Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0030193 (pain)
 261,466 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The study of mitotic transduction of the signal showed that overexpression of pAkt and reduction in pERK expression would be associated a biological relapse. For tumors T1-3 N0M0 at the high risk of local relapse after prostatectomy, an immediate radiotherapy compared with a differed radiotherapy (at the time of PSA relapse), showed a significant reduction in the rate of local relapse and an ameliorated progression free survival. The effectiveness of the docetaxel was confirmed in two phase III randomized clinical trials : TAX-327 with 3 arms compared docetaxel every 21 days, docetaxel every 7 days and mitoxantrone. All arms were prednisone-based. An increase in overall survival, PSA progression free survival, PSA response rate and a pain reduction were highlighted in the docetaxel arm every 21 days. Docetaxel obtained at the end of this study the marketing authorization in this indication and became the treatment of reference. The SWOG 99-16 study compared the docetaxel estramustine association with the same arm of reference, mitoxantrone and prednisone, with similar results. The addition of estramustine to the docetaxel seems to improve the PSA response rate and progression free survival, but with a greater embolic toxicity. The addition of an antiangiogenic agent, the thalidomide, to docetaxel, improves progression free survival and overall survival. PSA responses were observed with an inhibitor of the proteasome, the bortezomib, in monotherapy, contrary to the imatinib which in monotherapy didn't have any effectiveness. Studies in association with docetaxel are ongoing. Some biological responses were observed with a vaccine anti MUC-1 and must be confirmed on a greater series of patients. The docetaxel impact on localized disease is actually evaluated.
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PMID:[Prostate cancer: update]. 1626 70

PSA-progression following primary ADT defines an androgen-refractory but still hormone sensitive PCA which might respond to secondary hormonal manipulations. Secondary hormonal manipulations will result in a PSA decline >50% in about 60-80% of the patients with a mean duration of 7-17 months depending on the type of treatment. PSA-progression following secondary endocrine treatment defines hormone-refractory prostate cancer (HRPCA) which might be treated by systemic chemotherapy. Based on the results of 2 prospective, randomized clinical phase-III trials comparing docetaxel and mitoxantrone, docetaxel results in a statistically significant survival benefit of 2.5 months, a significantly higher PSA- and pain response and represents the treatment of choice in the management of HRPCA. Bisphosphonates such as zoledronate represent another cornerstone in the management of PSA-progressive PCA demonstrating a significant benefit with regard to the prevention of skeletal related events. Furthermore, bisphosphonates might be indicated in the treatment of symptomatic bone pain. The current article critically reflects the various therapeutic options in the management of PSA progression following primary androgen deprivation for advanced prostate cancer.
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PMID:[Therapy of hormone-refractory prostate cancer]. 1631 9

A systematic review was performed to evaluate the clinical effectiveness of docetaxel in combination with prednisolone (docetaxel is licensed in the UK for use in combination with prednisone or prednisolone for the treatment of patients with metastatic hormone-refractory prostate cancer. Prednisone is not used in the UK, but it is reasonable to use docetaxel plus prednisone data in this review of docetaxel plus prednisolone) for the treatment of metastatic hormone-refractory prostate cancer. A scoping search identified a trial of docetaxel plus prednisone vs mitoxantrone plus prednisone, but did not identify any trials comparing docetaxel plus prednisolone/prednisone with any other treatments. Therefore, we considered additional indirect evidence that would enable a comparison of docetaxel plus prednisolone/prednisone with other chemotherapy regimens and active supportive care. Systematic searching (upto April 2005) identified seven randomised controlled trials. One large well-conducted trial assessed docetaxel plus prednisone vs mitoxantrone plus prednisone; this showed statistically significant improvements with 3-weekly docetaxel in terms of overall survival, quality of life, pain response and PSA decline. Two other chemotherapy regimens that included docetaxel with estramustine also showed improved outcomes in comparison with mitoxantrone plus prednisone. Three trials that compared mitoxantrone plus corticosteroids with corticosteroids alone were identified and their results for overall survival combined, which showed very little difference between the two groups. The addition of clodronate to mitoxantrone plus prednisone showed no significant differences in comparison with mitoxantrone plus prednisone alone. The evidence suggests that chemotherapy regimens containing 3-weekly docetaxel are superior to mitoxantrone or corticosteroids alone.
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PMID:A systematic review of the effectiveness of docetaxel and mitoxantrone for the treatment of metastatic hormone-refractory prostate cancer. 1688 Jul 88

