Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0001418 (adenocarcinoma)
 68,496 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Cystosarcoma phyllodes of the prostate is a rare neoplasm, occurring in adult men. It closely resembles the not uncommon tumor of the female breast and usually behaves in a similar manner. This case of benign cystosarcoma phyllodes of the prostate occurred in a 53-year-old man who presented with increasing abdominal girth and underwent exploratory laparotomy and removal of the 11.2-kg tumor. It was remarkable for its very large size and the presence of foci of well-differentiated adenocarcinoma, prostatic acinar type. The glandular epithelium of both the phyllodes tumor and the carcinoma were immunoreactive for cytokeratin, epithelial membrane antigen, prostate-specific antigen, and prostate-specific acid phosphatase. The presence of typical prostatic type adenocarcinoma and this immunoreactivity pattern strongly supports a prostatic origin for this rare neoplasm.
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PMID:Giant cystosarcoma phyllodes of the prostate associated with adenocarcinoma. 131 Feb 47

Kallikreins are involved in the posttranslational processing of a number of specific polypeptide precursors. Previously, human glandular kallikrein (hGK-1) mRNA has been identified in the prostate; however, the hGK-1 protein has not been identified and characterized. Therefore, its physiologic function in the prostate is not known. In this study, we have isolated a full-length hGK-1 cDNA from a human adenocarcinoma cell line, LNCaP. In vitro translation experiments demonstrated that the molecular size of the hGK-1 protein generated from this cDNA is similar to that of prostate-specific antigen (PSA), a protein which is produced exclusively in the prostate. In situ hybridization with a hGK-1-specific oligonucleotide probe (77 bases), which can differentiate hGK-1 mRNA from PSA mRNA, demonstrated the hGK-1 mRNA to be located in the prostate epithelium. The hGK-1 mRNA was colocalized with PSA mRNA in prostatic epithelia. Moreover, in situ hybridization studies revealed that the level of hGK-1 mRNA in human benign prostatic hyperplasia tissues is approximately half that of PSA mRNA. Furthermore, we have demonstrated that hGK-1 mRNA is under androgenic regulation in LNCaP cells. Time course analysis revealed that hGK-1 mRNA levels increased significantly at 5 h of mibolerone treatment and reached maximal levels by 9 h. In addition, hGK-1 mRNA levels were increased by dihydrotestosterone, but not by dexamethasone or diethylstilbestrol treatments. Flutamide, a nonmetabolized anti-androgen, repressed the androgenic effects. These studies suggest that expression of hGK-1 mRNA is regulated by androgen via the androgen receptor.
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PMID:Tissue-specific and hormonal regulation of human prostate-specific glandular kallikrein. 137 Jun 33

Prostate-specific antigen (PSA) is the most sensitive marker available for monitoring the progression of prostate cancer and response to therapy. In a previous study, we demonstrated tissue-specific expression of PSA glycoprotein and mRNA and its regulation through the androgen receptor. In this study, we examine the effects of protein kinase A (PKA) and protein kinase C (PKC) on the androgen regulation of PSA in a human adenocarcinoma cell line, LNCaP. Northern blot analysis demonstrated that forskolin, an activator of PKA, had no effect on the androgen regulation of PSA. However, the phorbol ester 12-O-tetradecanoyl-phorbol-13-acetate (TPA), a direct activator of PKC, showed a time- and dose-dependent repression of the androgen regulation of PSA glycoprotein and mRNA. The biologically inactive phorbol ester, 4 alpha-phorbol-12,13-didecanoate, had no effect. Staurosporine, a PKC inhibitor, blocked the TPA-mediated repression of the androgenic stimulation of PSA glycoprotein. In addition, the calcium ionophore, A23187, was able to simulate the actions of TPA, presumably through activation of PKC via calcium mobilization. In summary, the androgenic regulation of PSA protein and mRNA is repressed by tumor-promoting phorbol esters through the PKC pathway. This indicates that the effects of TPA may be secondary to repressed gene transcription or altered mRNA stability. In addition, this study emphasizes that the androgenic regulation of PSA is complex and may involve other extracellular transduction signals.
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PMID:Tumor-promoting phorbol ester down-regulates the androgen induction of prostate-specific antigen in a human prostatic adenocarcinoma cell line. 137 17

External beam radiotherapy was administered to 39 patients after radical prostatectomy for adenocarcinoma. Thirty-seven of 39 patients had detectable levels of serum prostate-specific antigen (PSA) prior to irradiation as evidence of residual carcinoma (biochemical evidence of disease). Two patients also had palpable recurrences. Pathologic analysis of the surgical specimens suggested that positive surgical margins, seminal vesicle or lymph node involvement, or high Gleason pattern scores are associated with measurable PSA after surgery. Follow-up ranged from two to seventy-four months (mean 26.8 months). To date, local control has been achieved in all but 1 patient (including 2 patients with palpable tumor prior to radiotherapy). Two distinct risk groups for the development of distant metastases based on the trend of the PSA in relation to the duration of follow-up after radiotherapy are defined. In the high-risk group (those patients with a rising PSA), in 9 of the 18 bone metastases have developed, while none of the 17 low-risk patients have metastatic disease.
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PMID:Serum prostate-specific antigen after post-prostatectomy radiotherapy. 137 76

