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Query: UMLS:C0027651 (tumor)
 685,946 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Radical prostatectomy with curative intent was performed in 13 patients with prostate cancer after local failure of radiotherapy. Of these patients, 2 underwent cystoprostatectomy for bladder neck involvement by the prostatic tumor. Local recurrence had been diagnosed twenty-one to one hundred sixty-eight months (mean 65.4 months) after completion of radiotherapy (6,000-7,000 cGy; mean 6,136 cGy). Three patients had radioactive implants. Rising prostate-specific antigen (PSA) was part of the indication for surgery in 5 patients. Complications included minor rectal injury (1 patient) and total incontinence (2/13 patients). Two patients had positive surgical margins and 6/13 patients had involvement of seminal vesicles, 2 of whom also had positive lymph nodes. The authors conclude that salvage prostatectomy is feasible after radiation failure. Transrectal ultrasound and careful monitoring of PSA after irradiation treatment may improve patient selection and minimize the risk of complications and incomplete excision.
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PMID:Salvage radical prostatectomy after failure of curative radiotherapy for adenocarcinoma of prostate. 152 39

The function of the pituitary-gonadal axis in normal (immunocompetent) and nude (immunocompromised) mice, like that of other species, can be suppressed by luteinizing hormone-releasing hormone (LH-RH) agonists and antagonists administered by continuous release systems and, therefore, nude mice provide a valuable model for investigation of the effects of LH-RH analogues on growth of xenografts of human cancers. To extend our findings further, we treated male nude mice bearing xenografts of human prostate adenocarcinoma PC-82, for 42 days, with sustained release formulations (microcapsules or microgranules) of the agonist [D-Trp6]LH-RH, the antagonist [Ac-D-Nal(2)1,D-Phe(4Cl)2,D-Pal(3)3,D-Cit6,D-Ala10]LH- RH (SB-75), or the somatostatin analogue D-Phe-Cys-Tyr-D-Trp-Lys-Val-Cys-Trp-NH2 (RC-160). At necropsy, in mice given microcapsules releasing 25 micrograms/day of [D-Trp6]-LH-RH, tumor weight and volume were significantly decreased, compared with control mice, and weights of testes, ventral prostate, and seminal vesicles were also reduced in this group. In mice which received microgranules liberating 50 micrograms/day of antagonist SB-75, there was a greater decrease in tumor weight and volume than that produced by the agonist and a significant reduction in the weight of the testes and accessory sex organs. Histological parameters also demonstrated significant tumor inhibition, with the best results being obtained by treatment with the antagonist SB-75. The tumor inhibition induced by SB-75 was demonstrated to be due to decreased cellular proliferation, with enhanced cellular death (i.e., apoptosis) of the PC-82 cells. Microcapsules releasing 50 micrograms/day of RC-160 decreased tumor weight and volume by 23% and 28%, respectively, but this reduction was not significant. Serum levels of testosterone were decreased by 90% in mice given the LH-RH agonist and by 94% in response to the antagonist SB-75. Serum levels of prostate-specific antigen were significantly lower in mice treated with LH-RH analogues, with the antagonist SB-75 causing a greater reduction. A ratio of prostate-specific antigen to tumor weight suggests that levels of serum prostate-specific antigen may be correlated with tumor mass. Using sensitive multipoint micromethods, one class of binding sites for LH-RH, with a dissociation constant of 7.8 +/- 1.2 nM and a maximal binding capacity of 126.4 +/- 23.1 fmol/mg protein, was found in the control tumors. Tumors from mice treated with either LH-RH agonist or antagonist, but not somatostatin analogue RC-160, showed a significant reduction in maximal binding capacity for LH-RH, compared to control tumors.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Sustained release formulations of luteinizing hormone-releasing hormone antagonist SB-75 inhibit proliferation and enhance apoptotic cell death of human prostate carcinoma (PC-82) in male nude mice. 156 23