The most common form of hormonal treatment for prostate cancer is luteinizing hormone-releasing hormone (LHRH)-agonist therapy. During the first 1 to 3 weeks of LHRH-agonist therapy, an initial increase in testosterone is associated with a condition known as "flare." Blockade of flare can be accomplished with a number of agents, including flutamide, bicalutamide, nilutamide, diethylstilbestrol, ketoconazole, and cyproterone acetate. Evidence from the early use of LHRHagonists suggested that flare could be serious in nature, with an exacerbation of pain, increase in uremia, development of neurologic sequelae, and possibly death. These events have been uncommonly reported of late, most probably owing to the use of flare blockade in most patients with advanced disease, as well as the fact that many patients are currently being treated with much earlier disease. Evidence is conflicting as to whether flare makes a difference in less advanced disease. A few reports have noted complications during flare in patients in whom a blockade of flare was not required, including two deaths from one institution. Reported series, however, seem to suggest that with flare blockade, acute complications are extremely uncommon. Evidence suggests that 1) advanced disease should be blocked; 2) blockade should probably include an antiandrogen beginning about 1 week prior to administration of the LHRH-agonist; and 3) that patients without advanced disease but with very high PSA levels should be considered for flare blockade.
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PMID:Flare Associated with LHRH-Agonist Therapy. 1698 3

The efficacy of the drug cernilton was studied in patients with prostatic adenoma (PA) and chronic bacterial prostatitis (CBP). One group and two subgroups of patients were studied: 31 men with PA received cernilton for 3 months (group 1); 32 patients with CBP received antibacterial treatment (for 8 months) and cernilton for 3 months (group IIa); 30 CBP patients received standard antibiotic treatment for 2 months maximally (group IIb). All the patients were examined before the treatment and 3 months later. According to IPSS, patients of group 1 showed a significant (p < 0.001) regress of low urinary tract symptoms and improvement of quality of life. PSA in the serum lowered by 21.2%. Qmax significantly increased (p < 0.001), Vprost and Vres diminished. According to the scale NIH-CPSI, relief of pain, dysuria was greater, quality of life improved more in patients of group IIa than in group IIb (p < 0.05). The same trend was in the values Qmax, Vres and Vprost. Thus, it is evident that cernilton is effective in monotherapy of PA and combined treatment of CBP.
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PMID:[Cernilton in the treatment of prostatic adenoma and chronic prostatitis]. 1747 1

Based on the pre-clinical spectrum of activity in taxane-resistant cell lines, we evaluated KOS-862 (epothilone D; 12,13-desoxyepothilone B) as second-line chemotherapy in androgen-independent prostate cancer.Thirty-eight men with metastatic androgen-independent prostate cancer and evidence of progression following docetaxel-based chemotherapy were treated with KOS-862, 100 mg/m(2) (maximum of 240 mg) i.v. weekly for 3 weeks, repeated every 4 weeks. The primary objective for this study was to determine the antitumor activity, measured by PSA decline by more then 50% confirmed 4 weeks later. Two patients (5.3%, 90% CI 1-16%) met criteria for confirmed PSA decline. While both of these patients had previously been treated with docetaxel, neither had confirmed docetaxel-refractory disease. None of the 24 patients with measurable disease had a confirmed partial response. Seventy-three percent of patients had an adverse event leading to dose delay, reduction, or treatment discontinuation. Neurological toxicity and fatigue predominated. Seventeen patients (44.7%) had treatment related grade 3 neurological adverse events including peripheral sensory neuropathy (n = 4, 10.5%), ataxia (n = 3, 7.9%), peripheral motor neuropathy (n = 1, 2.6%), involuntary muscle contractions (n = 1, 2.6%) and neuropathic pain (n = 1, 2.6%). One subject (2.6%) had a grade 4 treatment peripheral motor neuropathy. Further study of this dose and schedule of KOS-862 in this patient population cannot be recommended due to both lack of activity and excessive toxicity.
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PMID:Phase II study of KOS-862 in patients with metastatic androgen independent prostate cancer previously treated with docetaxel. 1761 7

