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Query: UMLS:C0376358 (prostate cancer)
 59,338 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Grading of the cribriform pattern of prostate cancer is controversial, and the genetic changes are largely unknown. Furthermore, the pathogenetic relationship between the cribriform pattern of high-grade prostatic intraepithelial neoplasia (PIN) and cribriform carcinoma is poorly understood. We used fluorescence in situ hybridization with centromere-specific probes for chromosomes 7, 8, 10, 12, and Y and a region-specific probe for c-myc to evaluate genetic changes in matched foci of high-grade PIN (48 foci) and prostatic carcinoma (71 foci) in 25 whole-mount radical prostatectomy specimens from patients with metastatic cancer. These cases included 10 foci of cribriform PIN and 10 foci of cribriform cancer. Numeric chromosomal anomalies were found in 67 and 68% of the high-grade PIN and carcinoma foci, respectively. Extra copies of the c-myc gene were identified in 52 and 44% of the high-grade PIN and carcinoma foci, respectively. The cribriform pattern of cancer had a higher percentage of foci with gain of chromosomes 7, 12, and Y, loss of chromosome 8, and extra copies of c-myc gene than other Gleason Primary Patterns 3 and 4; there was no difference, however, for all paired comparisons of genetic changes between the cribriform pattern of cancer and Gleason Primary Pattern 5 cancer. Cribriform PIN and cribriform cancer generally exhibited similar anomalies, although the percentage of foci with gain of chromosomes 10 and 12 was higher in cribriform cancer. Our results indicate that the cribriform pattern of prostate cancer shares genetic changes with Gleason Primary Pattern 5 and that both contain more genetic changes than the cribriform pattern of PIN. These findings suggest that the cribriform pattern of prostate cancer has biologic similarity with Gleason Pattern 5 carcinoma and that the cribriform pattern of PIN is closely associated with the cribriform pattern of prostatic carcinoma.
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PMID:Detection of chromosomal anomalies and c-myc gene amplification in the cribriform pattern of prostatic intraepithelial neoplasia and carcinoma by fluorescence in situ hybridization. 938 62

Comparison of different screening methods including digital rectal examination (DRE) and estimation of serum prostate specific antigen (PSA) had been done for detection of cancer prostate at initial stages in 186 patients presenting with prostatism. The detection rate of raised serum PSA (> 4 ng/dl) was found significantly higher than that of abnormal DRE because it could detect cases of prostate cancer at very early stages. On the other hand using abnormal DRE alone as criteria for biopsy, large number of these cases, specially at early stages, would have remained undetected (36.9%) thereby giving false low incidence. Serum PSA was found raised in pre neoplastic conditions (73.9%) like PIN and AAH also, majority of which were missed on DRE (65.2%). Raised serum PSA was found in many benign conditions (36.7%, false positive) also, hence prostatic biopsy is advised to confirm malignancy.
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PMID:Screening of prostate cancer in males with prostatism. 944 53

p27Kip1 is a cyclin-dependent kinase inhibitor that negatively regulates cell proliferation by mediating cell cycle arrest in G1. This study was undertaken to assess the prognostic value of p27Kip1 in localized human prostate cancer. Archival material from 113 radical prostatectomy specimens obtained between 1985 and 1993 was stained immunohistochemically for p27Kip1 protein using a commercially available antibody. Patient charts were reviewed for preoperative serum prostate-specific antigen, clinical and pathological staging, Gleason tumor grade, time to biochemical and clinical recurrence, and survival. Strong p27Kip1 staining was uniformly seen in benign prostatic epithelial components in all tumor sections. p27Kip1 staining was reduced in most prostate cancers and was variable in prostatic intraepithelial neoplasia. Decreased p27Kip1 staining (<25% of nuclei stained positive for p27Kip1) correlated with seminal vesicle involvement (P = 0.0032) and with higher Gleason grade (P = 0.0114). On univariate analysis, low p27Kip1 predicted an increased risk of treatment failure in the node-negative cohort (P = 0.0037) and in the subset who did not receive neoadjuvant hormonal therapy (P = 0.049). Low p27Kip1 expression was an independent predictor of treatment failure on multivariate analysis of lymph node negative prostate cancers following radical retropubic prostatectomy (n = 102; P = 0.047). Seminal vesicle involvement (P = 0.034) and positive surgical margins (P = 0.047) were also independent prognostic factors for disease recurrence. In patients who received preoperative neoadjuvant hormonal therapy, low p27Kip1 in the pathological specimen was an even stronger predictor of outcome than it was in the entire group (n = 23, P = 0.015).
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PMID:Loss of cyclin-dependent kinase inhibitor p27Kip1 is a novel prognostic factor in localized human prostate adenocarcinoma. 945 3

