Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0027627 (metastases)
 103,950 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

As longevity has improved and mortality from cardiovascular and other diseases has declined, the risk of death from prostate cancer has increased steadily. Though slow growing, prostate cancer is not a benign disease. Nearly 10% of men in Western countries will be diagnosed with prostate cancer sometime during their life and 3% will die of the disease. The prospects for long-term control of prostate cancer diminish rapidly once the cancer has spread beyond the immediate periprostatic tissue. The 5-year survival rate for men with metastases is less than 30% and almost all will eventually die of their disease. A simple blood test, prostate-specific antigen (PSA), is available. This test, when used in conjunction with ultrasound-guided systematic needle biopsy of the prostate, will detect potentially lethal prostate cancers earlier than digital rectal examination (DRE). Definitive treatment, especially with radical prostatectomy, can eradicate the tumor in 90% of patients if the cancer is still confined to the prostate pathologically, regardless of the tumor grade. Randomized, prospective clinical trials are now underway to demonstrate conclusively whether screening or early definitive therapy will substantially reduce the mortality rate from this disease. Until the results of these trials are available, we recommend that healthy men over age 50, who have a life expectancy of 10 years or longer, have an annual PSA and DRE to detect prostate cancer while it is still curable.
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PMID:Current controversies in the management of localized prostate cancer. 852 48

To date androgen receptor (AR) expression and structure in human prostatic cancer have been studied in primary tumor specimens and in cell lines. Investigation of alterations in the androgen-signalling transduction cascade in prostatic carcinoma metastases is important to improve our understanding of tumor progression towards androgen insensitivity. In the present study we have collected data comparing AR expression in both the primary tumors and the respective pelvic lymph node metastases. Formalin-fixed and paraffin-embedded tissues derived from the primary tumors and positive lymph nodes of 12 patients undergoing radical prostatectomy were immunostained for the AR and prostate-specific antigen (PSA). AR expression was evaluated with the polyclonal antibody PG-21, which is directed against amino acid 1-21 in the N-terminal region of the AR. All primary tumors stained for the AR. In 8 of the 12 lymph nodes examined more than 50% of the tumor cells were AR positive and displayed a uniform staining pattern; in one lymph node metastasis remarkable heterogeneity in AR expression was observed. In two cases less than 10% of the tumor cells stained for the AR. In one case the lymph node metastasis was immunohistochemically negative for the AR, whereas the primary tumor obtained from the same patient displayed intense staining for the AR. PSA was expressed in all metastases and primary tumors. Our data demonstrate that loss of the AR in lymph node metastases from prostatic carcinoma is a rare event.
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PMID:Androgen receptor status of lymph node metastases from prostate cancer. 860 94

We report a new method for lymphadenectomy, the minilaparotomy (inguinal) pelvic lymph node dissection (MLPLND), and compare it with laparoscopic pelvic lymph node dissection (LPLND) in terms of cost, effectiveness, operation time and morbidity. We reviewed a series of 111 consecutive patients: 51 had MLPLND and 60 had LPLND. All patients had proved adenocarcinoma of the prostate by biopsy. Of the MLPLND patients, only 1 had to stay overnight in the hospital, and all left within 24 hours. Pelvic lymphadenectomy consisted of nodal removal along the internal iliac vessels and the external iliac vein, and nodes of the obturator foramen. A total of 14% of the patients had disease involving the lymph nodes. The cost of MLPLND was 50% of the cost of LPLND, with no interoperative or postoperative morbidity. This new operation can be performed thoroughly an inexpensively in approximately 35 minutes, with little or no morbidity. Since the drawbacks of laparoscopic techniques associated with instrument costs and the learning curve for this technically difficult operation are eliminated, staging pelvic lymphadenectomy can be performed routinely on a wider variety of patients with potential metastatic disease. Currently, we recommend MLPLND to any patient with a tumor of Gleason score 7 or higher or a serum prostate-specific antigen value of 15 ng/mL or higher.
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PMID:A new minimally invasive open pelvic lymphadenectomy surgical technique for the staging of prostate cancer. 863 13

