Susan L Dalrymple

Summary

Affiliation: Johns Hopkins University
Country: USA

Publications

  1. doi request reprint Tasquinimod prevents the angiogenic rebound induced by fractionated radiation resulting in an enhanced therapeutic response of prostate cancer xenografts
    Susan L Dalrymple
    Department of Oncology, The Sidney Kimmel Comprehensive Cancer Center at Johns Hopkins, The Johns Hopkins University School of Medicine, Baltimore, Maryland, USA
    Prostate 72:638-48. 2012
  2. pmc Loss of androgen receptor-dependent growth suppression by prostate cancer cells can occur independently from acquiring oncogenic addiction to androgen receptor signaling
    Jason M D'Antonio
    Department of Oncology, The Sidney Kimmel Comprehensive Cancer Center, The Johns Hopkins University School of Medicine, Baltimore, Maryland, United States of America
    PLoS ONE 5:e11475. 2010
  3. ncbi request reprint The quinoline-3-carboxamide anti-angiogenic agent, tasquinimod, enhances the anti-prostate cancer efficacy of androgen ablation and taxotere without effecting serum PSA directly in human xenografts
    Susan L Dalrymple
    Department of Urology, The Sidney Kimmel Comprehensive Cancer Center and the Brady Urological Institute, The Johns Hopkins University School of Medicine, Baltimore, Maryland, USA
    Prostate 67:790-7. 2007
  4. pmc Amino acid containing thapsigargin analogues deplete androgen receptor protein via synthesis inhibition and induce the death of prostate cancer cells
    Donald J Vander Griend
    The Sidney Kimmel Comprehensive Cancer Center, The Brady Urological Institute, The Johns Hopkins University School of Medicine, Baltimore, Maryland, USA
    Mol Cancer Ther 8:1340-9. 2009
  5. ncbi request reprint Identification of ABR-215050 as lead second generation quinoline-3-carboxamide anti-angiogenic agent for the treatment of prostate cancer
    John T Isaacs
    The Sidney Kimmel Comprehensive Cancer Center, The Johns Hopkins University School of Medicine, Baltimore, Maryland, USA
    Prostate 66:1768-78. 2006
  6. ncbi request reprint Low-calcium serum-free defined medium selects for growth of normal prostatic epithelial stem cells
    Ivan V Litvinov
    Chemical Therapeutics Program, The Sidney Kimmel Comprehensive Cancer Center at Johns Hopkins, The Johns Hopkins University School of Medicine, Baltimore, MD 21231, USA
    Cancer Res 66:8598-607. 2006
  7. pmc Tasquinimod Is an Allosteric Modulator of HDAC4 survival signaling within the compromised cancer microenvironment
    John T Isaacs
    Sidney Kimmel Comprehensive Cancer Center at Johns Hopkins, The Johns Hopkins University, 1650 Orleans St, Baltimore, MD 21287, USA
    Cancer Res 73:1386-99. 2013
  8. ncbi request reprint PC3, but not DU145, human prostate cancer cells retain the coregulators required for tumor suppressor ability of androgen receptor
    Ivan V Litvinov
    Chemical Therapeutics Program, The Sidney Kimmel Comprehensive Cancer Center at Johns Hopkins, Baltimore, Maryland 21231, USA
    Prostate 66:1329-38. 2006
  9. doi request reprint Detection and quantification of the evolution dynamics of apoptosis using the PET voltage sensor 18F-fluorobenzyl triphenyl phosphonium
    Igal Madar
    Russell H Morgan Department of Radiology, Johns Hopkins Medical Institutions, Baltimore, MD, USA
    J Nucl Med 50:774-80. 2009
  10. ncbi request reprint Pharmacologic basis for the enhanced efficacy of dutasteride against prostatic cancers
    Yi Xu
    Sidney Kimmel Comprehensive Cancer Center at Johns Hopkins, Baltimore, Maryland 21231, USA
    Clin Cancer Res 12:4072-9. 2006

