PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 19239458-11 2009 CONCLUSIONS: Our analysis suggests the therapeutic value of low-dose flutamide alone or combined with finasteride as first-line agents in a possible graduated approach for treating PSA-only recurrent prostate cancer. Flutamide 69-78 kallikrein related peptidase 3 Homo sapiens 181-184 15661065-3 2005 His serum prostate-specific antigen level was reduced to below the normal range after a combination treatment of a luteinizing hormone-releasing hormone agonist and flutamide for prostate carcinoma. Flutamide 165-174 kallikrein related peptidase 3 Homo sapiens 10-35 19389135-6 2009 RESULTS: Flutamide, but not hydroxyflutamide, successfully suppressed the transcription of all of the mutant androgen receptors examined in this study and also showed suppressive effects on PSA secretion by LNCaP cells treated with dihydrotestosterone. Flutamide 9-18 kallikrein related peptidase 3 Homo sapiens 190-193 18497080-5 2008 Herein, we have elucidated the effects of flutamide (a defined anti-androgen) and DHT on the expression of PSA and Zinc finger E-box Binding factor (ZEB-1). Flutamide 42-51 kallikrein related peptidase 3 Homo sapiens 107-110 18497080-9 2008 In the current study, the effects of 1 and 10 nM flutamide, in combination with 1 and 10 nM DHT, on expression of ZEB-1 and PSA, were investigated in 22Rv1, an androgen-responsive human PC cell line. Flutamide 49-58 kallikrein related peptidase 3 Homo sapiens 124-127 16153201-1 2005 OBJECTIVE: To determine the prostate-specific antigen (PSA) response and time to PSA or radiographic progression in men with prostate cancer refractory to bicalutamide and/or flutamide therapy. Flutamide 175-184 kallikrein related peptidase 3 Homo sapiens 28-59 16153202-10 2005 CONCLUSIONS: MAB using flutamide as second-line hormonal therapy can give a comparatively favourable PSA response with no severe side-effects; therefore, this therapy may be suitable for patients with HRPC after primary MAB using bicalutamide has failed, particularly in those with no bone metastases or whose disease has progressed for >1 year after first-line therapy. Flutamide 23-32 kallikrein related peptidase 3 Homo sapiens 101-104 16275987-6 2005 Analysis of androgen receptor and RNA polymerase II binding to the endogenous PSA gene by chromatin immunoprecipitation revealed that flutamide treatment and androgen withdrawal have different molecular mechanisms. Flutamide 134-143 kallikrein related peptidase 3 Homo sapiens 78-81 14635088-9 2003 In LNCaP prostate carcinoma cells, I3C treatment inhibited production of PSA, whereas combinations of I3C and the androgen antagonist flutamide more effectively inhibited DNA synthesis and PSA levels compared with either agent alone. Flutamide 134-143 kallikrein related peptidase 3 Homo sapiens 189-192 15223852-7 2004 Testosterone and PSA levels show a dose-dependent response to flutamide monotherapy. Flutamide 62-71 kallikrein related peptidase 3 Homo sapiens 17-20 14616448-1 2003 OBJECTIVE: To investigate the efficacy of low-dose flutamide (125 mg twice daily) in the treatment of prostate-specific antigen (PSA) recurrence after definitive treatment with radical retropubic prostatectomy (RRP), external-beam radiation therapy (RT), or cryotherapy. Flutamide 51-60 kallikrein related peptidase 3 Homo sapiens 102-133 14616448-2 2003 PATIENTS AND METHODS: In this phase II prospective trial, patients who had a PSA recurrence after definitive treatment for prostate cancer were treated with flutamide. Flutamide 157-166 kallikrein related peptidase 3 Homo sapiens 77-80 14616448-9 2003 CONCLUSIONS: The administration of low-dose flutamide (125 mg) was clinically effective in treating PSA recurrence after definitive treatments for prostate cancer, and was well tolerated. Flutamide 44-53 kallikrein related peptidase 3 Homo sapiens 100-103 11316974-9 2001 In patients who had been treated with flutamide in combination with leuprorelin, the mean PSA level did not exceed the pretreatment levels after leuprorelin administration. Flutamide 38-47 kallikrein related peptidase 3 Homo sapiens 90-93 11706524-9 2001 CONCLUSION: These results clearly demonstrate that, in patients