Therapeutic effects of finasteride: inhibition of disease progression and serum prostate-specific antigen reduction in patients with prostatic intraepithelial neoplasia.

The objective of this study was to evaluate the impact of finasteride on the progression of prostate intraepithelial neoplasia and levels of prostate-specific antigen (PSA) in patients. A total of 120 patients with high-grade prostatic intraepithelial neoplasia were included in this study from January 2013 to January 2018. All patients underwent prostate biopsies. Among them, 60 patients were assigned to the observation group and received a daily dosage of 5 mg finasteride for 60 months, while the remaining 60 patients were assigned to the control group and did not receive finasteride. PSA levels were measured every six months, and imaging scans were conducted throughout the five-year study period. Additional biopsies were performed if PSA levels exceeded 10 ng/mL or imaging suggested the presence of prostate cancer. Statistical analysis was applied to the collected data. In total, 25 cases of prostate cancer were identified in this study. Of these cases, 7 patients belonged to the observation group, whereas the remaining 18 patients were from the control group. The observation group exhibited significantly lower levels of total serum PSA (p < 0.001) and Gleason scores (p < 0.001) compared to the control group. Our study, which involved 120 participants, demonstrated that finasteride effectively reduces serum PSA levels and mitigates the severity of prostate cancer. These findings suggest that finasteride holds potential as a treatment option for patients with -high-grade prostatic intraepithelial neoplasia.

DIAGNOSTIC UTILITY OF IMMUNOHISTOCHEMICAL EXPRESSION OF KI!67, P63 AND AMACR IN PROSTATE INTRAEPITHELIAL NEOPLASIA.

OBJECTIVE: The aim: To determine malignant transformation and progression ability of high grade and low grade prostate intraepithelial neoplasia with the help of immunohistochemical method. PATIENTS AND METHODS: Materials and methods: The results of examination of 93 patients with PIN (50 patients with high grade PIN and 43 patients with low grade PIN) were assessed comparatively using immunohistochemical markers. Semiquantitative method was used to evaluate !"-67, #63 and AMACR tissue expression with four grades from "+" to "++++" or from 1 to 4 points: '+' - low reaction, '++' - poor reaction, '+++' - moderate reaction and '++++" - intense reaction. RESULTS: Results: There were statistically significant differences in immunohistochemical expression rates between HGPIN and LGPIN. Patients with HGPIN had higher Ki-67 and AMACR expression rate and lower p63 expression rate than patients with LGPIN. Intense and moderate Ki-67 expression was detected in HGPIN more often, in 24 % and 11 % respectively. Low and moderate AMACR expression was determined in HGPIN more often, in 28 % and 5 % respectively. Low and not evident p63 expression was observed in HGPIN more often, in 36 % and 8 % respectively. CONCLUSION: Conclusions: HGPIN has common morphological peculiarities with prostate adenocarcinoma. Immunohistochemical detection of Ki-67, p63 and AMACR is aimed to differentiate among patients with PIN a group of high malignant transformation risk.

The changes and updates in the fifth edition of the WHO Classification of prostate tumors.

The fifth edition of the WHO classification of prostate tumors provides new insight into prostate cancer pathogenesis supported by molecular data. It discards the terms low-grade PIN and high-grade PIN. The new entity „Treatment-related neuroendocrine prostatic carcinoma“ is introduced. The importance of the diagnosis of intraductal carcinoma is highlighted. The terminology of prostatic basocellular carcinoma is upgraded. Some cancer subtypes are being relocated to different chapters based on new findings. Also, the role of the prostate as an origin of hereditary cancer is stressed. Finally, the new therapeutic approaches are mentioned.

Implications of a diagnosis of atypical small acinar proliferation (ASAP) and high-grade prostatic intraepithelial neoplasia (HGPIN) on prostate biopsy: a 5-year follow-up study.