So far, no curative treatment is available for hormone-refractory prostate carcinoma. Therapy is thus focused on alleviating symptomatic tumor progression with the aim of improving quality of life. Therefore, anthracyclin-derived mitoxantrone was administered to 25 patients with hormone-refractory prostate carcinoma and symptomatic progressive disease. After a median treatment of 13 weeks, a median of 4 cycles and a follow-up of 14 months, 48% of the patients (12/25) reported improvement in tumor-related pain; in 60% (15/25) there was improvement of the self-assessment symptom score and 32% of the patients (8/25) gained weight. Additionally, partial tumor response with regression of lymph-node metastases occurred in 3/25 patients (12%). In 10/25 patients the serum level of prostate-specific antigen (PSA) decreased as well as the alkaline phosphatase (AP) in 7/25 patients. Side effects subsequent to chemotherapy were leucopenia WHO grade III in 25% of the patients and thrombocytopenia WHO grade III in 3/25 and grade V (treatment-related death) in 1/25 patients. Non-hematological toxicity occurred in 2 patients (cardiotoxicity n = 1, nephrotoxicity n = 1, WHO grade II each).
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PMID:[Therapy of hormone refractory prostate carcinoma with mitoxantrone. A clinical phase II study]. 865 Aug 48

The staging, screening and diagnosis, and treatment of prostate cancer are discussed. Prostate cancer kills about 40,000 men in the United States each year. Signs and symptoms range from dysuria to features of advanced metastatic disease. The American Urological System of staging prostate cancer designates four stages, A through D. The tumor is graded histologically with the Gleason scale. Methods used in the screening and diagnosis of prostate cancer include digital rectal examination, the prostate-specific antigen (PSA) assay, biopsy, transrectal ultrasonography, and determination of PSA density, velocity, and age specificity. The value of screening and treatment remains controversial because tumors are generally slow-growing and conclusive data showing an effect on survival time are lacking. Treatment methods consist of prostatectomy, radiation therapy, and hormonal drug therapy or bilateral orchiectomy. The choice is influenced primarily by the stage of the disease but also by the patient's age, physical condition, and response to prior therapy. Patients with stage A or B disease are considered for prostatectomy or radiation therapy. The primary treatment for stage C disease is radiation therapy. For stage D, the main approaches are watchful waiting and bilateral orchiectomy or hormonal drug therapy to reduce androgenic stimulation of prostate tissue. Long-term survival rates are high for stages A and B and considerably lower for stages C and D. Prostate cancer responds to estrogens, but adverse effects are frequent and potentially severe. Luteinizing hormone-releasing hormone agonists (leuprolide and goserelin) are as effective as estrogens but have less toxicity; a disadvantage of these agents is an initial flaring of the disease. Other hormonal agents used include antiandrogens-progestins, flutamide, and bicalutamide. Secondary hormonal treatments (aminoglutethimide and ketoconazole) are less effective than initial hormonal therapy. Antineoplastic agents have little or no effectiveness in prostate cancer. Although the value of screening for and treating prostate cancer continues to be debated, many experts recommend annual screening for all men over 50. Research to identify more effective drugs for treating advanced disease continues.
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PMID:Prostate cancer: current and evolving strategies. 867 58

The role of prostate-specific antigen in the management of prostatic adenocarcinoma is still not fully ascertained. Its place in the monitoring of patients who have undergone radical treatment is without question but its role in the primary assessment of a lesion is a point of continuous discussion. This study reports the analysis of prostate-specific antigen (PSA) in 92 patients with different stages of prostatic adenocarcinoma prior to treatment; in the case of the localized lesions, this was based to a great extent on the findings at lymphadenectomy. Apart from PSA analysis, deoxythymidine kinase (dTK) analyses were also performed in an attempt to discover whether the latter could provide additional information about the tumor load in the different patient categories, viz. those with lymph node involvement (group 1), those with lymph node involvement but without distant metastases (group 2), and those with disseminated disease (group 3). The median PSA and dTK values in groups 1-3 were 6.5 micrograms/L and 2.7 U/microliter, 16 micrograms/L and 2.6 U/microL, and 90 micrograms/L and 7.8 U/microL, respectively. If the two analyses were used concomitantly, they could differentiate true localized disease from metastatic in approximately 92% of cases. The combination should prove of value in the primary assessment of a patient with a newly diagnosed prostatic adenocarcinoma.
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PMID:Deoxythymidine kinase in the staging of prostatic adenocarcinoma. 868 50