with prostatic cancer, the administration of FLU for 2 weeks prior to the first LH-RHa administration is effective in preventing PSA flare, as well as in inducing an early decline in PSA levels. Flutamide 109-112 kallikrein related peptidase 3 Homo sapiens 193-196 11706524-9 2001 CONCLUSION: These results clearly demonstrate that, in patients with prostatic cancer, the administration of FLU for 2 weeks prior to the first LH-RHa administration is effective in preventing PSA flare, as well as in inducing an early decline in PSA levels. Flutamide 109-112 kallikrein related peptidase 3 Homo sapiens 247-250 14624911-0 2003 Combination of low-dose flutamide and finasteride for PSA-only recurrent prostate cancer after primary therapy. Flutamide 24-33 kallikrein related peptidase 3 Homo sapiens 54-57 14624911-1 2003 OBJECTIVES: To evaluate the efficacy and tolerability of combined finasteride and low-dose flutamide for prostate-specific antigen (PSA)-only recurrence after definitive therapy and to determine the predictors of recurrence-free survival. Flutamide 91-100 kallikrein related peptidase 3 Homo sapiens 105-137 14624911-12 2003 CONCLUSIONS: The combination of finasteride and flutamide showed a moderate efficacy in patients with PSA-only recurrence after definitive therapy. Flutamide 48-57 kallikrein related peptidase 3 Homo sapiens 102-105 11706524-0 2001 Inhibition of PSA flare in prostate cancer patients by administration of flutamide for 2 weeks before initiation of treatment with slow-releasing LH-RH agonist. Flutamide 73-82 kallikrein related peptidase 3 Homo sapiens 14-17 11706524-1 2001 BACKGROUND: A prospective randomized study was designed to determine whether flutamide (FLU) administered before treatment with a luteinizing hormone-releasing hormone agonist (LH-RHa) prevented prostate-specific antigen (PSA) flare in prostate cancer patients. Flutamide 77-86 kallikrein related peptidase 3 Homo sapiens 195-226 11706524-1 2001 BACKGROUND: A prospective randomized study was designed to determine whether flutamide (FLU) administered before treatment with a luteinizing hormone-releasing hormone agonist (LH-RHa) prevented prostate-specific antigen (PSA) flare in prostate cancer patients. Flutamide 88-91 kallikrein related peptidase 3 Homo sapiens 195-226 11706524-5 2001 RESULTS: Treatment with FLU prior to LH-RHa induced an early decline in PSA level. Flutamide 24-27 kallikrein related peptidase 3 Homo sapiens 72-75 11706524-8 2001 However, the number of patients with PSA flare was significantly lower in patients with prior FLU administration than in those with LH-RHa alone. Flutamide 94-97 kallikrein related peptidase 3 Homo sapiens 37-40 11316974-10 2001 The rate of decrease in PSA in the group receiving simultaneous administration of flutamide with leuprorelin showed a decline comparable to that during the period before leuprorelin administration in the flutamide pretreatment groups. Flutamide 82-91 kallikrein related peptidase 3 Homo sapiens 24-27 11316974-10 2001 The rate of decrease in PSA in the group receiving simultaneous administration of flutamide with leuprorelin showed a decline comparable to that during the period before leuprorelin administration in the flutamide pretreatment groups. Flutamide 204-213 kallikrein related peptidase 3 Homo sapiens 24-27 11085345-11 2000 Cessation of flutamide for at least 4 weeks and, in the case of bicalutamide, even 8 weeks, is mandatory before antiandrogen withdrawal syndrome can be excluded as the cause of decreasing PSA values. Flutamide 13-22 kallikrein related peptidase 3 Homo sapiens 188-191 11062382-8 2000 CONCLUSIONS: When combined with castration, 500 mg of flutamide appears to be equally effective in lowering serum PSA and is not significantly more toxic than conventional dosing. Flutamide 54-63 kallikrein related peptidase 3 Homo sapiens 114-117 10851326-2 1999 In the 26 patients with stage T(2) disease who have received continuous CAB with an LHRH agonist and flutamide, progression of cancer, as evidenced by rising serum prostate specific antigen (PSA), was observed in only one patient receiving CAB, occurring after 7.3 years of continuous CAB treatment. Flutamide 101-110 kallikrein related peptidase 