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6 results on '"Hagen, Jussara"'

1. RABL6A Promotes G1–S Phase Progression and Pancreatic Neuroendocrine Tumor Cell Proliferation in an Rb1-Dependent Manner

Author

Hagen, Jussara, primary, Muniz, Viviane P., additional, Falls, Kelly C., additional, Reed, Sara M., additional, Taghiyev, Agshin F., additional, Quelle, Frederick W., additional, Gourronc, Francoise A., additional, Klingelhutz, Aloysius J., additional, Major, Heather J., additional, Askeland, Ryan W., additional, Sherman, Scott K., additional, O'Dorisio, Thomas M., additional, Bellizzi, Andrew M., additional, Howe, James R., additional, Darbro, Benjamin W., additional, and Quelle, Dawn E., additional

Published
2014
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2. Abstract LB-162: Translational imaging of tumorigenesis in a TP53 porcine cancer model

Author

Sieren, Jessica C., primary, Wang, Xiao-Jun, additional, Davis, Bryan, additional, Newell, John D., additional, Hammond, Emily, additional, Rohret, Judy, additional, Rohret, Frank, additional, Struzynski, Jason, additional, Goeken, Adam, additional, Naumann, Paul, additional, Leidinger, Mariah, additional, Hagen, Jussara, additional, Rheeden, Richard Van, additional, Darbro, Benjamin W., additional, Quelle, Dawn E., additional, Meyerholz, David K., additional, and Rogers, Christopher S., additional

Published
2014
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3. Abstract 712: Parf-1A (Partner of ARF isoform 1A) promotes oxaliplatin resistance and is a new prognostic marker of survival in pancreatic ductal adenocarcinoma

Author

Muniz, Viviane P., primary, Zhang, Xuefeng, additional, Reed, Sara M., additional, Tompkins, Van S., additional, Smith, Tarik, additional, Hagen, Jussara KF, additional, Fitzgerald, Matthew, additional, Button, Anna, additional, Smith, Brian, additional, Zamba, Kokou D., additional, Domann, Frederick E., additional, Mezhir, James J., additional, Weydert, Jamie, additional, Askeland, Ryan A., additional, and Quelle, Dawn E., additional

Published
2012
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5. Large-Scale Molecular Comparison of Human Schwann Cells to Malignant Peripheral Nerve Sheath Tumor Cell Lines and Tissues

Author

Miller, Shyra J., primary, Rangwala, Fatima, additional, Williams, Jon, additional, Ackerman, Peter, additional, Kong, Sue, additional, Jegga, Anil G., additional, Kaiser, Sergio, additional, Aronow, Bruce J., additional, Frahm, Silke, additional, Kluwe, Lan, additional, Mautner, Victor, additional, Upadhyaya, Meena, additional, Muir, David, additional, Wallace, Margaret, additional, Hagen, Jussara, additional, Quelle, Dawn E., additional, Watson, Mark A., additional, Perry, Arie, additional, Gutmann, David H., additional, and Ratner, Nancy, additional

Published
2006
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6. RABL6A Promotes G1-S Phase Progression and Pancreatic Neuroendocrine Tumor Cell Proliferation in an Rb1-Dependent Manner.

Author

Hagen, Jussara, Muniz, Viviane P., Falls, Kelly C., Reed, Sara M., Taghiyev, Agshin F., Quelle, Frederick W., Gourronc, Francoise A., Klingelhutz, Aloysius J., Major, Heather J., Askeland, Ryan W., Sherman, Scott K., O'Dorisio, Thomas M., Bellizzi, Andrew M., Howe, James R., Darbro, Benjamin W., and Quelle, Dawn E.

Subjects
*NEUROENDOCRINE tumors, *CELL proliferation, *CANCER invasiveness, *GENE amplification, *PANCREATIC cancer, *CELL death, *TUMOR treatment
Abstract

Mechanisms of neuroendocrine tumor (NET) proliferation are poorly understood, and therapies that effectively control NET progression and metastatic disease are limited. We found amplification of a putative oncogene, RABL6A, in primary human pancreatic NETs (PNET) that correlated with high-level RABL6A protein expression. Consistent with those results, stable silencing of RABL6A in cultured BON-1 PNET cells revealed that it is essential for their proliferation and survival. Cells lacking RABL6A predominantly arrested in G1 phase with a moderate mitotic block. Pathway analysis of microarray data suggested activation of the p53 and retinoblastoma (Rb1) tumor-suppressor pathways in the arrested cells. Loss of p53 had no effect on the RABL6A knockdown phenotype, indicating that RABL6A functions independent of p53 in this setting. By comparison, Rb1 inactivation partially restoredG1 to S phase progression in RABL6A-knockdown cells, although it was insufficient to override the mitotic arrest and cell death caused by RABL6A loss. Thus, RABL6A promotesG1 progression in PNET cells by inactivating Rb1, an established suppressor of PNET proliferation and development. This work identifies RABL6A as a novel negative regulator of Rb1 that is essential for PNET proliferation and survival. We suggest RABL6A is a new potential biomarker and target for anticancer therapy in PNET patients. [ABSTRACT FROM AUTHOR]

Published
2014
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