenesis
Abstract

IntroductionThe 'MINO' (mammary intraepithelial neoplasia outgrowth) mouse model of ductal carcinoma in situ (DCIS) consists of six lines with distinct morphologic phenotypes and behavior, each meeting experimentally defined criteria for 'precancer'. Specifically, these lines grow orthotopically in cleared mammary fat pads and consistently progress to an invasive phenotype that is capable of ectopic growth. Transition to carcinoma has a consistent latency for each line, and three of the lines also exhibit pulmonary metastatic potential.MethodsGland cleared orthotopic transplanted precancer MINO tissues were analyzed by bacterial artifical chromosome and oligo array comparative genomic hybridization, microsatellite PCR, and telomerase repeat amplification assay. MINO cells were dissociated and cultured in three dimensional culture and transplanted in syngeneic gland cleared mammary fat pads.ResultsComparative genomic hybridization shows that the precancer and invasive tumors are genetically stable, with low level changes including whole chromosome gains in some lines. No changes are associated with progression, although spontaneous focal amplifications and deletions were detected occasionally. Microsatellite analysis shows a low frequency of alterations that are predominantly permanent within a MINO line. Telomerase activity is increased in both the MINO and the derived tumors when compared with normal mouse mammary gland. Dissociation of the precancer lesion cells and three dimensional 'spheroid' culture of single cells reveals a bipotential for myoepithelial and luminal differentiation and the formation of unique three-dimensional 'MINOspheres'. These MINOspheres exhibit features that are intermediate between spheroids that are derived from normal and carcinoma cells. Transplantation of a single cell derived MINOsphere recapitulates the outgrowth of the precancer morphology and progression to carcinoma.ConclusionThese data establish a precancer 'stem' cell that is capable of self-renewal and multilineage differentiation as the origin of invasive cancer. Within the context of this model, these cells have programmed potential for latency and metastasis that does not appear to require sequential genetic 'hits' for transformation.

Published
2008

10. Compound mutations in BCR-ABL1 are not major drivers of primary or secondary resistance to ponatinib in CP-CML patients

Author

Deininger, Michael W., Hodgson, J. Graeme, Shah, Neil P., Cortes, Jorge E., Kim, Dong-Wook, Nicolini, Franck E., Talpaz, Moshe, Baccarani, Michele, Müller, Martin C., Li, Jin, Parker, Wendy T., Lustgarten, Stephanie, Clackson, Tim, Haluska, Frank G., Guilhot, Francois, Kantarjian, Hagop M., Soverini, Simona, Hochhaus, Andreas, Hughes, Timothy P., Rivera, Victor M., and Branford, Susan

Published
2016
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11. Supplementary Figure 1 from Targeted Therapy for BRAFV600E Malignant Astrocytoma

Author

Nicolaides, Theodore P., primary, Li, Huifang, primary, Solomon, David A., primary, Hariono, Sujatmi, primary, Hashizume, Rintaro, primary, Barkovich, Krister, primary, Baker, Suzanne J., primary, Paugh, Barbara S., primary, Jones, Chris, primary, Forshew, Tim, primary, Hindley, Guy F., primary, Hodgson, J. Graeme, primary, Kim, Jung-Sik, primary, Rowitch, David H., primary, Weiss, William A., primary, Waldman, Todd A., primary, and James, C. David, primary

Published
2023
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12. Supplementary Figure 9 from Targeted Therapy for BRAFV600E Malignant Astrocytoma

Author

Nicolaides, Theodore P., primary, Li, Huifang, primary, Solomon, David A., primary, Hariono, Sujatmi, primary, Hashizume, Rintaro, primary, Barkovich, Krister, primary, Baker, Suzanne J., primary, Paugh, Barbara S., primary, Jones, Chris, primary, Forshew, Tim, primary, Hindley, Guy F., primary, Hodgson, J. Graeme, primary, Kim, Jung-Sik, primary, Rowitch, David H., primary, Weiss, William A., primary, Waldman, Todd A., primary, and James, C. David, primary

Published
2023
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13. Supplementary Table 1 from Targeted Therapy for BRAFV600E Malignant Astrocytoma