3 Homo sapiens 164-189 10705202-8 2000 PSA at diagnosis and PSA at the start of flutamide use were significantly lower for patients with CR. Flutamide 41-50 kallikrein related peptidase 3 Homo sapiens 21-24 10705202-9 2000 However, the results of multivariate logistic regression analysis demonstrated that only the post-treatment nadir PSA level was significantly correlated with prognosis of flutamide use. Flutamide 171-180 kallikrein related peptidase 3 Homo sapiens 114-117 10705202-10 2000 CONCLUSIONS: Flutamide use as second-line hormone therapy should be limited to cases in which first-line hormone therapy has been highly effective and for whom the post-treatment nadir PSA level was within normal limits, and other patients should undergo other therapies. Flutamide 13-22 kallikrein related peptidase 3 Homo sapiens 185-188 10634368-10 2000 A 6-month course of antiandrogen treatments with spironolactone, flutamide, or finasteride determines a reduction of PSA levels in these subjects. Flutamide 65-74 kallikrein related peptidase 3 Homo sapiens 117-120 11095136-5 2000 The testosterone and prostate-specific antigen (PSA) levels in patients administered flutamide (Group II) increased significantly 3 days after the first dose of LH-RH analog, whereas no such increase was observed in patients administered CMA (Group I), indicating that CMA prevented the flare-up. Flutamide 85-94 kallikrein related peptidase 3 Homo sapiens 21-52 10851326-2 1999 In the 26 patients with stage T(2) disease who have received continuous CAB with an LHRH agonist and flutamide, progression of cancer, as evidenced by rising serum prostate specific antigen (PSA), was observed in only one patient receiving CAB, occurring after 7.3 years of continuous CAB treatment. Flutamide 101-110 kallikrein related peptidase 3 Homo sapiens 191-194 9750522-1 1998 The antiandrogen withdrawal syndrome was first reported in patients with prostate cancer who manifested disease progression after total androgen blockage therapy with medical or surgical castration and pure antiandrogen, flutamide; discontinuation of flutamide resulted in a decline in prostate specific antigen and, in some cases, with clinical response. Flutamide 251-260 kallikrein related peptidase 3 Homo sapiens 286-311 9187700-15 1997 Mean percent decline in PSA value from baseline was 87.0 +/- 3.1% with flutamide alone and 94.0 +/- 1.9% with both flutamide and finasteride (P = 0.001). Flutamide 71-80 kallikrein related peptidase 3 Homo sapiens 24-27 9224356-0 1997 Re: Characterization of patients with androgen independent prostatic carcinoma whose serum prostate specific antigen decreased following flutamide withdrawal. Flutamide 137-146 kallikrein related peptidase 3 Homo sapiens 91-116 9186348-4 1997 In terms of biological response 11 of 20 patients (55%) receiving prednisolone and 10 of 20 (50%) receiving flutamide exhibited prostate specific antigen (PSA) suppression. Flutamide 108-117 kallikrein related peptidase 3 Homo sapiens 128-153 9186348-4 1997 In terms of biological response 11 of 20 patients (55%) receiving prednisolone and 10 of 20 (50%) receiving flutamide exhibited prostate specific antigen (PSA) suppression. Flutamide 108-117 kallikrein related peptidase 3 Homo sapiens 155-158 9186348-5 1997 Average minimum PSA was 54 and 52% of the initial PSA in patients receiving prednisolone and flutamide, respectively. Flutamide 93-102 kallikrein related peptidase 3 Homo sapiens 16-19 9634122-1 1998 Flutamide withdrawal syndrome is characterized by a decrease in prostate-specific antigen (PSA) after flutamide withdrawal in a subset of patients with progressing metastatic carcinoma of the prostate. Flutamide 0-9 kallikrein related peptidase 3 Homo sapiens 64-95 9634122-3 1998 We describe a patient with androgen-independent prostate cancer in whom PSA continued to decrease for a period of 15 months after flutamide withdrawal. Flutamide 130-139 kallikrein related peptidase 3 Homo sapiens 72-75 9471771-5 1997 Eight (22.9%) of 35 patients showed a decline in PSA levels following flutamide withdrawal. Flutamide 70-79 kallikrein related peptidase 3 Homo sapiens 49-52 9187700-15 1997 Mean percent decline in PSA value from baseline was 87.0 +/- 