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)

Both the polyclonal anti-c-erbB-2 peptide antiserum pAB 60 and the monoclonal anti-c-erbB-2 protein antibody mAB-1 detect the c-erbB-2 protein in human breast adenocarcinomas. We investigated c-erbB-2 expression in adult human benign hyperplastic and neoplastic prostates, using the avidin-biotin complex immunoperoxidase method. Formalin-fixed, paraffin-embedded specimens of benign hyperplastic prostate (13), prostatic adenocarcinoma (22), and prostatic adenocarcinoma lymph node metastases (two) were tested with pAB 60. Ten formalin-fixed, paraffin-embedded specimens of prostate adenocarcinoma, 11 frozen sections of benign hyperplastic specimens, and eight frozen sections of prostate adenocarcinoma were tested with mAB-1. Our results demonstrated consistent detection of c-erbB-2 immunohistochemically in frozen sections of both benign and malignant prostate. Preincubation of pAB 60 with the immunizing peptide blocked subsequent reactivity with prostatic tumor tissue, indicating specificity. However, fixation and processing protocols significantly affected the reactivity of the antigenic determinants detected by these antibodies, as mAB-1 was nonreactive with formalin-fixed, paraffin-embedded prostatic tissues. Differential reactivity of pAB 60 with malignant rather than benign glands was maximized by exposure of the specimen to the antibody at 4 degrees C rather than 22 degrees C. The most frequently observed staining pattern with both antibodies was cytoplasmic. However, mAB-1 produced distinctly membranous staining in two frozen specimens of benign hyperplasia and one specimen of prostate cancer.
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PMID:Immunohistochemical detection of c-erbB-2 protein in human benign and neoplastic prostate. 167 81

Immunosuppressive acidic protein (IAP) is a non-specific immunoreactive protein arising from inflammatory or malignant conditions in the human body. We determined the IAP levels in 65 cases with urological malignancies and in 31 cases with benign diseases as a control group during a 9-month period. There were significantly higher serum levels of IAP in cases of bladder transitional cell carcinoma (p = 0.025), prostate adenocarcinoma (p less than 0.00001) and upper urinary tract urothelial cancer (kidney and/or ureter, p = 0.013) as compared with those of the control group. Significant differences in IAP between different tumor stages were found in the bladder cancer group with high stage cases having higher IAP levels (p less than 0.0005). However, no significant differences were found between different tumor gradings. Most of the prostate cancer patients had extremely high IAP values (1,029 +/- 490 micrograms/ml) in this study. Renal cell carcinoma and testicular tumors showed no statistical differences from the control group (p = 0.89 and 0.37, respectively). No differences could be found in the different age groups (by decades) or sexes. The serum IAP level can be a good non-specific tumor marker for bladder cancer staging and probably a good follow-up tool for most urological malignancy patients.
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PMID:Serum level of immunosuppressive acidic protein in patients with urological malignancies. 168 Sep 90

Monoclonal antibodies (MAbs) to specific keratin subtypes were prepared and characterized by immunoblotting and immunohistochemical assays on human cell cultures and normal and malignant human tissues. Chain-specific MAbs to keratin 7 (RCK 105, OV-TL 12/30) and keratin 18 (RGE 53, RCK 106, CK18-2), as well as broadly cross-reacting keratin MAbs (RCK 102, OV-TL 12/5) could be shown to react with different types of human epithelial tissues and were therefore tested for their usefulness in the differential diagnosis of carcinomas. The two broad-spectrum antibodies stained virtually all of the more than 350 carcinomas tested, especially when combined, and distinguished them from most nonepithelial tumors. The keratin 18 MAbs distinguished adenocarcinomas (which are keratin 18 positive) from most squamous cell carcinomas (which are generally keratin 18 negative). The MAbs to keratin 7 could be shown to recognize specific subtypes of adenocarcinoma and could, for example, distinguish between ovarian carcinomas (keratin 7 positive) and carcinomas of the gastrointestinal tract (keratin 7 negative), or between transitional cell carcinomas (keratin 7 positive) and prostate cancer (keratin 7 negative). In general, malignancies showed the expected keratin reactivity pattern as concluded from the keratin pattern of its cell of origin or its type of differentiation. The use of an extended series of malignancies did, however, also illustrate that exceptions to this rule exist. For example, certain antibodies to keratin 18 stained tumor areas in squamous cell carcinomas of the lung. Also a certain percentage of tumors, which generally showed no keratin 7 expression, were positive with RCK 105 or OV-TL 12/30. On the other hand, a certain percentage of tumors, which were generally positive for keratin 7, did not show a staining reaction with these MAbs. Furthermore subtle differences between reactivity patterns of different MAbs recognizing the same keratin protein were observed, both in the normal and malignant human tissues, indicating that specific keratin epitopes may be masked in certain tissues and that unmasking of such epitopes can occur with malignant progression. This phenomenon may be of some use in a further subtyping of carcinomas, especially those of the gastrointestinal tract. Despite these exceptional staining patterns, the keratin MAbs described above have proved to be useful tools in the characterization of epithelial tumors in routine histopathology and cytopathology, in which they add to a more refined diagnosis of (adeno)carcinomas.
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PMID:Use of monoclonal antibodies to keratin 7 in the differential diagnosis of adenocarcinomas. 169 May 12