The identification of cell surface antigens is critical to the development of new diagnostic and therapeutic modalities for the management of prostate cancer. Prostate stem cell antigen (PSCA) is a prostate-specific gene with 30% homology to stem cell antigen 2, a member of the Thy-1/Ly-6 family of glycosylphosphatidylinositol (GPI)-anchored cell surface antigens. PSCA encodes a 123-aa protein with an amino-terminal signal sequence, a carboxyl-terminal GPI-anchoring sequence, and multiple N-glycosylation sites. PSCA mRNA expression is prostate-specific in normal male tissues and is highly up-regulated in both androgen-dependent and -independent prostate cancer xenografts. In situ mRNA analysis localizes PSCA expression in normal prostate to the basal cell epithelium, the putative stem cell compartment of the prostate. There is moderate to strong PSCA expression in 111 of 126 (88%) prostate cancer specimens examined by in situ analysis, including high-grade prostatic intraepithelial neoplasia and androgen-dependent and androgen-independent tumors. Flow cytometric analysis demonstrates that PSCA is expressed predominantly on the cell surface and is anchored by a GPI linkage. Fluorescent in situ hybridization analysis localizes the PSCA gene to chromosome 8q24.2, a region of allelic gain in more than 80% of prostate cancers. A mouse homologue with 70% amino acid identity and similar genomic organization to human PSCA has also been identified. These results support PSCA as a target for prostate cancer diagnosis and therapy.
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PMID:Prostate stem cell antigen: a cell surface marker overexpressed in prostate cancer. 946 86

From March 1994 to September 1996 485 patients of median age 67 years (range 49-82) underwent transrectal prostate needle biopsy at the Urological Clinic JLF UK in Martin. PIN was detected in 31 (6.4%) patients. Median age of patients with PIN was 67 years (range 58-75). There were 21 (68%) patients with low-grade PIN and 10 (32%) patients with high-grade PIN. In this group concomitant invasive cancer of the prostate was detected in 6 (19.4%) patients with PIN, of whom 5 (16.0%) had high-grade PIN and 1 (3.4%) nad low-grade PIN. Median concentration of PSA in patients with PIN was 9.1 ng/ml (range 1.3-85 ng/ml), significantly higher (p < 0.001) than PSA concentration in patients with BPH. We did not find significant differences between PSA concentrations in patients with PIN and in those with prostate cancer (p = 0.77). In conclusion we recommend clinical management of patients newly diagnosed with PIN.
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PMID:[Occurrence of prostatic intraepithelial neoplasia in needle biopsy of the prostate and its clinical significance]. 947 72

