Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0376358 (prostate cancer)
 59,338 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Flutamide, an anti-androgen used in prostate cancer therapy, is also a derivative of aniline. Mild, usually asymptomatic, methaemoglobinaemia has been reported. We report a patient receiving flutamide therapy who developed cyanosis, dyspnoea and anaemia, initially attributed to marked methaemoglobinaemia by the CO-Oximeter method. An unsuccessful trial of methylene blue therapy led to the finding of marked sulphaemoglobinaemia. Sulphaemoglobinaemia has not previously been reported with flutamide use. Recognition of this association is important, given the refractoriness of sulphaemoglobinaemia to methylene blue therapy.
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PMID:Flutamide-induced cyanosis refractory to methylene blue therapy. 875 11

Flutamide is a nonsteroidal antiandrogen commonly used in the treatment of prostate cancer. Hepatic toxicity associated with flutamide has been reported with an incidence from less than 1% to about 5%. Ursodeoxycholic acid (UDCA), a hydrophilic bile acid, has been widely used in the treatment of cholesterol gallstones and of several liver diseases, but few data are now available concerning its use in the management of drug-induced hepatitis. The case of a patient who presented severe hepatitis with jaundice following use of flutamide is reported. UDCA treatment was started on admission and, contemporaneously, flutamide was withdrawn. Clinical and biochemical improvement was progressively observed, and the patient was discharged six weeks after the admission. Since fatal flutamide-related hepatitis has been reported, monitoring of serum liver tests is advocated during flutamide administration, and the effectiveness of UDCA in the treatment of drug-induced hepatotoxicity requires further study.
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PMID:Flutamide-induced toxic hepatitis. Potential utility of ursodeoxycholic acid administration in toxic hepatitis. 894 75

The utility of monotherapy with antiandrogens in prostate cancer is under investigation. Flutamide (Eulexin, Schering-Plough International) appears equally effective to castration in prolonging progression-free survival. Nilutamide (Anandron, Roussel) has been studied less widely, but may represent a valid treatment option in advanced prostate cancer. Preliminary results suggest that bicalutamide (Casodex, Zeneca Ltd) is as effective as castration in non-metastatic disease. Monotherapy with non-steroidal antiandrogens may offer successful palliative management of advanced prostate cancer with significant value in enhancing certain aspects of quality of life.
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PMID:Antiandrogen monotherapy in the management of advanced prostate cancer. 907 6

Flutamide is a non-steroid antiandrogen used in advanced prostate cancer. This drug induces liver toxicity. Other side effects have been reported, especially four cases of photosensitivity. Our patient presented a sun-exposed eruption that disappeared when flutamide was discontinued and relapsed when it was rechallenged. Photopatch tests were negative. UVA MED was much lower during the treatment and the rechallenge of flutamide. The action spectrum of the drug seems to be in the UVA range. According to the literature, this photosensitivity is probably due to a photo-allergic mechanism.
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PMID:Flutamide photosensitivity. 911 81

Occult dissemination of tumor cells mainly determines the prognosis of patients with primary prostate cancer. The effect of androgen deprivation on micrometastatic tumor cells in these patients is currently unknown. We therefore used an immunocytochemical assay with monoclonal antibodies (MAbs) directed against epithelial cytoskeleton proteins (i.e., cytokeratins) to monitor the concentration of isolated tumor cells in the bone marrow of 36 prostate cancer patients (stage C), who underwent hormonal androgen deprivation with Flutamide and Leuprorelin acetate. Tumor cells in cytologic bone marrow preparations were detected using an assay that employed the MAb CK2 directed against cytokeratin (CK) 18 and the alkaline anti-alkaline phosphatase staining method. Prior to therapy, we detected between 1 and 38 CK-positive cells per sample of 2 x 10(6) nucleated cells in 21 patients, while the remaining 15 patients displayed tumor-free marrow samples. There was no significant correlation between the concentration of CK-positive cells and the volume of hypo-echogenic lesions as an indicator of the primary tumor volume or the serum level of prostate-specific antigen (PSA). After androgen deprivation, 20 of the 21 initially positive patients either became negative (n = 16) or showed at least a reduction in the concentration of CK-positive cells (n = 4). Moreover, only 2 of the 15 patients with negative pre-treatment findings became positive. All of the 7 patients with remaining tumor cells in the bone marrow after therapy showed no detectable amounts of PSA in their serum. Our findings suggest that serum PSA concentration is no indicator of micrometastatic disease in bone marrow. Neoadjuvant androgen deprivation appears to eliminate disseminated CK-positive tumor cells present in bone marrow, a preferred site of overt metastasis in prostate cancer patients.
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PMID:Immunocytochemical monitoring of micrometastatic disease: reduction of prostate cancer cells in bone marrow by androgen deprivation. 917 3

The literature contains many accounts of studies in which tumour growth has been accelerated by administration of a particular mitogen and the response then inhibited by co-administration of the corresponding antagonist. Much effort has been focused on the development of cytokine or growth factor antagonists. Like most other cancer therapies, biological therapies will undoubtedly have undesirable toxicities because the proteins they target may not be unique to malignant cells. We reviewed the clinical and therapeutic potential of growth factor agonists and antagonists in some non urologic and urologic diseases. In a recent report we demonstrated that both androgen and antiandrogen treatments enhance the proliferation rate of the hormone-dependent prostate cancer cell line LNCaP, expressing a mutated androgen receptor. Simultaneous treatment with 1 nM R1881 and 100 nM OH-Flutamide, completely counteracted the androgen-induced increase of Epidermal Growth Factor (EGF) levels. Moreover we found that Testosterone, DHT and EGF are mainly concentrated in the periurethral zone in human BPH and long term treatment with Finasteride and with Flutamide modify the distribution and concentration of these factors. Some authors analyzed whether and addition of aurin tricarboxylic acid (ATA) can reduce the growth rate of basic FGF-dependent cells in a manner similar to suramin.
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PMID:Peptide growth factors: clinical and therapeutic strategies. 922 27