In a 44-year-old man with persistent back-pain for 3 months duration, radiological and echological investigations revealed prostatic mass lesion with multiple osteoblastic involvements. Transrectal biopsy to the prostate demonstrated pathohistologically poorly differentiated adenocarcinoma (Gleason's score 4-4:8). Serum ACP, ALP and IAP were elevated at the initial diagnosis pathologically. The clinical and pathological stage was D2, without metastasis to lung and liver. Combination chemo-endocrine therapy (methotrexate, adriamycin, pepleomycin, Estracyt and tegafur) with bilateral orchiectomies was performed exclusively as initial treatment. These consecutive treatments brought remarkable reduction of the prostatic mass lesion, decrease of tumor markers to normal range, rapid improvement of subjective symptoms and distinct decrease of abnormal activity in bone scintigram. More than 3 years survival was obtained, and normal performance-status was kept. Prostatic cancer in middle-aged adults is reviewed and discussed.
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PMID:[A case of advanced prostatic cancer in a 44-year-old treated effectively with combination chemo-endocrine therapy]. 169 64

In this study, a site-specific immunoconjugate, designated CYT-356, of the prostate-reactive monoclonal antibody 7E11-C5 was characterized by immunohistological methods for reactivity with normal and neoplastic human tissues. In addition, CYT-356 labeled with 111In was assessed by in vivo imaging and pharmacokinetic studies for localization to human tumor xenografts in nude mice. The native antibody and the site-specific immunoconjugate exhibited similar patterns of reactivity with normal human tissues. Although the majority of tissues tested were negative, weak reactivity with cardiac muscle, proximal kidney tubules, and sweat glands was observed. Positive staining of normal prostate epithelial cells and glandular lumina and strong reactivity with a subset of skeletal muscle cells were also observed. CYT-356 reacted with 100% of prostate tumors examined but was negative on a variety of other neoplasms. Following i.v. administration, CYT-356-111In rapidly localized to and imaged LNCaP human prostate adenocarcinoma xenografts in nude mice, reaching maximal levels of about 30% of injected dose/g of tumor within 3 days. No unusual localization was seen to any nontumor tissue or organ; the level of radioactivity in the normal tissues and organs was at or below that seen in the blood. The localization to xenografts was antigen specific and the accessible binding sites in 100-200-mg tumors appeared to be saturated at an antibody dose between 10 and 100 micrograms. These findings suggest that the CYT-356 immunoconjugate may be useful in the diagnosis and therapy of prostate cancer.
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PMID:Immunohistochemical and pharmacokinetic characterization of the site-specific immunoconjugate CYT-356 derived from antiprostate monoclonal antibody 7E11-C5. 169 22

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

Prostatic acid phosphatase (PAP), gamma-seminoprotein (gamma-Sm) and prostate specific antigen (PSA) were examined on 120 cases of stage D2 prostate cancer between 1979 and 1989. All patients received endocrine therapy as the first treatment; castration and immediate administration of estrogen or antiandrogen (101), LH-RH analogs (13), estrogen (3) and antiandrogen (3). The actuarial survival rates were calculated by the cause-specific survival method. Pretreatment levels of PAP, gamma-Sm and PSA did not influence prognosis. After start of treatment, the relationship between the changes of the markers and prognosis were examined. At 1 month after the start of the treatment, normalization of PAP or gamma-Sm was not reflected in the following course. On the contrary, at 3 and 6 months, groups with normalization of PAP or gamma-Sm showed better prognosis than those with elevated levels. The same tendency of PSA was obtained at 6 months after start of treatment. In patients with normalized PAP at 3 months, abnormal gamma-Sm showed worse prognosis than normalized gamma-Sm. Therefore, the significance of determination on the two markers was manifested. As histological grade influenced the following course, poorly differentiated adenocarcinoma with normalized PAP at 3 months showed better prognosis than those with elevated levels. In conclusion, it is worthwhile to measure multiple markers for predicting the prognosis of stage D2 prostate cancer treated with endocrine therapy.
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PMID:[Changes in prostatic acid phosphatase, gamma-seminoprotein and prostate specific antigen after endocrine therapy for stage D2 prostate cancer]. 170 May 88

