Search

Your search keyword '"Smeester, Branden A."' showing total 16 results
Start Over Author "Smeester, Branden A." Search Limiters Full Text
16 results on '"Smeester, Branden A."'

3. 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
Full Text
View/download PDF

7. 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
Full Text
View/download PDF

8. 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
Full Text
View/download PDF

10. 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
Full Text
View/download PDF

12. 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

16. SEMA4C is a novel target to limit osteosarcoma growth, progression, and metastasis.

Author

Smeester BA, Slipek NJ, Pomeroy EJ, Bomberger HE, Shamsan GA, Peterson JJ, Crosby MR, Draper GM, Becklin KL, Rahrmann EP, McCarthy JB, Odde DJ, Wood DK, Largaespada DA, and Moriarity BS

Subjects
Carcinogenesis, Cell Line, Tumor, Cell Proliferation, Cell Transformation, Neoplastic, Gene Expression Regulation, Neoplastic, Gene Knockdown Techniques, Humans, Lung Neoplasms secondary, Neoplasm Metastasis, Semaphorins deficiency, Semaphorins genetics, Bone Neoplasms pathology, Disease Progression, Osteosarcoma pathology, Semaphorins metabolism
Abstract

Semaphorins, specifically type IV, are important regulators of axonal guidance and have been increasingly implicated in poor prognoses in a number of different solid cancers. In conjunction with their cognate PLXNB family receptors, type IV members have been increasingly shown to mediate oncogenic functions necessary for tumor development and malignant spread. In this study, we investigated the role of semaphorin 4C (SEMA4C) in osteosarcoma growth, progression, and metastasis. We investigated the expression and localization of SEMA4C in primary osteosarcoma patient tissues and its tumorigenic functions in these malignancies. We demonstrate that overexpression of SEMA4C promotes properties of cellular transformation, while RNAi knockdown of SEMA4C promotes adhesion and reduces cellular proliferation, colony formation, migration, wound healing, tumor growth, and lung metastasis. These phenotypic changes were accompanied by reductions in activated AKT signaling, G1 cell cycle delay, and decreases in expression of mesenchymal marker genes SNAI1, SNAI2, and TWIST1. Lastly, monoclonal antibody blockade of SEMA4C in vitro mirrored that of the genetic studies. Together, our results indicate a multi-dimensional oncogenic role for SEMA4C in metastatic osteosarcoma and more importantly that SEMA4C has actionable clinical potential.

Published
2020
Full Text
View/download PDF

Catalog

Books, media, physical & digital resources
See catalog results