From January, 1991, to December, 1995, forty-two patients with prostatic cancer (T2-T4: 40 patients) were treated with a luteinizing hormone-releasing hormone (LHRH) analog (2 administrations before and 3 during irradiation), Flutamide (1 month) and external beam radiation therapy (45 Gy to the whole pelvis and a 20 Gy boost). All patients completed the protocol and the LHRH analog was continued for 1-6 months in 5 patients with partial response at the end of radiotherapy. The incidence of acute toxicity was low according to the Radiation Therapy Oncology Group and European Organization for Research and Treatment in Cancer score (grades 1-2; 19% hematologic, 36% intestinal and 38% urological toxicity). At a median follow-up of 21 months (range: 1-60 months), one patient had local disease progression and lung metastases and two had bone metastases; the three relapsing patients were given the LHRH analog and exhibited partial response to rectal examination (1 case) and to bone scan (2 cases). Pain disappeared completely in both the patients with bone metastases. Overall 3-year survival and disease-free survival rates were 97% and 79%, respectively. Disease-free survival was significantly related to cT (at 3 years: cT2: 100%; cT3: 81.2%; log rank test: 0.0081). Late toxicity was observed in two patients: rectal bleeding in one case and chronic diarrhea in the other. The combined protocol used in this study was feasible and well tolerated. Our results seem to confirm the promising preliminary results of Radiation Therapy Oncology Group 8610 study.
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PMID:[Neoadjuvant combined hormonal therapy and radiotherapy with external beam irradiation in prostatic carcinoma]. 924 24

Flutamide is a non-steroidal anti-androgen used in the treatment of prostate cancer, usually in combination with LHRH-analogs. Incidence of hepatotoxicity associated to Flutamide in the literature is very low and does not exceed 0.18%. Between February 1989 and December 1994, the FDA was reported 20 cases of patients who had died and 26 who had been hospitalized due to hepatotoxicity secondary to Flutamide. We contribute two cases of patients diagnosed with prostate adenocarcinoma following treatment with flutamide and LHRH-analogs who presented liver failure; one with signs and symptoms of acute hepatitis that recovered after discontinuation of the drug, and a second one who developed micronodular cirrhosis and later died of icteroascitic decompensation and hepatorenal syndrome. Including a review of the literature, the paper comments on the likely biological mechanisms for liver toxicity caused by Flutamide. The authors conclude that clinical and laboratory monitoring of patients who either will receive or are receiving treatment with Flutamide is necessary, and withdrawal of drug imperative as soon as certain symptoms of hepatic dysfunction become apparent.
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PMID:[Liver failure caused by flutamide]. 932 96

Combined androgen blockade using a pure antiandrogen in association with a LHRH agonist or surgical castration is the most logical approach. This paper demonstrated that flutamide combined with leuprorelin acetate produced a significant reduction in the growth rate of Dunning R3327-H prostatic adenocarcinoma. Dunning R3327-H prostatic adenocarcinoma, provided by Dr. Norman H. Altmann (University of Miami, USA) was subcutaneously inoculated into the lateral region of male Copenhagen x Fischer F1 hybrid rat abdomen. The efficacy of the tumor growth rate was evaluated by measuring tumor size at 10 weeks after the inoculation. Flutamide was orally administered for 10 weeks and leuprorelin acetate was subcutaneously administered every 4 weeks. The effective dose of flutamide and leuprorelin acetate was determined in preliminary studies, and the following doses were used in the study; 15 mg/kg for flutamide, 0.1 mg/kg or 0.4 mg/kg for leuprorelin acetate. In combination of flutamide with leuprorelin acetate at 0.1 mg/kg and 0.4 mg/kg, the tumor inhibition was 94% and 97%, respectively. In addition, the weight of accessory sex organs coincided with the antitumor effect. Taking the above results into consideration, combined androgen blockade using flutamide and leuprorelin acetate may have some beneficial effect on prostatic cancer.
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PMID:[Combination effect of flutamide and leuprorelin acetate on growth of Dunning R3327-H prostatic adenocarcinoma in rats]. 953 Mar 63

Androgen receptors are present in both pancreatic cancer tissue and cell lines. Flutamide is a potent antiandrogen widely used in clinical practice for patients with metastatic prostate cancer. This Phase II trial was undertaken to evaluate the impact of flutamide in patients with advanced pancreatic adenocarcinoma who had developed progressive disease following therapy with one 5-FU-based regimen. Fourteen patients were treated with flutamide, 250 mg orally three times per day. Therapy was generally well tolerated. No patients achieved objective tumor response. No patient had improvement in tumor-related symptoms as measured by improvement in pain intensity, analgesic requirement, performance status, or nutritional status. Median survival was 4.7 months. We conclude that flutamide is ineffective second line therapy for patients with advanced pancreatic adenocarcinoma.
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PMID:Phase II study of flutamide as second line chemotherapy in patients with advanced pancreatic cancer. 954 80


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