Research Topics
Genomes and Genes | Susan L DalrympleSummaryAffiliation: Johns Hopkins University Country: USA Publications
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Publications
Tasquinimod prevents the angiogenic rebound induced by fractionated radiation resulting in an enhanced therapeutic response of prostate cancer xenograftsSusan 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....
Loss of androgen receptor-dependent growth suppression by prostate cancer cells can occur independently from acquiring oncogenic addiction to androgen receptor signalingJason 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...
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 xenograftsSusan 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...
Amino acid containing thapsigargin analogues deplete androgen receptor protein via synthesis inhibition and induce the death of prostate cancer cellsDonald 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...
Identification of ABR-215050 as lead second generation quinoline-3-carboxamide anti-angiogenic agent for the treatment of prostate cancerJohn 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...
Low-calcium serum-free defined medium selects for growth of normal prostatic epithelial stem cellsIvan 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....
PC3, but not DU145, human prostate cancer cells retain the coregulators required for tumor suppressor ability of androgen receptorIvan 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...
Detection and quantification of the evolution dynamics of apoptosis using the PET voltage sensor 18F-fluorobenzyl triphenyl phosphoniumIgal 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...
Pharmacologic basis for the enhanced efficacy of dutasteride against prostatic cancersYi 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...