Author

Nicolaides, Theodore P., primary, Li, Huifang, primary, Solomon, David A., primary, Hariono, Sujatmi, primary, Hashizume, Rintaro, primary, Barkovich, Krister, primary, Baker, Suzanne J., primary, Paugh, Barbara S., primary, Jones, Chris, primary, Forshew, Tim, primary, Hindley, Guy F., primary, Hodgson, J. Graeme, primary, Kim, Jung-Sik, primary, Rowitch, David H., primary, Weiss, William A., primary, Waldman, Todd A., primary, and James, C. David, primary

Published
2023
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14. Supplementary Figure 2 from Targeted Therapy for BRAFV600E Malignant Astrocytoma

Author

Nicolaides, Theodore P., primary, Li, Huifang, primary, Solomon, David A., primary, Hariono, Sujatmi, primary, Hashizume, Rintaro, primary, Barkovich, Krister, primary, Baker, Suzanne J., primary, Paugh, Barbara S., primary, Jones, Chris, primary, Forshew, Tim, primary, Hindley, Guy F., primary, Hodgson, J. Graeme, primary, Kim, Jung-Sik, primary, Rowitch, David H., primary, Weiss, William A., primary, Waldman, Todd A., primary, and James, C. David, primary

Published
2023
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15. Supplementary Figure 7 from Targeted Therapy for BRAFV600E Malignant Astrocytoma

Author

Nicolaides, Theodore P., primary, Li, Huifang, primary, Solomon, David A., primary, Hariono, Sujatmi, primary, Hashizume, Rintaro, primary, Barkovich, Krister, primary, Baker, Suzanne J., primary, Paugh, Barbara S., primary, Jones, Chris, primary, Forshew, Tim, primary, Hindley, Guy F., primary, Hodgson, J. Graeme, primary, Kim, Jung-Sik, primary, Rowitch, David H., primary, Weiss, William A., primary, Waldman, Todd A., primary, and James, C. David, primary

Published
2023
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16. Supplementary Figure 6 from Targeted Therapy for BRAFV600E Malignant Astrocytoma

Author

Nicolaides, Theodore P., primary, Li, Huifang, primary, Solomon, David A., primary, Hariono, Sujatmi, primary, Hashizume, Rintaro, primary, Barkovich, Krister, primary, Baker, Suzanne J., primary, Paugh, Barbara S., primary, Jones, Chris, primary, Forshew, Tim, primary, Hindley, Guy F., primary, Hodgson, J. Graeme, primary, Kim, Jung-Sik, primary, Rowitch, David H., primary, Weiss, William A., primary, Waldman, Todd A., primary, and James, C. David, primary

Published
2023
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17. Supplementary Figure 3 from Targeted Therapy for BRAFV600E Malignant Astrocytoma

Author

Nicolaides, Theodore P., primary, Li, Huifang, primary, Solomon, David A., primary, Hariono, Sujatmi, primary, Hashizume, Rintaro, primary, Barkovich, Krister, primary, Baker, Suzanne J., primary, Paugh, Barbara S., primary, Jones, Chris, primary, Forshew, Tim, primary, Hindley, Guy F., primary, Hodgson, J. Graeme, primary, Kim, Jung-Sik, primary, Rowitch, David H., primary, Weiss, William A., primary, Waldman, Todd A., primary, and James, C. David, primary

Published
2023
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18. Supplementary Figure 8 from Targeted Therapy for BRAFV600E Malignant Astrocytoma

Author

Nicolaides, Theodore P., primary, Li, Huifang, primary, Solomon, David A., primary, Hariono, Sujatmi, primary, Hashizume, Rintaro, primary, Barkovich, Krister, primary, Baker, Suzanne J., primary, Paugh, Barbara S., primary, Jones, Chris, primary, Forshew, Tim, primary, Hindley, Guy F., primary, Hodgson, J. Graeme, primary, Kim, Jung-Sik, primary, Rowitch, David H., primary, Weiss, William A., primary, Waldman, Todd A., primary, and James, C. David, primary

Published
2023
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19. Supplementary Table 2 from Targeted Therapy for BRAFV600E Malignant Astrocytoma

