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PubMed2006

DNA methylation paradigm shift: 15-lipoxygenase-1 upregulation in prostatic intraepithelial neoplasia and prostate cancer by atypical promoter hypermethylation.

Fifteen (15)-lipoxygenase type 1 (15-LO-1, ALOX15), a highly regulated, tissue- and cell-type-specific lipid-peroxidating enzyme has several functions ranging from physiological membrane remodeling, pathogenesis of atherosclerosis, inflammation and carcinogenesis. Several of our findings support a possible role for 15-LO-1 in prostate cancer (PCa) tumorigenesis. In the present study, we identified a CpG island in the 15-LO-1 promoter and demonstrate that the methylation status of a specific CpG within this island region is associated with transcriptional activation or repression of the 15-LO-1 gene. High levels of 15-LO-1 expression was exclusively correlated with one of the CpG dinucleotides within the 15-LO-1 promoter in all examined PCa cell-lines expressing 15-LO-1 mRNA. We examined the methylation status of this specific CpG in microdissected high grade prostatic intraepithelial neoplasia (HGPIN), PCa, metastatic human prostate tissues, normal prostate cell lines and human donor (normal) prostates. Methylation of this CpG correlated with HGPIN, PCa and metastatic human prostate tissues, while this CpG was unmethylated in all of the normal prostate cell lines and human donor (normal) prostates that either did not display or had minimal basal 15-LO-1 expression. Immunohistochemistry for 15-LO-1 was performed in prostates from PCa patients with Gleason scores 6, 7 [(4+3) and (3+4)], >7 with metastasis, (8-10) and 5 normal (donor) individual males. Quantitative reverse transcription-polymerase chain reaction (qRT-PCR) was used to detect 15-LO-1 in PrEC, RWPE-1, BPH-1, DU-145, LAPC-4, LNCaP, MDAPCa2b and PC-3 cell lines. The specific methylated CpG dinucleotide within the CpG island of the 15-LO-1 promoter was identified by bisulfite sequencing from these cell lines. The methylation status was determined by COBRA analyses of one specific CpG dinucleotide within the 15-LO-1 promoter in these cell lines and in prostates from patients and normal individuals. Fifteen-LO-1, GSTPi and beta-actin mRNA expression in BPH-1, LNCaP and MDAPCa2b cell lines with or without 5-aza-2'-deoxycytidine (5-aza-dC) and trichostatin-A (TSA) treatment were investigated by qRT-PCR. Complete or partial methylation of 15-LO-1 promoter was observed in all PCa patients but the normal donor prostates showed significantly less or no methylation. Exposure of LNCAP and MDAPCa2b cell lines to 5-aza-dC and TSA resulted in the downregulation of 15-LO-1 gene expression. Our results demonstrate that 15-LO-1 promoter methylation is frequently present in PCa patients and identify a new role for epigenetic phenomenon in PCa wherein hypermethylation of the 15-LO-1 promoter leads to the upregulation of 15-LO-1 expression and enzyme activity contributes to PCa initiation and progression.

Adult↗
PubMed2006

Pathological changes of high-grade prostatic intraepithelial neoplasia and prostate cancer after monotherapy with bicalutamide 150 mg.

OBJECTIVES: To evaluate the morphological changes induced by a 3-month course of neoadjuvant bicalutamide 150 mg/day before radical prostatectomy (RP) on prostatic adenocarcinoma and high-grade prostatic intraepithelial neoplasia (HGPIN). PATIENTS AND METHODS: In all, 90 patients with cT1-T2 prostate cancer and HGPIN on prostatic biopsy were randomized to receive bicalutamide (150 mg/day for 3 months) before RP, or to have immediate surgery. Surgical specimens were assessed for the histopathological features of cancer, HGPIN and benign epithelium in a blinded manner. The volumes of prostate cancer and HGPIN were evaluated using a stereological (i.e. grid) method. RESULTS: Compared with the bicalutamide-treated group, the ratio of stroma to epithelium, evaluated by visual microscopic assessment in the normal epithelium of the three prostate zones, was significantly lower in the control group, at 2.27 (sd 1.13), than in the treated group, at 1.87 (sd 0.72) (P = 0.048). The mean (sd) tumour volume was significantly lower in the bicalutamide-treated than in the control group, at 0.914 (0.13) vs 1.47 (0.24) mL (P = 0.044). Similarly, the mean (sd) volume of HGPIN was significantly lower in the bicalutamide-treated than in the control group, at 0.34 (0.06) vs 0.62 (0.07) mL (P = 0.003). At RP, specimen Gleason scores in the bicalutamide-treated group were similar to those in the control group, and were no different from the biopsy Gleason scores. CONCLUSIONS: Involution and epithelial shrinkage of prostate cancer and HGPIN were evident after neoadjuvant treatment with bicalutamide 150 mg. There was no evidence of the emergence of higher-grade cancer after treatment.

