SEARCH · PubMed Health

Results for “Prostatic Intraepithelial Neoplasia”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 19 recordsLinked to original sources

PubMed1998

CG island methylation changes near the GSTP1 gene in prostatic intraepithelial neoplasia.

Prostate intraepithelial neoplasia (PIN) is a purported prostate cancer precursor lesion and a candidate biomarker for efficacy assessment in prostate cancer chemoprevention trials. Loss of expression of the pi-class glutathione S-transferase enzyme GSTP1, which is associated with the hypermethylation of deoxycytidine residues in the 5'-regulatory CG island region of the GSTP1 gene, is a near-universal finding in human prostate cancer. GSTP1 expression was assessed by immunohistochemistry in 60 high-grade PIN samples adjacent to and distant from prostate adenocarcinoma. Whereas abundant enzyme polypeptide expression was evident in all normal prostatic tissues, all samples of high-grade PIN and adenocarcinoma were completely devoid of GSTP1. DNA from 10 high-grade PIN lesions was analyzed for GSTP1 CG island methylation changes using a PCR technique targeting a polymorphic (ATAAA)n repeat sequence in the promoter region of the GSTP1 gene. Somatic GSTP1 CG island methylation changes were detected in DNA from 7 of the 10 PIN lesions. Allele discrimination was possible for 5 of the 10 DNA samples: 2 of the 5 samples exhibited DNA methylation changes at both alleles; whereas 3 samples displayed no DNA methylation changes at either allele. GSTP1 CG island methylation changes were present in each of the five homozygous samples. Hypermethylation of the 5'-regulatory region of the GSTP1 gene may serve as an important molecular genetic biomarker for both prostate cancer and PIN. The finding of frequent GSTP1 methylation changes in PIN and prostate cancer supports a role for PIN lesions as a prostate cancer precursor and may provide insight to the molecular pathogenesis of prostate cancer.

Adenocarcinoma↗

PubMed1996

Clinical prognostic criteria for later diagnosis of prostate carcinoma in patients with initial isolated prostatic intraepithelial neoplasia.

Prostatic intraepithelial neoplasia (PIN) is considered as a precursor of prostate cancer and is frequently associated with it. Diagnosis of PIN on a prostate needle biopsy without associated carcinoma is a difficult problem since high-grade PIN does not necessarily mean that prostate cancer is always present and low-grade PIN is associated with cancer as well. Definition of parameters predictive of the later finding of prostate cancer on repeat biopsy in patients with PIN is of evident interest and we have reviewed our experience and recent data from the literature on this topic. High grade is a strong predictor of later cancer found on repeat biopsy (50-100%) and in these patients, serum prostate-specific antigen (PSA), digital rectal examination and transrectal ultrasound are predictors of later cancer found on repeat biopsy. High-grade PIN is, however, frequently associated with later cancer whatever PSA, even when < or = ng/ml. Low-grade PIN seems to behave like BPH since the incidence of later cancer is extremely low when PSA is < 4 ng/ml and is high when PSA > 10 ng/ml. Patients with high-grade PIN should systematically be rebiopsied after 3-6 months to exclude cancer because they are likely to have undiagnosed cancer. Patients with low-grade PIN and low PSA seem to have a low risk of later cancer found on repeat biopsy. Patients with low-grade PIN and high serum PSA should have repeat biopsies because the incidence of subsequent cancer is high and comparable to high-grade PIN. Further investigations are needed to optimize the management of patients with low-grade PIN and intermediate PSA level.

Biopsy, Needle↗

PubMed1998

Evaluation of needle biopsy in the diagnosis of prostatic carcinoma in men with prostatic intraepithelial neoplasia.

Prostatic intraepithelial neoplasia (PIN) is considered a premalignant lesion of the prostate. It is often encountered in prostate needle biopsy in cases where no cancer is identified. In order to evaluate its importance 25 patients with PIN in a former prostate needle biopsy underwent a second ultrasound guided needle biopsy. The first biopsy was performed in all patients as a result of positive DRE. In 13 patients (52%), prostate cancer was identified in the second specimen. All presented with high or intermediate grade PIN in the first biopsy. PSA values were compared with PIN grade and cancer presentation in the second biopsy, although no statistically significant difference was proven. In conclusion, when PIN is discovered in prostate needle biopsy in patients with positive DRE, a second biopsy has to be performed in order to exclude the possibility of a prostate carcinoma.

