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)

Localization of gamma-seminoprotein (gamma-Sm) was examined using horseradish peroxidase-labeled anti-gamma-Sm antibody (Chugai Corp. Ltd., Tokyo, Japan) by the enzyme-labeled antibody method in paraffin embedded specimens of 18 benign prostatic hyperplasias and 32 untreated prostatic cancers. The level of serum gamma-Sm was also determined by enzyme immunoassay in 10 untreated patients with prostatic cancer and 18 with benign prostatic hyperplasia. Specific gamma-Sm staining was detected in prostatic glandular epithelial cells and prostatic secretion of all specimens of benign prostatic hyperplasias and a half of the specimens of prostatic cancers. Specific gamma-Sm staining was shown to correlate with histological differentiation of the prostatic cancer, but no correlation was found between specific gamma-Sm staining and the level of serum gamma-Sm.
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PMID:[Clinical studies of gamma-seminoprotein in prostatic disease. II. Immunohistochemical study of gamma-seminoprotein]. 332 54

A patient who was treated with estrogens for carcinoma of the prostate was later diagnosed with apparent primary cancer of the male breast. He received chest-wall radiation therapy with curative intent. Later, immunodiagnosis by immunoperoxidase staining for human prostate-specific acid phosphatase of the breast tissue revealed that the patient actually had metastatic prostate cancer to the breast rather than primary breast cancer secondary to estrogen therapy. Use of highly specific peroxidase-antiperoxidase tissue staining for human prostate-specific acid phosphatase is recommended to differentiate primary male breast cancer from metastatic prostate cancer.
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PMID:Immunodiagnosis by prostatic acid phosphatase to differentiate primary male breast cancer from metastatic prostate cancer. 353 33

Human prostatic acid phosphatase isoenzyme 2 (HPAcP-2) was isolated from semen. This purified enzyme was immunized to rabbit to produce polyclonal antibodies. The specificity of the antibodies was tested by Western blot transfer method. Rabbit IgG-peroxidase conjugate was prepared from the antiserum and used to localize HPAcP-2 in prostatic carcinoma. It was found that in the tumor glandular acinus the normal basal cells were replaced by tumor cells containing reaction product. In the tumor cells, the reaction product was seen in the cisternae of rough endoplasmic reticulum (ER) and Golgi apparatus. The secretory vesicles which contained reaction product-stained granules and some amorphous material were seen to fuse with the apical plasma membrane and discharged their content into the glandular lumen. On the other hand, some secretory vesicles in the tumor cells facing to the basement membrane also discharged their similar content into the extracellular spaces. Reaction product-stained granules were found in the interstitial spaces surrounding the tumor cells. These findings suggest that HPAcP-2 is synthesized on the bound ribosomes and discharged into the cisternae of rough ER. The molecules are transported to the Golgi cisternae. After concentration and packaging, HPAcP-2 molecules are then transferred to the secretory vesicles, and discharged into the glandular lumen and to the extracellular spaces. The isoenzyme released in the extracellular space may reach the blood stream through the interstitial spaces or the lymphatic system, resulting in the elevation of serum HPAcPase level in some prostatic cancer patients.
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PMID:Immunoultrastructural demonstration of prostatic acid phosphatase isoenzyme 2 in prostatic carcinoma. 371 7

The acid phosphatase (AcP) isoenzyme in a human prostatic cancer cell line was compared to that of prostatic tissue extract by electrophoresis. The major isoenzyme by prostatic tissue extract is the AcP isoenzyme 2, while only AcP isoenzyme 4 (AcP-4) was observed in the human prostatic cancer cell line. A monoclonal antibody specific to AcP-4 was used to investigate the ultrastructural distribution of AcP-4 in a prostatic cancer cell line. The peroxidase staining pattern indicates that AcP-4 is synthesized on bound ribosomes, discharged into the cisternae of rough endoplasmic reticulum, transported to the cisternae of Golgi apparatus for concentration and packaging, and transferred to the secretory vesicles for exocytosis. It is well known that synthesis and secretion of AcP-2 are the major characteristics of the highly differentiated prostatic epithelial cells. The present data demonstrate the loss of this specific function in the prostatic cancer cell line. Instead of AcP-2, the dedifferentiated cancer cell line synthesizes and secretes AcP-4, which is a common AcP isoenzyme of many nonprostatic tissues.
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PMID:Alteration of acid phosphatase isoenzyme in a human prostatic cancer cell line. 378 36