Author

Nicolaides, Theodore P., primary, Li, Huifang, primary, Solomon, David A., primary, Hariono, Sujatmi, primary, Hashizume, Rintaro, primary, Barkovich, Krister, primary, Baker, Suzanne J., primary, Paugh, Barbara S., primary, Jones, Chris, primary, Forshew, Tim, primary, Hindley, Guy F., primary, Hodgson, J. Graeme, primary, Kim, Jung-Sik, primary, Rowitch, David H., primary, Weiss, William A., primary, Waldman, Todd A., primary, and James, C. David, primary

Published
2023
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20. Supplementary Table 4 from Targeted Therapy for BRAFV600E Malignant Astrocytoma

Author

Nicolaides, Theodore P., primary, Li, Huifang, primary, Solomon, David A., primary, Hariono, Sujatmi, primary, Hashizume, Rintaro, primary, Barkovich, Krister, primary, Baker, Suzanne J., primary, Paugh, Barbara S., primary, Jones, Chris, primary, Forshew, Tim, primary, Hindley, Guy F., primary, Hodgson, J. Graeme, primary, Kim, Jung-Sik, primary, Rowitch, David H., primary, Weiss, William A., primary, Waldman, Todd A., primary, and James, C. David, primary

Published
2023
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21. Supplementary Figure 4 from Targeted Therapy for BRAFV600E Malignant Astrocytoma

Author

Nicolaides, Theodore P., primary, Li, Huifang, primary, Solomon, David A., primary, Hariono, Sujatmi, primary, Hashizume, Rintaro, primary, Barkovich, Krister, primary, Baker, Suzanne J., primary, Paugh, Barbara S., primary, Jones, Chris, primary, Forshew, Tim, primary, Hindley, Guy F., primary, Hodgson, J. Graeme, primary, Kim, Jung-Sik, primary, Rowitch, David H., primary, Weiss, William A., primary, Waldman, Todd A., primary, and James, C. David, primary

Published
2023
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22. Supplementary Figure 5 from Targeted Therapy for BRAFV600E Malignant Astrocytoma

Author

Nicolaides, Theodore P., primary, Li, Huifang, primary, Solomon, David A., primary, Hariono, Sujatmi, primary, Hashizume, Rintaro, primary, Barkovich, Krister, primary, Baker, Suzanne J., primary, Paugh, Barbara S., primary, Jones, Chris, primary, Forshew, Tim, primary, Hindley, Guy F., primary, Hodgson, J. Graeme, primary, Kim, Jung-Sik, primary, Rowitch, David H., primary, Weiss, William A., primary, Waldman, Todd A., primary, and James, C. David, primary

Published
2023
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23. Supplementary Table 3 from Targeted Therapy for BRAFV600E Malignant Astrocytoma

Author

Nicolaides, Theodore P., primary, Li, Huifang, primary, Solomon, David A., primary, Hariono, Sujatmi, primary, Hashizume, Rintaro, primary, Barkovich, Krister, primary, Baker, Suzanne J., primary, Paugh, Barbara S., primary, Jones, Chris, primary, Forshew, Tim, primary, Hindley, Guy F., primary, Hodgson, J. Graeme, primary, Kim, Jung-Sik, primary, Rowitch, David H., primary, Weiss, William A., primary, Waldman, Todd A., primary, and James, C. David, primary

Published
2023
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24. Supplementary Table 1 from Oncogenic BRAF Mutation with CDKN2A Inactivation Is Characteristic of a Subset of Pediatric Malignant Astrocytomas

Author

Schiffman, Joshua D., primary, Hodgson, J. Graeme, primary, VandenBerg, Scott R., primary, Flaherty, Patrick, primary, Polley, Mei-Yin C., primary, Yu, Mamie, primary, Fisher, Paul G., primary, Rowitch, David H., primary, Ford, James M., primary, Berger, Mitchel S., primary, Ji, Hanlee, primary, Gutmann, David H., primary, and James, C. David, primary

Published
2023
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25. Data from Whole-Body Sleeping Beauty Mutagenesis Can Cause Penetrant Leukemia/Lymphoma and Rare High-Grade Glioma without Associated Embryonic Lethality

