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Shari Meyers - One of the best experts on this subject based on the ideXlab platform.

  • runx1 aml 1 and runx2 aml 3 cooperate with prostate derived ets factor to activate transcription from the psa upstream regulatory region
    Journal of Cellular Biochemistry, 2006
    Co-Authors: Marcie Fowler, Erkut Borazanci, Laura L Mcghee, Shannon Walls Pylant, Jill B Williams, Jonathan D Glass, Nathan J Davis, Shari Meyers
    Abstract:

    The RUNX transcription factors (RUNX1, RUNX2, and RUNX3) play essential roles in hematopoiesis and skeletal development. Consistent with these roles in differentiation and Cell cycle, the activity of both RUNX1 and RUNX3 is perturbed in cancer. To determine a role for the RUNX factors in prostate biology, we investigated the expression of RUNX factors in prostate epithelial Cell Lines and normal prostate tissue. RUNX1, RUNX2, and RUNX3 were expressed in both normal prostate tissue and an immortalized, non-Transformed Cell Line. We found that prostate cancer-derived Cell Lines expressed RUNX1 and RUNX2, but not RUNX3. Next, we sought to identify prostate-specific genes whose expression could be regulated by RUNX proteins. Four consensus RUNX sites are located within the prostate-specific antigen (PSA) regulatory region. Chromatin immunoprecipitation (ChIP) analysis showed that RUNX1 is specifically bound to the PSA regulatory region in LNCaP Cells. RUNX1 and RUNX2 activated the PSA regulatory region alone or cooperatively with prostate-derived ETS factor (PDEF) and RUNX1 physically associated with PDEF. Taken together, our results suggest that RUNX factors participate in prostate epithelial Cell function and cooperate with an Ets transcription factor to regulate PSA gene expression.

  • runx1 aml 1 and runx2 aml 3 cooperate with prostate derived ets factor to activate transcription from the psa upstream regulatory region
    Journal of Cellular Biochemistry, 2006
    Co-Authors: Marcie Fowler, Erkut Borazanci, Laura L Mcghee, Shannon Walls Pylant, Jill B Williams, Nathan J Davis, Shari Meyers, Jonathan Glass
    Abstract:

    The RUNX transcription factors (RUNX1, RUNX2, and RUNX3) play essential roles in hematopoiesis and skeletal development. Consistent with these roles in differentiation and Cell cycle, the activity of both RUNX1 and RUNX3 is perturbed in cancer. To determine a role for the RUNX factors in prostate biology, we investigated the expression of RUNX factors in prostate epithelial Cell Lines and normal prostate tissue. RUNX1, RUNX2, and RUNX3 were expressed in both normal prostate tissue and an immortalized, non-Transformed Cell Line. We found that prostate cancer-derived Cell Lines expressed RUNX1 and RUNX2, but not RUNX3. Next, we sought to identify prostate-specific genes whose expression could be regulated by RUNX proteins. Four consensus RUNX sites are located within the prostate-specific antigen (PSA) regulatory region. Chromatin immunoprecipitation (ChIP) analysis showed that RUNX1 is specifically bound to the PSA regulatory region in LNCaP Cells. RUNX1 and RUNX2 activated the PSA regulatory region alone or cooperatively with prostate-derived ETS factor (PDEF) and RUNX1 physically associated with PDEF. Taken together, our results suggest that RUNX factors participate in prostate epithelial Cell function and cooperate with an Ets transcription factor to regulate PSA gene expression. J. Cell. Biochem. © 2005 Wiley-Liss, Inc.

Marcie Fowler - One of the best experts on this subject based on the ideXlab platform.

  • runx1 aml 1 and runx2 aml 3 cooperate with prostate derived ets factor to activate transcription from the psa upstream regulatory region
    Journal of Cellular Biochemistry, 2006
    Co-Authors: Marcie Fowler, Erkut Borazanci, Laura L Mcghee, Shannon Walls Pylant, Jill B Williams, Jonathan D Glass, Nathan J Davis, Shari Meyers
    Abstract:

    The RUNX transcription factors (RUNX1, RUNX2, and RUNX3) play essential roles in hematopoiesis and skeletal development. Consistent with these roles in differentiation and Cell cycle, the activity of both RUNX1 and RUNX3 is perturbed in cancer. To determine a role for the RUNX factors in prostate biology, we investigated the expression of RUNX factors in prostate epithelial Cell Lines and normal prostate tissue. RUNX1, RUNX2, and RUNX3 were expressed in both normal prostate tissue and an immortalized, non-Transformed Cell Line. We found that prostate cancer-derived Cell Lines expressed RUNX1 and RUNX2, but not RUNX3. Next, we sought to identify prostate-specific genes whose expression could be regulated by RUNX proteins. Four consensus RUNX sites are located within the prostate-specific antigen (PSA) regulatory region. Chromatin immunoprecipitation (ChIP) analysis showed that RUNX1 is specifically bound to the PSA regulatory region in LNCaP Cells. RUNX1 and RUNX2 activated the PSA regulatory region alone or cooperatively with prostate-derived ETS factor (PDEF) and RUNX1 physically associated with PDEF. Taken together, our results suggest that RUNX factors participate in prostate epithelial Cell function and cooperate with an Ets transcription factor to regulate PSA gene expression.