Aged↗

PubMed1998

[Diagnostic criteria and differential diagnosis of prostatic intraepithelial neoplasia].

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.

Biopsy↗

PubMedDate not supplied

Free and total serum PSA values in patients with prostatic intraepithelial neoplasia (PIN), prostate cancer and BPH. Is F/T PSA a potential probe for dormant and manifest cancer?

Free and total PSA serum concentrations were retrospectively measured in 106 subjects: 45 patients with intraepithelial prostatic neoplasia (PIN), 30 subjects with benign prostatic hypertrophy (BPH) and 31 subjects with untreated prostatic carcinoma. The (F/T) x 100 PSA value is recorded in subjects with the elevated total PSA level (> 4 ng/ml). PIN patients were divided into two groups: a low grade PIN (PIN 1) and high grade PIN (PIN II-III) patients. The mean (F/T) x 100 PSA value in low grade PIN patients was 27.9 +/- 16.2 (range 17.1-41.2, median 25.1) and has been numerically similar to the respective value in BPH subjects (29.1 +/- 13.2, 15.8-48.0, 27.7). These parameters differed markedly (P < 0.01) from the mean (F/T) x 100 PSA value in high grade PIN patients (16.9 +/- 9.0, range 9.9-24.9, median 16.5). The later values were in turn comparable (P > > 0.05) with the respective value measured in untreated prostate cancer patients (14.4 +/- 10.8, 6.6-21.4, 12.6). Hence, values derived from the measurement of free and total serum PSA level may distinguish low grade PIN that prevailingly remains latent disease from high grade PIN that is in most cases not only early prostatic carcinoma but that is often a precursor of an aggressive neoplasm. The published literature is incoherent regarding the influence of tumor spread on F/T PSA level. The cutoff point that divides BPH from cancer may depend on tumor stage. We have not investigated F/T PSA values related to different stages and grades of prostate cancer. The cutoff point of (F/T) x 100 PSA in our study that divides malignant from benign prostate, or latent from manifest cancer, was tentatively assigned as 18 with a specificity of 91% and selectivity of 69%. Our data are based on the application of the CIS assay that, according to the literature, gives higher F-PSA % compared to other respective kits.

Alkaline Phosphatase↗

PubMed1996

Repeat biopsy strategy in men with isolated prostatic intraepithelial neoplasia on prostate needle biopsy.

PURPOSE: Isolated high grade prostatic intraepithelial neoplasia on needle biopsy of the prostate is a strong predictor of malignancy on repeat biopsy. However, the optimal repeat biopsy technique for these patients has not been defined. MATERIALS AND METHODS: We reviewed the records of 66 men in whom isolated prostatic intraepithelial neoplasia was found on needle biopsy of the prostate. We evaluated the side and/or quadrant and grade of prostatic intraepithelial neoplasia on initial biopsy, and compared the findings to the location of cancer on repeat biopsy. RESULTS: Of 66 men 31 (47%) had cancer on repeat biopsy, with disease on the same side of the prostate as prostatic intraepithelial neoplasia in 20 (64%). The quadrant locations of prostatic intraepithelial neoplasia and cancer matched in 6 of 12 cases (50%). Low and high grade prostatic intraepithelial neoplasia predicted the side of cancer on repeat biopsy in 3 of 5 (60%) and 17 of 26 (65%) cases, respectively. CONCLUSIONS: Directing repeat biopsy solely to the side with prostatic intraepithelial neoplasia will miss cancer in approximately 35% of cases. The optimal repeat biopsy technique for patients with high grade prostatic intraepithelial neoplasia should include systematic biopsy of the prostate.

Aged↗

PubMed1994

Effects of combination endocrine treatment on normal prostate, prostatic intraepithelial neoplasia, and prostatic adenocarcinoma.