BACKGROUND: In the era of active surveillance of low- and intermediate-risk prostatic cancer, a reconsideration of the implications of a biopsy report of ASAP and/or HGPIN may be timely. AIMS: We investigated the implications of a diagnosis of atypical small acinar proliferation (ASAP) and high-grade prostatic intraepithelial neoplasia (HGPIN) on prostate biopsy. METHODS: The rate of re-biopsy and the incidence of carcinoma on repeat biopsy for benign, HGPIN, and ASAP groups were compared. Mean PSA and PSA velocity was also compared between groups. RESULTS: There was an increased risk of developing prostate cancer in the following 5 years with a biopsy diagnosis of ASAP compared to benign (20% vs 5.9%, p = 0.009), and with a biopsy of HGPIN compared with benign (14.8% vs 5.9%, p = 0.005). The frequency of repeat biopsy following a diagnosis of ASAP (54.2%) vs. HGPIN (37%) was not significantly different (p = 0.079). The risk of developing prostate cancer was highest following a biopsy with concomitant ASAP and HGPIN compared to benign (50% vs 5.9%, p < 0.001). There was no significant difference in PSA values between the 3 diagnostic groups at the time of initial biopsy (p = 0.206). CONCLUSION: The findings of this study suggest that a biopsy diagnosis of ASAP ± HGPIN, on either initial or surveillance biopsy, provides support for earlier repeat mpMRI and/or re-biopsy. This may assist in directing to early re-biopsy those patients likely to have intermediate- and high-risk prostate cancer.

CDK19 as a diagnostic marker for high-grade prostatic intraepithelial neoplasia.

High-grade prostatic intraepithelial neoplasia (HGPIN) is a facultative precursor lesion of prostate cancer (PCa). Multifocal HGPIN in needle biopsies in the absence of PCa indicates a higher risk of cancer detection in subsequent biopsies. Therefore, a reliable diagnosis of HGPIN is of high clinical relevance guiding the management of patients with cancer-negative biopsies. Detection of HGPIN is merely based on morphological features while biomarkers aiding in the diagnosis of HGPIN and its differentiation from benign glands and other glandular lesions are lacking yet. Here, we investigated the expression of cyclin-dependent kinase 19 (CDK19) by immunohistochemistry on prostate needle biopsies of 140 patients who were all diagnosed with PCa using whole-tissue sections and compared CDK19 levels between HGPIN, PCa, and adjacent benign glands. In addition, CDK19 was compared with AMACR expression in a subset of intraductal carcinomas (IDCs) on radical prostatectomy (RP) specimens. HGPIN was present in 65.7% of biopsies and in 88% associated to adjacent PCa. CDK19 overexpression defined as moderate to high CDK19 expression visible at low magnification was found in 82.6% of HGPIN. In contrast, 89.3% of benign glands were CDK19-negative or demonstrated only low CDK19 expression highlighting a high sensitivity and specificity to accurately detect HGPIN based on CDK19 expression levels. CDK19 was overexpressed in 59% of PCa but did not correlate significantly with the expression of intermingled HGPIN. On RP, CDK19 and AMACR showed no significant difference in the detection rate of IDC. In summary, assessment of CDK19 facilitates accurate and simplified diagnosis of HGPIN with high sensitivity and specificity and aides the differentiation to non-neoplastic glandular alterations. Considering the high clinical significance of diagnosis HGPIN that still has a limited reproducibility among pathologists, we suggest CDK19 as diagnostic biomarker for HGPIN.

Comparative study of immunohistochemical expression of ERG and MAGI2 in prostatic carcinoma.

Diagnosis of Prostatic adenocarcinoma (PAC) is still a problematic issue. The objective of this study was to evaluate the diagnostic and prognostic value of ERG immunohistochemical (IHC) expression compared to MAGI2. MATERIALS AND METHODS: This study was conducted on 56 cases of PAC and 29 cases of nodular prostatic hyperplasia (NPH). IHC staining for ERG and MAGI2 was applied to archival formalin-fixed paraffin-embedded blocks. Semi-quantitative scoring was compared and correlated with clinicopathologic parameters and the Ki-67 index. RESULTS: Revealed positive ERG in 51.8% of PAC while all NPH cases were negative. On the other hand, MAGI2 was detected in 91.1% of PAC versus 17.2% of NPH. Using ROC curve, the ERG showed 53.6% sensitivity, 100% specificity, 76.5% diagnostic accuracy (DA) and area under the ROC curve 0.768 in comparison to MAGI2 that showed (91.1%, 86.2%, 88.25% and 0.948 respectively). Analysis of the combined use of the two markers revealed 95% sensitivity, 100% specificity, and 94% DA when tested synchronously. Moreover, a statistically significant inverse relationship could be detected between ERG expression and the Gleason grading group (P = 0.01) and Ki-67 index (P < 0.001). In addition, high-grade prostatic intraepithelial neoplasia (HGPIN) adjacent to carcinoma; showed positive expressions in (1/11 cases, 9.11%) for ERG and (6/11 cases, 54%) for MAGI2. CONCLUSION: This study recommends using both ERG and MAGI2 in a cocktail for better diagnostic validity of PAC. Only ERG expression could be a good prognostic indicator.

Small Cell-like Change in Central Zone Histology-A New Observation Mimicking Cribriform Intraductal Prostatic Adenocarcinoma.

