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)

Preliminary results are presented after measuring Pregnancy alpha 2 glycoprotein (P.A.G.) in a series of healthy males and those with cancer of the prostate, some of whom were being treated with oestrogens. Serum P.A.G. levels were measured in 21 patients with cancer of the prostate to observe any changes occurring during treatment with oestrogens. There was no significant difference between the P.A.G levels in healthy males and those with untreated prostatic cancer. Treatment however causes increased P.A.G. levels with wide individual variations. There is no apparent relationship between P.A.G. levels and the tumor stage, or efficacy of treatment. A relationship does exist however between the curves of serum P.A.G. levels in pregnant women and patients with prostatic cancer treated with oestrogens. Until proved otherwise, these measurements are of no practical value in patients with prostatic cancer, and future confirmation of these results by the study of a larger number of cases would be of value only in that they avoid other teams from repeating the same investigations.
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PMID:[Assay of "pregnancy alpha 2 glycoprotein" in the serum of prostatic cancer patients and changes during estrogen therapy]. 9 Jul 38

Immunochemical determinations of serum proteinase inhibitors in human semen showed the presence of alpha1-antitrypsin and alpha1,x-antichymotrypsin, whereas inter-alpha-trypsin inhibitor, antithrombin III, alpha2-neuramino-glycoprotein and alpha2-macroglobulin could not be detected. Both serum proteinase inhibitors were determined in the seminal vesicle secretions of two patients with prostatic cancer. Employing the Ouchterlony double immunodiffusion technique pattern of identity was found between alpha1-antitrypsin resp. alpha1,x-antichymotrypsin in seminal plasma, seminal vesicle secretions and serum. Mean alpha1-antitrypsin concentration in seminal plasma of 129 andrological patients was 97.7 mug/ml and that of alpha1,x-antichymotrypsin 32.8 mug/ml. There were no differences in the mean alpha1-antitrypsin concentrations of normozoospermic and oligozoospermic ejaculates and those with seminal plasma fructose deficiency. Azoospermic ejaculates, however, showed a significant decrease of the mean alpha1-antitrypsin concentration (p less than 0.05). Alpha1,x-antichymotrypsin concentrations of normozoospermic ejaculates were significantly higher compared to those of oligozoospermia and azoospermia (p less than 0.05). Alpha1,x-antichymotrypsin levels in semen samples were fructose deficiency were not different from those of the total ejaculate population. The cause and significance of the observed differences in the inhibitor concentrations within the different ejaculate types is not known. However, there are no indications for the involvement of both proteinase inhibitors in male reproductive processes.
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PMID:Quantitative determination of high molecular weight serum proteinase inhibitors in human semen. 108 38

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

Prostatic specific antigen (PSA) can be detected in normal and benign hypertrophic prostates, as well as in prostatic cancer and its metastases. Since it appears in the serum, this glycoprotein has become an established marker for the detection and monitoring of prostate cancer. Using a radioimmunoassay (CIS--Biointernational, France), we found serum PSA levels higher than 4 ng/ml in 55 of 58 patients with prostatic cancer. The concentrations were proportional to tumor stage: significantly higher in stages C and D than in stages A and B (p less than 0.002). In all 6 cases with occult prostatic carcinoma (stage A), levels were higher than 15 ng/ml. PSA was found to be a good indicator of response to therapy, as well as a marker of tumor progression during follow-up. After radical prostatectomy serum PSA levels decreased to below 1 ng/ml. Following radiotherapy levels returned to normal within 1-6 months in 8 of 11 patients. In 21 of 23 with metastases serum PSA decreased during hormonal treatment. In 3 who responded initially to hormonal therapy, levels increased before clinical manifestation of tumor progression. We conclude that PSA is a sensitive serum marker for the diagnosis of prostatic cancer in cases of metastatic disease of unknown origin, as well as for monitoring the response to treatment of prostatic carcinoma. The use of PSA serum levels for screening for prostatic cancer is still controversial.
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PMID:[Prostatic specific antigen for detection and monitoring of prostatic cancer]. 137 29

