Other Publications (1)
Articles by Taylor Polk in JoVE
In Vivo Model for Testing Effect of Hypoxia on Tumor Metastasis Sung-Hyeok Hong*1, Jason U. Tilan*2,3, Susana Galli1, Rachel Acree3, Katherine Connors4, Akanksha Mahajan1, Larissa Wietlisbach3, Taylor Polk3, Ewa Izycka-Swieszewska5, Yi-Chien Lee6, Luciane R. Cavalli6, Olga C. Rodriguez6, Chris Albanese6,7, Joanna B. Kitlinska1 1Department of Biochemistry and Molecular & Cellular Biology, Georgetown University Medical Center, 2Department of Nursing, Georgetown University, School of Nursing and Health Studies, 3Department of Human Science, Georgetown University, School of Nursing and Health Studies, 4School of Medicine, Georgetown University Medical Center, 5Department of Pathology and Neuropathology, Medical University of Gdańsk, 6Department of Oncology, Georgetown University Medical Center, 7Department of Pathology, Georgetown University Medical Center This manuscript describes the development of an animal model that allows for the direct testing of the effects of tumor hypoxia on metastasis and the deciphering the mechanisms of its action. Although the experiments described here focus on Ewing sarcoma, a similar approach can be applied to other tumor types.
Other articles by Taylor Polk on PubMed
High Neuropeptide Y Release Associates with Ewing Sarcoma Bone Dissemination - in Vivo Model of Site-specific Metastases Oncotarget. Mar, 2015 | Pubmed ID: 25714031 Ewing sarcoma (ES) develops in bones or soft tissues of children and adolescents. The presence of bone metastases is one of the most adverse prognostic factors, yet the mechanisms governing their formation remain unclear. As a transcriptional target of EWS-FLI1, the fusion protein driving ES transformation, neuropeptide Y (NPY) is highly expressed and released from ES tumors. Hypoxia up-regulates NPY and activates its pro-metastatic functions. To test the impact of NPY on ES metastatic pattern, ES cell lines, SK-ES1 and TC71, with high and low peptide release, respectively, were used in an orthotopic xenograft model. ES cells were injected into gastrocnemius muscles of SCID/beige mice, the primary tumors excised, and mice monitored for the presence of metastases. SK-ES1 xenografts resulted in thoracic extra-osseous metastases (67%) and dissemination to bone (50%) and brain (25%), while TC71 tumors metastasized to the lungs (70%). Bone dissemination in SK-ES1 xenografts associated with increased NPY expression in bone metastases and its accumulation in bone invasion areas. The genetic silencing of NPY in SK-ES1 cells reduced bone degradation. Our study supports the role for NPY in ES bone invasion and provides new models for identifying pathways driving ES metastases to specific niches and testing anti-metastatic therapeutics.