AIMS: To investigate the effect of combination endocrine treatment (CET) or luteinising hormone releasing hormone agonist and flutamide on non-neoplastic prostate, prostatic intraepithelial neoplasia, and prostatic adenocarcinoma. METHODS: The morphology, including the mitotic activity, of 12 radical prostatectomies from patients with prostatic adenocarcinoma pretreated for three months with CET was evaluated in haematoxylin and eosin stained sections and compared with an untreated age and stage matched control group. RESULTS: A differential effect on the non-neoplastic prostate was observed. In fact, the transition zone of the treated prostate showed simplification of the glandular lobules: the ducts and acini were small without undulations of the epithelial border and with a prominent basal cell layer. Within the peripheral zone there was inconspicuous branching of the ducts and acini which looked dilatated and lined by flattened atrophic epithelium. Prostatic intraepithelial neoplasia occurred in scattered ducts and acini in the peripheral zone of 10 of the 12 patients. The epithelial cell lining showed a prominent basal cell layer. A certain degree of secretory cell type stratification was always present. However, crowding was less evident than in the untreated prostate because of cytoplasmic clearing and enlargement as a result of coalescence of vacuoles. The treated adenocarcinomas had neoplastic acini which looked small and shrunken, and areas of individual infiltrating tumour cells separated by abundant interglandular connective tissue. The secretory cells of the nonneoplastic, prostatic intraepithelial neoplasia, and prostatic adenocarcinoma lesions had inconspicuous nucleoli, nuclear shrinkage, chromatin condensation, and cytoplasmic clearing. Apoptotic bodies were easily identifiable in all the cell layers. The lumina were rich in macrophages, sloughed secretory cells with degenerative features, and apoptotic bodies. Mitoses were not observed in any of the treated non-neoplastic prostate, prostatic intraepithelial neoplasia, or prostatic adenocarcinomas, whereas the mitotic frequency increased from non-neoplastic prostate through prostatic intraepithelial neoplasia up to prostatic adenocarcinomas in the untreated specimens. CONCLUSIONS: CET before radical prostatectomy causes regressive epithelial changes together with enhanced apoptosis and blocked mitotic activity.

Adenocarcinoma↗

PubMed1995

A unifying hypothesis that links benign prostatic hyperplasia and prostatic intraepithelial neoplasia with prostate cancer. Invited comments.

Prostatic Intraepithelial Neoplasia (PIN) and prostatic cancer (PCA) are not caused by infection, allergic reaction, inadequate immunological response, ischemia, ageing, systemic hormones, carcinogens, nor prostatic ductal contents. PIN and PCA are apparently caused by increased inner acinar pressure due to partially blocked draining ducts. Only this explanation can account for all the observations about PIN and PCA. All other possible causes are disproved by specific observations. In order to further clarify the cause of PIN and PCA, it is important to discover if peripheral zone lesions cluster around ducts or blood vessels. PIN patterns are the morphological precursors of both PCA and prostatic cysts. Different PIN patterns represent different adaptive stages to increasing inner acinar pressure. The immediate tissue cause of PCA is PIN disruption seeding the stroma with high-grade PIN (HGPIN) cells. These cells, programmed for adaptive proliferation and mobility in PIN, are sufficient in the stroma to cause all stages and patterns of invasive PCA. No mutated cells are necessary. For reasons given, the primary cause of the initial ductal blockage that results in PIN and PCA cannot be inflammation, stones, proteineous plugs, infarction, venus thrombosis, ductal hyperplasia, nor a constricted penis at ejaculation. Only benign prostatic hyperplasia (BPH) can explain all the facts and is thus the primary cause of the ductal blockage resulting in cysts, PIN and PCA. The main causes of BPH are apparently disuse atrophy of sexual and abdominal muscles, and atherosclerosis of the capsular branch of the prostatic artery, causes atypical adenomatous hyperplasia (AAH) in the transition zone. The resulting muscular and glandular atrophy decreases local and general growth inhibitors. New growth in the adult prostate is abnormal because epithelial cells grow into ducts rather into the stroma. In such ducts, the growths cannot receive stromal growth inhibitory signals, and thus continue to grow indefinitely and result in BPH, AAH-adenosis, blockage of ducts, cysts, PIN and PCA.

Adult↗

PubMed1991

Significance of prostatic intraepithelial neoplasia on prostate needle biopsy.

Prostatic intraepithelial neoplasia (PIN) is a putative premalignant change in the human prostate. Previously, the spatial association of PIN with invasive carcinoma has been described in the study of total prostatectomies. PIN is frequently recognized in prostate needle biopsy specimens in which no carcinoma is apparent. To further define the potential significance of PIN, we performed repeat ultrasound-guided prostate needle biopsy in 21 men who had PIN identified on prostate biopsy performed because of an abnormal finding on digital rectal examination. Twelve patients (57%) had carcinoma identified on their second procedure including all who had intermediate- and high-grade PIN on the initial procedure. Prostate-specific antigen correlated with PIN grade and carcinoma on the secondary procedure, although this did not achieve statistical significance. Men with PIN on prostate needle biopsy should undergo repeat sampling to exclude missed carcinoma.