Rabbit antibodies raised against the major isozymes of cytochrome P-450 isolated from hepatic microsomes of beta-naphthoflavone- (BNF) and phenobarbital-treated rats (cytochrome P-450 BNF-B2 and cytochrome P-450 PB-B2, respectively) and against rat liver NADPH-cytochrome P-450 reductase were used to localize these enzymes immunohistochemically in the rat ventral prostate. Using the unlabeled antibody peroxidase-antiperoxidase technique, NADPH-cytochrome P-450 reductase was detected exclusively in the epithelial cells of the gland to the same magnitude in untreated, phenobarbital-, and BNF-treated rats. Cytochrome P-450 BNF-B2-like immunoreactivity was exclusively present in the glandular epithelium in BNF-treated rats, whereas staining could not be visualized in untreated or in phenobarbital-treated rats. The staining for NADPH-cytochrome P-450 reductase was more uniformly distributed within the epithelium than was the cytochrome P-450 BNF-B2-like immunoreactivity. Cytochrome P-450 PB-B2-like immunoreactivity was not found, regardless of animal pretreatment. These findings support our previous results (Haaparanta, T., Halpert, J., Glaumann, H., and Gustafsson, J-A., Cancer Res. 43: 5131-5137, 1983) demonstrating the presence of constitutive NADPH-cytochrome P-450 reductase in the prostate and that an isozyme of cytochrome P-450 is highly inducible by BNF in this gland. The significance of these findings are discussed in view of the essentially unknown etiology of human prostatic cancer.
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PMID:Immunohistochemical localization of cytochrome P-450 and reduced nicotinamide adenine dinucleotide phosphate:cytochrome P-450 reductase in the rat ventral prostate. 391 91

A prostate-specific antigen, distinct from acid phosphatase, was identified by immunologic procedures in prostate tissues (normal, benign hypertrophic, and cancerous) and seminal plasma, as well as in sera of patients with prostatic cancer and of nude mice bearing human prostatic tumor. This antigen was shown by immunoperoxidase staining to be confined to epithelial cells comprising the prostatic ductal elements. Prostate antigen was purified from prostatic tissue and seminal plasma, and it was shown to have a molecular weight of 33,000-34,000 with no subunit component. The isoelectric point of purified antigen was around 6.9, though several unpurified isomers with different isoelectric points also were observed. Serum-borne prostate antigen showed a molecular weight of 90,000-100,000 but it exhibited a molecular weight of 36,000 in the presence of sodium dodecyl sulfate. A sandwich-type, peroxidase-linked immunosorbent assay capable of detecting 0.1 ng of the antigen per milliliter of blood was developed. With this technique, serum level of the antigen was found to increase in patients with prostatic cancer as compared with normal males. The prostate-specific antigen can be a useful marker for detection of prostatic cancer.
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PMID:Prostate antigen: a new potential marker for prostatic cancer. 616 79

The unlabeled antibody peroxidase-antiperoxidase technique was used to examine human malignant prostatic tissue (primary tumors) for the presence of prostate-specific antigen (PSA), carcinoembryonic antigen (CEA), nonspecific cross-reacting antigen (NCA), and beta-chorionic gonadotrophin (HCG). The results were compared to those obtained with normal and hyperplastic prostate tissue (BPH). All specimens of neoplastic, hyperplastic, and normal prostate tissue showed immunostaining reactions for PSA. Immunostaining for PSA was relatively uniform among samples of normal and BPH tissue, but variations with respect to intensity of PSA immunostaining were noted among prostate tumors as well as between the neoplastic cells of individual tumors. Some areas of normal or hyperplastic prostatic epithelium within tumors showed stronger staining reactions for PSA than the tumor cells themselves. Using an antiserum which was able to detect both NCA and CEA, it was found that 16 of 38 tumors (42%) had positive immunostaining reactions. Of these, 15 were subsequently shown to contain only NCA immunoreactivity, and 1 tumor had both NCA and CEA immunoreactivity. NCA, but not CEA, immunoreactivity was identified in hyperplastic prostate tissue within tumor specimens and in BPH specimens. Neither antigen was detected in normal prostatic epithelium. Three of 38 tumors (8%) were found to contain neoplastic cells with HCG immunoreactivity. HCG immunoreactivity was not identified in BPH or normal prostatic tissue. Therefore, HCG and CEA immunoreactivity appear to be tumor-associated antigens in prostate cancer which are expressed with a low incidence. The results of the study identified prostate tumors with different patterns of immunocytochemical markers: 22 of 38 tumors (58%) contained only PSA immunoreactivity; 13 of 38 tumors (34%) contained PSA and NCA immunoreactivity; 2 of 38 tumors (5%) were positive for PSA, NCA, and HCG immunoreactivity; and 1 of 38 tumors (3%) contained PSA, NCA, HCG, and CEA immunoreactivity. Apart from PSA, which was present in all tumors, the markers studied here appeared to be more frequently expressed in well-differentiated tumors than in less-differentiated tumors. Our results suggest the possibility of subclassifying prostate tumors by means of immunocytochemistry.
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PMID:Immunocytochemical evaluation of human prostatic carcinomas for carcinoembryonic antigen, nonspecific cross-reacting antigen, beta-chorionic gonadotrophin, and prostate-specific antigen. 619 63

