James R Lambert

Summary

Affiliation: University of Colorado Health Sciences Center
Country: USA

Publications

  1. ncbi Prostate derived factor in human prostate cancer cells: gene induction by vitamin D via a p53-dependent mechanism and inhibition of prostate cancer cell growth
    James R Lambert
    Department of Pathology, University of Colorado Health Sciences Center, Aurora, Colorado 80045, USA
    J Cell Physiol 208:566-74. 2006
  2. ncbi p53 controls prostate-derived factor/macrophage inhibitory cytokine/NSAID-activated gene expression in response to cell density, DNA damage and hypoxia through diverse mechanisms
    Julie A Kelly
    Department of Pathology, University of Colorado Denver, 12801 E 17th Avenue, Aurora, CO 80045, USA
    Cancer Lett 277:38-47. 2009
  3. ncbi Aberrant HOXC expression accompanies the malignant phenotype in human prostate
    Gary J Miller
    Department of Pathology, University of Colorado Health Sciences Center, Denver, Colorado 80262, USA
    Cancer Res 63:5879-88. 2003
  4. ncbi HOXC8 inhibits androgen receptor signaling in human prostate cancer cells by inhibiting SRC-3 recruitment to direct androgen target genes
    Sunshine Daddario Axlund
    Department of Pathology, University of Colorado Denver, Anschutz Medical Campus, 12801 E 17th Ave, Aurora, CO 80045, USA
    Mol Cancer Res 8:1643-55. 2010
  5. ncbi Mechanistic and pharmacodynamic studies of a 25-hydroxyvitamin D3 derivative in prostate cancer cells
    James R Lambert
    Department of Pathology, University of Colorado Health Science Center, Aurora, CO, USA
    Biochem Biophys Res Commun 361:189-95. 2007
  6. ncbi Glucocorticoid receptor-DNA interactions: binding energetics are the primary determinant of sequence-specific transcriptional activity
    David L Bain
    Department of Pharmaceutical Sciences, University of Colorado Anschutz Medical Campus, Aurora, CO 80045, USA
    J Mol Biol 422:18-32. 2012
  7. ncbi Growth differentiation factor-15 (GDF-15) suppresses in vitro angiogenesis through a novel interaction with connective tissue growth factor (CCN2)
    Ramon J Whitson
    Department of Pathology, University of Colorado Denver, Anschutz Medical Campus, Aurora, Colorado 80045
    J Cell Biochem 114:1424-33. 2013
  8. ncbi Growth factors in benign prostatic hyperplasia: basic science implications
    M Scott Lucia
    Department of Pathology, University of Colorado DHSC, 12800 East 19th Avenue, PO Box 6511, Aurora, CO 80045, USA
    Curr Urol Rep 9:272-8. 2008
  9. ncbi The anticancer agent prodigiosin induces p21WAF1/CIP1 expression via transforming growth factor-beta receptor pathway
    Vanessa Soto Cerrato
    Department of Pathology and Experimental Therapeutics, Cancer Cell Biology Research Group, Universitat de Barcelona, and Laboratori de Recerca Translacional, ICO IDIBELL, L Hospitalet de Llobregat, Barcelona, Spain
    Biochem Pharmacol 74:1340-9. 2007
  10. ncbi Prodigiosin induces the proapoptotic gene NAG-1 via glycogen synthase kinase-3beta activity in human breast cancer cells
    Vanessa Soto-Cerrato
    Department of Pathology and Experimental Therapeutics, Cancer Cell Biology Research Group, Universitat de Barcelona, Pavelló Central, 5a planta, LR 5101 C Feixa Llarga s n, E 08907 L Hospitalet, Barcelona, Spain
    Mol Cancer Ther 6:362-9. 2007