Author

Collier, Lara S., primary, Adams, David J., primary, Hackett, Christopher S., primary, Bendzick, Laura E., primary, Akagi, Keiko, primary, Davies, Michael N., primary, Diers, Miechaleen D., primary, Rodriguez, Fausto J., primary, Bender, Aaron M., primary, Tieu, Christina, primary, Matise, Ilze, primary, Dupuy, Adam J., primary, Copeland, Neal G., primary, Jenkins, Nancy A., primary, Hodgson, J. Graeme, primary, Weiss, William A., primary, Jenkins, Robert B., primary, and Largaespada, David A., primary

Published
2023
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29. Data from Oncogenic BRAF Mutation with CDKN2A Inactivation Is Characteristic of a Subset of Pediatric Malignant Astrocytomas

Author

Schiffman, Joshua D., primary, Hodgson, J. Graeme, primary, VandenBerg, Scott R., primary, Flaherty, Patrick, primary, Polley, Mei-Yin C., primary, Yu, Mamie, primary, Fisher, Paul G., primary, Rowitch, David H., primary, Ford, James M., primary, Berger, Mitchel S., primary, Ji, Hanlee, primary, Gutmann, David H., primary, and James, C. David, primary

Published
2023
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30. Supplementary Table 3 from Whole-Body Sleeping Beauty Mutagenesis Can Cause Penetrant Leukemia/Lymphoma and Rare High-Grade Glioma without Associated Embryonic Lethality

Author

Collier, Lara S., primary, Adams, David J., primary, Hackett, Christopher S., primary, Bendzick, Laura E., primary, Akagi, Keiko, primary, Davies, Michael N., primary, Diers, Miechaleen D., primary, Rodriguez, Fausto J., primary, Bender, Aaron M., primary, Tieu, Christina, primary, Matise, Ilze, primary, Dupuy, Adam J., primary, Copeland, Neal G., primary, Jenkins, Nancy A., primary, Hodgson, J. Graeme, primary, Weiss, William A., primary, Jenkins, Robert B., primary, and Largaespada, David A., primary

Published
2023
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31. Supplementary Figure 1 from Oncogenic BRAF Mutation with CDKN2A Inactivation Is Characteristic of a Subset of Pediatric Malignant Astrocytomas

Author

Schiffman, Joshua D., primary, Hodgson, J. Graeme, primary, VandenBerg, Scott R., primary, Flaherty, Patrick, primary, Polley, Mei-Yin C., primary, Yu, Mamie, primary, Fisher, Paul G., primary, Rowitch, David H., primary, Ford, James M., primary, Berger, Mitchel S., primary, Ji, Hanlee, primary, Gutmann, David H., primary, and James, C. David, primary

Published
2023
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32. Supplementary Figure 2 from Whole-Body Sleeping Beauty Mutagenesis Can Cause Penetrant Leukemia/Lymphoma and Rare High-Grade Glioma without Associated Embryonic Lethality

Author

Collier, Lara S., primary, Adams, David J., primary, Hackett, Christopher S., primary, Bendzick, Laura E., primary, Akagi, Keiko, primary, Davies, Michael N., primary, Diers, Miechaleen D., primary, Rodriguez, Fausto J., primary, Bender, Aaron M., primary, Tieu, Christina, primary, Matise, Ilze, primary, Dupuy, Adam J., primary, Copeland, Neal G., primary, Jenkins, Nancy A., primary, Hodgson, J. Graeme, primary, Weiss, William A., primary, Jenkins, Robert B., primary, and Largaespada, David A., primary

Published
2023
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33. Supplementary Table 2 from Whole-Body Sleeping Beauty Mutagenesis Can Cause Penetrant Leukemia/Lymphoma and Rare High-Grade Glioma without Associated Embryonic Lethality

Author

Collier, Lara S., primary, Adams, David J., primary, Hackett, Christopher S., primary, Bendzick, Laura E., primary, Akagi, Keiko, primary, Davies, Michael N., primary, Diers, Miechaleen D., primary, Rodriguez, Fausto J., primary, Bender, Aaron M., primary, Tieu, Christina, primary, Matise, Ilze, primary, Dupuy, Adam J., primary, Copeland, Neal G., primary, Jenkins, Nancy A., primary, Hodgson, J. Graeme, primary, Weiss, William A., primary, Jenkins, Robert B., primary, and Largaespada, David A., primary

