Benjamin Bryson, PhD

Benjamin Bryson, PhD

Postdoctoral Researcher

blb74@case.edu

216.368.5924 (o)

I was born and raised in Greenville, Ohio where my passion for science was ignited by my high school science teachers Mr. Rismiller and Mr. Palmer. I obtained my B.S. in Microbiology from The Ohio State University and conducted research for 1 year under Dr. Christopher Pierson at The Research Institute at Nationwide Children's Hospital, Center for Childhood Cancer, where we investigated the mechanisms underlying a rare genetic disorder called X-Linked Myotubular Myopathy (XLMTM). My graduate research was performed at Case Western Reserve University in Dr. Mark Jackson’s lab in the Department of Pathology and the Comprehensive Cancer Center (CCC)’s shared Cancer Biology Training Program. My Ph.D. studies mostly focused on utilizing a refined model of human mammary epithelial cell (HMEC) transformation to define the roles of a novel oncogene FAM83B and the cytokine Oncostatin M (OSM) in breast cancer development and progression. I started my postdoc research in Dr. Jackson’s lab where I continued my work focusing on the molecular links between senescence, EMT, and stemness during breast tumorigenesis. I joined Dr. Ruth Keri's lab as a postdoc in order to gain more experience utilizing in vivo cancer models and to expand on my training using various molecular biology techniques. I like to approach my research studies with a mixture of rationale-based science combined with more “outside-the-box” ideas or strategies. Under Dr. Keri’s mentorship, my ultimate goal is to identify novel therapeutic targets or regimens that will lead to improved outcomes and extended lives for breast cancer patients.

Current Research Activities

  • Developing and utilizing novel experimental models which are more physiologically relevant and recapitulate the cellular biology that exists within patients' tumors

  • Assessing the effectiveness of combinatorial treatment regimens for breast cancer patients that involve both targeted and systemic therapies

Awards and Honors

  • 2019: First Place Poster Award, Great Lakes Breast Cancer Research Symposium

  • 2018: Short-Talk Podium Presentation Award, Cancer Stem Cell Conference

  • 2018: Case CCC Distinguished Trainee Short-Talk Podium Presentation, Case Comprehensive Cancer Center Annual Scientific Retreat

  • 2018: First Place Poster Award, Case Comprehensive Cancer Center Annual Scientific Retreat

  • 2018: Postdoctoral Scholar First Place Poster Presentation Award, Research ShowCASE

  • 2016: First Place Poster Award, Department of Pathology Annual Research Retreat

  • 2016: Short-Talk Podium Presentation Award, Department of Pathology Annual Research Retreat

  • 2016: Short-Talk Podium Presentation Award, Cancer Stem Cell Conference

  • 2016: Graduate Student First Place Poster Presentation Award, Research ShowCASE

  • 2015: First Place Poster Award, Case Comprehensive Cancer Center Annual Scientific Retreat

  • 2014: Short-Talk Podium Presentation Award, Cancer Stem Cell Conference

Publications

  • O'Connor C, Leonard D, Wiredja D, Avelar R, Wang Z, Schlatzer D, Bryson BL, Tokala E, Taylor S, Upadhyay A, Sangodkar J, Gingras AC, Westermarck J, Xu W, DiFeo A, Brautigan D, Haider S, Jackson MW, and Narla G. Inactivation of PP2A by a recurrent mutation drives resistance to MEK inhibitors. Oncogene 2019. DOI: 10.1038/s41388-019-1012-2

  • Smigiel JM, Taylor SE, Bryson BL, Tamagno I, Polak K, Jackson MW. Cellular plasticity and metastasis in breast cancer: a pre- and post-malignant problem. J Cancer Metastasis Treat 2019. DOI: 10.20517/2394-4722.2019.26

  • Doherty MR, Parvani JG, Tamagno I, Junk DJ, Bryson BL, Cheon H, Stark GR, Jackson MW. The opposing effects of Interferon-beta and Oncostatin-M as regulators of cancer stem cell plasticity in Triple Negative Breast Cancer. Breast Cancer Research 2019. PMID: 31036052; DOI: 10.1186/s13058-019-1136-x

  • Dashzeveg NK, Taftaf R, Ramos EK, Torre-Healy L, Chumakova A, Silver DJ, Alban TJ, Sinyuk M, Thiagarajan PS, Jarrar AM, et al. New Advances and Challenges of Targeting Cancer Stem Cells. Cancer Res 2017; 77:5222-7.