A better understanding is needed of the role of pre-analytical factors if prostate-specific antigen (PSA) is to be reliably used as a tumor marker. Reports on the analytical performance of TANDEM-R PSA (Hybritech, Inc., San Diego, CA) differ considerably with respect to detection limit and imprecision, differences that might be due (e.g.) to the use of different control matrices, to between-batch variations in reagent composition, or to nonrobustness of the assay. During nine months we determined PSA in 986 serum samples from 728 male urology patients and 54 samples from women (25 assay runs). As controls we used two serum pools with low PSA concentration and two widely used commercial controls. The within-assay CV for patients' samples was similar to that found with the commercial controls: 2.6% to 3.4% in the upper part of the normal reference interval. Precision was worse at lower concentrations (CVs 5-10% at about 0.5 micrograms/L). Imprecision tended to be higher at the end of runs. Assay drift for 100-tube runs was -4%. PSA was stable at -20 degrees C during six months. Neither the polyester polymer in SST tubes nor a hemolysate had any detectable effect on PSA values. Clinical analysis of the first 322 patients and all patients with PSA less than or equal to 0.20 micrograms/L highlighted the requirements for strict adherence to sampling instructions and to stringent quality control also at low analyte concentrations (analyte-free sera and sera with PSA concentrations 0.2-0.5 micrograms/L). Values with TANDEM-R PSA and IRMA-Count PSA (Diagnostic Products Corp., Los Angeles, CA) correlated well with no difference in detection limit or with samples from women. Within-assay precision was better with IRMA-Count PSA in the upper part of the normal reference interval and above. The designs of the two assays were compared in a format that is generally applicable for immunoassay kits (NORDKEM kit group, unpublished), and subjective impressions were recorded.
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PMID:Determination of prostate-specific antigen in serum by immunoradiometric assay. 168 45

Noninvasive methods for the diagnosis of prostatic cancer, its staging and evaluation of response to therapy are often not sufficiently sensitive or specific. Prostate-specific antigen (PSA) was identified in 1979 and has been evaluated since then as a marker, both at the serum and the tissue level. A review is presented in this article. PSA is an organ-specific glycoprotein presented in most prostatic carcinomas, but also in normal prostatic tissue and in benign prostatic hypertrophy (BPH). The monitoring of serum PSA concentrations by serial measurement can be used for the detection of residual or recurrent tumor after primary treatment and for the evaluation of response to systemic treatment of advanced disease. At the tissue level immunohistochemical detection of PSA may help to identify metastatic tumor of unknown origin. PSA serum assays have not been sufficiently sensitive and specific for staging of the primary tumor or for screening purposes. PSA is an equally specific, but more sensitive marker of prostatic carcinoma compared to prostatic acid phosphatase.
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PMID:Prostate-specific antigen (PSA). A tissue-specific and sensitive tumor marker. 168 77

A mucinous adenocarcinoma of the prostate is rate, and a doubtful diagnosis should be verified to determine that the tumor surely does arise from the prostate, since a mucinous adenocarcinoma arising from the gastrointestinal tract is not as rare and often metastasizes to the prostate. We herein report on a case of a mucinous adenocarcinoma of the prostate, the origin of which was proved to be the prostate by immunohistochemical staining for a prostate-specific antigen and prostate-specific acid phosphatase.
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PMID:[A case of mucinous adenocarcinoma of the prostate]. 169 Aug 26

Recent advances in the diagnosis and treatment of patients with prostate cancer have altered clinical management of the disease. Although direct rectal examination remains the standard clinical tool for staging prostate cancer, transrectal ultrasound appears to be about twice as sensitive for detection. Prostate-specific antigen (PSA) has replaced prostate-specific acid phosphatase as a serum tumor marker for prostate cancer. When used in conjunction with measurement of prostate volume by transrectal ultrasound, PSA values may identify patients at increased risk for occult cancer. Use of transrectal ultrasound and PSA values has also improved the accuracy of clinical staging. Modifications in the technique of radical prostatectomy have minimized the morbidity associated with this procedure, making it a more attractive therapeutic option in patients with localized prostate cancer. In patients with metastatic disease, total androgen blockade is an option that appears superior to standard hormonal therapy.
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PMID:Prostate cancer. Promising advances that may alter survival rates. 169 Aug 83

Serum prostate-specific antigen (PSA) levels were determined in four groups of patients with prostatic carcinoma: 230 untreated patients with adenocarcinoma of the prostate after careful clinical staging; in 102 patients with localized prostatic carcinoma who were treated by radical prostatectomy; in 183 patients after radiation therapy for adenocarcinoma of the prostate; and in 45 antiandrogen-treated patients with documented metastatic disease. Within each treatment modality PSA proved to be a powerful tool in predicting stage and prognosis of each patient. In the untreated group the PSA level was directly proportional to advancing clinical stage and Gleason score. The rate of increase of PSA in clinical stage A and B cancer patients suggested a doubling time of at least 2 years. In the group of patients who underwent radical prostatectomy, PSA correlated extremely well with the tumor volume and had a high predictive value for pelvic lymph node metastasis. No patient with pelvic lymph node metastasis achieved an undetectable PSA level following radical prostatectomy without adjunctive therapy. Both anti-androgen and radiation treatment were followed initially by dramatic falls in serum PSA concentrations, but the majority of patients soon experienced a reversal of this initial response, signifying early failure and again providing new information unavailable from any other source.
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PMID:[The role of prostate-specific antigen in the diagnosis and treatment of prostatic adenocarcinoma]. 169 83