  • runx1 aml 1 and runx2 aml 3 cooperate with prostate derived ets factor to activate transcription from the psa upstream regulatory region
    Journal of Cellular Biochemistry, 2006
    Co-Authors: Marcie Fowler, Erkut Borazanci, Laura L Mcghee, Shannon Walls Pylant, Jill B Williams, Nathan J Davis, Shari Meyers, Jonathan Glass
    Abstract:

    The RUNX transcription factors (RUNX1, RUNX2, and RUNX3) play essential roles in hematopoiesis and skeletal development. Consistent with these roles in differentiation and Cell cycle, the activity of both RUNX1 and RUNX3 is perturbed in cancer. To determine a role for the RUNX factors in prostate biology, we investigated the expression of RUNX factors in prostate epithelial Cell Lines and normal prostate tissue. RUNX1, RUNX2, and RUNX3 were expressed in both normal prostate tissue and an immortalized, non-Transformed Cell Line. We found that prostate cancer-derived Cell Lines expressed RUNX1 and RUNX2, but not RUNX3. Next, we sought to identify prostate-specific genes whose expression could be regulated by RUNX proteins. Four consensus RUNX sites are located within the prostate-specific antigen (PSA) regulatory region. Chromatin immunoprecipitation (ChIP) analysis showed that RUNX1 is specifically bound to the PSA regulatory region in LNCaP Cells. RUNX1 and RUNX2 activated the PSA regulatory region alone or cooperatively with prostate-derived ETS factor (PDEF) and RUNX1 physically associated with PDEF. Taken together, our results suggest that RUNX factors participate in prostate epithelial Cell function and cooperate with an Ets transcription factor to regulate PSA gene expression. J. Cell. Biochem. © 2005 Wiley-Liss, Inc.

Scott K Durum - One of the best experts on this subject based on the ideXlab platform.

  • inhibiting janus kinase 1 and bcl 2 to treat t Cell acute lymphoblastic leukemia with il7 rα mutations
    Oncotarget, 2018
    Co-Authors: Emilee Senkevitch, Julie A Hixon, Gary T Pauly, Timothy C Back, Kelli Czarra, Caroline Andrews, Sarah Cramer, Scott K Durum
    Abstract:

    Acute lymphoblastic leukemia (ALL) is the most common cancer in children. Current chemotherapy is quite toxic in growing children and more directed therapeutics are being sought. The IL-7R pathway is a major driver of ALL and here we evaluate two drugs directed to that pathway using a model of T Cell ALL. Mutant gain-of-function IL-7Rα was transduced into an IL-7-dependent murine thymocyte Line conferring ligand-independent survival and growth. JAK1 is associated with IL-7Rα and mediates signaling from the mutant receptor. In vitro, treating the Transformed Cell Line with the JAK1/2 inhibitor ruxolitinib inhibited ligand-independent signaling and induced Cell death. Transfer of the Transformed Cell Line into mice resulted in aggressive leukemia and untreated mice succumbed in about three weeks. Treatment with ruxolitinib incorporated into chow showed a potent therapeutic benefit with reduction in leukemic burden and extension of survival. BCL-2 is an anti-apoptotic downstream mediator of the IL-7R survival mechanism. Venetoclax, an inhibitor of BCL-2, showed activity against the Transformed Cell Line in vitro and could be combined with ruxolitinib in vivo. These findings support the therapeutic potential of treating T-ALL by targeting the IL-7R pathway.