    ***Tumor MICROENVIRONMENT: Bryson BL

  • Junk DJ*, Bryson BL*, Smigiel JM, Parameswaran N, Bartel CA, and Jackson MW. Oncostatin M promotes cancer cell plasticity through cooperative STAT3-SMAD3 signaling. Oncogene 2017. PMID: 28288136; DOI: 10.1038/onc.2017.33

  • La Belle AA, Schiemann WP. Oncostatin M Activation of Stat3:Smad3 Complexes Drives Senescence. Cell Cycle 2017. PMID: 28129030; DOI: 10.1080/15384101.2017.1287862; NEWS and VIEWS to:

    Bryson BL, Junk DJ, Cipriano R, Jackson MW. STAT3-mediated SMAD3 activation underlies Oncostatin M-induced Senescence. Cell Cycle 2016. PMID: 27892764; DOI: 10.1080/15384101.2016.1259037

  • Bryson BL, Junk DJ, Cipriano R, Jackson MW. STAT3-mediated SMAD3 activation underlies Oncostatin M-induced Senescence. Cell Cycle 2016; 16(4):319-334. PMID: 27892764; DOI: 10.1080/15384101.2016.1259037

  • Adorno-Cruz V, Kibria G, Liu X, Doherty M, Junk DJ, Guan D, Hubert C, Venere M, Mulkearns-Hubert E, Sinyuk M, Alvarado A, Caplan AI, Rich J, Gerson SL, Lathia J, Liu H. Cancer stem cells: targeting the roots of cancer, seeds of metastasis, and sources of therapy resistance. Cancer Res 2015; 75(6):924-9. PMID: 25604264; PMCID: PMC4359955; DOI: 10.1158/0008-5472.CAN-14-3225; ***Epithelial Tumor Stem Cells and Metastasis: Bryson BL

  • Cipriano R, Miskimen KL, Bryson BL, Foy CR, Bartel CA, Jackson MW. Conserved oncogenic behavior of the FAM83 family regulates MAPK signaling in human cancer. Mol Cancer Res 2014; 12(8):1156-65. PMID: 24736947; PMCID: PMC4135001; DOI: 10.1158/1541-7786.MCR-13-0289

  • Cipriano R, Bryson BL, Miskimen KL, Bartel CA, Hernandez-Sanchez W, Bruntz RC, Scott SA, Lindsley CW, Brown HA, Jackson MW. Hyperactivation of EGFR and downstream effector phospholipase D1 by oncogenic FAM83B. Oncogene 2014; 33(25):3298-306. PMID: 23912460; PMCID: PMC3923847; DOI: 10.1038/onc.2013.293

  • Junk DJ, Bryson BL, Jackson MW. HiJAK'd Signaling; the STAT3 Paradox in Senescence and Cancer Progression. Cancers (Basel) 2014; 6(2):741-55. PMID: 24675570; PMCID: PMC4074801; DOI: 10.3390/cancers6020741

  • Junk DJ, Cipriano R, Bryson BL, Gilmore HL, Jackson MW. Tumor Microenvironmental Signaling Elicits Epithelial-Mesenchymal Plasticity through Cooperation with Transforming Genetic Events. Neoplasia 2013; 15(9):1100-9. PMID: 24027434; PMCID: PMC3769888

  • Cipriano R, Miskimen KL, Bryson BL, Foy CR, Bartel CA, Jackson MW. FAM83B-mediated activation of PI3K/AKT and MAPK signaling cooperates to promote epithelial cell transformation and resistance to targeted therapies. Oncotarget 2013; 4(5):729-38. PMID: 23676467; PMCID: PMC3742833; DOI: 10.18632/oncotarget.1027

  • Cipriano R, Graham J, Miskimen KL, Bryson BL, Bruntz RC, Scott SA, Brown HA, Stark GR, Jackson MW. FAM83B mediates EGFR- and RAS-driven oncogenic transformation. J Clin Invest 2012; 122(9):3197-210. PMID: 22886302; PMCID: PMC3428078; DOI: 10.1172/JCI60517

  • Pierson CR, Dulin-Smith AN, Durban AN, Marshall ML, Marshall JT, Snyder AD, Naiyer N, Gladman JT, Chandler DS, Lawlor MW, Buj-Bello A, Dowling JJ, Beggs AH. Modeling the human MTM1 pR69C mutation in murine Mtm1 results in exon 4 skipping and a less severe myotubular myopathy phenotype. Hum Mol Genet 2012; 21(4):811-25. PMID: 22068590; PMCID: PMC3263994; DOI: 10.1093/hmg/ddr512; ***ACKNOWLEDGEMENTS: Bryson BL