Adenocarcinoma↗
PubMed2001

Repeat biopsy strategy in patients with atypical small acinar proliferation or high grade prostatic intraepithelial neoplasia on initial prostate needle biopsy.

PURPOSE: Isolated high grade prostatic intraepithelial neoplasia and/or atypical small acinar proliferation on prostate biopsy increases the risk of identifying cancer on repeat biopsy. We report the results of repeat prostate biopsy for high grade prostatic intraepithelial neoplasia and/or atypical small acinar proliferation, and propose an optimal repeat biopsy strategy. MATERIALS AND METHODS: Of 1,391 men who underwent standard systematic sextant biopsy of the prostate 137 (9.8%) had isolated high grade prostatic intraepithelial neoplasia or atypical small acinar proliferation, including 100 who underwent repeat prostate biopsy within 12 months of the initial biopsy. RESULTS: Adenocarcinoma was detected in 47 of the 100 patients who underwent repeat biopsy. The initial biopsy site of high grade prostatic intraepithelial neoplasia and/or atypical small acinar proliferation matched the sextant location of cancer on repeat biopsy in 22 cases (47%). Repeat biopsy directed only to the high grade prostatic intraepithelial neoplasia and/or atypical small acinar proliferation site on initial biopsy would have missed 53% of cancer cases. In 12 of the 47 men (26%) cancer was limited to the side of the prostate contralateral to the side of high grade prostatic intraepithelial neoplasia and/or atypical small acinar proliferation. Of the 31 patients with cancer in whom the transition zone was sampled cancer was limited to the transition zone in 4 (13%) and evident at other biopsy sites in 13 (42%). The only significant predictor of positive repeat biopsy was mean prostate specific antigen velocity plus or minus standard error (1.37 +/- 1.4 versus 0.52 +/- 0.8 ng./ml. per year, p <0.001). CONCLUSIONS: Patients with isolated high grade prostatic intraepithelial neoplasia and/or atypical small acinar proliferation on prostate biopsy are at 47% risk for cancer on repeat biopsy. The optimal repeat biopsy strategy in this setting should include bilateral biopsies of the standard sextant locations. We also strongly recommend that transition zone sampling should be considered.

Adenocarcinoma↗
PubMed1993

PSA in benign prostatic hyperplasia and prostatic intraepithelial neoplasia.

Prostate specific antigen has become an important adjunct to the digital rectal examination in screening for prostate cancer. The clinician should be familiar with interpretation of this test. Many men with BPH have elevated serum PSA concentrations; however, the majority of these men will have other pathologic processes such as occult cancer, PIN, or acute inflammation that may account for the elevations in serum PSA. Certainly, serial increases in serum PSA should increase concern that occult carcinoma is present. Patients with PIN may also have elevated PSA concentrations. When PIN is associated with elevated PSA, a high incidence of invasive carcinoma is noted on subsequent biopsy. Further investigation into the associations will further refine the clinical utility of this powerful tumor marker.

Aged↗
PubMed2006

Periacinar Clefting and p63 Immunostaining in Prostatic Intraepithelial Neoplasia and Prostatic Carcinoma.