A monoclonal antibody (MAb) designated PD41 (IgG1k) was generated by hyperimmunizing BALB/c mice with a membrane preparation prepared from a moderately to poorly differentiated prostate carcinoma surgical specimen. The immunohistochemical reactivity of MAb PD41 was shown to be highly restricted to the ductal epithelia and secretions of prostate adenocarcinoma tissues. Sixty-five % of the prostate tumor specimens were stained with MAb PD41, whereas no staining of the fetal or benign prostate specimens was observed. PD41 reacted minimally with normal prostate tissues, with less than 1% of the epithelial cells staining. This MAb did not react with nonprostate carcinomas or to a variety of normal human tissues. Using both radioimmunoassay and immunofluorescent procedures, several cultured human tumor cell lines, human blood cells, and purified antigens to prostate-specific antigen and prostatic acid phosphatase also were found not to express the PD41 antigen. MAb PD41 also was shown to bind to the target antigen present in seminal plasma obtained from prostate carcinoma patients but not to seminal plasma from normal donors. Immunoblots of gel-separated components of prostate carcinoma tissue extracts indicate that the molecular weight of the proteins carrying the PD41 antigenic determinant can differ among individual tumors, ranging from Mr 90,000 to greater than 400,000. However, in seminal plasma from prostate cancer patients, the predominant component recognized by PD41 is the diffuse Mr greater than 400,000 band. It appears that this monoclonal antibody may recognize a prostate carcinoma-associated mucin-like antigen, which is preferentially expressed on prostate carcinomas, and therefore, may be a useful marker to distinguish benign prostate hyperplasia from prostate carcinoma.
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PMID:Monoclonal antibody PD41 recognizes an antigen restricted to prostate adenocarcinomas. 170 72

In an attempt to induce prostatic adenocarcinoma at higher incidence in a shorter period, we administered diet containing 0.75 ppm of ethinyl estradiol (EE) for three weeks to ACI/Seg rats, which are predisposed to develop a high incidence of microscopic adenocarcinoma of the prostate at higher age. Then, feeding was changed to basal diet and a single subcutaneous injection of 50 mg/kg body weight of 3,2'-dimethyl-4-aminobiphenyl (DMAB) was given two days after the change. We repeated this schedule 10 times. The rats were killed in week 60 of the experiment and subjected to routine autopsy. The average body weight of rats in group 1 given EE and DMAB was lower than that of control rats in group 2. The incidence of adenocarcinoma was not significantly different in the two groups, i.e., 6/74 (8.1%) in group 1 and 2/54 (3.7%) in group 2. The lesions were all microscopic. The incidence of atypical hyperplasia was significantly higher in group 1 at 17 of 74 rats (23.0%) whereas in group 2, it was only 2 of 54 rats (3.7%). Simple hyperplasia was also observed in 25 of 74 rats (33.8%) in group 1, which was significantly higher than that in group 2, where six of 54 rats (11.1%) had this lesion. The reduced growth of animals due to treatments with EE and DMAB probably suppressed the development of prostate cancer in this experiment. Further studies are needed to develop an appropriate model to induce prostate carcinoma at higher incidence in a shorter period.
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PMID:Trial to induce prostatic cancer in ACI/Seg rats treated with a combination of 3,2'-dimethyl-4-aminobiphenyl and ethinyl estradiol. 170 55

Serum levels of prostatic acid phosphatase (PAP), gamma-seminoprotein (gamma-Sm) and prostate-specific antigen (PSA) were determined simultaneously in 57 patients with benign prostatic hyperplasia (BPH) and in 50 untreated patients with prostatic cancer (adenocarcinoma, N = 47 and non-adenocarcinoma, N = 3). The correlations between the serum levels of gamma-Sm and PSA in these patients were assessed by linear regression analysis. Some fundamental studies were added for explaining the causes of discrepancy between the serum levels of gamma-Sm and PSA. All of BPH group underwent transurethral resection of the prostate (TURP) and the sera were obtained for measurements before, immediately after and 18 hours after TURP. The gamma-Sm correlated well with the PSA in the sera obtained before (r = 0.76) and 18 hours after (r = 0.73) TURP. However, there was no correlation (r = 0.26) between them in the sera obtained immediately after TURP. In 47 untreated patients with adenocarcinoma of the prostate, no significant correlation (r = 0.19) between serum levels of gamma-Sm and PSA was observed, although there was correlation (r = 0.51) between those of PAP and PSA. When these patients were classified into two groups, M0 (stage A-C; N = 26) and M1 (stage D; N = 21), however, the serum gamma-Sm correlated with the serum PSA in M0 group (r = 0.57), but didn't in M1 group (r = 0.11). Furthermore, the differences in the means of PAP (p less than 0.05) and PSA (p less than 0.001) between M0 group and M1 group were statistically significant, although the serum gamma-Sm failed to distinguish M0 from M1. The anti-PSA antibody of "PSA Kit" reacted against the standard gamma-Sm adopted from "gamma-Sm Kit". Surprisingly, the anti-gamma-Sm antibody of "gamma-Sm Kit" also reacted against the standard PSA adopted from "PSA Kit". The gamma-Sm and PSA apparently cross-reacted each other. The quantitative analyses with serial dilution of the sera were done by using each assay in 3 patients whose serum levels of gamma-Sm were markedly different from those of PSA. The dilution curve for PAP appeared to be rectilineal, and that for PSA also appeared to be approximately rectilineal. However, the gamma-Sm assay failed to be proportional. In conclusion, the correlation between serum levels of gamma-Sm and PSA was absent in certain circumstances, when the true values of them were expected to be much higher than those determined.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[Discrepancy between the serum levels of gamma seminoprotein and prostate-specific antigen in patients with prostatic neoplasms. Both true or either untrue]. 171 Nov 33


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