Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0007112 (prostatic adenocarcinoma)
 2,574 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In recent years we have made great strides in our understanding of various atypical lesions within the prostate. This clarity originated with the recognition that lesions of atypical hyperplasia of the prostate are diverse both in their histology and in their potential relationship to adenocarcinoma. While the possible relationship of adenosis to carcinoma is still somewhat controversial, there has been a growing body of histological, histochemical, and immunohistological evidence demonstrating that intraductal dysplasia (PIN) is closely linked to some forms of adenocarcinoma of the prostate. Whether there are significant differences in the relationship of intraductal dysplasia to clinically detectable peripherally located adenocarcinoma and centrally located incidentally found carcinomas needs additional clarification. Further studies on all forms of atypical hyperplasia are still required to determine their relative risk of developing carcinoma, similar to those that have been recently published on various atypical hyperplastic lesions within the breast. In order for these studies to be successful, better imaging techniques of the prostate must become available to rule out invasive carcinoma already being present when one of the forms of atypical hyperplasia is identified on biopsy. Additional directions of research in the future will also undoubtedly probe the molecular biology of various forms of atypical hyperplasia, in particular intraductal dysplasia and its relationship to carcinoma, although at this time the molecular characteristics of adenocarcinoma of the prostate is still in its infancy.
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PMID:Controversies in prostate pathology: dysplasia and carcinoma in situ. 140 40

Using a silver staining technique, Nucleolar Organizer Region-associated proteins (NORs) were evaluated on paraffin sections of 16 resected prostatic adenocarcinomas stage A1. Then 30 histological areas was selected which comprised 6 areas for each grade of Prostatic Intraepithelial Neoplasia: PIN 1, PIN 2, PIN 3, 6 areas of normal glandular prostatic epithelium and 6 areas of well differentiated prostatic adenocarcinoma (Gleason I). The mean numbers of argyrophilic nucleolar organizer regions (AgNORs) increased from normal glandular prostatic epithelium to PIN 3, while the mean numbers of well differentiated prostatic adenocarcinoma was similar to PIN 1. A statistically significant difference (P less than 0.01) for AgNORs was found between normal glandular epithelium, PIN 1, PIN 2 and PIN 3 and between PIN 3 and well differentiated adenocarcinoma. It was concluded that AgNORs counts provide to significant kinetic evaluation of PIN and prostatic adenocarcinoma besides to supply a better definition of PIN.
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PMID:[Nucleolus organizer regions in prostatic intraepithelial neoplasm]. 228 42

The necessity of early detection of prostate cancer renewed interest regarding putative premalignant lesions in the tumorigenesis of the prostate. Prostatic intraepithelial neoplasia (PIN) is one potential precursor for prostatic adenocarcinoma. The term PIN has been adopted to replace a wide range of synonyms in the literature that describe potential precursors. PIN is an intraluminal proliferation of the secretory cells lining architecturally benign prostatic ducts and acini that exhibit cytologic atypia. In this review, we discuss the histologic features, the differential diagnosis, the evidence that PIN is a precursor of prostatic carcinoma, and the clinical significance of PIN.
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PMID:Prostatic intraepithelial neoplasia: a potential precursor lesion of prostatic adenocarcinoma. 766 Jun 73