The aim of the present study was to correlate the presence and extent of retraction clefting and the expression of p63 in neoplastic glands and glands with prostatic intraepithelial neoplasia (PIN) in needle core biopsies. We analyzed needle core biopsies from 28 patients with PIN and 41 patients with adenocarcinoma. Neoplastic glands and those with PIN were analyzed on high power field (400x) and classified in three groups according to the extent of clefting. Immunohistochemical staining was performed following Microwave Streptavidin ImmunoPeroxidase (MSIP) protocol on DAKO TechMate Horizon automated immunostainer. Periacinar retraction clefting was significantly more prominent in prostatic carcinoma compared to PIN (p<0.0001) and nonneoplastic glands (p<0.0001). There was no difference between normal glands and PIN regarding clefting (p=0.8064). p63 was positive around the whole circumference in 12 out of 28 cases with PIN, and discontinuously positive in remaining 16 PIN cases suggesting initial disruption of the basal cell layer. p63 immunostaining was also positive in all nonneoplastic glands, and negative in all carcinomas. We conclude that retraction clefting was associated with cancer and lack of basal cells, but not with PIN. The relationship between clefting and p63 immunostaining in prostatic cancer should be further analyzed.

Adenocarcinoma↗
PubMed2006

Widespread high-grade prostatic intraepithelial neoplasia on prostatic needle biopsy: a significant likelihood of subsequently diagnosed adenocarcinoma.

In comparison with earlier studies, recent reports have demonstrated a lower incidence of prostate carcinoma after an initial diagnosis of high-grade prostatic intraepithelial neoplasia (HGPIN). The latter has led to a general tendency to reconsider the absolute need for a rebiopsy in this setting. The current retrospective study assesses the subsequent likelihood of identifying prostatic adenocarcinoma (PCa) in 41 patients with an initial diagnosis of "widespread" HGPIN defined as HGPIN present in 4 or more biopsy cores. All patients underwent at least 1 follow-up (F/U) sampling procedure in a period of 1 to 41 months. PCa was found in 16/41 patients (39%), all except 1 identified on the first F/U biopsy with the remaining patients diagnosed on a transurethral resection after a negative first F/U biopsy. All but 1 prostatic carcinoma diagnoses were obtained within 2 years from initial biopsy with 10 rendered within the first year. On average, prostate cancer was identified at 10.4 months (range: 1 to 36). One-fourth of all identified prostatic carcinomas were of Gleason score 7 or more. In 4 additional patients (9.7%), F/U biopsy revealed HGPIN with adjacent atypical small glands suspicious but not diagnostic of carcinoma (PINATYP). Of 41 patients, 10 (24.3%) continued to show HGPIN with the remaining 11/41 patients (26.8%) showing benign prostatic tissue. Patients >or=70 years of age at the time of initial biopsy had a statistically significant higher rate of PCa or HGPIN/PINATYP diagnosis on repeat biopsy compared with younger patients (P=0.02), with 55% of older men being diagnosed with cancer as compared with 33% in younger men. Patients with fewer cores sampled on initial biopsy were more likely to be diagnosed with carcinoma as opposed to HGPIN/PINATYP on F/U (P=0.015). Other factors such as the number of F/U procedures, serum prostate-specific antigen level before initial HGPIN biopsy, number of cores per F/U biopsy, and F/U interval length did not affect the likelihood of finding carcinoma. In summary, our study reveals a 39% risk of finding PCa on repeat biopsies obtained after an initial diagnosis of widespread HGPIN. Our findings support the need for a repeat biopsy in this subset of patients.

Adenocarcinoma↗
PubMed2006

Immunohistochemical study of the expression of epidermal growth factor receptor in benign prostatic hypertrophy, prostatic intraepithelial neoplasia and prostatic carcinoma.

