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J I Epstein

Publications and source records attributed to J I Epstein.

At least 73 records · Page 4Linked to original sources

Extensively necrotic cystic renal cell carcinoma: a clinicopathologic study with comparison to other cystic and necrotic renal cancers.

Renal cell carcinomas often show varying degrees of necrosis and cystic change. The prognostic importance of necrosis so extensive that only a few tumor cells can be identified is not clear. We gathered clinicopathologic and follow-up data on a group of eight such cases ("type I"). These patients were compared with two other groups of renal cell carcinomas: those with extensive necrosis (>50%), yet with readily identifiable tumor ("type II"), and cancers with extensive cystic change not resulting from necrosis, usually multiloculated ("type III"). The groups showed similar demographic characteristics, and within each group there was great variation in tumor size. Conventional (clear cell) histology was more common than papillary morphology in all groups. The type II neoplasms tended to be of higher nuclear grade and pathologic stage than the other groups. While one of six type I patients with follow up progressed 131 months after diagnosis, eight of 20 type II patients showed progression. None of the six type III patients with follow up progressed. We conclude that renal cell carcinomas showing extensive necrosis are capable of aggressive behavior, and patients with these lesions cannot be assured of cure following surgery. Pathologists must be aware of this entity and extensively sample any renal lesion showing extensive necrosis. The tumors showing a greater amount of viable neoplastic cells yet at least 50% necrosis had a higher rate of progression than did the type I patients. The lack of progression of any of the type III cases supports the idea that type III multiloculated cystic renal cell carcinomas may carry a distinctly better prognosis than other forms of renal cell carcinoma.

Adult↗

Pseudohyperplastic prostatic adenocarcinoma on needle biopsy and simple prostatectomy.

Prostatic adenocarcinoma resembling benign hyperplastic glands architecturally is a recently recognized entity. In the only prior study on this entity, 100 needle biopsies were studied and only two contained carcinoma with pseudohyperplastic features, which occupied a small percentage of the cancer. The current study investigates histologic attributes of pseudohyperplastic prostatic adenocarcinoma on needle biopsy and simple prostatectomy in which the pseudohyperplastic regions represent the majority of the cancer. The authors reviewed outside cases received in consultation by one of the authors (J.I.E.) and the surgical pathology files of Johns Hopkins Hospital from January 1991 to August 1998 and identified 20 cases of needle biopsy and simple prostatectomy in which > or =60% of the cancer had benign architectural features. The majority (19 of 20) were consult cases. Of the 20 cases studied, 16 were needle biopsies, two were transurethral resections of the prostate, and two were enucleations. Cancer involved one core in 75% of the needle biopsies. In 13 of the 20 cases (65%), > or =90% of the cancer had pseudohyperplastic features. Benign features included papillary infoldings in all cases, large atypical glands in 95% of cases, branching in 45% of cases, and corpora amylacea in 20% of cases. The extent of pseudohyperplastic cancer ranged from 1.0 to 10.0 mm (average, 3.7 mm). Within the pseudohyperplastic foci, features helpful in establishing a malignant diagnosis were nuclear enlargement in 95% of cases, pink amorphous secretions in 70% of cases, occasional to frequent nucleoli in 45% of cases, and crystalloids in 45% of cases. Other features associated with malignancy (mitoses, blue-tinged mucin, adjacent high-grade prostatic intraepithelial neoplasia, and perineural invasion) were seen infrequently. Immunohistochemical stains for high-molecular weight keratin showed an absence of basal cells in the pseudohyperplastic areas in all 20 cases, confirming the diagnosis of cancer. It is critical to recognize pseudohyperplastic prostatic adenocarcinoma and the features needed to establish a malignant diagnosis so these carcinomas are not misdiagnosed as benign.

Adenocarcinoma↗

Primary renal synovial sarcoma: molecular and morphologic delineation of an entity previously included among embryonal sarcomas of the kidney.