We studied 33 cases with an initial needle biopsy of the prostate that showed only high-grade prostatic intraepithelial neoplasia (PIN 2-3), for which follow-up biopsies were available. Twenty-four men (73%) were shown to have adenocarcinoma either on a simultaneous (14 patients) or subsequent (10 patients) biopsy. The grade of PIN (grade 2 v 3), rectal examination findings, and transrectal ultrasound results proved not to be significantly different in patients with proven adenocarcinoma compared with those without proven carcinoma. In contrast, serum prostate-specific antigen (PSA) concentrations were elevated in 90% of patients with carcinoma compared with only 50% of those with a benign follow-up biopsy. Persistent elevation of serum PSA concentration was seen in only one of three patients with serial PSA measurements and a benign follow-up biopsy. Notably, all patients with carcinoma for whom we had serial measurements of serum PSA levels had persistent elevation. The finding of high-grade PIN on needle biopsy often represents a sampling problem with carcinoma nearby. Consequently, the finding of high-grade PIN on needle biopsy merits vigorous follow-up, including rebiopsy. In particular, patients with increased serum PSA appear to be at greater risk of harboring prostatic adenocarcinoma. However, a significant number of patients with high-grade PIN on initial biopsy may not have evidence of carcinoma on repeat biopsy. Thus, radical prostatectomy or radiotherapy for PIN is not warranted.
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PMID:Significance of high-grade prostatic intraepithelial neoplasia on needle biopsy. 768 99

The frequency and location of apoptotic bodies (AB) were evaluated in hematoxylin- and eosin-stained sections of 12 radical prostatectomies from patients with prostatic adenocarcinoma pre-treated for 3 months with total androgen ablation. Results were compared with an untreated age-, morphology- and stage-matched control group. Treated prostates showed involutional changes, with cytoplasmic vacuolization and chromatin changes ranging from mild to severe condensation, similar to that observed in apoptosis. In treated benign prostatic epithelium, the mean number of AB was 1.64% (standard error (SE), 0.19%), 6.3 times greater than in the untreated group (mean, 0.26%; SE, 0.03%). AB were more frequent in the basal cell layer than in the lumenal cell layer, whereas in the untreated group, AB were almost exclusively found in the basal cell layer. In treated prostatic intraepithelial neoplasia (PIN present in 10 cases), the mean number of AB was 1.74% (SE, 0.04%), which was 2.56 and 2.32 times greater than in untreated low grade PIN (mean, 0.68%; SE, 0.15%) and high grade PIN (mean, 0.75%; SE, 0.11%), respectively. In treated and untreated PIN, the number of AB was greatest in the basal cell layer, less in the intermediate cell layer and lowest in the cell layer bordering the lumen. The mean number of AB in the 12 treated cancers was 1.35 times greater than in untreated cancers (1.80% [SE, 0.12%] versus 1.33% [SE, 0.32%], respectively). The number of AB in treated cases of the acinar pattern of cancer (present in 7 cancer cases) was 1.78 times greater than in untreated cases, and in treated cases of the cribriform pattern of cancer (present in four cases), the mean number of AB was 1.39 times greater than in untreated cases. The number of AB was greatest in the outermost cell layer, with progressive decrease in layers closer to the lumen. In the one treated case with solid/trabecular pattern of cancer, the number of AB was 1.08 times greater than in untreated cases. The gland lumina was rich in macrophages, sloughed secretory cells with degenerative features and AB. The number of AB in the lumina increased from normal epithelium through PIN to cancer, and was greater in treated cases than in untreated cases.
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PMID:Apoptotic bodies in prostatic intraepithelial neoplasia and prostatic adenocarcinoma following total androgen ablation. 860 68

High-grade PIN is the most likely precursor of prostatic adenocarcinoma, according to virtually all available evidence to date. The clinical importance of recognizing PIN is based on its strong association with prostatic carcinoma. PIN has a high predictive value as a marker for adenocarcinoma. Its identification in biopsy specimens of the prostate warrants further search for concurrent invasive carcinoma. PIN is associated with progressive abnormalities of phenotype and genotype intermediate between normal prostatic epithelium and cancer, indicating impairment of cell differentiation and regulatory control with advancing stages of prostatic carcinogenesis. There is progressive gain or loss of a wide variety of biomarkers, including morphometric markers, differentiation markers, stromal markers, growth factors and associated receptors, oncogenes, tumor suppressor genes, and chromosomes. Abnormalities in expression of most biomarkers are amplified in the progression from high-grade PIN to localized cancer, metastatic cancer, and hormone-refractory cancer. Oncogenesis of prostatic carcinoma probably occurs through the selection of several genetic changes, each modifying the expression or function of genes controlling cell growth and differentiation. Further studies are needed to evaluate the function and prognostic value of oncogene expression in the normal, preneoplastic, and neoplastic prostate.
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PMID:Molecular biology of prostatic intraepithelial neoplasia. 870 Aug 1