Improvement of the sensitivity and specificity of a simultaneous stress-free screening method for catechol estrogens as a potential prostate cancer marker in urine has been accomplished by HPLC with a diamond-electrode electrochemical detector and a fluorescence detector. Since taking urine samples generates less stress (or pain) than the drawing of blood, the method can readily be applied to almost any patient, and will also assist in improving the sensitivity and specificity of the prostatic specific antigen test. Catechol estrogens (2-hydroxyestrone, 4-hydroxyestrone, 2-methoxyestrone, 2-hydroxyestradiol, 4-hydroxyestradiol, 2-methoxyestradiol, and 2-hydroxyestriol) and estrogens (estrone, estradiol, estriol) were separated on an Inertsil ODS-II column with acetonitrile-potassium dihydrogen phosphate (pH 3.0). The diamond-electrode electrochemical detector used had the great advantage of being a maintenance-free system, and could sequentially analyze hundreds of samples. Fluorescence detection improved the sensitivity 10-500 times (e. g., the LOD of 2-hydroxyestriol was improved 250 times) compared to previous electrochemical detection reports, and dual detection improved peak identification in the urine samples. The proposed method was applied to the simultaneous determination of catechol estrogens in spiked urine in a preliminary study on estrogens and PSA values in biopsy and prostate cancer patients.
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PMID:HPLC for stress-free screening of potential prostate cancer marker catechol estrogens in urine using a diamond-electrode electrochemical and a fluorescence detector. 1766 12

We report a very rare case of triple primary neoplasia synchronously originating in the prostate, kidney and thyroid, in a 79-year-old male who presented with hematuria and continuous pain at the right hip. Examination revealed an enlarged nodular thyroid, while digital rectal examination showed prostatic enlargement with elevated PSA (16.7 ng/mL). Plain radiography showed an osteolytic lesion in the right ischium. Ultrasonography and CT scan of left kidney suggested renal cell carcinoma (RCC), which was subsequently confirmed on histopathology of the left radical nephrectomy specimen. Biopsies from prostate showed adenocarcinoma, along with deposits in ischial biopsy. Fine needle aspiration cytology (FNAC) of neck swellings suggested deposits from thyroid follicular carcinoma, which was subsequently confirmed by histopathology of the near-total thyroidectomy specimen. Currently, the patient is on regular follow-up since the past 24 months.
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PMID:Synchronous primary triple neoplasia (renal cell carcinoma and prostate cancer in combination with thyroid neoplasm). Report of an unusual case. 1794 62

Endothelins are a family of peptide compounds which exert regulatory control over cellular processes important for growth, survival, invasion, and angiogenesis. In particular, endothelin-1, acting primarily through the endothelin-A receptor, is implicated in the neoplastic growth of multiple tumor types. In preclinical models, endothelin antagonism inhibits tumor cell proliferation, invasiveness, and new vessel formation, as well as attenuates osteoblastic and pain-related responses to tumor. Clinical testing of an orally bioavailable endothelin antagonist has demonstrated benefit in PSA progression, markers of bone turnover, and pain in men with prostate cancer, but has not demonstrated significant improvement in survival or time to cancer progression. Although this class of drugs is promising for targeted anti-cancer therapy, their role in treatment remains to be defined by completion of future clinical trials.
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PMID:Endothelin receptor antagonists in cancer therapy. 1805 75

For many years the benefit of chemotherapy in patients with prostate cancer was thought to be limited to palliation of late-stage disease, and thus this treatment option only became involved in patient care towards the end of the disease process, if at all. However, two landmark phase-III trials with docetaxel-based therapy (TAX 327 and Southwest Oncology Group, SWOG, 9916) have shown a survival benefit for patients with hormone refractory prostate cancer (HRPC) thus prompting a change in patterns of care. With raising interest for chemotherapeutic options and clinical trials for new drugs and new indications (neoadjuvant therapy, adjuvant therapy, increasing PSA levels after local treatment, and hormone sensitive cancer) under way our goal was to review within the context of a multidisciplinary team the available evidence and explore the standard for the medical treatment of prostate cancer outside of clinical trials. We are carefully evaluating the current treatment recommendations based on the available evidence and highlight potential future treatment options but also discuss important clinical topics (treatment until progression versus the advantage of chemo holidays, definition of particular patient subgroups and potential second line options) for which there are no clear cut answers to date. The role and importance of radiotherapy, biphosphonate treatment and the medical management of pain and side effects is also discussed. The multitude of treatment options for patients with advanced prostate cancer clearly asks for a close collaboration between urologists, medical oncologists and radiation therapists.
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PMID:[Chemotherapy for prostate cancer]. 1872 72


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