Collaborators

Detail Information

Publications10

  1. doi request reprint Tasquinimod prevents the angiogenic rebound induced by fractionated radiation resulting in an enhanced therapeutic response of prostate cancer xenografts
    Susan L Dalrymple
    Department of Oncology, The Sidney Kimmel Comprehensive Cancer Center at Johns Hopkins, The Johns Hopkins University School of Medicine, Baltimore, Maryland, USA
    Prostate 72:638-48. 2012
    ....
  2. pmc Loss of androgen receptor-dependent growth suppression by prostate cancer cells can occur independently from acquiring oncogenic addiction to androgen receptor signaling
    Jason M D'Antonio
    Department of Oncology, The Sidney Kimmel Comprehensive Cancer Center, The Johns Hopkins University School of Medicine, Baltimore, Maryland, United States of America
    PLoS ONE 5:e11475. 2010
    ..Thus, patients with prostate cancer cells harboring such AR loss-of-function mutations will not benefit from aggressive hormone or anti-AR therapies even though they express AR protein...
  3. ncbi request reprint The quinoline-3-carboxamide anti-angiogenic agent, tasquinimod, enhances the anti-prostate cancer efficacy of androgen ablation and taxotere without effecting serum PSA directly in human xenografts
    Susan L Dalrymple
    Department of Urology, The Sidney Kimmel Comprehensive Cancer Center and the Brady Urological Institute, The Johns Hopkins University School of Medicine, Baltimore, Maryland, USA
    Prostate 67:790-7. 2007
    ..Androgen ablation and taxanes are standard therapies for metastatic prostate cancer. This raises the issue of whether combining tasquinimod with either of these approaches enhances therapeutic efficacy...
  4. pmc Amino acid containing thapsigargin analogues deplete androgen receptor protein via synthesis inhibition and induce the death of prostate cancer cells
    Donald J Vander Griend
    The Sidney Kimmel Comprehensive Cancer Center, The Brady Urological Institute, The Johns Hopkins University School of Medicine, Baltimore, Maryland, USA
    Mol Cancer Ther 8:1340-9. 2009
    ..Based on these results, these prodrugs are undergoing clinical development...
  5. ncbi request reprint Identification of ABR-215050 as lead second generation quinoline-3-carboxamide anti-angiogenic agent for the treatment of prostate cancer
    John T Isaacs
    The Sidney Kimmel Comprehensive Cancer Center, The Johns Hopkins University School of Medicine, Baltimore, Maryland, USA
    Prostate 66:1768-78. 2006
    ..MS clinical trials were discontinued because of unacceptable toxicity, due to dose-dependent induction of proinflammation...
  6. ncbi request reprint Low-calcium serum-free defined medium selects for growth of normal prostatic epithelial stem cells
    Ivan V Litvinov
    Chemical Therapeutics Program, The Sidney Kimmel Comprehensive Cancer Center at Johns Hopkins, The Johns Hopkins University School of Medicine, Baltimore, MD 21231, USA
    Cancer Res 66:8598-607. 2006
    ....
  7. pmc Tasquinimod Is an Allosteric Modulator of HDAC4 survival signaling within the compromised cancer microenvironment
    John T Isaacs
    Sidney Kimmel Comprehensive Cancer Center at Johns Hopkins, The Johns Hopkins University, 1650 Orleans St, Baltimore, MD 21287, USA
    Cancer Res 73:1386-99. 2013
    ..Cancer Res; 73(4); 1386-99. ©2012 AACR...
  8. ncbi request reprint PC3, but not DU145, human prostate cancer cells retain the coregulators required for tumor suppressor ability of androgen receptor
    Ivan V Litvinov
    Chemical Therapeutics Program, The Sidney Kimmel Comprehensive Cancer Center at Johns Hopkins, Baltimore, Maryland 21231, USA
    Prostate 66:1329-38. 2006
    ..While these cells do not express AR, it is unclear whether they retained the coactivators necessary for AR-dependent tumor suppression. To answer this question the response to AR protein expression by PC3 and DU145 cells was evaluated...
  9. doi request reprint Detection and quantification of the evolution dynamics of apoptosis using the PET voltage sensor 18F-fluorobenzyl triphenyl phosphonium
    Igal Madar
    Russell H Morgan Department of Radiology, Johns Hopkins Medical Institutions, Baltimore, MD, USA
    J Nucl Med 50:774-80. 2009
    ..Here, we have characterized the ability of the novel PET voltage sensor (18)F-fluorobenzyl triphenyl phosphonium ((18)F-FBnTP) to quantify the time-dependent apoptotic action of the taxanes paclitaxel and docetaxel in vitro and in vivo...
  10. ncbi request reprint Pharmacologic basis for the enhanced efficacy of dutasteride against prostatic cancers
    Yi Xu
    Sidney Kimmel Comprehensive Cancer Center at Johns Hopkins, Baltimore, Maryland 21231, USA
    Clin Cancer Res 12:4072-9. 2006
    ..Therefore, the levels of expression SRD5A1 and SRD5A2 and the antiprostatic cancer growth response to finasteride, a selective SRD5A2 inhibitor, versus the dual SRD5A1 and SRD5A2 inhibitor, dutasteride, were compared...