"Estramustine phosphate" from_date:2012

Estramustine Phosphate Inhibits TGF-β-Induced Mouse Macrophage Migration and Urokinase-Type Plasminogen Activator Production Transforming growth factor-beta (TGF-) has been demonstrated as a key regulator of immune responses including monocyte/macrophage functions. TGF- regulates macrophage cell migration and polarization, as well as it is shown to modulate macrophage urokinase-type plasminogen activator (uPA) production, which also contributes to macrophage chemotaxis and migration toward damaged or inflamed tissues. Microtubule (MT) cytoskeleton dynamic plays a key role during the cell motility, and any interference on the MT network profoundly affects cell migration. In this study, by using estramustine phosphate (EP), which modifies MT stability, we analysed whether tubulin cytoskeleton

Weekly paclitaxel/estramustine phosphate plus carboplatin administered either weekly or every 4 weeks in the treatment of hormone refractory prostate cancer (HRPC): A randomized phase II trial of the Minnie Pearl Cancer Research Network.

Multi-institutional trial of the epothilone B analogue BMS-247550 with or without estramustine phosphate (EMP) in patients with progressive castrate-metastatic prostate cancer (PCMPC): Updated results.

Neoadjuvant luteinizing-hormone-releasing hormone agonist plus low-dose estramustine phosphate improves prostate-specific antigen-free survival in high-risk prostate cancer patients: a propensity score-matched analysis. The optimal treatment for high-risk prostate cancer (Pca) remains to be established. We previously reported favorable biochemical recurrence-free survival (BRFS) in high-risk Pca patients treated with a neoadjuvant therapy comprising a luteinizing-hormone-releasing hormone (LHRH) agonist plus low dose estramustine phosphate (EMP) (LHRH+EMP) followed by radical prostatectomy (RP). In the present study, we used a retrospective design via propensity score matching to elucidate the clinical benefit of neoadjuvant LHRH+EMP for high-risk Pca. The Michinoku Urological Cancer Study Group

Clinical outcomes and toxicity of estramustine phosphate (EP) addition to docetaxel (D) as first-line therapy for castration-resistant prostate cancer (CRPC): A cumulative analysis on 243 patients (pts) from two randomized phase II trials.

Short-term clinicopathological outcome of neoadjuvant chemohormonal therapy comprising complete androgen blockade, followed by treatment with docetaxel and estramustine phosphate before radical prostatectomy in Japanese patients with high-risk localized p To assess the outcome of neoadjuvant chemohormonal therapy comprising complete androgen blockade followed by treatment with docetaxel and estramustine phosphate before radical prostatectomy in Japanese patients with a high risk of localized prostate cancer (PCa). Complete androgen blockade followed by 6 cycles of docetaxel (30 mg/m2) with estramustine phosphate (560 mg) were given to 18 PCa patients before radical prostatectomy. Subsequently, the clinical and pathological outcomes were analyzed. No patients had severe adverse events during

, no protocol has been established. This study aimed to assess the effect of androgen deprivation therapy combined with low-dose estramustine phosphate (EMP) on BCR compared with androgen deprivation therapy (ADT) alone in high- and very high-risk patients with PC. This retrospective study targeted patients with PC meeting the National Comprehensive Cancer Network high-risk criteria (cT1-4N0M0), with 173

, carmustine, and vincristine (PBV) for chemotherapy pre-treated patients with recurrent glioblastoma: a single-institution analysis. J Neurooncol 109(2):433–438 CAS PubMed Article Google Scholar 89. Rosenthal MA, Gruber ML, Glass J et al (2000) Phase II study of combination taxol and estramustine phosphate in the treatment of recurrent glioblastoma multiforme. J Neurooncol 47(1):59

in 2005-2011 at four hospitals in Ibaraki, Japan were analyzed. We determined the cause-specific survival (CSS) from the start of docetaxel therapy and the time point of CRPC diagnosis, and we compared the CSS achieved with/without prior classical SHTs, which were defined as low-dose steroid and estramustine phosphate. Of the 73 enrolled patients, 26 underwent docetaxel therapy (DOC group), and 47

Ablation of the ATP-binding cassette transporter, Abca2 modifies response to estrogen-based therapies The ATP-binding cassette transporter 2 (ABCA2) is an endolysosomal protein expressed in oligodendrocytes and Schwann cells, prostate, ovary and macrophages. In cell cultures, ABCA2 over-expression has been linked with resistance to the anticancer agent, estramustine phosphate (EMP; a nor-nitrogen

been used include diethylstilbestrol, fosfestrol, ethinylestradiol, ethinylestradiol sulfonate, polyestradiol phosphate, and estradiol undecylate, as well as the dual estrogenic and cytostatic agent estramustine phosphate.[54][55] Newer estrogens with improved tolerability and safety like GTx-758 have also been studied.[56][57] Estrogens are effective in prostate cancer because they are functional 5 mg/day Fosfestrol 100–480 mg 1–3x/day Chlorotrianisene 12–48 mg/day Quadrosilan 900 mg/day Estramustine phosphate