The present study provides an analysis of immunohistochemical expression and localization of epidermal growth factor receptor (EGFR) in formalin fixed paraffin embedded specimens of prostate. Thirty-five cases each of benign prostatic hypertrophy (BPH) and prostatic carcinoma and 30 cases of prostatic intraepithelial neoplasia (PIN) were taken up for study. Streptavidin biotin peroxidase method was employed for immunohistochemical staining. EGFR positivity was observed in all the cases (100%) of BPH and PIN and in only 10 cases (28.5%) of prostatic carcinoma. In both BPH and PIN the basal cells revealed significantly higher intensity and percentage cell positivity than the luminal cells. Intensity and percentage of positively stained basal cells in BPH was higher than PIN basal cells but the difference was not statistically significant. The intensity and percentage cell positivity of BPH basal cells and PIN basal and luminal cells were significantly greater than the epithelial cells of prostatic carcinoma. Presently, the significance of variable expression of EGFR in various types of prostatic lesions is unknown.

Aged↗
PubMed2003

Distinguishing atrophy and high-grade prostatic intraepithelial neoplasia from prostatic adenocarcinoma with and without previous adjuvant hormone therapy with the aid of cytokeratin 5/6.

We evaluated the sensitivity and specificity of cytokeratin (CK) 5/6 for distinguishing foci of atrophy from prostatic adenocarcinoma with and without previous hormonal adjuvant therapy and observed the intensity and pattern of staining in mimickers of prostatic adenocarcinoma (basal cell hyperplasia, atypical adenomatous hyperplasia, and tangentially cut high-grade prostatic intraepithelial neoplasia [PIN]). We reviewed 146 acinar proliferations in 81 specimens (radical prostatectomy, previously untreated, 41; radical prostatectomy, following androgen-deprivation therapy, 11; transurethral resection, previously untreated, 29). All benign acinar proliferations stained positively for CK5/6, with immunoreactivity restricted to basal cells. Untreated and androgen-deprived prostatic adenocarcinomas were invariably negative. The pattern of staining was continuous in 79% of the atrophy cases (15/19), and all foci stained with CK5/6. Characteristic double-layer staining in basal cell hyperplasia was observed in 93% of cases (13/14), and foci of high-grade PIN had a characteristic "checkerboard" staining with areas of discontinuity. Foci of atypical adenomatous hyperplasia showed continuous staining, including cauterized acini in 53% of cases (8/15), with a fragmented basal cell layer pattern in 47% of cases (7/15). CK5/6 staining of the basal cells in foci of atrophy is sensitive and specific for excluding prostatic adenocarcinoma with and without androgen-deprivation effect.

Adenocarcinoma↗
PubMed1995

Apoptotic bodies in prostatic intraepithelial neoplasia and prostatic adenocarcinoma following total androgen ablation.

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.

Adenocarcinoma↗
PubMed1997

Argyrophilic nucleolar organizer regions in atypical adenomatous hyperplasias, prostatic intraepithelial neoplasias and prostatic neoplasms.

Sections from 104 cases of benign, preneoplastic and neoplastic lesions of the prostate were studied for argyrophilic nucleolar organizer regions (AgNORs). The mean NOR counts in normal controls (2.87) and benign prostatic hyperplasia with or without chronic prostatitis (4.90 and 3.84 NORs/nucleus, respectively) were found to be significantly less (p < 0.001) than that in prostatic intraepithelial neoplasia (PIN) and adenocarcinoma of the prostate (5.65 and 5.78 NORs/nucleus, respectively). The mean AgNOR count of a section with atypical adenomatous hyperplasia was significantly lower than that in PIN. No statistically significant difference was observed between AgNOR counts of high-grade PIN and well-differentiated adenocarcinoma (WDAC; 5.67 vs. 5.78 NORs/nucleus, respectively), however the difference between low-grade PIN and WDAC was statistically significant (5.46 vs. 5.78 NORs/nucleus, p < 0.005). The increase in NOR counts occurred concomitantly with the decrease in the degree of differentiation of adenocarcinoma. Thus, NOR was found to be a good adjuvant to the existing diagnostic parameters to pick up more cases at the stage of PIN when prognosis is better.

Adenocarcinoma↗
PubMed1992

New relationships between prostatic intraepithelial neoplasia and prostatic carcinoma.