Adenocarcinoma↗

PubMed1996

Strategy for repeat biopsy of patients with prostatic intraepithelial neoplasia detected by prostate needle biopsy.

PURPOSE: We evaluated the strategy for repeat biopsy of patients with prostatic intraepithelial neoplasia without concurrent carcinoma detected on prostate needle biopsy. MATERIALS AND METHODS: Of 1,275 consecutive patients undergoing prostate needle biopsy 61 were identified with prostatic intraepithelial neoplasia but without concurrent prostate carcinoma. Of the 61 patients 53 had undergone repeat biopsy. The medical records, transrectal ultrasound, and operative and pathological reports of these patients were reviewed. RESULTS: Repeat biopsy was done in 53 patients with prostatic intraepithelial neoplasia, yielding carcinoma in 15, prostatic intraepithelial neoplasia without carcinoma in 8 and benign tissue in 30. The yield of carcinoma from repeat biopsy of a prostatic intraepithelial neoplasia site was 8.3% (7 of 84 sites). A total of 18 sites of carcinoma was detected by repeat biopsy of a previous random biopsy site (8), a prostatic intraepithelial neoplasia site only (5), a transrectal ultrasound nodule (3), a palpable nodule and prostatic intraepithelial neoplasia site (1), and a transrectal ultrasound nodule and prostatic intraepithelial neoplasia site (1). Carcinoma was as frequently detected by repeat biopsy of a prostatic intraepithelial neoplasia site (6 patients) as by random repeat biopsy (6 patients). CONCLUSIONS: Repeat prostate needle biopsy of patients with prostatic intraepithelial neoplasia should include random repeat biopsy and repeat biopsy of transrectal ultrasound abnormalities as well as previous sites of prostatic intraepithelial neoplasia.

Adenocarcinoma↗

PubMed1996

Comparative analysis of the nuclear proliferative index (Ki-67) in benign prostate, prostatic intraepithelial neoplasia, and prostatic carcinoma.

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.

Adenocarcinoma↗

PubMed1997

The relationship between prostatic intraepithelial neoplasia and prostate cancer: critical issues.

PURPOSE: Prostatic intraepithelial neoplasia (PIN) is often considered to be a premalignant lesion and the main precursor of invasive carcinoma of the prostate. We evaluated the evidence for and against PIN as a premalignant lesion and determined guidelines for the clinical management of PIN. MATERIALS AND METHODS: Literature analysis of histopathological, morphometric, phenotypic and molecular genetic evidence of progression and of clinical findings regarding PIN was done. Literature searches were performed on MEDLINE with relevant key words. RESULTS: PIN, like prostate cancer, occurs most frequently in the peripheral zone of the prostate and is usually located in close proximity to prostate cancer. The relative PIN and prostate cancer volumes vary inversely. Prostate specific antigen in cases of PIN appears to be intermediate between prostate cancer and normal levels, although this elevation may be explained by concomitant prostate cancer or benign prostatic hyperplasia. Deoxyribonucleic acid ploidy in PIN follows the aneuploid proportion as in the concomitant prostate cancer. Prostate cancer and PIN show evidence of loss of putative tumor suppressor genes on chromosome 8p. The clinical relevance of PIN biopsy findings is based on the association of neoplasia and prostate cancer. High grade PIN in core biopsies without concomitant prostate cancer has a substantial risk for prostate cancer in subsequent biopsies (24 to 73%, up to 100% when the digital rectal examination is suspicious) and should cause further biopsy sampling. CONCLUSIONS: There is convincing evidence that PIN is a precursor lesion to prostate cancer, with a close association of PIN and prostate cancer in biopsy and prostatectomy specimens. A biopsy finding of high grade PIN necessitates further investigation in patients who are candidates for radical treatment for localized prostate cancer.

Algorithms↗

PubMed2000

Nuclear volume estimates in prostatic intraepithelial neoplasia.