We report 15 primary renal neoplasms with morphologic, immunohistochemical, and molecular features identical to those of synovial sarcoma. These tumors form a distinct subset of the entity previously designated as embryonal sarcoma of the kidney. Most were diagnosed between the ages of 20 and 50 years. On gross examination, tumors are large, partially necrotic, and usually contain smooth-walled cysts. Microscopically, tumors are characterized by mitotically active, monomorphic plump spindle cells with indistinct cell borders growing in short, intersecting fascicles. Grossly identified cysts are lined by mitotically inactive polygonal eosinophilic cells with apically oriented nuclei ("hobnailed epithelium"). The spindle cells are immunoreactive for vimentin, often immunoreactive for EMA, but typically non-immunoreactive for desmin, actin, S100, or cytokeratins, whereas the cyst epithelium is cytokeratin-positive. These findings are consistent with monophasic, spindled synovial sarcoma encircling dilated native renal collecting ducts. The presence of an SYT-SSX gene fusion resulting from the t(X;18) characteristic of synovial sarcoma was demonstrated by reverse transcriptase polymerase chain reaction in three of three tumors in which adequate RNA could be obtained from paraffin blocks. An additional case demonstrated the characteristic t(X; 18) translocation on cytogenetic analysis, but adequate material to perform molecular studies was not available in this case or the remaining 11 cases. Primary renal synovial sarcoma is a distinctive clinicopathologic entity confirmed by molecular detection of SYT-SSX fusion transcripts.

Adult↗

Infarct of the prostate gland: experience on needle biopsy specimens.

Prostatic infarcts are uncommon and in the past have only been reported on transurethral resections of the prostate. We reviewed 13 consults and 2 nonconsult cases of needle biopsies showing prostatic infarcts from two institutions. The incidence of infarcts on biopsy were 2 in 2958 (0.07%) and 1 in 108,586 (0.0009%) in our nonconsult cases. Men averaged 71 years of age (range, 57-84 yrs). No relationship was seen with histories of hypertension, diabetes, atherosclerotic coronary vascular disease, recent surgery, and steroid use. Four of 12 men with available information had acute urinary retention, with markedly enlarged prostates in three (90 cc, 92 cc, 94 cc); two of these men had hematuria. An additional two men also had large glands (84 cc, 150 cc), one also with hematuria. Of eight men without acute urinary retention, three had sudden prostate-specific antigen (PSA) rises (increases of 199 ng/mL, 219 ng/mL, 287 ng/mL). Infarcts were usually an isolated focus on one core and varied from 1 mm to 11 mm (mean, 6.3 mm). Six cases showed earlier-aged infarcts with coagulative necrosis and recent hemorrhage and six showed intermediate-aged infarcts with reactive stroma and epithelium without necrosis. In the remaining three cases, there were remote infarcts characterized by replacement of the stroma by dense fibrosis with metaplastic glands. Adjacent tissue revealed reactive nests of immature squamous metaplasia in 14 of 15 cases with visible nucleoli (12 cases), squamous atypia (7 cases), and mitoses ranging from 1-10 (7 cases). Pathologists sent in 10 of 13 consult cases (77%) for problems with interpretation of the infarcts; remaining consults had other pathology of concern. One case was misdiagnosed as urothelial cancer. Features helpful in recognizing infarcts' benign nature were cyst formation containing cellular debris with or without neutrophils (73%), corpora amylacea (20%), and rings of collagen around squamous islands (40%). Infarcts are typically, although not exclusively, found in large prostates and may result in sudden rises in serum PSA. Infarcts' distinctive histology must be recognized and distinguished from necrosis resulting from infection and prior cryotherapy, as we have seen such misdiagnoses. Pathologists' awareness of prostatic infarcts on needle biopsy and their potential for atypical histology can prevent the misdiagnosis of cancer.

Aged↗

Tubulocystic clear cell adenocarcinoma arising within the prostate.

