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33 results on '"Smeester, Branden A."'

2. PLX3397 treatment inhibits constitutive CSF1R-induced oncogenic ERK signaling, reduces tumor growth, and metastatic burden in osteosarcoma

Author

Smeester, Branden A., Slipek, Nicholas J., Pomeroy, Emily J., Laoharawee, Kanut, Osum, Sara H., Larsson, Alex T., Williams, Kyle B., Stratton, Natalie, Yamamoto, Kenta, Peterson, Joseph J., Rathe, Susan K., Mills, Lauren J., Hudson, Wendy A., Crosby, Margaret R., Wang, Minjing, Rahrmann, Eric P., Moriarity, Branden S., and Largaespada, David A.

Published
2020
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4. CRISPR-Cas9 cytidine and adenosine base editing of splice-sites mediates highly-efficient disruption of proteins in primary and immortalized cells

Author

Kluesner, Mitchell G., Lahr, Walker S., Lonetree, Cara-lin, Smeester, Branden A., Qiu, Xiaohong, Slipek, Nicholas J., Claudio Vázquez, Patricia N., Pitzen, Samuel P., Pomeroy, Emily J., Vignes, Madison J., Lee, Samantha C., Bingea, Samuel P., Andrew, Aneesha A., Webber, Beau R., and Moriarity, Branden S.

Published
2021
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10. Data from Breast Tumor Kinase (Brk/PTK6) Mediates Advanced Cancer Phenotypes via SH2-Domain Dependent Activation of RhoA and Aryl Hydrocarbon Receptor (AhR) Signaling

Author

Dwyer, Amy R., primary, Kerkvliet, Carlos Perez, primary, Krutilina, Raisa I., primary, Playa, Hilaire C., primary, Parke, Deanna N., primary, Thomas, Warner A., primary, Smeester, Branden A., primary, Moriarity, Branden S., primary, Seagroves, Tiffany N., primary, and Lange, Carol A., primary

Published
2023
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11. Supplemental Methods including references, Supplemental Table 1, and Supplemental Figures 1-5 from Breast Tumor Kinase (Brk/PTK6) Mediates Advanced Cancer Phenotypes via SH2-Domain Dependent Activation of RhoA and Aryl Hydrocarbon Receptor (AhR) Signaling

Author

Dwyer, Amy R., primary, Kerkvliet, Carlos Perez, primary, Krutilina, Raisa I., primary, Playa, Hilaire C., primary, Parke, Deanna N., primary, Thomas, Warner A., primary, Smeester, Branden A., primary, Moriarity, Branden S., primary, Seagroves, Tiffany N., primary, and Lange, Carol A., primary

Published
2023
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12. Supplementary Data from Implication of ZNF217 in Accelerating Tumor Development and Therapeutically Targeting ZNF217-Induced PI3K–AKT Signaling for the Treatment of Metastatic Osteosarcoma

Author

Smeester, Branden A., primary, Draper, Garrett M., primary, Slipek, Nicholas J., primary, Larsson, Alex T., primary, Stratton, Natalie, primary, Pomeroy, Emily J., primary, Becklin, Kelsie L., primary, Yamamoto, Kenta, primary, Williams, Kyle B., primary, Laoharawee, Kanut, primary, Peterson, Joseph J., primary, Abrahante, Juan E., primary, Rathe, Susan K., primary, Mills, Lauren J., primary, Crosby, Margaret R., primary, Hudson, Wendy A., primary, Rahrmann, Eric P., primary, Largaespada, David A., primary, and Moriarity, Branden S., primary

Published
2023
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13. Data from Implication of ZNF217 in Accelerating Tumor Development and Therapeutically Targeting ZNF217-Induced PI3K–AKT Signaling for the Treatment of Metastatic Osteosarcoma

Author

Smeester, Branden A., primary, Draper, Garrett M., primary, Slipek, Nicholas J., primary, Larsson, Alex T., primary, Stratton, Natalie, primary, Pomeroy, Emily J., primary, Becklin, Kelsie L., primary, Yamamoto, Kenta, primary, Williams, Kyle B., primary, Laoharawee, Kanut, primary, Peterson, Joseph J., primary, Abrahante, Juan E., primary, Rathe, Susan K., primary, Mills, Lauren J., primary, Crosby, Margaret R., primary, Hudson, Wendy A., primary, Rahrmann, Eric P., primary, Largaespada, David A., primary, and Moriarity, Branden S., primary