3.1% with flutamide alone and 94.0 +/- 1.9% with both flutamide and finasteride (P = 0.001). Flutamide 115-124 kallikrein related peptidase 3 Homo sapiens 24-27 9112515-0 1997 Prostate specific antigen decreases after withdrawal of antiandrogen therapy with bicalutamide or flutamide in patients receiving combined androgen blockade. Flutamide 98-107 kallikrein related peptidase 3 Homo sapiens 0-25 9112515-1 1997 PURPOSE: We determined whether decreases in prostate specific antigen (PSA) would occur after withdrawal of double-blinded antiandrogen therapy with flutamide or bicalutamide for clinical progression or increasing PSA concentration in patients receiving combined androgen blockade for advanced prostate cancer. Flutamide 149-158 kallikrein related peptidase 3 Homo sapiens 44-69 9112515-1 1997 PURPOSE: We determined whether decreases in prostate specific antigen (PSA) would occur after withdrawal of double-blinded antiandrogen therapy with flutamide or bicalutamide for clinical progression or increasing PSA concentration in patients receiving combined androgen blockade for advanced prostate cancer. Flutamide 149-158 kallikrein related peptidase 3 Homo sapiens 71-74 9112515-6 1997 PSA responses after withdrawal of flutamide therapy occurred within the first few days, whereas those after withdrawal of bicalutamide therapy occurred within 4 to 8 weeks. Flutamide 34-43 kallikrein related peptidase 3 Homo sapiens 0-3 9112515-9 1997 CONCLUSIONS: For patients with stage D2 prostate cancer and disease progression or an increasing PSA concentration, withdrawal of antiandrogen therapy with bicalutamide or flutamide may result in a PSA response. Flutamide 172-181 kallikrein related peptidase 3 Homo sapiens 97-100 9112515-9 1997 CONCLUSIONS: For patients with stage D2 prostate cancer and disease progression or an increasing PSA concentration, withdrawal of antiandrogen therapy with bicalutamide or flutamide may result in a PSA response. Flutamide 172-181 kallikrein related peptidase 3 Homo sapiens 198-201 9112515-10 1997 The time to PSA response is longer with bicalutamide than with flutamide. Flutamide 63-72 kallikrein related peptidase 3 Homo sapiens 12-15 8558675-0 1996 Characterization of patients with androgen-independent prostatic carcinoma whose serum prostate specific antigen decreased following flutamide withdrawal. Flutamide 133-142 kallikrein related peptidase 3 Homo sapiens 87-112 9144890-2 1997 A "flutamide withdrawal syndrome" was first described by Kelly and Scher [15], who reported a decrease in serum prostate-specific antigen (PSA) levels after the removal of flutamide from the treatment regimen. Flutamide 3-12 kallikrein related peptidase 3 Homo sapiens 112-143 8973674-3 1996 Flutamide (250 mg three times a day) was added after serum PSA levels stabilized. Flutamide 0-9 kallikrein related peptidase 3 Homo sapiens 59-62 8973674-5 1996 Combined finasteride and flutamide resulted in a mean 91% reduction in serum PSA levels, with 85% of men achieving a nadir serum PSA level of less than 4.0 ng/mL and 46% achieving undetectable levels (0.2 ng/mL or less). Flutamide 25-34 kallikrein related peptidase 3 Homo sapiens 77-80 8973674-5 1996 Combined finasteride and flutamide resulted in a mean 91% reduction in serum PSA levels, with 85% of men achieving a nadir serum PSA level of less than 4.0 ng/mL and 46% achieving undetectable levels (0.2 ng/mL or less). Flutamide 25-34 kallikrein related peptidase 3 Homo sapiens 129-132 8558675-1 1996 PURPOSE: We confirmed the reported rate of prostate specific antigen (PSA) suppression after flutamide withdrawal in patients with metastatic prostatic carcinoma, increasing serum PSA and tumor progression following treatment with total androgen blockade (castration and flutamide). Flutamide 93-102 kallikrein related peptidase 3 Homo sapiens 43-68 8558675-1 1996 PURPOSE: We confirmed the reported rate of prostate specific antigen (PSA) suppression after flutamide withdrawal in patients with metastatic prostatic carcinoma, increasing serum PSA and tumor progression following treatment with total androgen blockade (castration and flutamide). Flutamide 93-102 kallikrein related peptidase 3 Homo sapiens 70-73 8558675-1 1996 