Published
2023
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34. Supplementary Table 2 from Oncogenic BRAF Mutation with CDKN2A Inactivation Is Characteristic of a Subset of Pediatric Malignant Astrocytomas

Author

Schiffman, Joshua D., primary, Hodgson, J. Graeme, primary, VandenBerg, Scott R., primary, Flaherty, Patrick, primary, Polley, Mei-Yin C., primary, Yu, Mamie, primary, Fisher, Paul G., primary, Rowitch, David H., primary, Ford, James M., primary, Berger, Mitchel S., primary, Ji, Hanlee, primary, Gutmann, David H., primary, and James, C. David, primary

Published
2023
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35. Supplementary Table 1 from Whole-Body Sleeping Beauty Mutagenesis Can Cause Penetrant Leukemia/Lymphoma and Rare High-Grade Glioma without Associated Embryonic Lethality

Author

Collier, Lara S., primary, Adams, David J., primary, Hackett, Christopher S., primary, Bendzick, Laura E., primary, Akagi, Keiko, primary, Davies, Michael N., primary, Diers, Miechaleen D., primary, Rodriguez, Fausto J., primary, Bender, Aaron M., primary, Tieu, Christina, primary, Matise, Ilze, primary, Dupuy, Adam J., primary, Copeland, Neal G., primary, Jenkins, Nancy A., primary, Hodgson, J. Graeme, primary, Weiss, William A., primary, Jenkins, Robert B., primary, and Largaespada, David A., primary

Published
2023
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37. Supplementary Figure 1 from Whole-Body Sleeping Beauty Mutagenesis Can Cause Penetrant Leukemia/Lymphoma and Rare High-Grade Glioma without Associated Embryonic Lethality

Author

Collier, Lara S., primary, Adams, David J., primary, Hackett, Christopher S., primary, Bendzick, Laura E., primary, Akagi, Keiko, primary, Davies, Michael N., primary, Diers, Miechaleen D., primary, Rodriguez, Fausto J., primary, Bender, Aaron M., primary, Tieu, Christina, primary, Matise, Ilze, primary, Dupuy, Adam J., primary, Copeland, Neal G., primary, Jenkins, Nancy A., primary, Hodgson, J. Graeme, primary, Weiss, William A., primary, Jenkins, Robert B., primary, and Largaespada, David A., primary

Published
2023
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38. Supplementary Table 4 from Whole-Body Sleeping Beauty Mutagenesis Can Cause Penetrant Leukemia/Lymphoma and Rare High-Grade Glioma without Associated Embryonic Lethality

Author

Collier, Lara S., primary, Adams, David J., primary, Hackett, Christopher S., primary, Bendzick, Laura E., primary, Akagi, Keiko, primary, Davies, Michael N., primary, Diers, Miechaleen D., primary, Rodriguez, Fausto J., primary, Bender, Aaron M., primary, Tieu, Christina, primary, Matise, Ilze, primary, Dupuy, Adam J., primary, Copeland, Neal G., primary, Jenkins, Nancy A., primary, Hodgson, J. Graeme, primary, Weiss, William A., primary, Jenkins, Robert B., primary, and Largaespada, David A., primary

Published
2023
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39. Supplementary Figure 3 from Whole-Body Sleeping Beauty Mutagenesis Can Cause Penetrant Leukemia/Lymphoma and Rare High-Grade Glioma without Associated Embryonic Lethality

Author

Collier, Lara S., primary, Adams, David J., primary, Hackett, Christopher S., primary, Bendzick, Laura E., primary, Akagi, Keiko, primary, Davies, Michael N., primary, Diers, Miechaleen D., primary, Rodriguez, Fausto J., primary, Bender, Aaron M., primary, Tieu, Christina, primary, Matise, Ilze, primary, Dupuy, Adam J., primary, Copeland, Neal G., primary, Jenkins, Nancy A., primary, Hodgson, J. Graeme, primary, Weiss, William A., primary, Jenkins, Robert B., primary, and Largaespada, David A., primary