OBJECTIVE: Prostatic intraepithelial neoplasia (PIN), the most likely precursor of prostatic adenocarcinoma, is divided into two grades, low and high. Pathologists may encounter difficulties in applying these criteria in daily practice. In view of the clinical significance of high grade PIN as strong predictor of carcinoma, the separation of low and high grade PIN plays an important role in patient management. The aim of the present study was to evaluate three-dimensional nuclear size estimation in normal prostatic glands, low and high grade PIN, and prostatic adenocarcinoma as an element in their classification. STUDY DESIGN: We studied 31 formalin-fixed, paraffin-embedded, whole-mounted radical prostastectomy specimens that contained foci of normal prostatic glands, low and high grade PIN, and prostatic adenocarcinoma. Hematoxylin-eosin-stained sections were selected for the stereologic estimation of volume-weighted mean nuclear volume by the "point-sampled intercepts" method. On each focus, an average of six fields of vision were systematically chosen. RESULTS: The quantitative results indicate a significant increase in nuclear volume from normal prostatic glands (mean, 209.0 micron 3; SD, 64.6 micron 3) to low grade PIN, high grade PIN and prostatic adenocarcinoma with increments of 49%, 88% and 109%, respectively (F = 29.1, P < .001). Two-group comparisons (Duncan procedure) showed differences between low and high grade PIN and prostatic adenocarcinoma (P < .01). The difference between high grade PIN and prostatic adenocarcinoma was not significant. CONCLUSION: Three-dimensional estimates of nuclear size discriminate low and high grade PIN. Lack of stereologic differences between high grade PIN and prostatic adenocarcinoma further supports high grade PIN as a precursor of prostatic adenocarcinoma.

Aged↗

PubMed1997

Ultrastructure of prostatic intraepithelial neoplasia.

BACKGROUND: Prostatic intraepithelial neoplasia (PIN) is the most likely precursor of prostatic adenocarcinoma. However, the ultrastructural features of PIN have not been defined in properly fixed tissues. METHODS: In this study, we examined a total of 84 acini from 11 cases of high-grade PIN and matched benign epithelium and adenocarcinoma from patients undergoing radical prostatectomy. Specimens from each case were immediately fixed in glutaraldehyde after surgical removal and processed routinely to ensure optimal preservation. RESULTS: High-grade PIN displayed ultrastructural features that were intermediate between those of benign epithelium and adenocarcinoma. These included the presence of cells with a variable number of cytoplasmic secretory vacuoles, luminal apocrine blebs, large nuclei with coarsely clumped chromatin, enlarged nucleoli, prominent apical microvilli, intact or discontinuous basal cell layer, and intact basement membrane. CONCLUSIONS: Our results indicate that PIN shares many ultrastructural characteristics with adenocarcinoma, supporting its role as a premalignant lesion.

Adenocarcinoma↗

PubMed1999

Prostatic intraepithelial neoplasia in prostate specimens: frequency, significance and relationship to the sampling of the specimen (a retrospective study of 121 cases).

OBJECTIVES: To determine the frequency of PIN (prostatic intraepithelial neoplasia) in prostate specimens and the relationship of PIN with PCA (prostatic carcinoma) and amount of sampling of the specimen. MATERIALS AND METHODS: All the haematoxylin-eosin stained slides of 121 cases diagnosed between 1990 and 1995 were re-examined retrospectively. The amount of sampling of prostate specimens was also re-examined. RESULTS: PIN was observed in 47.9% of all prostate specimens. The frequency of incidental PIN was 71.4% in cystoprostatectomy specimens. PIN was present in 58.3% of the cases with PCA. We observed foci of high-grade PIN adjacent to sites of invasive carcinoma in 100.0% of prostatectomy specimens with PCA. PIN was high-grade in 100.0% of the carcinomatous prostates with PIN. It was multifocal in 53.4% of 58 cases with PIN. Incidental PCA was identified in 14.3% of cytoprostatectomies for bladder cancer. The average number of paraffin blocks of prostatic tissue was 4.1 (+/-2.6) in cases with PIN and 3.2 (+/-1.4) in cases without PIN. CONCLUSION: In prostate specimens, the determination of PIN is very important since it is the most likely precursor of PCA. The probability of detecting PIN and PCA in a prostate specimen is directly related to the amount of sampling.

Adult↗

PubMed1995

High grade prostatic intraepithelial neoplasia in prostates removed following irradiation failure in the treatment of prostatic adenocarcinoma.