Our group has been studying the progressive molecular changes in prostatic epithelium which precede the invasive phenotype. Initial studies revealed similar alterations in cytoskeletal proteins between high grade prostatic intraepithelial neoplasia (PIN) lesions and invasive carcinoma. Specifically we observed an increased expression of certain cytokeratins and decreased expression of vimentin. We also noted a change in glycosylation as detected by Ulex europaeus staining. Using the latter technique we were able to microdissect and isolate nuclei from areas of low and high grade PIN lesions as well as from invasive carcinoma for morphometric analysis. Similarities in nuclear size, chromatin heterogeneity, and nuclear DNA content between low and high grade PIN and invasive carcinoma in carcinomatous specimens were noted. In contrast, these parameters were significantly different in low grade PIN lesions obtained from benign prostatic transurethral resection (TURP) specimens. In addition, DNA histograms revealed similar proliferative indices between high grade PIN and invasive carcinoma, which differed significantly from low grade PIN. Parameters thought to be relative to the invasive phenotype were also examined, such as the members of the metalloproteinase family; although normal luminal cells fail to express detectable levels of these enzymes, invasive carcinoma and even low grade PIN lesions express both the 72 kDa and 92 kDa type IV collagenase. Taken together, these data indicate that the dysplastic cells of PIN lesions and carcinomas are similar in nuclear and genomic features as well as protease expression. Our current working hypothesis is that these cells are already armed with the necessary proteases to invade the basal lamina but in an inactive form. Tumor progression requires an additional event of protease activation.

Carcinoma↗
PubMed1995

Expression of tumor-associated glycoprotein 72 in prostatic intraepithelial neoplasia and prostatic adenocarcinoma.

Tumor-associated glycoprotein 72 is a high-molecular-weight sialomucin that is expressed selectively in various adenocarcinomas, including those of the prostate. We utilized the monoclonal antibodies B72.3 and CC49 to examine the expression of TAG-72 in high-grade prostatic intraepithelial neoplasia (PIN), localized adenocarcinomas (pathologic stages B and C), as well as matching primary and nodal lesions from patients with stage D adenocarcinomas. Immunoreactivity within PIN lesions was detected within 20 (87%) and 17 (74%) of 23 specimens immunostained with B72.3 and CC49, respectively. Benign epithelium and stromal tissue did not immunostain with either antibody at the concentrations tested. Immunostaining was detected within the malignant cells in 30 (77%) and 35 (90%) of 39 localized adenocarcinomas using B72.3 and CC49, respectively. Immunostaining was localized to the cytoplasm and cellular membranes of the malignant cells and within the lumen of malignant glands. Seven of 17 (41%) primary lesions from patients with stage D adenocarcinomas demonstrated immunoreactivity when stained with B72.3. Immunoreactivity was detected in 8 of 10 (80%) of these tissues immunostained with CC49. Within nodal lesions obtained from these patients, immunostaining was observed in 3 of 17 (18%) and 6 of 10 (60%) of the specimens immunostained with B72.3 and CC49, respectively. We used a semiquantitative technique to compare the extent of immunoreactivity among well-differentiated (Gleason score < 6), moderately differentiated (Gleason 6-7), and poorly differentiated (Gleason score > 7) tumors. We observed an inverse correlation of TAG-72 expression to Gleason scores. Furthermore, TAG-72 expression was reduced in the matching primary and metastatic lesions of stage D adenocarcinomas as compared to localized lesions.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenocarcinoma↗
PubMed1994

Expression of p160erbB-3 and p185erbB-2 in prostatic intraepithelial neoplasia and prostatic adenocarcinoma.