Intraluminal prostatic crystalloids (IPC) are more common in prostate cancer acini than in benign acini. This study was undertaken to evaluate the hypothesis that crystalloids seen in a benign biopsy may indicate an increased risk of a concomitant prostatic carcinoma. A total of 600 patients underwent more than one prostate biopsy. For 394 patients the results of the biopsy were either negative or positive for prostate cancer. After exclusion of patients whose biopsy results were considered negative but coded as high-grade prostatic intraepithelial neoplasia or were suspicious for cancer or whose slides were unavailable for review, 331 patients remained. Biopsy results for these patients were evaluated for the presence of IPC. Also, 18 completely-embedded benign prostates from cystoprostatectomy specimens from patients with bladder cancer were evaluated for the presence of IPC. Seven hundred twenty-five biopsy specimens were reviewed; 51 (7%) contained crystalloids. Thirty-two of 634 (5%) benign biopsy specimens and 19 of 91 (21%) prostatic carcinoma biopsy specimens contained crystalloids. Sixteen of 331 patients (5%) had crystalloids in the initial benign biopsy specimen; 6 patients subsequently were determined to have carcinoma (38%), and 10 continued to have negative results (62%). Three hundred fifteen initial benign biopsies did not show crystalloids; 83 (26%) patients were subsequently diagnosed as having prostatic carcinoma (p = 0.238, Fisher's Exact Test, chi-square test). The IPC were found in 5 of 18 cystoprostatectomy prostates (28%). In this study, the presence of IPC on the initial biopsy specimens was not a significant risk factor for a subsequent diagnosis of prostate cancer. The IPC were not uncommon in prostates without cancer.
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PMID:The significance of intraluminal prostatic crystalloids in benign needle biopsies. 1019 82

Enlargement of the prostate is an age-related, physiological process that is unique in human tissue. The prostate gland is the most common site of neoplastic disorders in men. Despite the growing impact of the various prostate diseases in terms of morbidity and mortality, the pathogenesis of benign prostate hyperplasia (BPH) and prostate cancer remains poorly understood. This reflects the complex composition of the gland with different anatomic, cellular and functional compartments that are differentially involved in benign and malignant disease processes. The present review summarizes new concepts on the morphogenesis of normal and abnormal growth in the human prostate. There is increasing evidence that prostatic stem cells are located in the basal cell layer that is basically involved in normal growth and the development of glandular hyperplasia and prostate cancer. High-grade prostatic intraepithelial neoplasia is considered the most likely precursor of clinically important cancer of the peripheral zone. Severe differentiation and proliferation abnormalities occur during malignant transformation of the prostatic epithelium. These premalignant changes are associated with abnormal expression of growth factor receptors, oncogene and suppressor gene products and genetic instability. During the process of stromal invasion the transformed cells lose their basal cell phenotype and produce basement membrane-like matrices. Common prostate cancer is mainly composed of exocrine cell types that remain androgen-responsive even in hormone-independent disease. The frequent occurrence of neuroendocrine differentiation in common prostate cancer reflects the differentiation potency of its stem cells. The endocrine phenotype derives from exocrine tumor cells via intermediate (amphicrine) cell types. Neuroendocrine tumor cells consistently lack the nuclear androgen receptor and represent an androgen-insensitive cell population in prostate cancer.
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PMID:[Morphogenesis of benign prostatic hyperplasia and prostatic carcinoma]. 954 38

Prostatic intraepithelial neoplasia (HGPIN) is considered the most likely precursor of clinically significant prostate cancer. Biopsy remains the only definitive method for detecting these premalignant lesions. In this article we review the diagnostic criteria of HGPIN and discuss histological features that allow their distinction from other benign and malignant lesions. PIN is recognised at low power magnification as a thickened, basophilic and hyperchromatic epithelium in pre-existing acinar duct structures. This important histological feature is due to nuclear crowding and stratification. Distinction between HGPIN and low grade PIN (LGPIN), a lesion with little clinical significance, is made mainly on the presence or absence of prominent nucleoli. HGPIN lesions always retain an intact or fragmented basal cell layer. The different growth patterns of HGPIN (tufting, micropapillary, cribriform and flat) have no clinical significance but should be considered in the differential diagnosis together with normal structures, and both benign and malignant lesions. HGPIN has a high predictive value as a marker for prostate cancer but should not influence therapeutic decisions. Its identification in biopsy specimens warrants close surveillance with repeated biopsy.
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PMID:[Diagnostic criteria and differential diagnosis of prostatic intraepithelial neoplasia]. 954 40