Neoplasms resembling ovarian common epithelial-type tumors, including clear cell adenocarcinomas, rarely occur in the lower urinary tract of men. When they do, they develop in the urethra or urinary bladder. We report a case of such a tumor arising within the prostate of a 47-year-old man. The tumor was a cystic mass in the left posterolateral region of the prostate. Histologically, the tumor was chiefly composed of tubulocystic and papillary glands lined by glycogen-rich, cuboidal or hobnail cells with clear to eosinophilic cytoplasm. The tumor cells were strongly positive for pan-cytokeratin, low molecular weight cytokeratin, and epithelial membrane antigen, and focally positive for high molecular weight keratin. The tumor did not immunohistochemically express prostate-specific antigen (PSA) and prostatic acid phosphatase. Serologically, the patient had increased levels of CA125 instead of PSA. The clinical as well as the pathologic features are consistent with a clear cell adenocarcinoma as seen in the female genital tract rather than a typical prostatic adenocarcinoma.

Adenocarcinoma, Clear Cell↗

Genetic alterations in urinary bladder carcinosarcoma: evidence of a common clonal origin.

The cellular origin of carcinosarcoma of the bladder is unknown. We addressed this issue by using microsatellite analysis for loss of heterozygosity (LOH) in both the carcinomatous and sarcomatous components of 6 bladder tumors. We tested 40 microsatellite markers from 19 human chromosomes and compared the genetic alterations between the two separately isolated components. The potential relevance of the E-cadherin pathway was also evaluated by immunohistochemistry. All 6 cases revealed identical LOH on chromosomal arms 9p, 9q, 8p, and 8q, corresponding to relatively early events in bladder carcinogenesis. Discordant losses between two alleles in the remaining chromosomes, associated with progression, were seen in all tumors with a trend toward a higher incidence in the more advanced tumors (N1M1 and N1Mx). E-cadherin was strongly expressed in the carcinomatous components (5 of 6), whereas most of sarcomatous elements displayed absence of the protein product (4 of 6). These results indicate that both the carcinomatous and sarcomatous components of carcinosarcoma are derived from a common stem cell. Downregulation of E-cadherin may define one of the pathways responsible for conversion of epithelial cells to the sarcomatous phenotype.

Aged↗

Effects of a saw palmetto herbal blend in men with symptomatic benign prostatic hyperplasia.

PURPOSE: We tested the effects of a saw palmetto herbal blend in men with symptomatic benign prostatic hyperplasia (BPH) via a randomized, placebo controlled trial. MATERIALS AND METHODS: We randomized 44 men 45 to 80 years old with symptomatic BPH into a trial of a saw palmetto herbal blend versus placebo. End points included routine clinical measures (symptom score, uroflowmetry and post-void residual urine volume), blood chemistry studies (prostate specific antigen, sex hormones and multiphasic analysis), prostate volumetrics by magnetic resonance imaging, and prostate biopsy for zonal tissue morphometry and semiquantitative histology studies. RESULTS: Saw palmetto herbal blend and placebo groups had improved clinical parameters with a slight advantage in the saw palmetto group (not statistically significant). Neither prostate specific antigen nor prostate volume changed from baseline. Prostate epithelial contraction was noted, especially in the transition zone, where percent epithelium decreased from 17.8% at baseline to 10.7% after 6 months of saw palmetto herbal blend (p <0.01). Histological studies showed that the percent of atrophic glands increased from 25. 2% to 40.9% after treatment with saw palmetto herbal blend (p <0.01). The mechanism of action appeared to be nonhormonal but it was not identified by tissue studies of apoptosis, cellular proliferation, angiogenesis, growth factors or androgen receptor expression. We noted no adverse effects of saw palmetto herbal blend. When the study was no longer blinded, 41 men elected to continue therapy in an open label extension. CONCLUSIONS: Saw palmetto herbal blend appears to be a safe, highly desirable option for men with moderately symptomatic BPH. The secondary outcome measures of clinical effect in our study were only slightly better for saw palmetto herbal blend than placebo (not statistically significant). However, saw palmetto herbal blend therapy was associated with epithelial contraction, especially in the transition zone (p <0.01), indicating a possible mechanism of action underlying the clinical significance detected in other studies.