BACKGROUND: Although prostatic adenocarcinoma is the most frequent malignancy among American men, little is known concerning the roles of growth factors, growth factor receptors, or proto-oncogene products in the development and progression of this malignancy. PURPOSE: We examined and compared the expression and cellular distribution of the erbB-3 protein (p160erbB-3) and the erbB-2 protein (p185erbB-2) in various stages of development and progression of prostatic adenocarcinoma. METHODS: Immunoperoxidase staining was used to determine the expression of p160erbB-3 and p185erbB-2 in benign prostatic epithelium, prostatic intraepithelial neoplasia, localized adenocarcinomas (pathologic stages B and C) as well as matching primary and lymph node lesions from patients with stage D adenocarcinoma. In order to test antibody specificity, we used Western blot analysis to examine the expression of p160erbB-3 and p185erbB-2 in selected prostatic adenocarcinomas. RESULTS: Within benign glands, immunostaining for p160erbB-3 or p185erbB-2 was strongest in the basal cells and was typically absent or weak in the luminal (secretory) cells. Expression of both proteins within luminal cells was localized to cell membranes. We examined the expression of p160erbB-3 and p185erbB-2 in the prostatic intraepithelial neoplastic lesions of 22 radical prostatectomy specimens. Like benign glands, the basal cells of these neoplastic lesions typically demonstrated strong to moderate immunostaining when stained with either antibody. In contrast to benign glands, moderate to strong immunostaining for p160erbB-3 and p185erbB-2 was frequently observed within the cytoplasm and cell membranes of the prostatic intraepithelial neoplastic luminal cells. p160erbB-3 and p185erbB-2 were detected within the malignant cells in 28 and 29 of 29 localized adenocarcinomas, respectively. Immunostaining with either antibody was typically moderate to strong in the malignant cells. Both proteins were expressed on the cellular membranes as well as in the cytoplasm of malignant cells. Immunostaining for p160erbB-3 was detected in the matching primary and metastatic lesions (lymph nodes) in 10 of 11 patients with stage D adenocarcinoma. Immunostaining for p185erbB-2 was detected in matching primary and metastatic lesions (lymph nodes) obtained from 16 patients with stage D adenocarcinoma. Western blot analysis confirmed the specificity of the antibodies. CONCLUSIONS: These results suggest that increased expression and changes in the subcellular distribution of both p160erbB-3 and p185erbB-2 represent early events in the development and progression of prostatic adenocarcinomas. The high expression and distribution of both p160erbB-3 and p185erbB-2 are retained both in advanced-stage primary and metastatic tumors.

Adenocarcinoma↗
PubMed1995

Morphometric analysis and clinical followup of isolated prostatic intraepithelial neoplasia in needle biopsy of the prostate.

PURPOSE: We evaluate the significance of grade and extent of isolated prostatic intraepithelial neoplasia in prostate needle biopsies as a predictor of cancer on repeat biopsy. MATERIALS AND METHODS: We reviewed our experience with 58 men 50 years or older who had isolated prostatic intraepithelial neoplasia on initial prostate needle biopsy during a prostate specific antigen (PSA) based screening trial for prostate cancer. All 58 men underwent repeat biopsy to follow the initial findings of prostatic intraepithelial neoplasia. We assessed the relationship of patient age, digital rectal examination, serum PSA concentration, PSA density, prostatic intraepithelial neoplasia grade, number of foci of neoplasia and linear extent of prostatic intraepithelial neoplasia in the initial biopsy specimen to the finding of cancer on the repeat biopsy. We also compared the cancer detection rate in the 58 men with and 427 without prostatic intraepithelial neoplasia in the same screening trial. RESULTS: Of 21 men with low grade and 37 with high grade prostatic intraepithelial neoplasia 4 (19%) and 19 (51%), respectively, had cancer on repeat biopsy (p < 0.02), compared to 82 of 427 (19%) without cancer or prostatic intraepithelial neoplasia on the initial biopsy. High grade prostatic intraepithelial neoplasia was a significant predictor of malignancy on repeat biopsy (p < 0.05). The number of foci of neoplasia and the linear extent of prostatic intraepithelial neoplasia on initial biopsy were not predictive of cancer on repeat biopsy. CONCLUSIONS: Our results demonstrate that the presence of high grade prostatic intraepithelial neoplasia is a strong predictor of prostate cancer in men with elevated serum PSA concentrations and they should be followed with repeat biopsy.

Aged↗
PubMed2006

Significance of atypical and suspicious small acinar proliferations, and high grade prostatic intraepithelial neoplasia on prostate biopsy: implications for cancer detection and biopsy strategy.

