Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C1519176 (PSA)
 5,490 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The asymptomatic patient who has been treated with a curative intent by surgery or irradiation for cancer of the prostate needs only a PSA and a baseline bone scan for his initial (post-treatment) follow-up. Rising serum PSA levels which still remain in the moderate range may signal a local recurrence, but this must be documented histologically. The therapeutic options to consider for a documented local recurrence include pelvic irradiation for the previously operated patient, or surgery for a post-irradiation recurrence. A serum PSA which rises to high levels following treatment will often be associated with distant metastases, and this is more certain if the original tumor was locally advanced and/or the histology was poorly differentiated or aneuploid. A newly elevated serum acid phosphatase in a treated patient with prostate cancer will usually signify disseminated disease also. Whether to wait until a patient becomes symptomatic from a recurrence or to initiate endocrine treatment solely on the basis of a rising serum marker still remains a point of controversy. The overall survival of Stage D2 patients has not been prolonged by endocrine manipulations which were instituted before symptoms of widespread dissemination appeared. The routine use of periodic imaging studies to follow asymptomatic patients with prostate cancer after they have received treatment cannot be justified for clinical decision-making purposes. On the other hand, in treated patients who develop new symptoms suggesting bone metastases, radionuclide scans which are correlated carefully with the patient's symptoms and with radiographs of "hot" areas on the scans are indicated. When a suspected diagnosis of metastatic disease still remains in doubt, elevated serum tumor markers may provide additional evidence. Imaging studies can also be used to guide percutaneous biopsies of suspected metastases in bones (radionuclide scans and radiographs), or of persistent tumor in an irradiated prostate gland or at the urethro-vesical junction after surgery (TRUS). Since cancer of the prostate often progresses slowly and disseminated disease remains incurable at this time, some degree of uncertainty about the presence of metastases or of recurrent local disease might be safer and less costly than the use of multiple diagnostic studies and aggressive treatment (including endocrine manipulations) in nonsymptomatic patients.
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PMID:Surveillance of patients with prostate cancer after treatment: the roles of serologic and imaging studies. 768 12

Transrectal ultrasound was performed on 15 men with clinical suspicion of local disease after radical retropubic prostatectomy. Clinical suspicion was defined as an elevation in serial serum prostate-specific antigen (PSA, above 0.4 ng/mL, Tandem-R + Assay) and/or palpable mass in the rectal vault. Post-radical prostatectomy ultrasound was normal if there was smooth tapering of the bladder neck to the urethra with no foci of variable echogenicity, and suspicious if any hyper- or hypo-echoic foci were present or if a mass was detected. Thirteen of 15 ultrasounds (87%) were described as suspicious while 2 of 15 (13%) were described as normal. Only 6 of 13 patients (46%) with suspicious findings on ultrasound had biopsy-proved carcinoma. Both patients with normal findings on post-radical prostatectomy ultrasound had biopsy-proved cancer. Transrectal ultrasound of the prostatic fossa when used independently is of no value in the diagnosis of local disease after radical prostatectomy. Transrectal ultrasound may help to direct systematic biopsies of the prostatic fossa in those patients in whom local disease is suspected on the basis of elevated serum PSA and/or a mass found on rectal examination.
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PMID:Value of transrectal ultrasound in identifying local disease after radical prostatectomy. 768 58

Pre- and post-treatment specimens from 47 patients with hormone resistant prostatic carcinoma were compared with each other regarding histological grade and immunoreactivity for p53 protein, neuron specific enolase and c-erbB-2 protein. Significantly more specimens expressed a high malignancy grade when the tumour had become hormone resistant than at the time of initial diagnosis (Gleason P: < 0.0001, WHO P:0.0003). p53 protein immunoreactivity increased significantly with disease progression (P:0.006), while tissue PSA immunoreactivity was reduced in post-treatment specimens (P:0.011). p53 protein expression did not correlate with histological grade or PSA expression and seems to be an independent parameter which participates late in the neoplastic transformation. Thirty-two percent of the tumours were neuron specific enolase positive, but this parameter did not correlate with development of hormone resistance. c-erbB-2 protein reactivity was not recognised.
Br J Cancer 1993 Aug
PMID:Hormone resistant prostatic adenocarcinoma. An evaluation of prognostic factors in pre- and post-treatment specimens. 768 48

Evidence is mounting indicating that screening for prostate cancer is rational and appropriate. More information is necessary to define the optimal ages at which screening should be performed and to determine the appropriate role of PSA, PSA velocity, and PSA density in serial screening. Formal demonstration of a significant screening-induced reduction in cancer-specific morbidity and mortality is necessary to unambiguously justify screening. A prospective, randomized trial evaluating prostate cancer screening will soon be underway.
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PMID:The case for prostate cancer screening. 768 38