Transrectal fine-needle aspiration biopsy (FNAB) of the prostate under digital control is a cheap and rapid method for diagnostic evaluation of palpable and non-palpable nodules, yielding high sensitivity (ca. 95%) and a low complication rate (< 1%). Its specificity amounts to > 97%. The scarcity of urologists trained in the FNAB method and of pathologists experienced in cytology of the prostate limit the clinical application so far. Besides various forms of prostatitis, five different types of cancer can cytologically be differentiated. While PIN I cannot be cytologically identified, PIN II/III lesions may lead to false-positive diagnoses. Cytologic grading of adenocarcinomas of the prostate is of statistically proven prognostic validity and strictly correlated with its histologic counterpart. Preoperative, radiologically controlled FNAB of pelvic and paraortal lymph nodes has sensitivity of ca.86% and specificity of 100%. It thus helps to avoid unnecessary prostatectomies if nodal tumor spread has preoperatively been proven. Diagnostic DNA cytometry is able to identify those prostatic cancer patients who do not reveal significantly increased risk of tumor progression or decreased survival probability, even without therapy (constantly and representatively diploid and tetraploid patterns). Patients with DNA tetraplid histograms may show deteriation of prognosis under hormonal therapy. DNA-aneuploid prostatic cancers should not be subjected to a "wait and see" strategy; they do not respond to hormonal therapy.
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PMID:[Cytopathology of the prostate]. 954 42

A wide variety of architectural patterns of adenocarcinoma may be seen in the prostate. We have recently encountered a hitherto-undescribed pattern of growth characterized by intraluminal ball-like clusters of cancer cells reminiscent of renal glomeruli, which we refer to as prostatic adenocarcinoma with glomeruloid features. To define the architectural features, frequency, and distribution of prostatic adenocarcinoma with glomeruloid features, we reviewed 202 totally embedded radical prostatectomy specimens obtained between October 1992 and April 1994 from the files of the Mayo Clinic. This series was supplemented by 100 consecutive needle biopsies with prostatic cancer from January to February 1996. Prostatic adenocarcinoma with glomeruloid features was characterized by round to oval epithelial tufts growing within malignant acini, often supported by a fibrovascular core. The epithelial cells were sometimes arranged in semicircular concentric rows separated by clefted spaces. In the radical prostatectomy specimens, nine cases (4.5%) had glomeruloid features. The glomeruloid pattern constituted 5% to 20% of each cancer (mean, 8.33%) and was usually located at the apex or in the peripheral zone of the prostate. Seven cases were associated with a high Gleason score (7 or 8), one with a score of 6, and one with a score of 5. All cases were associated with high-grade prostatic intraepithelial neoplasia and extensive perineural invasion. Pathological stages included T2c (three cases), T3b (four cases), and T3c (two cases); one of the T3b cases had lymph node metastases (N1). Three (3%) of 100 consecutive routine needle biopsy specimens with cancer showed glomeruloid features, and this pattern constituted 5% to 10% of each cancer (mean, 6.7%). The Gleason score was 6 for two cases and 8 for one case. Two cases were associated with high-grade prostatic intraepithelial neoplasia, and one case had perineural invasion. Glomeruloid features were not observed in any benign or premalignant lesions, including hyperplasia and intraepithelial neoplasia. Glomeruloid structures in the prostate represent an uncommon but distinctive pattern of growth that is specific for malignancy. Glomeruloid features may be a useful diagnostic clue for malignancy, particularly in some challenging needle biopsy specimens. This pattern of growth is usually seen in high-grade adenocarcinoma, often with extraprostatic extension. Further investigations are required to determine its independent predictive value and correlation with stage and Gleason score.
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PMID:Prostatic adenocarcinoma with glomeruloid features. 992 39


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