PURPOSE: We reviewed our results from a urological pathology reference laboratory with respect to the incidence of HGPIN, and atypical and suspicious lesions in the spectrum of ASAP. Subsequent CaP findings on repeat biopsy with relevant clinical implications were assessed. MATERIALS AND METHODS: A review of 42,667 prostate biopsies was performed. We defined atypical and suspicious as variants of ASAP with suspicious being more worrisome for CaP. Findings were correlated with the location of CaP on repeat prostate biopsy. RESULTS: The rate of subsequent CaP detection was significantly higher for an initial diagnosis of suspicious findings (51% or 54 of 107 cases) than for atypical findings (34% or 39 of 116) or HGPIN (22% or 79 of 358, p < 0.001). CaP was found on the same side of the prostate in 61 of 78 (78%), 30 of 39 (77%) and 41 of 54 patients (76%) with initial HGPIN, atypical and suspicious biopsies, respectively. There was no significant difference among the 3 groups in the likelihood of future CaP at the same site or the same side of the prostate. CONCLUSIONS: Patients with a suspicious biopsy were significantly more likely to have CaP on future biopsy than those with atypical findings or HGPIN, suggesting that there may be divisions with prognostic significance in the larger category of ASAP. To our knowledge the reproducibility of recognizing such divisions remains to be established. Neither atypical nor suspicious lesions were more likely than HGPIN to predict CaP at the same site or side of the prostate as the original diagnosis. Repeat biopsy may be indicated in any patient with HGPIN, or atypical or suspicious lesions and this biopsy should not be limited to the site or side of the original pathological findings.

Aged↗
PubMed1993

Prostatic intraepithelial neoplasia and prostate-specific antigen.

Prostatic intraepithelial neoplasia (PIN) is a putative premalignant lesion of the prostate gland. PIN has been demonstrated to share morphologic and phenotypic similarities to invasive carcinoma of the prostate. In addition, PIN is spatially related to invasive carcinoma and occurs with greater frequency in men whose prostates harbor carcinoma. Prostate-specific antigen (PSA) is a glycoprotein produced by the prostatic epithelium. For PSA to be detected in the serum, it must traverse several tissue layers to reach the circulatory system. PSA levels associated with PIN are intermediate between those of benign and malignant prostate tissue. Spatially associated occult carcinoma, disruption of the basal cell layer, and increased vascularity may account for elevated PSA values in PIN.

Humans↗
PubMed2005

[Isolated intraepithelial prostatic neoplasia and positive prostate adenocarcinoma results at repeated biopsy. Review of our series].

OBJECTIVE: To review the incidence of isolated prostatic intraepithelial neoplasia (PIN) as well as the positive prostate cancer results in repeat biopsy in our series of transrectal biopsy of the prostate. We compare these results with the actual literature. MATERIALS AND METHODS: We review the 2.475 transrectal ultrasound guided biopsies of the prostate made in our department from January 1992 to June 2004 looking for intraepithelial neoplasia and looking in particular for isolated High-grade PIN (HGPIN). We review repeat biopsies made at this patients and the likelihood of detecting prostate cancer in them. RESULTS: The diagnosis of PIN was found in 31 biopsies, 13 of them were isolated HGPIN what means a 0.52% incidence of the total biopsies performed in our department. We performed 7 repeat biopsies of the 13 cases in a period from 3 months to 2 years after the first biopsy, and we found 3 cases of prostate cancer what means that 43% of isolated HGPIN with repeated biopsy showed prostate cancer. The mean age of the patients studied was 67 years (range 53-88). The median PSA value of the studied cases was 9.8 ng/ml. The Gleason score of the positive biopsies was always between 3 and 7. In our series, age and PSA levels did not have correlation with the positive results for prostate cancer in repeated biopsies. CONCLUSIONS: In spite of a lower number of HGPIN cases in our series, the positive for prostate cancer in repeated biopsy (43%) is similar to the incidence reported in literature so it is advisable rigorous controls and repeated biopsies for these patients.

Adenocarcinoma↗