Published
2023
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40. Supplementary Figure 4 from Whole-Body Sleeping Beauty Mutagenesis Can Cause Penetrant Leukemia/Lymphoma and Rare High-Grade Glioma without Associated Embryonic Lethality

Author

Collier, Lara S., primary, Adams, David J., primary, Hackett, Christopher S., primary, Bendzick, Laura E., primary, Akagi, Keiko, primary, Davies, Michael N., primary, Diers, Miechaleen D., primary, Rodriguez, Fausto J., primary, Bender, Aaron M., primary, Tieu, Christina, primary, Matise, Ilze, primary, Dupuy, Adam J., primary, Copeland, Neal G., primary, Jenkins, Nancy A., primary, Hodgson, J. Graeme, primary, Weiss, William A., primary, Jenkins, Robert B., primary, and Largaespada, David A., primary

Published
2023
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41. Integrated Genomic Analysis Identifies Clinically Relevant Subtypes of Glioblastoma Characterized by Abnormalities in PDGFRA, IDH1, EGFR, and NF1

Author

Verhaak, Roel G.W., Hoadley, Katherine A., Purdom, Elizabeth, Wang, Victoria, Qi, Yuan, Wilkerson, Matthew D., Miller, C. Ryan, Ding, Li, Golub, Todd, Mesirov, Jill P., Alexe, Gabriele, Lawrence, Michael, O'Kelly, Michael, Tamayo, Pablo, Weir, Barbara A., Gabriel, Stacey, Winckler, Wendy, Gupta, Supriya, Jakkula, Lakshmi, Feiler, Heidi S., Hodgson, J. Graeme, James, C. David, Sarkaria, Jann N., Brennan, Cameron, Kahn, Ari, Spellman, Paul T., Wilson, Richard K., Speed, Terence P., Gray, Joe W., Meyerson, Matthew, Getz, Gad, Perou, Charles M., and Hayes, D. Neil

Published
2010
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45. Discovery and Characterization of SY-1365, a Selective, Covalent Inhibitor of CDK7

Author

Hu, Shanhu, primary, Marineau, Jason J., additional, Rajagopal, Nisha, additional, Hamman, Kristin B., additional, Choi, Yoon Jong, additional, Schmidt, Darby R., additional, Ke, Nan, additional, Johannessen, Liv, additional, Bradley, Michael J., additional, Orlando, David A., additional, Alnemy, Sydney R., additional, Ren, Yixuan, additional, Ciblat, Stephane, additional, Winter, Dana K., additional, Kabro, Anzhelika, additional, Sprott, Kevin T., additional, Hodgson, J. Graeme, additional, Fritz, Christian C., additional, Carulli, John P., additional, di Tomaso, Emmanuelle, additional, and Olson, Eric R., additional

Published
2019
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46. miR-124 and miR-137 inhibit proliferation of glioblastoma multiforme cells and induce differentiation of brain tumor stem cells

Author

Costello Joseph F, James C David, Ginzinger David G, Vandenberg Scott R, Yu Mamie, Maunakea Alika K, Persson Anders I, Petritsch Claudia, Lim Daniel A, Silber Joachim, Bergers Gabriele, Weiss William A, Alvarez-Buylla Arturo, and Hodgson J Graeme

