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)

The inversion of PSA/PAP ratio is not common in patients with prostate cancer. Of 215 patients, 7 showed PSA levels below those of PAP (3.2%). All patients had metastatic disease at the time of diagnosis, 57% in multiple organs and tissues, with a Gleason value in all cases 4. Forty-three percent showed no early response to hormone therapy; mean survival interval recorded in these 7 patients was 21 months. Such a situation may suggest a poor prognosis for this neoplasia.
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PMID:[The clinical and prognostic value of inversion of the PSA/PAP ratio in prostatic cancer]. 752 63

The present status of tumor markers in prostate cancer, especially prostate-specific antigen (PSA), for diagnosis and follow-up of prostate cancer patients was reviewed. Due to tissue-specific protein of PSA as well as PAP, serum PSA levels may increase in patients with benign hyperplasia (BPH) which is the disease necessary for differential diagnosis from prostate cancer. Therefore, it has been believed to be difficult to differentiate early stages of prostate cancer from BPH using only PSA determination. However, with the use of recently developed assay systems, the detection of PSA-protease inhibitor complex, or PSA-density, the detection of early stages of prostate cancer may be possible. In following up prostate cancer patients, serially determined PSA is one of the best tools to evaluate treatment response and early detection of disease progression.
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PMID:[Tumor markers in prostate cancer]. 752 99

The TOSOH II PA (AIA-PACK PA in the U.S.A.) monoclonal immunoenzyme assay was used and the clinical usefulness of prostate specific antigen (PSA) was evaluated in 39 men with prostatic cancer and 32 men with benign prostatic hyperplasia (BPH) confirmed pathologically. We evaluated the lower limit of detection in this assay by the mean PSA level plue 3 standard deviations in 5 separate experiments with a zero control sera as well as the mean PSA level minus 3 standard deviations in 5 separate experiments with serial dilutions of a known concentration of PSA. PSA concentrations of 0 to 0.25 ng/ml could not be distinguished from the zero control. Therefore, we set the lower limit of detection for the assay as 0.25 ng/ml. At our laboratory, the normal standard value was determined by the mean PSA level plus 3 standard deviations in 79 healthy men as 2.3 ng/ml. Of patients that underwent radical cystoprostatectomy for bladder cancer, all had PSA levels less than 0.25 ng/ml, while only 6% had PAP levels less than 0.11 ng/ml, the lower limit of detection in the TOSOH II PAP assay. We compared TOSOH II PA with Markit PA, a commonly used assay in Japan. Although there was a close linear correlation (r = 0.90) between the TOSOH II PA and Markit PA, the difference of slope in the linear regression lines was great, it was thought due to anti-PSA antibodies in each assay recognizing different epitopes of PSA in the blood.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Prostate specific antigen in patients with prostatic cancer--clinical usefulness of its measurement with sensitive enzyme immunoassay, TOSOH II PA assay]. 752 70

PSA is a 34-kDa 240-amino-acid glycoprotein produced exclusively by prostatic epithelial cells. PSA is a serine protease, is a member of the kallikrein gene family, and has a high sequence homology with human glandular kallikrein. It has chymotrypsin-, trypsin-, and esterase-like activities. In the serum it is present mainly in a complex form with alpha 1-antichymotrypsin. It is secreted in the seminal plasma and is responsible for liquefaction of the seminal coagulum. The production of PSA proteins appears to be under the control of circulating androgens acting through the androgen receptors. The PSA gene is up-regulated predominantly by androgens at both the protein and mRNA levels. DRE causes minimal changes in the PSA level, while prostate massage, ultrasonography, systoscopic examination, and prostate biopsy can all cause clinically significant elevations. Other conditions, such as prostatitis, prostate intraepithelial neoplasia, acute urinary retention, and renal failure can also elevate the PSA level. The value of PSA as a screening tool is questionable because of the great deal of overlap in PSA levels between BPH and prostate cancer. However, if used in men over 50, in conjunction with DRE and/or ultrasonography, it may become a vital part of the early detection program. PSA's role in determining the clinical and pathological stage is also limited, in spite of the direct correlation between the pathological stage and the PSA level, because of great overlap in the PSA levels in various stages. The most important clinical utility of PSA is in monitoring patients after definitive therapy. PSA is most sensitive and reliable in the detection of a residual tumor, possibly recurrence, or disease progression following treatment, irrespective of the treatment modality. PSA can accurately predict the tumor status and can detect recurrence several months before its detection by any other method. PSA is also a very sensitive and specific immunohistochemical marker for tumors of prostatic origin. Compared to PAP, PSA is a more precise and meaningful marker in all clinical situations. With the development of ultrasensitive assays and the adoption of an international standard PSA calibrator, so that results from multicenter studies can be compared, PSA could become one of the most useful tumor marker in cancer biology.
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PMID:Prostatic specific antigen. 753 74

The tumor marker study attempts to make a diagnosis before the clinical diagnosis. We have studied some of these tumor markers (PSA, PAP and acid phosphatase) in 97 patients who suffered from benign prostatic hypertrophy, prostatic cancer and other non-prostatic pathologies. PSA appears to be the best marker, as reported in the literature. The sensitivity and specificity for two different cut off levels (5 and 10 ng/ml) were analyzed in order to determine the best. The statistical analysis was done by the chi-square method. The differences between the tumor markers were not significant for sensitivity. PSA appears to be more sensitive than PAP. Although there are no significant differences for sensitivity between both cut-off levels, and between PSA and PAP. We consider that the 10 ng/ml cut off is better assuming we will have a higher percentage of specificity (p < 0.05).
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PMID:[Determination of tumor markers in the diagnosis of prostatic cancer]. 768 85