The aim of the study was to investigate the location of the expression of 72-kd metalloproteinase (MMP-2) in relation to the distribution of type IV collagen in untreated prostatic adenocarcinoma (PAc). Twenty formalin-fixed, paraffin-embedded PAc cases, in which high grade prostatic intraepithelial neoplasia (PINhigh) was occasionally present, were immunohistochemically examined. Type IV collagen immunoreactivity showed the presence of a basement membrane (BM) at the epithelial-stromal junction. In cribriform and solid/trabecular PAc, the staining was focally disrupted. In acinar PAc, the BM immunostained by anti-type IV collagen was observed around the individual acini, with occasional thinning and fragmentation. Immunostaining for MMP-2 was heterogeneous in intensity and location. Cribriform and solid/trabecular PAc showed weak cytoplasmic immunostaining for MMP-2; both moderately and intensely stained cells were seen in the cell layer adjacent to the stroma; intense immunostaining was shown by small clusters of neoplastic cells or single neoplastic cells located in the stroma which also showed thinning and fragmentation of BM staining. In acinar PAc, weak cytoplasmic immunostaining for MMP-2 was seen throughout most areas of the tumours, whereas moderately and intensely stained cells were observed less frequently than in cribriform and solid/trabecular adenocarcinoma. Intense immunostaining of single or small clusters of neoplastic cells located in the stroma was rarely observed and, as for cribriform and solid/trabecular PAc, mainly located towards the periphery of the tumour nodules. BM stained by anti-type IV collagen was preserved in normal prostate and in PIN, some thinning being present in the latter. The pattern and intensity of immunoreactivity for MMP-2 in PIN was similar to that of cribriform and solid/trabecular PAc, whereas normal ducts and acini showed weak immunostaining in most of the secretory cells and moderate to strong immunoreactivity in scattered basal cells. Thus, MMP-2 appeared basically expressed in cells which lie in direct contact with the stroma. This underlined the importance of evaluating the MMP-2 location in relation to basement membrane degradation and tumour invasion.
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PMID:Location of 72-kd metalloproteinase (type IV collagenase) in untreated prostatic adenocarcinoma. 882 16

High-grade prostatic intraepithelial neoplasia (HG-PIN) lies in the morphologic continuum between benign and carcinomatous prostate, but its status as a neoplastic precursor remains only putative. We measured nuclear proliferative activity using MIB-1 antibody to further characterize the cell kinetics of HG-PIN and to assess its relationship to prostatic adenocarcinoma. We studied 36 specimens from randomly selected patients who underwent radical prostatectomies for prostatic adenocarcinoma. Sections of formalin-fixed, paraffin-embedded tissue pretreated by a citric acid monohydrate antigen retrieval method were immunostained with the mouse monoclonal antibody MIB-1, which detects the Ki-67 antigen in formalin-fixed tissue. The Ki-67 antigen is expressed by non-G0 proliferating cells and has been used to assess cellular proliferative activity. A maximum of either 20,400 x fields or 100 positively stained nuclei in benign glands, areas of HG-PIN, and adenocarcinoma were counted to obtain an immunohistologic proliferation index for each case. For benign prostate, HG-PIN, and adenocarcinoma, the mean positivity was 0.4 +/- 0.42 cells per field (range, 0-2), 2.5 +/- 3.79 cells per field (range, 0-16.6), and 13.8 +/- 15.05 cells per field (range, 0.25-73.66), respectively. Using a Kruskall-Wallis analysis of variance (chi 2 = 58, P < 0.05) and the t test for dependent samples, we found that the mean Ki-67 antigen expression significantly differs between histologic categories (P < 0.01, all three comparisons). In addition, the proliferative index consistently increased along the continuum from benign to malignant. We conclude that the MIB-1 proliferative index of HG-PIN lies between that of benign and carcinomatous prostate, supporting the assertion that HG-PIN is a biologic intermediate in the multistep process of transformation into carcinoma.
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PMID:Comparative analysis of the nuclear proliferative index (Ki-67) in benign prostate, prostatic intraepithelial neoplasia, and prostatic carcinoma. 890 40