Published
2023
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14. Table S2 from Implication of ZNF217 in Accelerating Tumor Development and Therapeutically Targeting ZNF217-Induced PI3K–AKT Signaling for the Treatment of Metastatic Osteosarcoma

Author

Smeester, Branden A., primary, Draper, Garrett M., primary, Slipek, Nicholas J., primary, Larsson, Alex T., primary, Stratton, Natalie, primary, Pomeroy, Emily J., primary, Becklin, Kelsie L., primary, Yamamoto, Kenta, primary, Williams, Kyle B., primary, Laoharawee, Kanut, primary, Peterson, Joseph J., primary, Abrahante, Juan E., primary, Rathe, Susan K., primary, Mills, Lauren J., primary, Crosby, Margaret R., primary, Hudson, Wendy A., primary, Rahrmann, Eric P., primary, Largaespada, David A., primary, and Moriarity, Branden S., primary

Published
2023
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19. Breast Tumor Kinase (Brk/PTK6) Mediates Advanced Cancer Phenotypes via SH2-Domain Dependent Activation of RhoA and Aryl Hydrocarbon Receptor (AhR) Signaling

Author

Dwyer, Amy R., primary, Kerkvliet, Carlos Perez, additional, Krutilina, Raisa I., additional, Playa, Hilaire C., additional, Parke, Deanna N., additional, Thomas, Warner A., additional, Smeester, Branden A., additional, Moriarity, Branden S., additional, Seagroves, Tiffany N., additional, and Lange, Carol A., additional

Published
2021
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20. Implication of ZNF217 in Accelerating Tumor Development and Therapeutically Targeting ZNF217-Induced PI3K–AKT Signaling for the Treatment of Metastatic Osteosarcoma

Author

Smeester, Branden A., primary, Draper, Garrett M., additional, Slipek, Nicholas J., additional, Larsson, Alex T., additional, Stratton, Natalie, additional, Pomeroy, Emily J., additional, Becklin, Kelsie L., additional, Yamamoto, Kenta, additional, Williams, Kyle B., additional, Laoharawee, Kanut, additional, Peterson, Joseph J., additional, Abrahante, Juan E., additional, Rathe, Susan K., additional, Mills, Lauren J., additional, Crosby, Margaret R., additional, Hudson, Wendy A., additional, Rahrmann, Eric P., additional, Largaespada, David A., additional, and Moriarity, Branden S., additional

Published
2020
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21. CRISPR-Cas9 cytidine and adenosine base editing of splice-sites mediates highly-efficient disruption of proteins in primary cells

Author

Kluesner, Mitchell G., primary, Lahr, Walker S., additional, Lonetree, Cara-Lin, additional, Smeester, Branden A., additional, Claudio-Vázquez, Patricia N., additional, Pitzen, Samuel P., additional, Vignes, Madison J., additional, Lee, Samantha C., additional, Bingea, Samuel P., additional, Andrews, Aneesha A., additional, Webber, Beau R., additional, and Moriarity, Branden S., additional

Published
2020
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23. SEMA4C is a novel target to limit osteosarcoma growth, progression, and metastasis

Author

Smeester, Branden A., primary, Slipek, Nicholas J., additional, Pomeroy, Emily J., additional, Bomberger, Heather E., additional, Shamsan, Ghaidan A., additional, Peterson, Joseph J., additional, Crosby, Margaret R., additional, Draper, Garrett M., additional, Becklin, Kelsie L., additional, Rahrmann, Eric P., additional, McCarthy, James B., additional, Odde, David J., additional, Wood, David K., additional, Largaespada, David A., additional, and Moriarity, Branden S., additional

Published
2019
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25. Human β-Defensin 1 and β-Defensin 3 (Mouse Ortholog mBD14) Function as Full Endogenous Agonists at Select Melanocortin Receptors

Author

Ericson, Mark D., primary, Singh, Anamika, additional, Tala, Srinivasa R., additional, Haslach, Erica M., additional, Dirain, Marvin L. S., additional, Schaub, Jay W., additional, Flores, Viktor, additional, Eick, Natalie, additional, Lensing, Cody J., additional, Freeman, Katie T., additional, Smeester, Branden A., additional, Adank, Danielle N., additional, Wilber, Stacey L., additional, Speth, Robert, additional, and Haskell-Luevano, Carrie, additional

Published
2018
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26. Osteosarcomagenesis : Biology, Development, Metastasis, and Mechanisms of Pain

Author

Smeester, Branden A.