Collaborators

Detail Information

Publications10

  1. ncbi Prostate derived factor in human prostate cancer cells: gene induction by vitamin D via a p53-dependent mechanism and inhibition of prostate cancer cell growth
    James R Lambert
    Department of Pathology, University of Colorado Health Sciences Center, Aurora, Colorado 80045, USA
    J Cell Physiol 208:566-74. 2006
    ..These data demonstrate that PDF exerts antitumorigenic properties on PCa cells and its regulation by 1,25D may provide insights into the action of 1,25D in PCa...
  2. ncbi p53 controls prostate-derived factor/macrophage inhibitory cytokine/NSAID-activated gene expression in response to cell density, DNA damage and hypoxia through diverse mechanisms
    Julie A Kelly
    Department of Pathology, University of Colorado Denver, 12801 E 17th Avenue, Aurora, CO 80045, USA
    Cancer Lett 277:38-47. 2009
    ..Thus, PDF may represent a novel target of p53 in response to cell stress...
  3. ncbi Aberrant HOXC expression accompanies the malignant phenotype in human prostate
    Gary J Miller
    Department of Pathology, University of Colorado Health Sciences Center, Denver, Colorado 80262, USA
    Cancer Res 63:5879-88. 2003
    ..We speculate that HOXC overexpression may predispose tumor cells to androgen independence by necessitating adaptation to diminished androgen signaling...
  4. ncbi HOXC8 inhibits androgen receptor signaling in human prostate cancer cells by inhibiting SRC-3 recruitment to direct androgen target genes
    Sunshine Daddario Axlund
    Department of Pathology, University of Colorado Denver, Anschutz Medical Campus, 12801 E 17th Ave, Aurora, CO 80045, USA
    Mol Cancer Res 8:1643-55. 2010
    ..A greater understanding of HOXC8 actions in the prostate and its interactions with androgen signaling pathways may elucidate mechanisms driving the onset and progression of prostate cancer...
  5. ncbi Mechanistic and pharmacodynamic studies of a 25-hydroxyvitamin D3 derivative in prostate cancer cells
    James R Lambert
    Department of Pathology, University of Colorado Health Science Center, Aurora, CO, USA
    Biochem Biophys Res Commun 361:189-95. 2007
    ..Furthermore, we carried out cellular uptake and serum stability studies of 25-OH-D(3)-3-BE to demonstrate potential therapeutic applicability of 25-OH-D(3)-3-BE in hormone-sensitive and hormone-insensitive prostate cancer...
  6. ncbi Glucocorticoid receptor-DNA interactions: binding energetics are the primary determinant of sequence-specific transcriptional activity
    David L Bain
    Department of Pharmaceutical Sciences, University of Colorado Anschutz Medical Campus, Aurora, CO 80045, USA
    J Mol Biol 422:18-32. 2012
    ..Thus, despite the complexity of GR function, DNA binding energetics are the primary determinant of sequence-specific transcriptional activity...
  7. ncbi Growth differentiation factor-15 (GDF-15) suppresses in vitro angiogenesis through a novel interaction with connective tissue growth factor (CCN2)
    Ramon J Whitson
    Department of Pathology, University of Colorado Denver, Anschutz Medical Campus, Aurora, Colorado 80045
    J Cell Biochem 114:1424-33. 2013
    ..Furthermore, antagonism of CCN2 mediated angiogenesis by GDF-15 may provide insight into the functional role of GDF-15 in disease states. J. Cell. Biochem. 114: 1424-1433, 2013. © 2012 Wiley Periodicals, Inc...
  8. ncbi Growth factors in benign prostatic hyperplasia: basic science implications
    M Scott Lucia
    Department of Pathology, University of Colorado DHSC, 12800 East 19th Avenue, PO Box 6511, Aurora, CO 80045, USA
    Curr Urol Rep 9:272-8. 2008
    ..As we begin to unravel the precise mechanisms involved, new treatments for BPH aimed at these interacting pathways may emerge...
  9. ncbi The anticancer agent prodigiosin induces p21WAF1/CIP1 expression via transforming growth factor-beta receptor pathway
    Vanessa Soto Cerrato
    Department of Pathology and Experimental Therapeutics, Cancer Cell Biology Research Group, Universitat de Barcelona, and Laboratori de Recerca Translacional, ICO IDIBELL, L Hospitalet de Llobregat, Barcelona, Spain
    Biochem Pharmacol 74:1340-9. 2007
    ..Taken together, these results suggest the TGF-beta pathway is required for induction of p21 expression after prodigiosin treatment of MCF-7 cells...
  10. ncbi Prodigiosin induces the proapoptotic gene NAG-1 via glycogen synthase kinase-3beta activity in human breast cancer cells
    Vanessa Soto-Cerrato
    Department of Pathology and Experimental Therapeutics, Cancer Cell Biology Research Group, Universitat de Barcelona, Pavelló Central, 5a planta, LR 5101 C Feixa Llarga s n, E 08907 L Hospitalet, Barcelona, Spain
    Mol Cancer Ther 6:362-9. 2007
    ..These findings suggest that prodigiosin-mediated GSK-3beta activation is a key event in regulating the molecular pathways that trigger the apoptosis induced by this anticancer agent...