The purpose of this study was to determine whether changes in the expression of platelet-derived growth factor (PDGF) and its receptors were associated with prostate cancer. Peroxidase-anti-peroxidase-immunoperoxidase labeling was used to detect the A and B chains and alpha and beta receptors of PDGF in 5 benign prostatic hyperplasias and 13 human prostate adenocarcinomas (Gleason grades 2 to 9). In all 5 benign prostatic hyperplasias, none of the PDGF antibodies (even at high titers, 1:50 dilutions) labeled the epithelial or the stromal cells. In adenocarcinomas, the A chain and alpha receptor antibodies labeled both epithelial and stromal cells. The intensity of the staining was relatively high in low Gleason grade (<6) and low in high Gleason grade (>7) tissue; however, the B chain and beta receptor antibodies failed to label either epithelial or stromal cells in any of the 13 adenocarcinomas. The data suggest that PDGF A and alpha receptor genes may be preferentially turned on in epithelial and stromal prostate tumor cells.
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PMID:Immunohistochemistry analysis of platelet-derived growth factor A and B chains and platelet-derived growth factor alpha and beta receptor expression in benign prostatic hyperplasias and Gleason-graded human prostate adenocarcinomas. 752 68

Nearly all primary prostatic carcinomas have been found to express the androgen receptor (AR) protein, which is the intracellular mediator of androgen action. To gain a better insight into the mechanisms of androgen independence of advanced prostatic carcinoma, it is important to know whether the AR is also present in metastases of androgen-independent tumors. We have assessed the status of the AR and the prostate-specific antigen in 22 metastases of 18 patients with progressive prostate cancer. In 18 cases, the metastases were localized in bone, in 3 cases in the epidural space, and in 1 case in the periosteum. All but one patient had received some kind of endocrine treatment for prostatic carcinoma. Paraffin-embedded tissue sections were stained for the AR following a streptavidinbiotin-peroxidase protocol with the polyclonal antibody PG-21, which is directed against amino acids 1 through 21 of the rat and the human AR. The percentage of AR-positive cells was evaluated on the basis of an arbitrary 4-point scale. All 22 tumor metastases displayed AR positivity. One AR-positive metastatic lesion did not stain for prostate-specific antigen, but in all other metastases, this protein was detected by means of immunohistochemistry. The present study provides evidence that, unlike androgen-independent prostatic carcinoma cell lines, distant prostatic carcinoma metastases do express the AR. These findings indicate that the AR may be involved in the progression of prostate cancer.
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PMID:Distant metastases from prostatic carcinoma express androgen receptor protein. 754 9

Anti-HNK-1 monoclonal antibody (MAb) was reactive with non-cancerous and cancerous prostatic epithelia, as well as natural killer cells, myelinated nerves and cells from APUD systems. The expression of HNK-1 antigen on prostate cancer was investigated immunohistochemically by avidinbiotin-peroxidase complex (ABC) method with anti-HNK-1 MAb to clarify the relationship between anti-HNK-1 immunostaining of the cancerous tissue and the tumor differentiation, and that between the former and the survival rate of patients. Of 52 patients with prostate cancer, 49 were reactive with anti-HNK-1 MAb, the positive rate being 94%. The well differentiated cancer showed the highest percentage of positive cancer cells and the strongest staining, while the poorly differentiated cancer had the lowest percentage of positive cancer cells and the weakest staining. HNK-1 antigen was highly expressed on prostate cancer, and the better differentiated the cancer, the more HNK-1 antigen expressed. We also analyzed the total 5-year survival rate of the 52 patients, and the average 5-year survival rate and non-progression rate of 32 patients in stage D2 who had received only endocrinotherapy. Significantly higher survival rate and non-progression rate were observed in the group with more than two-thirds positive cancer cells as compared with the group with less than two-thirds positive cancer cells. The results suggest that the expression of HNK-1 antigen on prostate cancer may be a useful prognostic factor for patients with prostate cancer.
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PMID:Immunohistochemical study of HNK-1 (Leu-7) antigen in prostate cancer and its clinical significance. 755 70


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