PSA-based screening substantially increases the prostate cancer detection rate and the percentage of organ-confined tumors. It appears that there is some benefit from screening for prostate cancer because of the increased amount of potentially curable disease discovered and the fact that 96% of the pathologically staged tumors detected have histologic features associated with aggressive cancer. Additional evidence that nearly all tumors detected on the basis of initial PSA screening are apt to be clinically significant may be derived from the information that PSA-based screening decreases the incidence of incidental A1 grade III and A2 tumors but does not increase the detection of clinically insignificant A1 grade I and II tumors. At this time, PSA represents the most effective and valuable tool to detect early prostate cancer; therefore, PSA should be used to improve early diagnosis of prostate cancer. Some advances have been made with the introduction of age-specific reference ranges and the ability to measure free to total PSA ratios. The data presented support the clinical usefulness of age-specific reference ranges for serum PSA. Calculation of the free to total PSA ratio is valuable in deciding which screening volunteers require further evaluation, increases the specificity of PSA screening, and as demonstrated may be useful in deciding which patients with isolated PIN should undergo repeat biopsies. Based on these facts, PSA truly can be described as the most important and useful marker for adenocarcinoma of the prostate. Based on these encouraging results and the obligingness of the social insurances, we will be able to continue PSA screening for early detection of prostate cancer for all concerned Tyrolean men in the future.
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PMID:Prostate-specific antigen as a screening test. The Austrian experience. 912 29

Mutational alterations involving the p53 and retinoblastoma (RB) tumor suppressor genes are implicated in the oncogenesis of a variety of tumors. Their role in the pathogenesis of prostatic adenocarcinoma remains to be fully elucidated, and their detection in high-grade prostatic intraepithelial neoplasia (HG-PIN) has not been closely examined. We studied the immunohistochemical expression of RB and p53 proteins in HG-PIN, benign prostate, and prostatic adenocarcinoma from 25 radical prostatectomy specimens. Formalin-fixed, paraffin-embedded tissue sections pretreated with antigen retrieval in citrate buffer were stained with anti-RB antibody RB-WL-1 and anti-p53 antibody DO-7. RB immunoreactivity was present in all of the cases in the foci of HG-PIN, benign prostate, and prostatic adenocarcinoma. Mutant p53 protein was detected in 56% of HG-PIN, 72% of prostatic adenocarcinomas, and 20% of benign prostatic glands. A multivariate analysis of variance showed an overall difference in p53 immunoreactivity between HG-PIN, benign prostate, and prostatic adenocarcinoma (P < .001). There was a statistically significant difference between immunoreactivity of the benign prostate and of HG-PIN (P < .001) and between the immunoreactivity of benign prostate and prostatic adenocarcinoma (P < .001). The immunoreactivities of HG-PIN and prostatic adenocarcinoma were not statistically different (P = .3). These data suggest that RB loss might not play a role in initiation of all cases of prostatic adenocarcinoma. The p53 immunoreactivity in HG-PIN was significantly different from that found in benign prostate and was similar to that of prostatic adenocarcinoma. This is in keeping with the putative premalignant character of HG-PIN.
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PMID:Immunohistochemical expression of retinoblastoma and p53 tumor suppressor genes in prostatic intraepithelial neoplasia: comparison with prostatic adenocarcinoma and benign prostate. 952 70


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