Prostatic Intraepithelial Neoplasia (PIN) is widely considered to be a precursor lesion for adenocarcinoma of the prostate. No information is available, however, on the sensitivity of PIN to irradiation or the distribution of residual PIN after radiotherapy. We studied a series of forty-six totally embedded, whole mounted, serially sectioned prostates removed by salvage radical retropubic prostatectomy following irradiation failure in which no hormonal therapy/ablation had been undertaken. The mean age of patients was 65 (56-74) years, the mean dose of radiotherapy was 7,266 (6,000-9,000) cGy (15 external beam, 27 external beam plus iridium or gold seed, 3 iodine, and 1 unknown) and the mean interval for irradiation therapy to prostatectomy was 60 (16-145) months. Thirty-two (70%) of the patients had high grade PIN within the prostatectomy specimen. The pattern of PIN was recorded as described by Bostwick and co workers. The frequency of the different patterns per positive case paralleled in rank those in Bostwick's series of non-irradiated prostates, with the most common to least common per patient being: tufting (78.1%), micropapillary (59.3%), cribriform (34.4%) and flat (15.6%). However, the mean number of foci of PIN per prostate was less than in Bostwick's series (7.1 foci vs. 17 foci). There was no statistically significant difference between groups with or without high grade PIN with regard to various clinical factors (last preoperative serum PSA, age, dose of radiotherapy, interval from irradiation therapy to prostatectomy, Kaplan-Meier survival), or pathologic factors (presence of confined tumor, extracapsular extension, positive surgical margins, seminal vesicle invasion, or positive lymph nodes on permanent sections). We conclude that high grade PIN is common in the prostates of patients who have failed irradiation therapy and that, theoretically, not all recurrent tumors derive from regrowth of the initial, incompletely eradicated tumor. However, because there was no significant difference between the two groups with regard to the clinical and pathologic parameters listed, we consider it likely that most recurrent tumors derive from the initial incompletely eradicated tumor.

Adenocarcinoma↗

PubMed1998

Altered expression of RET proto-oncogene product in prostatic intraepithelial neoplasia and prostate cancer.

BACKGROUND: The RET proto-oncogene encodes a protein that belongs to the tyrosine kinase growth factor receptor family. Germline point mutations in RET are found in individuals with multiple endocrine neoplasia (MEN) syndromes, and gene rearrangements have been reported in papillary thyroid cancers. We recently identified transcripts of the RET proto-oncogene in human prostate cancer xenografts and prostate cancer cell lines by means of reverse transcription-polymerase chain reaction analyses. The purpose of this study was to investigate Ret protein expression in human prostate tissue. METHODS: Ret protein expression was evaluated immunohistochemically in formalin-fixed, paraffin-embedded whole-prostate sections. The prostate specimens were obtained from 30 patients with prostate cancer after radical prostatectomies. Ret protein expression was compared in tumor foci and benign prostatic tissue. Medullary thyroid carcinoma tissue associated with an MEN syndrome and papillary thyroid cancer tissue served as positive controls. RESULTS: Ret appeared to be overexpressed in high-grade (histopathologically advanced) prostatic intraepithelial neoplasia (PIN) and prostate cancer when compared with its expression level in benign prostatic secretory epithelium. In addition, there was an apparent increase in Ret protein expression with decreased cellular differentiation, i.e., increasing Gleason pattern. CONCLUSION: Expression of the RET proto-oncogene in benign prostatic epithelium, high-grade PIN, and histopathologically advanced prostate cancer suggests that RET may play a role in the growth of both benign and neoplastic prostate epithelial cells.

Drosophila Proteins↗

PubMed1993

Concordance of DNA content between prostatic intraepithelial neoplasia and concomitant invasive carcinoma. Evidence that prostatic intraepithelial neoplasia is a precursor of invasive prostatic carcinoma.

It has been postulated that prostatic intraepithelial neoplasia (PIN) is a precursor lesion to invasive carcinoma in the prostate, yet there has been little direct evidence for this relationship. Therefore, we studied the DNA content of the epithelial cells in PIN lesions with accompanying invasive carcinoma in seven cases. DNA content of nuclei in Feulgen-stained tissue sections was performed using the CAS200 System (Cell Analysis Systems Inc, Elmhurst, Ill), with normal and hyperplastic glands serving as controls for diploid DNA content. In four cases, the cells of both lesions (PIN and invasive carcinoma) contained only diploid DNA; in one case, an additional aneuploid tumor stem line was present only in the invasive component; and in two cases, both PIN and carcinoma cells contained aneuploid cells having similar DNA content. The concordance of DNA content between PIN and invasive carcinoma in these cases provides evidence that PIN is a precursor lesion for invasive carcinoma.

Adenocarcinoma↗