The authors consider fundamentals of hormone therapy in prostate cancer, mechanism of long-term androgenic stimulation, detail mechanism of action of antiandrogen (ciproteron acetate-androcur) on the basis of discovered key role of cellular receptor in endocrine regulation of physiological functions in metabolism. Monotherapy with androcur-depo (300 mg once a week) was given to 24 patients with prostatic cancer stage T2-T4. Eight patients had metastases to the bones. The age of the patients ranged from 58 to 80 years. Alleviation of pain, reduction of the prostate size and density, positive uroflowmetric changes (maximal urination rate increased from 2-5 to 10-15 ml/s), residual urine fall occurred as early as treatment week 5-7. There was also a decrease in the activity of acid phosphotase from 5-10 to 0.3-0.8 units according to Bodansky. Serum level of prostate-specific antigen (PSA) dropped from 388-23 to 116-4 ng/ml. Androcur-depo monotherapy demonstrated high efficacy in the treatment of local prostatic cancer.
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PMID:[Cyproterone acetate (Androcur-depo) in the treatment of inoperable prostatic cancer]. 868 22

Combined androgen blockade (CAB), the addition of an antiandrogen to castration (medical or surgical), is becoming a well-established option for advanced prostate cancer. CAB with leuprolide and flutamide was found to improve both progression-free and overall survival, compared with leuprolide alone, particularly in patients with minimal metastatic disease. These findings have led to an intergroup study in more than 1,300 men, including 300 with minimal disease, of orchidectomy with flutamide versus orchidectomy with placebo, which will examine which patient subgroups benefit most from CAB. This intergroup study has already provided important information regarding prostate-specific antigen as a surrogate marker for response and progression. The success with CAB in lengthening survival and improving quality of life in metastatic prostate cancer has stimulated enthusiasm for broadening the base of clinical studies for the management of this disease.
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PMID:Combined androgen blockade. 871 65

The detection of blood-borne prostate cancer (PCA) cells may help with clinical staging and the further understanding of PCA metastases. We discovered prostate-specific antigen (PSA)-positive stained but not PSA mRNA-expressing blood cells by means of cell sorting and PSA reverse transcription-PCR in patients. Therefore, we developed a cytokeratin immunomagnetic method to isolate PSA-positive epithelial cells from the circulating blood of PCA patients. We obtained blood-borne single cells from 6 of 10 PCA patients and clustered cells from 8 of 10 PCA patients. Patients with benign prostate hyperplasia tested negative for cell clusters. The reported isolation method yielded prostate-derived cells or clusters of them from PCA-diagnosed patients.
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PMID:Isolation of prostate-derived single cells and cell clusters from human peripheral blood. 884 Sep 59

The utility of monoclonal antibody (MAb) imaging for detection of occult recurrent prostate cancer was investigated in 14 patients with elevated serum prostate-specific antigen at least 3 months after therapy. All were imaged with capromab pendetide (CYT-356) and subsequently had biopsies of the prostate bed. Ten also had PET scans with F-18 fluorodeoxyglucose. Ten MAb scans were positive for tumor in the prostate bed and eight showed lymph node metastases. Six of the seven patients with positive biopsies had positive MAb scans, one had a negative scan. Three of the seven patients with negative biopsies had negative MAb scans, four had positive scans. Of the six patients with positive biopsies who had PET scans, one was positive, five were negative. Two of four patients with negative biopsies had negative positron emission tomography scans, two were positive. MAb imaging is superior to PET scan for identifying recurrent disease in the prostate bed. Assuming no false-negative biopsies, the positive predictive values for MAb and PET scan are 60% and 33%, negative predictive values are 75% and 29% and sensitivities are 86% and 17%. Additional investigation is necessary to determine if MAb uptake in lymph nodes is predictive of metastatic disease.
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PMID:Monoclonal antibody imaging of occult prostate cancer in patients with elevated prostate-specific antigen. Positron emission tomography and biopsy correlation. 887 71


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