We report our experience in the follow-up of 63 patients with advanced prostate adenocarcinoma. We used prostate-specific antigen and prostatic acid phosphatase in 27 patients; in 36 patients we evaluated osteocalcin and bone isoenzyme of alkaline phosphatase, two markers of bone metabolism which seem to be good markers in the follow-up of patients with bone metastases.
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PMID:Advanced prostate cancer follow-up with prostate-specific antigen, prostatic acid phosphatase, osteocalcin and bone isoenzyme of alkaline phosphatase. 138 27

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

We used the method of Rudolph et al. (Clin Chem 1988; 34:2031-8) to find information in the data from correlated determinations of acid phosphatase (PAP, EC 3.1.3.2; DuPont aca) and prostate-specific antigen (PSA, Hybritech). We described there how we assign medical decision limits for two or more correlated variables and convert the database to a binary coded message, allowing separation of a selected disease class with minimum error. The decision point, analogous to a percentile upper limit on the ordered values of each variable in the reference group, satisfies the maximum entropy constraints of reference, producing a minimum entropy for the binary coded patient database. We found maximum entropy decision points at PAP = 0.75 U/L and PSA = 22.8 micrograms/L. Patients with PSA values exceeding 22.8 micrograms/L had no benign prostatic disease except for five patients with benign prostate hyperplasia (BPH) with adjacent colon carcinoma (95.3), BPH with infarction (27.6), BPH (23.4) 28.1), or acute prostatitis (34.6). We consider PSA exceeding 22.8 micrograms/L as indicative of carcinoma of the prostate, stage C or D, in the absence of disconfirming evidence. Another decision value for PSA is 11.3 micrograms/L. This bounds the region between 11.3 and 22.8 micrograms/L, where the frequency of BPH is 1.5 times that for adenocarcinoma. At PSA less than 11.3 micrograms/L there is a high frequency of BPH. PSA concentration is not correlated with prostatic size (mass) or with prostatitis. A metastatic carcinoma is as likely to be nonprostatic as prostatic when the PSA concentration is less than 11.3 micrograms/L.
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PMID:Medically significant concentrations of prostate-specific antigen in serum assessed. 169 92

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

Human glandular kallikrein-1 gene (hGK-1) is closely related to the gene of human prostate-specific antigen (PSA) and both genes are expressed in the human prostate. We have studied PSA and hGK-1 mRNAs in human prostatic tissue samples from patients with benign prostatic hyperplasia (BPH) or adenocarcinoma (CA), using Northern and slot-blot analysis in order to gain insight into the expression of these highly similar genes. Multiple mRNAs were found to originate from both genes. The major mRNA species of 1.6 kb accounted for 57% to 76% of the total coding capacity for PSA in different tissue specimens, but a variant mRNA species of 1.9 kb was also abundant. Most of the BPH samples contained marked amounts of an aberrant 0.9 kb mRNA, and long PSA mRNAs of 6.1 kb, 4.5 kb and 3.1 kb were found in elevated amounts in some of the CA samples. The amount of PSA mRNAs that would produce aberrant PSA proteins if translated into protein varied from 18% to 38% in these tissue samples. The major mRNA species originating from hGK-1 was of 1.6 kb, but other less abundant mRNA species could also be observed. The amount of PSA and hGK-1 mRNAs was determined from slot blots hybridized with specific oligonucleotide probes. No significant differences could be found in the PSA gene expression between BPH and CA samples. The total amount of the PSA mRNAs in all the different BPH specimens was fairly similar, but there was a 3-fold difference between the highest and lowest PSA mRNA levels in the CA samples. The hGK-1 mRNA levels in the BPH specimens studied demonstrated greater variance than the PSA mRNA levels in the same samples. The correlation between PSA gene and hGK-1 expression in the BPH samples was good, suggesting that there are similarities in the regulation of these genes. However, the lack of correlation between the amounts of PSA and hGK-1 mRNAs in the CA samples except in sample C1 indicates that there are also differences in the gene regulation. The observed 3.7- to 6.5-fold excess of PSA mRNAs as compared with the amount of hGK-1 mRNAs present in the same tissue specimen also indicated differences in the cis- or trans-acting regulatory elements of these genes.
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PMID:Expression of the gene coding for human prostate-specific antigen and related hGK-1 in benign and malignant tumors of the human prostate. 169 Nov 51

A total of 58 cases with prostatic diseases including benign hypertrophy (BPH) (n = 10) and adenocarcinoma (n = 48) were studied as to prostate-specific antigen (PA) with indirect enzyme immunohistochemistry. The expression of PA in the prostate, as well as the localization of PA in the tissue, was also studied in regard to cell differentiations, clinical stages, serum PA levels, with or without endocrine therapy, and prognosis of prostate cancer. Strong staining of PA was noted in epithelial cells of the gland, particularly on the ductal cavity, except for patients in the poorly differentiated carcinoma group. The overall positive rate for expression of PA was 100% in BPH and 73% (35/48) in prostate cancer. When prostate cancer was classified by cell differentiation, the positive rate was 100% (17/17) in the patients with well, 83% (10/12) moderately, and 42% (8/19) poorly differentiated carcinoma. When divided by clinical stages, the positive rate was 100% (1/1 and 9/9) in stages A and B each, 69% (9/13) in stage C, and 65% (17/26) in stage D. Of 33 cases whose serum PA values were determined, the histochemistry was positive in 67% of 12 patients with normal serum PA levels and in 86% of 21 in the elevated group. The prior to endocrine therapy group showed the presence of PA in 22 of 27 cases (82%) and a positive rate of 62% (13/21) was observed in the group during the treatment.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[The histological expression of prostate-specific antigen and its clinical significance in patients with prostate cancer]. 169 32


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