Aged↗

Correlation of serum prostate specific antigen and quantitative immunohistochemistry.

PURPOSE: Serum prostate specific antigen (PSA) in patients with prostate carcinoma is influenced by prostate size, transition zone volume, and tumor differentiation and volume. Immunohistochemistry studies have demonstrated an inverse correlation between PSA staining intensity and tumor grade, yet to our knowledge tissue expression of PSA has never been correlated with serum PSA. MATERIALS AND METHODS: In 47 radical prostatectomy cases serum PSA was corrected for gland size and tumor volume. Standard immunohistochemistry staining techniques were applied to specimens using monoclonal antibodies to PSA and cytokeratin CAM5.2. Color images of PSA and CAM5.2 immunohistochemistry stained slides were digitally acquired and analyzed using a standard image analysis system. Representative tumor foci in each slide were imaged with a 20x objective and 10x eyepiece. Staining extent and intensity of the tumor epithelium were measured, and stromal elements and luminal areas were excluded from analysis. For each case quantitative PSA staining intensity was expressed relative to keratin staining in adjacent benign epithelium. RESULTS: Gland volume and tumor volume independently correlated with serum PSA. Furthermore, tissue PSA intensity inversely correlated with histological grade of the tumor (p <0.00001). After gland size, tumor volume and grade were considered, corrected quantitative tissue PSA intensity did not significantly correlate with corrected serum PSA. CONCLUSIONS: Immunohistochemistry expression of tissue PSA in prostate carcinoma cannot be used to explain variations in serum PSA. This discrepancy may relate to differences between the amount of PSA produced by prostatic tumors and the amount secreted, and/or the sensitivity of detecting various tissue isoforms of PSA with immunohistochemistry.

Adenocarcinoma↗

Neural network prediction of prostate tissue composition based on magnetic resonance imaging analysis. A pilot study.

OBJECTIVE: To develop a neural network model that estimates prostate histology using magnetic resonance imaging (MRI). STUDY DESIGN: Fifty-three men with lower urinary tract symptoms (average age = 63.8 +/- 8.9 years) underwent a prostate MRI (T2) and sextant biopsy of the prostate. Masson Trichome and immunohistochemical prostate-specific antigen staining of the biopsy material were used to calculate the amount of stroma and epithelium in the inner gland (central plus transition zone). MRIs were normalized to the mean intensity of the obturator internus muscle for comparative analyses. Gray scale and texture features were extracted from the inner gland in the midsection transverse MRI slice. Clinical and image variables were used in two neural networks predicting a high amount of stroma and a high amount of epithelium, respectively. RESULTS: The positive and negative predictive values of the stroma and epithelium neural networks were 95%, 69% and 65%, 92%, respectively. CONCLUSION: These data suggest that the combined use of these neural networks may predict patient response to medical therapy targeting prostatic stroma or epithelium.

Adult↗

Seminal vesicle invasion by prostate cancer: prognostic significance and therapeutic implications.

When the pathologist's report following radical prostatectomy describes seminal vesicle invasion (SVI), generally the outlook for the patient is poor. But are we all on the same page of the same book when we talk about SVI? Does it mean muscular wall invasion? Does it include the ejaculatory duct? Getting a clear definition can have far-reaching clinical implications for patient prognosis and treatment.

Journal Article↗

Nuclear morphometry predicts disease-free interval for clinically localized adenocarcinoma of the prostate treated with definitive radiation therapy.