PURPOSE: We confirmed the reported rate of prostate specific antigen (PSA) suppression after flutamide withdrawal in patients with metastatic prostatic carcinoma, increasing serum PSA and tumor progression following treatment with total androgen blockade (castration and flutamide). Flutamide 93-102 kallikrein related peptidase 3 Homo sapiens 180-183 8558675-1 1996 PURPOSE: We confirmed the reported rate of prostate specific antigen (PSA) suppression after flutamide withdrawal in patients with metastatic prostatic carcinoma, increasing serum PSA and tumor progression following treatment with total androgen blockade (castration and flutamide). Flutamide 271-280 kallikrein related peptidase 3 Homo sapiens 43-68 8558675-1 1996 PURPOSE: We confirmed the reported rate of prostate specific antigen (PSA) suppression after flutamide withdrawal in patients with metastatic prostatic carcinoma, increasing serum PSA and tumor progression following treatment with total androgen blockade (castration and flutamide). Flutamide 271-280 kallikrein related peptidase 3 Homo sapiens 70-73 8558675-2 1996 The value of clinical variables in predicting the rate of PSA decrease after flutamide withdrawal was assessed and adrenal androgen metabolism was correlated with the rate of PSA suppression following flutamide withdrawal. Flutamide 77-86 kallikrein related peptidase 3 Homo sapiens 58-61 8558675-2 1996 The value of clinical variables in predicting the rate of PSA decrease after flutamide withdrawal was assessed and adrenal androgen metabolism was correlated with the rate of PSA suppression following flutamide withdrawal. Flutamide 201-210 kallikrein related peptidase 3 Homo sapiens 175-178 8558675-7 1996 RESULTS: Of 39 patients studied 11 (28.2%, 95% confidence internal 14 to 45%) had a PSA decrease (more than 50% from baseline) following flutamide withdrawal and they were treated with initial complete androgen blockade. Flutamide 137-146 kallikrein related peptidase 3 Homo sapiens 84-87 8558675-10 1996 No statistical correlation between endocrine studies or serum bombesin secretion and PSA decrease was found, although patients with a PSA decrease after flutamide withdrawal tended to have a lower dehydroepiandrosterone concentration than those with PSA progression. Flutamide 153-162 kallikrein related peptidase 3 Homo sapiens 134-137 8558675-10 1996 No statistical correlation between endocrine studies or serum bombesin secretion and PSA decrease was found, although patients with a PSA decrease after flutamide withdrawal tended to have a lower dehydroepiandrosterone concentration than those with PSA progression. Flutamide 153-162 kallikrein related peptidase 3 Homo sapiens 134-137 8558675-12 1996 CONCLUSIONS: We confirmed the existence of the reported paradoxical PSA decrease in patients with androgen-independent carcinoma of the prostate, and that the delivery of simultaneous initial flutamide with castration predicts for PSA decrease. Flutamide 192-201 kallikrein related peptidase 3 Homo sapiens 231-234 8995493-9 1996 In addition, prostate-specific antigen (PSA)-defined responses were observed in six patients receiving therapy at 175 microg/ml, but these responses were confounded by cessation of therapy with flutamide during suramin treatment. Flutamide 194-203 kallikrein related peptidase 3 Homo sapiens 13-45 7510915-4 1994 CONCLUSIONS: The relationship between antiandrogen withdrawal and a change in PSA may be a general phenomenon, not unique to flutamide. Flutamide 125-134 kallikrein related peptidase 3 Homo sapiens 78-81 8620419-2 1995 BACKGROUND: Flutamide withdrawal has been reported to be therapeutically efficacious for patients with hormone-refractory prostate cancer, with a reported prostate specific antigen (PSA) response rate of 29%. Flutamide 12-21 kallikrein related peptidase 3 Homo sapiens 155-180 8620419-2 1995 BACKGROUND: Flutamide withdrawal has been reported to be therapeutically efficacious for patients with hormone-refractory prostate cancer, with a reported prostate specific antigen (PSA) response rate of 29%. Flutamide 12-21 kallikrein related peptidase 3 Homo sapiens 182-185 7541862-1 1995 PURPOSE: We assess the impact of deferred flutamide treatment on the