Stage A1 prostate cancer implies indolence. If only well-differentiated low-volume tumors are considered, the rate of cancer growth, clinical progression, and prostate cancer death is exceedingly low. All but a very few of these patients will need observation alone. Younger patients (those less than 60 years of age) and those with more moderately differentiated tumors or with serological or ultrasound evidence of residual cancer need further evaluation. It is likely that patients within this group are those who have in past studies experienced a higher degree of progression and cancer mortality. A stepped-up effort to detect nonpalpable prostate cancer has included PSA and transrectal ultrasound with random biopsies. Prostate cancer screening using a serum test and/or ultrasound has allowed increased detection of otherwise clinically silent cancer (stage A). Occult prostate cancer identified by needle biopsy or detected through elevated PSA levels most often is peripheral zone cancer and more aggressive than that arising in the transitional zone. A reclassification of stage A is therefore needed and a new scheme for TNM staging was recently introduced (Table 4). Because of its more aggressive potential, the new stage T1c will likely require different treatment recommendations than those for traditional stage A1 (T1a). More time and evaluation will be needed to estimate the prognosis of those diagnosed with minimal stage T1c prostate cancer.
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PMID:Treatment of stage A1 prostate cancer: the case for observation. 768 40

Many questions still exist about the etiology of prostate cancer. Prostate cancer screening methods continue to evolve. The following four findings are important to remember: (1) PSA is organ specific, not cancer specific, (2) DRE remains the standard method for screening, (3) TRUS continues to evolve but is currently too expensive to use as a screening modality, and (4) a combination of DRE and PSA is the most effective and cost-efficient screening method. Although screening methods are controversial, mass screening for prostate cancer is already occurring in several cities in the United States. An understanding of the value and limitations of the available screening tools is essential.
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PMID:Prostate cancer: screening and early detection update. 769 77

We have established organ cultures of human prostate for in vitro analysis of the hormone responsiveness of prostatic carcinoma. Tissue samples were obtained from total prostatectomies for localized cancer. Normal prostate tissues with age-related hyperplastic changes were obtained from cystoprostatectomies of bladder cancer patients representing the same age group, and they wer cultivated as controls. The explants of prostates were cultured for 7 days in basal medium containing 5% dextran charcoal-treated fetal calf serum, insulin (0.08 IU/ml), and dexamethasone (10(-7) M) with or without dihydrotestosterone (DHT) (10(-7) M) or estradiol (10(-9) M). Control prostates showed involutive changes of morphology when cultured in basal medium. These changes were prevented by DHT, which also maintained a strong epithelial immunostaining for PSA (prostate specific antigen), which was used as a marker for tissue-specific functions. The concentration of PSA in the medium was high. The rate of [3H]thymidine incorporation into DNA was stimulated by DHT in some cultures of control prostates, but no increase was seen in the others. Androgen stimulation of [3H]thymidine incorporation was consistently inhibited by the antihormone cyproterone acetate. The main morphological response of cultured control prostates to estradiol was induction of squamous metaplasia. This was associated with increased incorporation of [3H]thymidine, which was radioautographically localized to the basal layer of epithelium. Estradiol effects were counteracted by the antihormone toremifene. The expression of androgen receptor mRNA and protein in cultured control prostate was demonstrated by Northern blotting and immunohistochemistry, respectively. Also, the expression of estrogen receptor was demonstrated by the polymerase chain reaction analysis of total mRNA from cultured control and cancer prostate. The cultured explants of prostate cancer maintained the overall morphology of the original carcinoma. However, the presence of DHT improved the morphology of cancerous acini in all better differentiated carcinomas (3 grade I and 5 grade II), and corresponding responses to DHT were observed in the rate of DNA labeling with [3H]thymidine. In 2 of 3 grade I carcinomas, DHT increased DNA synthesis, but in grade II cancers the patterns of hormone responses were more variable. The poorly differentiated grade III prostatic carcinomas did not respond to either hormone as measured by [3H]thymidine uptake, and no hormone effects could be seen in morphology. Immunostaining for PSA differed from that in control prostates: besides cancerous acini, the surrounding stroma was also intensively stained, which suggests unpolarized and impaired secretion of PSA by the cancer cells.(ABSTRACT TRUNCATED AT 400 WORDS)
Cancer Res 1993 Nov 01
PMID:Hormone regulation of human prostate in organ culture. 769 34