To evaluate the clinical and prognostic value of prostate-specific antigen (PSA) for the detection of tumor and tumor growth after therapy, 520 sera from 246 patients with prostatic carcinoma, 990 sera from patients with BPH, and 1,488 sera from patients with other urological diseases were analyzed. The values ranged from 0.1 to 1,828.9 ng/ml. 51% of all values were about 2.5 ng/ml, and 76.8% of all values about 10 ng/ml. The commercial recommendation for the cutoff values is 2.5 ng/ml (IBL, FRG). In patients with benign prostatic hypertrophy this cutoff means 61% false-positive results, which makes the test highly sensitive but unspecific. In prostatic carcinoma patients this borderline means a false-negative result in 9.75% (24 of 246). By determining the cutoff at 10 ng/ml in our series, a false-negative result appeared in 14.6%. Therefore a plea is made for the 10-ng/ml cutoff. In follow-up studies a marked decline in PSA values after transurethral resection or antiandrogen therapy (orchiectomy/Zoladex/ICI/flutamide, Essex). Generally, the greater the PSA levels the more advanced the stage of disease. These data suggest that PSA may be a useful adjuvant marker for monitoring tumor growth in patients with regionally confined tumor.
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PMID:Prostate-specific antigen in prostatic carcinoma. 169 55

Twelve patients with primary mucinous adenocarcinoma of the prostate were included in a clinicopathologic study; criteria included a total tumor volume more than 25% mucinous and single or clustered tumor cells floating in mucin lakes. Patient ages were 57 to 81 years; tumor stages were C (three), D (five), and unknown (four). Bone was the most frequent metastatic site (usually osteoblastic), followed by lymph nodes and lungs. Serum levels of prostatic acid phosphatase and prostate-specific antigen were frequently elevated (five of 10 and three of three measured, respectively). All mucinous adenocarcinomas also contained other histologic patterns: microglandular (four), cribriform (three), comedo (two), solid (two), and hypernephroid (one). Mucinous components composed less than 50% of three tumors, 50% and 75% of six, and more than 75% of three. No tumor contained signet-ring cells. Immunoperoxidase staining was positive for prostatic acid phosphatase and prostate-specific antigen and negative for carcinoembryonic antigen. Treatment was radiation, estrogen, orchiectomy, or a combination. In two of four patients, serum prostatic acid phosphatase levels normalized after therapy. Seven patients died of disease (mean follow-up, 56 months), and five patients are alive with disease (mean, 32.2 months). The proportion of mucinous component did not affect prognosis.
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PMID:Mucinous adenocarcinoma of the prostate: histochemical and immunohistochemical studies. 169 91

The serum prostate-specific antigen (PSA) of 58 men with benign prostatic hypertrophy (BPH) and 17 men with carcinoma of the prostate (CaP) was correlated with the weight of prostatic tissue resected at transurethral prostatectomy (TURP). A significant correlation was identified between the weight of resected BPH tissue and the serum PSA (p less than or equal to 0.001; r = 0.54). No such correlation was seen in the CaP patients. By arbitrarily dividing the serum PSA by the prostate weight, it was possible to devise an index. This index corrected PSA in relation to prostatic size and unlike PSA in isolation did not differ significantly between normal controls and those with BPH. The index in CaP was significantly greater than that of either controls or BPH (p less than or equal to 0.001). Furthermore the index of metastatic CaP (M1) was significantly higher than that of nonmetastatic disease (MO) (p = 0.05). The higher index found in CaP would seem to be related to the bulk metastatic tumor, either manifest or occult. Comparing the index of CaPs to that found in normal and benign disease (a constant) offers a possible means of estimating the extent of local and metastatic tumor mass.
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PMID:Quantification of prostatic cancer metastatic disease using prostate-specific antigen. 169 96


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