Subjects
Medical / Prosthesis
Abstract

Osteosarcoma is the most common primary cancer of the bone and third most common cancer in children and adolescents with approximately 900 new cases annually in the United States. A major facet of osteosarcoma is its high level of genomic instability, in particular chromosomal instability, which is the result of increased or decreased chromosome number in a cell. Furthermore, pain is the most common symptomatic feature of osteosarcoma that lacks effective therapy. Pain in osteosarcoma is relatively more complicated than many other painful conditions requiring a more thorough understanding of its etiology, pathobiology, and neurobiology to allow the development of better therapies for reducing pain in osteosarcoma patients. Studies are underway to define the diverse modalities of presentation, growth, development, metastases, and nociception in osteosarcoma. New data from human studies in combination with data from studies incorporating transgenic mouse models of osteosarcoma are providing valuable insights into the mechanisms underlying the development of both the tumor and the tumor-induced pain. These new data will undoubtedly lead to improved prognoses, as well as the development of novel therapeutics that will significantly decrease bone cancer pain.

Published
2017

32. Functional Validation Of Candidate Osteosarcoma Genes Identified Via Sleeping Beauty Mutagenesis

Author

Smeester, Branden

Abstract

PURPOSE The work presented throughout this thesis sought to functionally, mechanistically, and therapeutically investigate a number of top candidate gene targets and associated signalling pathways in osteosarcoma (OSA) that were originally identified using the Sleeping Beauty (SB) transposon system. Chapter 1 begins with a current overview of OSA biology, metastasis, therapeutic treatments, and mechanisms of pain. Chapter 2 focuses on how new candidate OSA genes were identified using the SB system. Subsequent chapters (3-5) are dedicated to the functional and mechanistic characterization of three top candidate genes (SEMA4C, CSF1R, and ZNF217) with the explicit goal of characterizing their biology in the context of OSA and ultimately exploiting their therapeutic potential. MAJOR FINDINGS In brief, 1) SEMA4C was found to be implicated in promoting OSA growth and metastasis. Cellular transformation associated with these cancer phenotypes could be reversed via administration of a monoclonal antibody against SEMA4C in vitro; 2) Active CSF1R was found to be involved in OSA growth and metastatic burden in part through enhanced ERK signalling which could be disrupted through small molecule CSF1R kinase blockade; 3) ZNF217 was found to accelerate OSA progression, growth, and metastasis through regulation of PI3K-AKT signalling, which could be therapeutically blocked via an AKT inhibitor.

Published
2020

33. Cancer Gene Discovery Utilizing Sleeping Beauty Transposon Mutagenesis.

Author

Becklin KL, Smeester BA, and Moriarity BS

Subjects
Genetic Engineering, Genome, Human, Humans, Neoplasms pathology, Recombination, Genetic, DNA Transposable Elements, Mutagenesis, Neoplasm Proteins genetics, Neoplasms genetics, Transposases metabolism
Abstract

Transposable elements are DNA sequences with the ability to move from one genomic location to another. The movement of class II transposable elements has been functionally harnessed and separated into two distinct DNA transposon components: the terminal inverted repeat sequences that flank genetic cargo to be mobilized and a transposase enzyme capable of recognizing the terminal inverted repeat sequences and catalyzing the transposition reaction. In particular, the Sleeping Beauty (SB) system was the first successful demonstration of transposon-based gene transfer in vertebrate species. Over the years, several improvements have been made to SB technology and more recent studies have demonstrated the versatility of the system for many applications including insertional mutagenesis, gene transfer, and transgenesis. These genetic engineering advances made available by SB both augment and advance large-scale efforts that have been directed toward identifying how genes and environmental factors influence human health in recent years. In the age of personalized medicine, the versatility of SB provides numerous genetic engineering avenues for answering novel questions in basic and applied research. This chapter discusses the use of SB-based insertional mutagenesis in mice for the efficient identification of candidate cancer genes across numerous types of cancers.

Published
2019
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