  • inhibiting janus kinase 1 and bcl 2 to treat t Cell acute lymphoblastic leukemia with il7 rα mutations
    Oncotarget, 2018
    Co-Authors: Emilee Senkevitch, Julie A Hixon, Sarah D Cramer, Gary T Pauly, Timothy C Back, Kelli Czarra, Caroline Andrews, Wenqing Li, Scott K Durum
    Abstract:

    // Emilee Senkevitch 1 , Wenqing Li 1 , Julie A. Hixon 1 , CaroLine Andrews 1, 2, 3 , Sarah D. Cramer 1, 2, 4 , Gary T. Pauly 6 , Timothy Back 1 , Kelli Czarra 5 and Scott K. Durum 1 1 Cytokines and Immunity Section, Cancer and Inflammation Program, National Cancer Institute, National Institutes of Health, Frederick, MD, USA 2 Comparative Biomedical Scientist Training Program, NIH, Bethesda, MD, USA 3 Michigan State University, East Lansing, MI, USA 4 Department of Veterinary Medicine, University of Maryland, College Park, MD, USA 5 Laboratory Animal Sciences Program, Cancer and Inflammation Program, National Cancer Institute, National Institutes of Health, Frederick, MD, USA 6 Chemical Biology Laboratory, National Cancer Institute, National Institutes of Health, Frederick, MD, USA Correspondence to: Scott K. Durum, email: durums@mail.nih.gov Keywords: JAK1; BCL-2; T-ALL; ruxolitinib; venetoclax Received: June 23, 2017      Accepted: April 04, 2018      Published: April 27, 2018 ABSTRACT Acute lymphoblastic leukemia (ALL) is the most common cancer in children. Current chemotherapy is quite toxic in growing children and more directed therapeutics are being sought. The IL-7R pathway is a major driver of ALL and here we evaluate two drugs directed to that pathway using a model of T Cell ALL. Mutant gain-of-function IL-7Rα was transduced into an IL-7-dependent murine thymocyte Line conferring ligand-independent survival and growth. JAK1 is associated with IL-7Rα and mediates signaling from the mutant receptor. In vitro , treating the Transformed Cell Line with the JAK1/2 inhibitor ruxolitinib inhibited ligand-independent signaling and induced Cell death. Transfer of the Transformed Cell Line into mice resulted in aggressive leukemia and untreated mice succumbed in about three weeks. Treatment with ruxolitinib incorporated into chow showed a potent therapeutic benefit with reduction in leukemic burden and extension of survival. BCL-2 is an anti-apoptotic downstream mediator of the IL-7R survival mechanism. Venetoclax, an inhibitor of BCL-2, showed activity against the Transformed Cell Line in vitro and could be combined with ruxolitinib in vivo . These findings support the therapeutic potential of treating T-ALL by targeting the IL-7R pathway.

Laura L Mcghee - One of the best experts on this subject based on the ideXlab platform.

  • runx1 aml 1 and runx2 aml 3 cooperate with prostate derived ets factor to activate transcription from the psa upstream regulatory region
    Journal of Cellular Biochemistry, 2006
    Co-Authors: Marcie Fowler, Erkut Borazanci, Laura L Mcghee, Shannon Walls Pylant, Jill B Williams, Jonathan D Glass, Nathan J Davis, Shari Meyers
    Abstract:

    The RUNX transcription factors (RUNX1, RUNX2, and RUNX3) play essential roles in hematopoiesis and skeletal development. Consistent with these roles in differentiation and Cell cycle, the activity of both RUNX1 and RUNX3 is perturbed in cancer. To determine a role for the RUNX factors in prostate biology, we investigated the expression of RUNX factors in prostate epithelial Cell Lines and normal prostate tissue. RUNX1, RUNX2, and RUNX3 were expressed in both normal prostate tissue and an immortalized, non-Transformed Cell Line. We found that prostate cancer-derived Cell Lines expressed RUNX1 and RUNX2, but not RUNX3. Next, we sought to identify prostate-specific genes whose expression could be regulated by RUNX proteins. Four consensus RUNX sites are located within the prostate-specific antigen (PSA) regulatory region. Chromatin immunoprecipitation (ChIP) analysis showed that RUNX1 is specifically bound to the PSA regulatory region in LNCaP Cells. RUNX1 and RUNX2 activated the PSA regulatory region alone or cooperatively with prostate-derived ETS factor (PDEF) and RUNX1 physically associated with PDEF. Taken together, our results suggest that RUNX factors participate in prostate epithelial Cell function and cooperate with an Ets transcription factor to regulate PSA gene expression.