Prostate-specific antigen (PSA) has emerged as the most useful marker for management of patients with prostate cancer. The regulation of this glycoprotein in vivo has important clinical implications. Indirect evidence indicates that the PSA glycoprotein might be regulated by androgens, and previous studies in this laboratory have demonstrated that PSA mRNA is upregulated by androgens. The current work reports a detailed study of PSA glycoprotein expression as influenced by steroid hormones in a human prostatic adenocarcinoma cell line, LNCaP. First, we have examined the steroid binding specificity of the androgen receptor in this cell line. In comparison with wild-type rat androgen receptor in prostate, the receptor in LNCaP cells has altered affinity for a number of steroids or analogs such as progesterone (R5020), antiprogesterone (RU486), two antiandrogens (cyperoterone acetate and hydroxyflutamide), and an androgen metabolite (epitestosterone). However, its affinity for androgens (mibolerone, dihydrotestosterone, and testosterone) is not changed. The receptor does not bind to the synthetic glucocorticoids (triaminolone acetonide and dexamethasone) nor to a synthetic estrogen DES (diethylstilbestrol). The change of the steroid binding specificity of the receptor is correlated with a single mutation (A----G at nucleotide #876 relative to the initiation codon) of the steroid binding domain of the receptor. The mutation and alteration of steroid-binding specificity of the androgen receptor is also correlated with PSA glycoprotein expression affected by different ligands tested. We have demonstrated that the PSA glycoprotein is upregulated by androgens and is affected by neither epidermal growth factor nor basic fibroblast growth factor. Moreover, PSA glycoprotein could be induced by R5020, estradiol, and epitestosterone; but neither glucocorticoids nor DES had any effect on PSA induction. Interestingly, although the antiandrogen, cyperotone acetate, had the ability to induce PSA, both RU486 and hydroxyflutamide could block androgen and progesterone induction of PSA glycoprotein. Therefore, we conclude that the PSA glycoprotein expression is influenced predominantly by androgens via its receptor, and the mutation of the receptor can affect the expression of this cellular gene by the steroids other than androgens.
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PMID:Hormonal regulation of prostate-specific antigen (PSA) glycoprotein in the human prostatic adenocarcinoma cell line, LNCaP. 137 63

Bone scintigraphy is the most sensitive imaging technique for the initial detection of bone metastases and is widely used in the staging of prostatic cancer. This study was performed to assess whether the development of further bone metastases can be detected by serial measurements of the serum glycoprotein prostate-specific antigen (PSA) as an alternative to follow-up scintigraphy. The bone scintigrams and PSA levels of 101 patients with metastatic prostate cancer entered into two therapeutic trials have been reviewed. Serial results of both investigations were available in 59 cases. In three cases new bone deposits were observed without a corresponding rise in PSA. In two other cases the scintigrams were considered to be suspicious of progression with no change in PSA levels; however, further follow-up indicated that these changes were not due to metastases. In 13 cases PSA levels were rising in advance of new deposits on the scintigrams. In the remaining 41 cases the PSA levels and scintigraphic findings paralleled each other. We conclude that serial estimation of PSA levels is a simpler marker for disease progression than bone scintigraphy in metastatic prostatic cancer, but that neither technique in isolation gives complete accuracy.
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PMID:Can serum prostate-specific antigen replace bone scintigraphy in the follow-up of metastatic prostatic cancer? 138 17

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

We surveyed the tumor-related proteins present in the urine specimens of 118 bladder cancer patients to seek a possible marker enabling future diagnosis and prognosis of this disease. We identified a protein of 180 kDa. by sodium dodecyl sulfate polyacrylamide gel electrophoresis in urine samples subjected to prior adsorption by protein-A conjugated to a sepharose bead. This protein appears to be a glycoprotein because it binds to concanavalin A-conjugated sepharose and can be eluted by alpha-methyl D-mannoside. It does not react immunochemically with antibodies prepared against either carcinoembryonic antigen or epidermal growth factor receptor, both of which have an apparent molecular weight close to 180 kDa. We found this protein in the urine of 74.3% of the patients with transitional cell carcinoma. It was not present in age-matched controls, patients with benign prostatic hyperplasia or patients with 10 other cancers. There was 1 false positive result in a patient with prostate cancer. It does not appear to be associated with urinary tract infection, blood contamination, premedication or anesthesia.
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PMID:A new 180 kDa. urine protein marker associated with bladder cancer. 235 80