Subjects
Medicine
Abstract

Abstract Background Glioblastoma multiforme (GBM) is an invariably fatal central nervous system tumor despite treatment with surgery, radiation, and chemotherapy. Further insights into the molecular and cellular mechanisms that drive GBM formation are required to improve patient outcome. MicroRNAs are emerging as important regulators of cellular differentiation and proliferation, and have been implicated in the etiology of a variety of cancers, yet the role of microRNAs in GBM remains poorly understood. In this study, we investigated the role of microRNAs in regulating the differentiation and proliferation of neural stem cells and glioblastoma-multiforme tumor cells. Methods We used quantitative RT-PCR to assess microRNA expression in high-grade astrocytomas and adult mouse neural stem cells. To assess the function of candidate microRNAs in high-grade astrocytomas, we transfected miR mimics to cultured-mouse neural stem cells, -mouse oligodendroglioma-derived stem cells, -human glioblastoma multiforme-derived stem cells and -glioblastoma multiforme cell lines. Cellular differentiation was assessed by immunostaining, and cellular proliferation was determined using fluorescence-activated cell sorting. Results Our studies revealed that expression levels of microRNA-124 and microRNA-137 were significantly decreased in anaplastic astrocytomas (World Health Organization grade III) and glioblastoma multiforme (World Health Organization grade IV) relative to non-neoplastic brain tissue (P < 0.01), and were increased 8- to 20-fold during differentiation of cultured mouse neural stem cells following growth factor withdrawal. Expression of microRNA-137 was increased 3- to 12-fold in glioblastoma multiforme cell lines U87 and U251 following inhibition of DNA methylation with 5-aza-2'-deoxycytidine (5-aza-dC). Transfection of microRNA-124 or microRNA-137 induced morphological changes and marker expressions consistent with neuronal differentiation in mouse neural stem cells, mouse oligodendroglioma-derived stem cells derived from S100β-v-erbB tumors and cluster of differentiation 133+ human glioblastoma multiforme-derived stem cells (SF6969). Transfection of microRNA-124 or microRNA-137 also induced G1 cell cycle arrest in U251 and SF6969 glioblastoma multiforme cells, which was associated with decreased expression of cyclin-dependent kinase 6 and phosphorylated retinoblastoma (pSer 807/811) proteins. Conclusion microRNA-124 and microRNA-137 induce differentiation of adult mouse neural stem cells, mouse oligodendroglioma-derived stem cells and human glioblastoma multiforme-derived stem cells and induce glioblastoma multiforme cell cycle arrest. These results suggest that targeted delivery of microRNA-124 and/or microRNA-137 to glioblastoma multiforme tumor cells may be therapeutically efficacious for the treatment of this disease.

Published
2008
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47. A murine leukemia virus with Cre-LoxP excisible coding sequences allowing superinfection, transgene delivery, and generation of host genomic deletions

Author

Pedersen Finn, Malek Tiffany, Hodgson J Graeme, Wang Clifford L, and Wabl Matthias

Subjects
Immunologic diseases. Allergy, RC581-607
Abstract

Abstract Background To generate a replication-competent retrovirus that could be conditionally inactivated, we flanked the viral genes of the Akv murine leukemia virus with LoxP sites. This provirus can delete its envelope gene by LoxP/Cre mediated recombination and thereby allow superinfection of Cre recombinase expressing cells. Results In our studies, the virus repeatedly infected the cell and delivered multiple copies of the viral genome to the host genome; the superinfected cells expressed a viral transgene on average twenty times more than non-superinfected cells. The insertion of multiple LoxP sites into the cellular genome also led to genomic deletions, as demonstrated by comparative genome hybridization. Conclusion We envision that this technology may be particularly valuable for delivering transgenes and/or causing deletions.

Published
2004
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48. Single-Molecule Sequencing Reveals Patterns of Preexisting Drug Resistance That Suggest Treatment Strategies in Philadelphia-Positive Leukemias

Author

Schmitt, Michael W., primary, Pritchard, Justin R., additional, Leighow, Scott M., additional, Aminov, Bella I., additional, Beppu, Lan, additional, Kim, Daniel S., additional, Hodgson, J. Graeme, additional, Rivera, Victor M., additional, Loeb, Lawrence A., additional, and Radich, Jerald P., additional

Published
2018
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50. Activity of brigatinib (BRG) in crizotinib (CRZ)-resistant ALK+ NSCLC patients (pts) according to ALK plasma mutation status.

Author

Bazhenova, Lyudmila, primary, Hodgson, J. Graeme, additional, Langer, Corey J., additional, Simon, George R., additional, Gettinger, Scott N., additional, Ou, Sai-Hong Ignatius, additional, Reckamp, Karen L., additional, West, Howard Jack, additional, Chiappori, Alberto, additional, Koh, Han A., additional, Molina, Julian R., additional, Shaw, Alice Tsang, additional, Patel, Jyoti D., additional, Favaro, Justin Peter, additional, Haney, Jeff, additional, Reichmann, William, additional, Kerstein, David, additional, Rivera, Victor M., additional, and Camidge, D. Ross, additional

Published
2017
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