  • runx1 aml 1 and runx2 aml 3 cooperate with prostate derived ets factor to activate transcription from the psa upstream regulatory region
    Journal of Cellular Biochemistry, 2006
    Co-Authors: Marcie Fowler, Erkut Borazanci, Laura L Mcghee, Shannon Walls Pylant, Jill B Williams, Nathan J Davis, Shari Meyers, Jonathan Glass
    Abstract:

    The RUNX transcription factors (RUNX1, RUNX2, and RUNX3) play essential roles in hematopoiesis and skeletal development. Consistent with these roles in differentiation and Cell cycle, the activity of both RUNX1 and RUNX3 is perturbed in cancer. To determine a role for the RUNX factors in prostate biology, we investigated the expression of RUNX factors in prostate epithelial Cell Lines and normal prostate tissue. RUNX1, RUNX2, and RUNX3 were expressed in both normal prostate tissue and an immortalized, non-Transformed Cell Line. We found that prostate cancer-derived Cell Lines expressed RUNX1 and RUNX2, but not RUNX3. Next, we sought to identify prostate-specific genes whose expression could be regulated by RUNX proteins. Four consensus RUNX sites are located within the prostate-specific antigen (PSA) regulatory region. Chromatin immunoprecipitation (ChIP) analysis showed that RUNX1 is specifically bound to the PSA regulatory region in LNCaP Cells. RUNX1 and RUNX2 activated the PSA regulatory region alone or cooperatively with prostate-derived ETS factor (PDEF) and RUNX1 physically associated with PDEF. Taken together, our results suggest that RUNX factors participate in prostate epithelial Cell function and cooperate with an Ets transcription factor to regulate PSA gene expression. J. Cell. Biochem. © 2005 Wiley-Liss, Inc.

Erkut Borazanci - One of the best experts on this subject based on the ideXlab platform.

  • runx1 aml 1 and runx2 aml 3 cooperate with prostate derived ets factor to activate transcription from the psa upstream regulatory region
    Journal of Cellular Biochemistry, 2006
    Co-Authors: Marcie Fowler, Erkut Borazanci, Laura L Mcghee, Shannon Walls Pylant, Jill B Williams, Jonathan D Glass, Nathan J Davis, Shari Meyers
    Abstract:

    The RUNX transcription factors (RUNX1, RUNX2, and RUNX3) play essential roles in hematopoiesis and skeletal development. Consistent with these roles in differentiation and Cell cycle, the activity of both RUNX1 and RUNX3 is perturbed in cancer. To determine a role for the RUNX factors in prostate biology, we investigated the expression of RUNX factors in prostate epithelial Cell Lines and normal prostate tissue. RUNX1, RUNX2, and RUNX3 were expressed in both normal prostate tissue and an immortalized, non-Transformed Cell Line. We found that prostate cancer-derived Cell Lines expressed RUNX1 and RUNX2, but not RUNX3. Next, we sought to identify prostate-specific genes whose expression could be regulated by RUNX proteins. Four consensus RUNX sites are located within the prostate-specific antigen (PSA) regulatory region. Chromatin immunoprecipitation (ChIP) analysis showed that RUNX1 is specifically bound to the PSA regulatory region in LNCaP Cells. RUNX1 and RUNX2 activated the PSA regulatory region alone or cooperatively with prostate-derived ETS factor (PDEF) and RUNX1 physically associated with PDEF. Taken together, our results suggest that RUNX factors participate in prostate epithelial Cell function and cooperate with an Ets transcription factor to regulate PSA gene expression.

  • runx1 aml 1 and runx2 aml 3 cooperate with prostate derived ets factor to activate transcription from the psa upstream regulatory region
    Journal of Cellular Biochemistry, 2006
    Co-Authors: Marcie Fowler, Erkut Borazanci, Laura L Mcghee, Shannon Walls Pylant, Jill B Williams, Nathan J Davis, Shari Meyers, Jonathan Glass
    Abstract:

    The RUNX transcription factors (RUNX1, RUNX2, and RUNX3) play essential roles in hematopoiesis and skeletal development. Consistent with these roles in differentiation and Cell cycle, the activity of both RUNX1 and RUNX3 is perturbed in cancer. To determine a role for the RUNX factors in prostate biology, we investigated the expression of RUNX factors in prostate epithelial Cell Lines and normal prostate tissue. RUNX1, RUNX2, and RUNX3 were expressed in both normal prostate tissue and an immortalized, non-Transformed Cell Line. We found that prostate cancer-derived Cell Lines expressed RUNX1 and RUNX2, but not RUNX3. Next, we sought to identify prostate-specific genes whose expression could be regulated by RUNX proteins. Four consensus RUNX sites are located within the prostate-specific antigen (PSA) regulatory region. Chromatin immunoprecipitation (ChIP) analysis showed that RUNX1 is specifically bound to the PSA regulatory region in LNCaP Cells. RUNX1 and RUNX2 activated the PSA regulatory region alone or cooperatively with prostate-derived ETS factor (PDEF) and RUNX1 physically associated with PDEF. Taken together, our results suggest that RUNX factors participate in prostate epithelial Cell function and cooperate with an Ets transcription factor to regulate PSA gene expression. J. Cell. Biochem. © 2005 Wiley-Liss, Inc.