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

Seventy-two patients were admitted in a multicentre trial with the purpose of assessing the clinical efficacy and safety of the hormonal control and tolerance of leuprolide acetate in a once-a-month depot injection formulation for the treatment of disseminated prostate cancer. During a 1-year follow-up, there were ten withdrawals for different reasons. At baseline and at 6 months of treatment the following parameters were evaluated: clinical examination, routine blood analysis, PAP, PSA, LH and testosterone, as well as bone scan. LH and testosterone determinations were repeated at 2, 4, 8, 12, 16, 20 and 24 weeks. Testosterone reached castration levels within the second week and was maintained until the end of the study. In agreement with the NPCP criteria, 65 patients were assessed as: complete response 3%, partial response 40%, disease stabilization 36%, and progression 21%. In summary, a once-a-month injection of leuprolide acetate offers a safe and effective alternative to surgical castration.
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PMID:[Treatment of metastatic prostatic cancer with monthly injections of leuprolide acetate depot]. 797 7

Seventy-seven cases of prostate cancer were treated for 5 years at our department and all cases were followed by bone scintigraphy and tumor markers. Of these cases on case of flare response on bone scintigraphy was recognized. A 51-year-old man was hospitalized with chief complaint of lumbago. Serum PAP and gamma-Sm levels were 320 ng/ml and 15 ng/ml, respectively. Prostate biopsy revealed moderately differentiated adenocarcinoma. Bone scintigraphy and CT scan demonstrated multiple bone metastases and lymph nodes involvements. Treatment was started with diethylstilbestrol diphosphate (DES). At one month after the initiation of treatment tumor markers fell down to the normal level and lumbago was diminished, but only serum alkaline phosphatase was elevated and bone scintigraphy showed apparent progression of individual lesions (flare response). The treatment was not altered. At the times after 2, 8, 12 and 36 months successful treatment the bone imaging improved with reduced tracer uptake and no new lesions. The flare response is a healing reaction and is followed apparent improvement. In general, serial bone scintigrams accurately depict the activity of bone metastases in the patients of prostate cancer, but between 1 and 3 months after starting treatment the paradoxical "flare phenomenon" should be taken care.
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PMID:[Flare response on bone scintigraphy in metastatic prostate cancer]. 802 46

The response of advanced prostatic cancer with metastatic chest wall tumor to high-dose diethylstilbestrol diphosphate (DESP) therapy was monitored by in vivo 31P magnetic resonance spectroscopy (31P MRS) study. A eighty-three year old man with Stage D2 prostatic cancer had been treated with chlormadinone acetate and cyclophosphamide since 1984. He was admitted to our hospital with a chest wall tumor and anemia on May 9, 1992. The elevated PAP, PSA and gamma-Sm levels were also observed. Needle biopsy of the tumor revealed poorly differentiated adenocarcinoma metastatic from the prostatic cancer. The patient received 500 mg of DESP by DIV daily for 10 days, and the tumor was reduced by 54% clinically. The abnormal PAP, PSA and gamma-Sm levels returned to almost normal range by three weeks after the initiation of high-dose DESP therapy, and regression of the tumor was confirmed by the MRI. After the first administration of DESP, the MR spectra of the chest wall tumor showed elevated peaks of phosphomonoesters and phosphodiesters. These substances are related to the membrane metabolism and their increase represents the membranous degeneration of tumor cells. The same changes continued consecuitively for three weeks, and corresponded with the regression of the tumor. In conclusion, these results suggest that in vivo 31P MRS of malignant tumors can be useful for evaluating early response to therapy prior to other clinical examinations.
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PMID:[Monitoring tumor response to therapy by means of 31P magnetic resonance spectroscopy. A case of advanced prostatic cancer with metastatic chest wall tumor]. 802 47

The principal role of PAP determinations in 1993 with the ready availability of reproducible serum PSA determinations would be in the identification of those patients with clinically localized prostate cancer who will not be candidates for surgical cure because of the high likelihood of having pathologic stage C or D disease. However, if you believe that radical prostatectomy offers good local control and palliation for clinically localized but pathologic stage C or D disease, then preoperative PAP determinations are not necessary. Also, if you believe that radical prostatectomy in conjugation with androgen deprivation therapy is appropriate for clinically localized but pathologic stage D1 disease, then, again, preoperative PAP determinations are not necessary. However, if you believe that radical prostatectomy is indicated only for those patients with organ-confined cancer, then ordering a preoperative staging Roy enzymatic PAP assay is indicated. Therefore, every urologist must know the type of assay and the substrate being used by his/her laboratory to interpret the PAP results properly; otherwise, patients with potentially curable cancer will not be offered a radical prostatectomy. In conclusion, PSA is superior to PAP for diagnosis, screening, and monitoring prostate cancer. Even though there are three assays for PSA, there is less confusion in interpreting the results than for PAP. The only specific area where the enzymatic PAP assay can be useful is in the identification of those patients with clinically localized disease but pathologically extensive disease; this is not important if you believe that radical prostatectomy offers good local control and palliation for pathologic stage C and D1 disease.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Prostatic acid phosphatase in 1993. Its limited clinical utility. 827 67


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