Men treated for prostate cancer often have unexpected outcomes despite predictive models based on stage, grade and prostate-specific antigen (PSA). Previous results have indicated that nuclear morphometry can predict patient outcome in urologic malignancies. Application of this analytical method in prostate cancer treated with radiation therapy is limited. We have evaluated the predictive ability of nuclear morphometry in such patients. Histologic sections from 23 men with clinically localized adenocarcinoma of the prostate treated with radiation therapy were studied. Nuclear morphometric parameters were assessed using a previously described and validated system. Univariate and multivariate logistic regression analyses and a Cox proportional hazards model were used to assess the ability of nuclear morphometric parameters to predict recurrence and disease-free interval. Ten patients had no recurrence with median follow-up of 47. 5 months, while 13 had recurrence. Gleason grade was not predictive of treatment outcome. Pre-treatment PSA data, available for only 11 patients, were predictive of treatment outcome. Several nuclear morphometric parameters predicted recurrence, including upper quartile of suboptimal circle fit and upper quartile of feret-diameter ratio. A prognostic factor score incorporating these 2 parameters was derived, which predicted disease-free interval (p = 0.0014). Int. J. Cancer (Pred. Oncol.) 84:594-597, 1999.

Adenocarcinoma↗

Mandatory second opinion surgical pathology at a large referral hospital.

BACKGROUND: When patients are referred to one's own institution for therapy based on a histopathologic diagnosis rendered at another institution, many hospitals require a second opinion of the surgical pathology material. This quality assurance practice has been threatened in the era of managed care and cost containment. METHODS: The authors reviewed the impact of mandatory second opinion surgical pathology at The Johns Hopkins Hospital. Cases were collected prospectively over a 21-month period from April 1995 to December 1996. For the purposes of this study, a changed diagnosis was defined as a discordant diagnosis resulting in a major modification in therapy or prognosis. The majority of cases involved a change between benign and malignant or a major change in tumor classification. Changes involving a modification of tumor grade or stage were not included. RESULTS: Of 6171 cases reviewed, second opinion surgical pathology resulted in 86 changed diagnoses (1.4%). Compared with the entire group, 2 organ systems were significantly more likely to undergo a change in diagnosis: serosal surfaces (9. 5%) (P < 0.0001) and the female reproductive tract (5.1%) (P < 0. 0001). Organ systems that were not more likely to undergo a change in diagnosis than the group as a whole included the skin (2.9%); central nervous system (2.8%); breast (1.4%); genitourinary system (1.2%); gastrointestinal tract (1.2%); hematologic system (1.1%); ear, nose, and throat (1.0%); bone/soft tissue (0.9%); lung (0.6%); endocrine (0%); mediastinum (0%); and cardiovascular system (0%). CONCLUSIONS: Second opinion surgical pathology can result in major therapeutic and prognostic modifications for patients sent to large referral hospitals. Although the overall percentage of affected cases is not large, the consistent rate of discrepant diagnosis uncovered by second opinion surgical pathology may have an enormous human and financial impact. Accordingly, the authors recommend that review of the original histologic material should be undertaken prior to the institution of a major therapeutic endeavor.

Adolescent↗

Monoclonal antibody to prostate cancer nuclear matrix protein (PRO:4-216) recognizes nucleophosmin/B23.

BACKGROUND: The nuclear protein B23, nucleophosmin, is an RNA-associated nucleolar phosphoprotein reported to be more abundant in malignant and growing cells than in normal nondividing cells. We examined the levels of B23 in fresh human prostate tissue and in five human prostate cancer cell lines with monoclonal antibodies (mAb) to nucleophosmin (alpha-B23) and to human prostate cancer nuclear matrix proteins (PRO:4-216). METHODS: mAb PRO:4-216 and mAb alpha-B23 were used for protein level detection. Nuclear matrix proteins (NMPs) were prepared from prostate tumor and five human prostate cancer cell lines: LNCaP, TSU, DU145, PC-3, and PPC-1. The NMPs were run on one-dimensional and two-dimensional (2D) electrophoresis gels for Western blot analysis with the two mAbs. Histologic sections from paraffin-embedded normal and cancerous prostate tissue were stained immunohistochemically with both mAbs. RESULTS: PRO:4-216 and B23 mAbs identified a 40-kD protein (pI approximately 5.0) by Western blot analysis in the human prostate cancer cell lines and on two-dimensional blots of human prostate cancer NMPs. Immunohistochemical staining demonstrated large punctate nuclear dots in most cancer nuclei, while staining of normal tissue was less intense or absent. Predominant reactivity was of epithelial nuclei, with some minor reactivity of stromal nuclei. Red blood cells (RBCs) and white blood cells (WBCs) were routinely negative. CONCLUSIONS: PRO:4-216, previously characterized as recognizing prostate cancer nuclear matrix proteins, recognized B23/nucleophosmin. PRO:4-216 and alpha-B23 showed intense immunohistochemical staining of B23/nucleophosmin in cancer nuclei compared to adjacent normal cells in paraffin-embedded prostate tissue. This preliminary study showed the potential of B23 as a tumor marker for human prostate cancer.