serum prostate specific antigen (PSA) level in patients with localized or metastatic cancer. Flutamide 42-51 kallikrein related peptidase 3 Homo sapiens 75-100 7541862-1 1995 PURPOSE: We assess the impact of deferred flutamide treatment on the serum prostate specific antigen (PSA) level in patients with localized or metastatic cancer. Flutamide 42-51 kallikrein related peptidase 3 Homo sapiens 102-105 7541862-3 1995 RESULTS: Of 40 evaluable patients with localized cancer and 50 with metastatic cancer 32 (80%) and 27 (54%), respectively, had a PSA decrease of 50% or more of baseline during flutamide treatment (p = 0.014). Flutamide 176-185 kallikrein related peptidase 3 Homo sapiens 129-132 7541862-4 1995 Among patients with localized cancer actuarial analysis of freedom from PSA elevation during flutamide treatment favored those with a 50% or greater PSA decrease (p = 0.006) but in patients with metastatic cancer the analysis revealed no significant difference. Flutamide 93-102 kallikrein related peptidase 3 Homo sapiens 72-75 7541862-4 1995 Among patients with localized cancer actuarial analysis of freedom from PSA elevation during flutamide treatment favored those with a 50% or greater PSA decrease (p = 0.006) but in patients with metastatic cancer the analysis revealed no significant difference. Flutamide 93-102 kallikrein related peptidase 3 Homo sapiens 149-152 7535978-0 1995 Prostate specific antigen decline following the discontinuation of flutamide in patients with stage D2 prostate cancer. Flutamide 67-76 kallikrein related peptidase 3 Homo sapiens 0-25 1948117-6 1991 The level of prostate-specific antigen was reduced markedly following 6 months" treatment with flutamide. Flutamide 95-104 kallikrein related peptidase 3 Homo sapiens 13-38 7679759-3 1993 We report 3 representative cases receiving complete androgen blockade with either gonadotropin-releasing hormone or orchiectomy plus the antiandrogen flutamide, which demonstrated sustained declines in serum PSA levels after discontinuation of the antiandrogen. Flutamide 150-159 kallikrein related peptidase 3 Homo sapiens 208-211 7679759-6 1993 The results suggest that a trial of flutamide withdrawal is justified in an asymptomatic patient with an increasing PSA before treatment with more toxic therapies. Flutamide 36-45 kallikrein related peptidase 3 Homo sapiens 116-119 31564004-7 2020 The 3- (80.8% vs. 35.3%; p < 0.001) and 6-month (73.1% vs. 31.4%; p < 0.001) prostate-specific antigen response rates were higher in the enzalutamide than in the flutamide group. Flutamide 168-177 kallikrein related peptidase 3 Homo sapiens 83-108 1693455-9 1990 In follow-up studies a marked decline in PSA values after transurethral resection or antiandrogen therapy (orchiectomy/Zoladex/ICI/flutamide, Essex). Flutamide 131-140 kallikrein related peptidase 3 Homo sapiens 41-44 30971225-10 2019 The expected results of this study will be that enzalutamide is superior to flutamide in terms of PSA response. Flutamide 76-85 kallikrein related peptidase 3 Homo sapiens 98-101 31262916-5 2019 RESULTS: Patients who responded well to flutamide (Flutamide effective) following initial maximum androgen blockade (MAB) showed significantly higher changes in serum PSA levels (p=0.039) and PSA-progression-free survival (PFS) rate (p=0.016) following enzalutamide therapy compared to those who did not respond well to flutamide. Flutamide 40-49 kallikrein related peptidase 3 Homo sapiens 167-170 31262916-5 2019 RESULTS: Patients who responded well to flutamide (Flutamide effective) following initial maximum androgen blockade (MAB) showed significantly higher changes in serum PSA levels (p=0.039) and PSA-progression-free survival (PFS) rate (p=0.016) following enzalutamide therapy compared to those who did not respond well to flutamide. Flutamide 40-49 kallikrein related peptidase 3 Homo sapiens 192-195 31262916-5 2019 RESULTS: Patients who responded well to flutamide (Flutamide effective) following initial maximum androgen blockade (MAB) showed significantly higher changes in serum PSA levels (p=0.039) and PSA-progression-free survival (PFS) rate (p=0.016) following enzalutamide therapy compared to those who did not respond well to