The levels of prostatic specific antigen (PSA) and prostatic acid phosphatase (PAP), both measured by radioimmunoassay, and two cancer indices given by the ratio of serum alpha-1 acid glycoprotein to prealbumin (AGP:Palb) and alpha-1 acid glycoprotein to alpha-2 HS globulin (AGP:HS) were evaluated as markers to assess the response of prostatic cancer to treatment with Zoladex, an LH-RH agonist. A rise in PSA and PAP occurred in 8/65 patients (12%) during the initial induction phase. In metastatic disease prior to treatment none of these indices was significantly different between patients who attained a sustained response and those whose response was nil or only transient. Responders and non-responders could, however, be distinguished by the levels of various analytes after treatment. At 6 months the median PSA in those who responded was 2.5 ng/ml compared with 51.5 ng/ml in the non-responders. At 12 months the figures were 3.0 and 155 ng/ml respectively. The corresponding median PAP levels were 1.4 and 19 ng/ml at 6 months and 1.3 and 18 ng/ml at 12 months. The AGP:Palb ratio was also significantly different in these two groups at 6 and 12 months. PSA appears to be the most sensitive indicator of the response to treatment. The likelihood of obtaining a prolonged clinical response can be assessed within 6 months of the start of treatment.
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PMID:Biochemical monitoring of carcinoma of prostate treated with an LH-RH analogue (Zoladex). 243 85

CA-549 is a circulating breast cancer-associated antigen that reacts with monoclonal antibody BC4E 549. Biochemical characterization of CA-549 revealed that it is an acidic (isoelectric point 5.2) glycoprotein that exhibits two bands by sodium dodecyl sulfate-polyacrylamide gel electrophoresis under reducing conditions of apparent molecular weights of 400,000 and 512,000. Immunohistochemical staining of unfixed frozen tissue sections of human breast tumors and a variety of benign tissues with BC4E 549 revealed no preferential staining of tumor over benign breast tissue and cross-reactivity with a wide range of other benign tissues including kidney, liver, lung, colon, pancreas, ovary, and spleen. Serum levels of CA-549 were initially tested by an enzyme-linked immunosorbent assay inhibition using BC4E 549. This assay showed that CA-549 concentrations were elevated in 19 of 27 sera from patients with advanced breast cancer compared to 0 of 22 and 0 of 129 sera from benign breast disease patients and healthy females, respectively. These preliminary data suggested that CA-549 was a useful breast tumor marker; thus BC4E 549 was adapted to a sandwich immunoradiometric assay format suitable for routine use in the clinical laboratory and its performance was evaluated on a panel of 668 serum samples. The test detected significant concentrations of CA-549 in the sera of 40 of 80 patients with advanced breast cancer, 1 of 30 with early breast cancer, 4 of 19 with advanced lung cancer, 2 of 40 with advanced colon cancer, and 5 of 29 with advanced prostate cancer. The test showed a high degree of specificity, producing false-positives in only 3 of 79 benign breast patients, 2 of 25 benign liver patients, 2 of 70 benign colon patients, 2 of 19 benign lung patients, 0 of 20 benign prostate patients, and 3 of 257 healthy individuals. These data represent an overall 50% sensitivity and 98% specificity as a test for advanced breast cancer. These data indicate that this immunoradiometric assay is a useful test for the detection of circulating CA-549 in advanced breast cancer patients and suggest that it may prove useful as a monitor in the management of that disease.
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PMID:Serum levels and biochemical characteristics of cancer-associated antigen CA-549, a circulating breast cancer marker. 244 35


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