Antibodies, Monoclonal↗

Bioimpedance: novel use of a minimally invasive technique for cancer localization in the intact prostate.

BACKGROUND: Prostate cancer is presently diagnosed by transrectal ultrasound (TRUS)-guided sextant needle biopsy. While echo texture of the tissue can prompt localization of tumor, it is presently imprecise. From 50-75% of men biopsied, based on an abnormal digital rectal examination (DRE) or elevated prostate-specific antigen (PSA) level, have negative biopsy results. Improvements in tumor localization during TRUS-guided prostate biopsy are greatly needed. Bioimpedance is an electrical property of biologic tissue. Electric current is limited in living tissue by highly insulating cell membranes; however, different tissue architecture such as cancer may impede current differently and allow detection of differences between normal and abnormal or malignant prostate tissue. Our goal was to assess the utility of bioimpedance measurements in differentiating tumor from normal prostatic tissue in an ex vivo model. METHODS: Bioimpedance was measured in six ex vivo prostates, which were removed for clinically localized prostate cancer. Two bioimpedance needles, 1 mm apart, were inserted 3 mm into the posterior surface of the prostate an average of 16 times per gland. Frequencies ranging from 100 kHz-4 MHz were used to obtain 594 bioimpedance measurements from the six glands. These measurements were then correlated with histology to determine the presence or absence of prostate cancer. RESULTS: Prostate cancer was found to have a higher impedance, of 932+/-170 ohms, compared to areas of no cancer within the same prostate, 751+/-151 ohms, P < 0.0001, at 2 MHz. This phenomenon was observed across all frequencies tested. CONCLUSIONS: This study demonstrates for the first time application of bioimpedance to distinguish areas of prostate cancer from areas of normal prostate. This technology may improve identification and localization of cancer within the prostate. Moreover, bioimpedance can potentially guide needle placement during prostate biopsy and thus improve sampling of tumors. Currently, our ex vivo model is limited by variables such as temperature and lack of blood flow. Further studies in an in vivo model will be needed to assess their effect.

Diagnostic Techniques and Procedures↗

Proliferative inflammatory atrophy of the prostate: implications for prostatic carcinogenesis.