Despite recent advances in imaging techniques, the staging process is still unsatisfactory in cancer of the prostate. The underestimation for stage B2 and C tumours in about 50%. We present our findings in a retrospective study analyzing the clinical and biological effects of complete androgen blockade before radical prostatectomy in patients with advanced stage localized tumours. We treated 21 patients from 1989 to 1993. All received preoperative homonotherapy by complete androgen block for at least 3 months before node dissection preceding suprapubic radical prostatectomy. Only 20 prostatectomies were performed as metastasis was found in the extemporaneous examination in 1 patient. The volume of the prostate gland had diminished in all patients after the hormonotherapy (27.8%) as did PSA (95%). When evaluated, the tumour stage of the surgical specimen was always more advanced than the needle biopsy. Only 1 tumour was strictly limited to the intracapsule and all the others had either invaded the capsule, reached the margins or had invaded the seminal vessels or lymph nodes. With a mean follow up of 45 months, recurrence rate is 50%, mainly due to tumours with positive margins or seminal invasion in patients who were not given adjuvant treatment. Our results are in agreement with those in the literature showing that although the volume of the prostate is reduced and PSA declines, no improvement in pathology staging is observed.
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PMID:[Radical prostatectomy after complete androgen blockade in stage B2 and C cancer]. 774 57

A 58-year-old male complaining of pollakisuria, miction pain and back pain visited us Dec. 26, 1979. Rectal examination revealed the prostate enlarged by 5 digital width, stony hard and irregular. Transrectal needle biopsy revealed moderately differentiated adenocarcinoma of the prostate. Bladder neck invasion, pelvic and mediastinal lymph node metastases and multiple bone metastases were found. The case was diagnosed with prostatic adenocarcinoma T3N2M1 (OSS, LYM) stage D2. Three courses of chemotherapy using ifosfamide applied from Feb. 2, 1980 showed no marked effect except for partial pain relief. Hormonal treatment with diethylstilbestrol diphosphate was started from May 28 and arterial infusion chemotherapy using CDDP and 5-FU was performed 2 months later, resulting in size reduction of the prostate and pelvic lymph node metastases and disappearance of mediastinal lymph node metastases. Needle biopsy of the prostate was negative for cancer cells. After 8 months, Tegafur was started, and 12 months later radiotherapy was added to the prostate and pelvic lymph nodes. The abnormal accumulation in bone scan began to decrease after 14 months and achieved complete remission 28 months after the initial therapy. We discontinued the hormonal therapy 31 months later because of his complaint of chest discomfort and palpitation. At the present time, 14 years after the initial therapy, the prostate was 35 x 29 x 19 mm in size on transrectal ultrasonography with undetectable serum PSA level and no tumor cells but only mass fibrosis has been seen by pathological examinations. We considered this patient to be with no evidence of disease.
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PMID:[A case of completely responding stage D2 prostatic cancer with no evidence of disease 14 years after diagnosis]. 780 48

Prostate cancer with marked neuroendocrine (NE) differentiation belongs to the hormone resistant carcinomas. We report the development of TSH-secreting small cell prostate cancer (SCPC) from high grade adenocarcinoma (Gleason score 8) with an elevated number of chromogranin A positive cells located in benign structures adjacent to the cancer. Conversion to SCPC was followed-up during 4 years. The initial adenocarcinoma exerted a stronger positivity for PAP than for PSA (respective staining indexes, Sls, 2.2 and 1.8, maximum staining 3.0). In the developed SCPC, 2 cell subpopulations that were derived from epithelial cells were found (positive stain for EMA and CEA, respectively) and from one of them originated CEA-positive liver metastases. Blood CEA and NSE levels were elevated in SCPC (284 ng/ml and 24.5 ng/ml). However, blood TPS level which reflects proliferation of epithelial cells was within the normal range. The development of a << pure >> sarcomatoid prostatic tumor from adenocarcinoma with 2 areas of similar differentiation grades (Gleason score 7 and 9-10) that initially differ in staining for PSA and PAP (SIs for PSA were 1.2 and 0.02 and for PAP were 1.6 and 0.02, respectively) was followed-up during 4 years of treatment with Estracyt. Adenocarcinoma tissue specimens was slightly CEA-positive. The disappearance of lower grade adenocarcinoma during treatment was accompanied by the development of sarcomatoid areas that were 100% vimentin positive. In the last year of follow-up the primary tumor was composed only of vimentin positive sarcomatoid cells with a slight positivity for Chromogranin A, NSE and ACTH. In parallel, normal serum PSA and PAP values and elevated CEA and NSE serotests (12.6 ng/ml and 24.7 ng/ml, respectively) were found. Blood TPS level was at the upper limit of the normal range. Scintigraphy revealed extensive liver metastases. The recorded data indicate (i) extremely poor prognoses associated with high grade adenocarcinomas that demonstrate stronger immunohistochemical positivity for PAP than that for PSA (ii), chromogranin A positive cells in benign structures adjacent to the cancer as a possible paracrine promoter of SCPC from poorly differentiated adenocarcinoma, and (iii) a high degree of heterogeneity of both SCPC and sarcomatoid prostatic neoplasms with some evidence for definite links (EMA and CEA) to secretory epithelial cells.
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PMID:Immunohistochemical staining and serotest markers during development of a sarcomatoid and small cell prostate tumor. 784 May 15


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