flutamide. Flutamide 51-60 kallikrein related peptidase 3 Homo sapiens 167-170 31262916-5 2019 RESULTS: Patients who responded well to flutamide (Flutamide effective) following initial maximum androgen blockade (MAB) showed significantly higher changes in serum PSA levels (p=0.039) and PSA-progression-free survival (PFS) rate (p=0.016) following enzalutamide therapy compared to those who did not respond well to flutamide. Flutamide 51-60 kallikrein related peptidase 3 Homo sapiens 192-195 31262916-6 2019 Multivariate analysis showed that the factor of Flutamide effective was significantly associated with a good PSA-PFS rate following enzalutamide therapy (HR=7.36, 95%CI=1.4-38.71, p=0.018). Flutamide 48-57 kallikrein related peptidase 3 Homo sapiens 109-112 31262916-7 2019 CONCLUSION: Patients showing good response to flutamide following initial MAB may achieve a satisfactory PSA-PFS rate with subsequent enzalutamide therapy. Flutamide 46-55 kallikrein related peptidase 3 Homo sapiens 105-108 27123292-5 2016 Following the introduction of alternative anti-androgen therapy with flutamide, PSA decline was observed in 185 patients (68.0%), including 103 (37.9%) who achieved a PSA reduction of >50%; however, the PSA level continued to elevate in the remaining 87 (32.0%). Flutamide 69-78 kallikrein related peptidase 3 Homo sapiens 80-83 29843816-4 2018 The response to flutamide therapy was defined as any decrease in prostate-specific antigen compared to baseline prostate-specific antigen. Flutamide 16-25 kallikrein related peptidase 3 Homo sapiens 65-90 29843816-4 2018 The response to flutamide therapy was defined as any decrease in prostate-specific antigen compared to baseline prostate-specific antigen. Flutamide 16-25 kallikrein related peptidase 3 Homo sapiens 112-137 29843816-5 2018 Among the abiraterone-treated patients, those for whom flutamide after bicalutamide was effective showed significantly lower prostate-specific antigen changes than those for whom it was ineffective (P = 0.0175). Flutamide 55-64 kallikrein related peptidase 3 Homo sapiens 125-150 29843816-6 2018 Prostate-specific antigen-progression-free survival was significantly higher in the abiraterone patients when flutamide was effective than in the patients when it was ineffective (P = 0.027). Flutamide 110-119 kallikrein related peptidase 3 Homo sapiens 0-25 27493956-1 2016 We determined whether prostate specific antigen (PSA) would decrease with immediate antiandrogen switching from bicalutamide (BCL) to flutamide (FLT) in patients receiving combined androgen blockade for advanced prostate cancer. Flutamide 134-143 kallikrein related peptidase 3 Homo sapiens 22-47 27493956-1 2016 We determined whether prostate specific antigen (PSA) would decrease with immediate antiandrogen switching from bicalutamide (BCL) to flutamide (FLT) in patients receiving combined androgen blockade for advanced prostate cancer. Flutamide 134-143 kallikrein related peptidase 3 Homo sapiens 49-52 27493956-1 2016 We determined whether prostate specific antigen (PSA) would decrease with immediate antiandrogen switching from bicalutamide (BCL) to flutamide (FLT) in patients receiving combined androgen blockade for advanced prostate cancer. Flutamide 145-148 kallikrein related peptidase 3 Homo sapiens 22-47 27493956-1 2016 We determined whether prostate specific antigen (PSA) would decrease with immediate antiandrogen switching from bicalutamide (BCL) to flutamide (FLT) in patients receiving combined androgen blockade for advanced prostate cancer. Flutamide 145-148 kallikrein related peptidase 3 Homo sapiens 49-52 22180287-13 2012 CONCLUSIONS: The use of the finasteride/flutamide combination is feasible, and results in PSA declines of >=80% in 96% of patients with serologic progression after definitive local therapy. Flutamide 40-49 kallikrein related peptidase 3 Homo sapiens 90-93 26024831-1 2015 The study aims to compare serial changes in prostate-specific antigen (PSA), testosterone, dehydroepiandrosterone (DHEA), and androstenedione in patients treated with either of the antiandrogen agents, bicalutamide or flutamide, using a randomized controlled study. Flutamide 218-227 kallikrein related peptidase 3 Homo sapiens 44-76