Proliferation in the setting of longstanding chronic inflammation appears to predispose to carcinoma in the liver, large bowel, urinary bladder, and gastric mucosa. Focal prostatic atrophy, which is associated with chronic inflammation, is highly proliferative (Ruska et al, Am J Surg Pathol 1998, 22:1073-1077); thus the focus of this study was to more fully characterize the phenotype of the atrophic cells to assess the feasibility of the proposal that they may be targets of neoplastic transformation. The pi-class glutathione S-transferase (GSTP1), a carcinogen-detoxifying enzyme, is not expressed in >90% of prostate carcinomas (CaPs). GSTP1 promoter hypermethylation, which appears to permanently silence transcription, is the most frequently detected genomic alteration in CaP (Lee et al, Proc Natl Acad Sci USA 1994, 91:11733-11737; >90% of cases). In high-grade prostatic intraepithelial neoplasia (PIN), this alteration is present in at least 70% of cases (Brooks et al, Cancer Epidemiol Biomarkers Prev, 1998, 7:531-536). Although normal-appearing prostate secretory cells rarely express GSTP1, they remain capable of expression, inasmuch as GSTP1 promoter hypermethylation is not detected in normal prostate. Fifty-five lesions from paraffin-embedded prostatectomy specimens (n = 42) were stained for GSTP1, using immunohistochemistry. Adjacent sections were stained for p27(Kip1), Ki-67, androgen receptor (AR), prostate-specific antigen (PSA), prostate-specific acid phosphatase (PSAP), Bcl-2, and basal cell-specific cytokeratins (34betaE12). With normal prostate epithelium as the internal standard, staining was scored for each marker in the atrophic epithelium. The lesions showed two cell types, basal cells staining positive for 34betaE12, and atrophic secretory-type cells staining weakly negative for 34betaE12. All lesions showed elevated levels of Bcl-2 in many of the secretory-type cells. All lesions had an elevated staining index for the proliferation marker Ki-67 in the secretory layer and decreased expression of p27(Kip1), a finding reminiscent of high-grade PIN (De Marzo et al, Am J Pathol 1998, 153:911-919). Consistent with partial secretory cell differentiation, the luminal cells showed weak to moderate staining for androgen receptor and the secretory proteins PSA and PSAP. All atrophic lesions showed elevated GSTP1 expression in many of the luminal secretory-type cells. Because all lesions are hyperproliferative, are associated with inflammation, and have the distinct morphological appearance recognized as prostatic atrophy, we suggest the term "proliferative inflammatory atrophy" (PIA). Elevated levels of GSTP1 may reflect its inducible nature in secretory cells, possibly in response to increased electrophile or oxidant stress. Elevated Bcl-2 expression may be responsible for the very low apoptotic rate in PIA and is consistent with the conclusion that PIA is a regenerative lesion. We discuss our proposal to integrate the atrophy and high-grade PIN hypotheses of prostate carcinogenesis by suggesting that atrophy may give rise to carcinoma either directly, as previously postulated, or indirectly by first developing into high-grade PIN.

Apoptosis↗

Can ploidy of prostate carcinoma diagnosed on needle biopsy predict radical prostatectomy stage and grade?

PURPOSE: Deoxyribonucleic acid ploidy correlates with the biological behavior of prostate carcinoma. However, the usefulness of ploidy on needle biopsies that show prostate cancer has not been established to our knowledge. MATERIALS AND METHODS: We retrospectively determined ploidy on needle biopsies of 159 men with prostate carcinoma treated surgically at Johns Hopkins Hospital. Ploidy was determined by image analysis of Feulgen stained slides. Needle ploidy and Gleason score were compared as prognostic tools in the prediction of grade and stage of subsequent prostatectomy. RESULTS: Of the 159 cases 98 (62%) were diploid, 16 (10%) tetraploid and 45 (28%) aneuploid. Of the diploid, tetraploid and aneuploid tumors 69, 50 and 44%, respectively, proved to be organ confined. Tetraploid and aneuploid tumors were grouped for the remaining analysis. Needle ploidy correlated significantly with pathological stage (p = 0.003). However, needle Gleason score correlated even more strongly (p <0.001), and on multivariate analysis ploidy was not further predictive of pathological stage once Gleason score was considered. Needle ploidy and Gleason score were predictive of prostatectomy Gleason score (6 or less versus 7 or greater), and on multivariate analysis ploidy was an independently significant predictor of this parameter (p = 0.04). In 13 cases (8%) there was an important grading discrepancy, in which needle ploidy would have accurately predicted prostatectomy grade. However, in 33 cases (21%) needle and prostatectomy Gleason scores were congruent, and needle ploidy did not accurately predict prostatectomy Gleason score. CONCLUSIONS: With accurate needle Gleason grading, ploidy is not helpful in predicting prostatectomy findings. However, ploidy correlates with prostatectomy stage and grade, and may be useful if accurate Gleason grading is a concern.

Aged↗