A small cell-like change in prostate has been described in high-grade prostatic intraepithelial neoplasia (PIN), intraductal prostatic adenocarcinoma, and invasive prostate cancer. It occurs when these processes have a cribriform architecture. To date, small cell-like change has not been described in benign glands. Herein, I describe such a change in cribriform central zone histology from a radical prostatectomy with a spatially remote treatment naïve Grade Group 3 prostate cancer. The cancer did not have cribriform morphology or intraductal prostatic adenocarcinoma. The small cell-like change was positive for racemase in PIN-4 cocktail and no nuclei were highlighted by Ki-67. This is the first report of a small cell-like change in benign prostate tissue. Although rare, such finding in cribriform architecture of central zone histology can potentially be misinterpreted as a neoplastic process.

PIN-like ductal carcinoma of the prostate has frequent activating RAS/RAF mutations.

AIMS: Prostatic intraepithelial neoplasia-like (PIN-like) ductal carcinoma is a rare tumour characterised by often cystically dilated glands architecturally resembling high-grade PIN, but lacking basal cells. These tumours are frequently accompanied by grade group 1 acinar cancer and behave relatively indolently. In contrast, conventional ductal adenocarcinoma of the prostate is an aggressive variant comparable to grade group 4 acinar cancer. Here, we used targeted next-generation sequencing to molecularly profile PIN-like ductal carcinoma cases at radical prostatectomy. METHODS AND RESULTS: Five PIN-like ductal carcinoma samples at radical prostatectomy with sufficient tumour tissue available were analysed for genomic alterations by targeted next-generation sequencing using the Johns Hopkins University (JHU) solid tumour panel. DNA was captured using SureSelect for 640 genes and sequenced on the Illumina HiSeq platform. Three of five (60%) of the PIN-like ductal carcinomas showed activating mutations in the RAS/RAF pathways, which are extraordinarily rare in conventional primary prostate carcinoma (<3% of cases), including an activating hot-spot BRAF mutation (p.K601E), an activating hot-spot mutation in HRAS (p.Q61K) and an in-frame activating deletion in BRAF (p.T488_Q493delinsK). An additional two cases lacked BRAF or HRAS mutations, but harboured in-frame insertions of uncertain significance in MAP2K4 and MAP3K6. One case had sufficient acinar tumour for sequencing, and showed a similar molecular profile as the concurrent PIN-like ductal carcinoma, suggesting a clonal relationship between the two components. CONCLUSIONS: PIN-like ductal carcinoma represents a molecularly unique tumour, enriched for potentially targetable oncogenic driver mutations in the RAS/RAF/MAPK pathway. This molecular profile contrasts with that of conventional ductal adenocarcinoma, which is typically enriched for pathogenic mutations in the mismatch repair (MMR) and homologous recombination (HR) DNA repair pathways.

Plasma Sarcosine Measured by Gas Chromatography-Mass Spectrometry Distinguishes Prostatic Intraepithelial Neoplasia and Prostate Cancer from Benign Prostate Hyperplasia.

OBJECTIVE: Sarcosine was postulated in 2009 as a biomarker for prostate cancer (PCa). Here, we assess plasma sarcosine as a biomarker that is complementary to prostate-specific antigen (PSA). METHODS: Plasma sarcosine was measured using gas chromatography-mass spectrometry (GC-MS) in adults classified as noncancerous controls (with benign prostate hyperplasia [BPH], n = 36), with prostatic intraepithelial neoplasia (PIN, n = 16), or with PCa (n = 27). Diagnostic accuracy was assessed using receiver operating characteristic curve analysis. RESULTS: Plasma sarcosine levels were higher in the PCa (2.0 µM [1.3-3.3 µM], P <.01) and the PIN (1.9 µM [1.2-6.5 µM], P <.001) groups than in the BPH (0.9 µM [0.6-1.4 µM]) group. Plasma sarcosine had "good" and "very good" discriminative capability to detect PIN (area under the curve [AUC], 0.734) and PCa (AUC, 0.833) versus BPH, respectively. The use of PSA and sarcosine together improved the overall diagnostic accuracy to detect PIN and PCa versus BPH. CONCLUSION: Plasma sarcosine measured by GC-MS had "good" and "very good" classification performance for distinguishing PIN and PCa, respectively, relative to noncancerous patients diagnosed with BPH.

Análisis del escenario microscópico de una biopsia prostática negativa como predictor del riesgo de cáncer de próstata. Una revisión sistemática / In Search for risk predictors at the microscopic scenario of a negative biopsy. A systematic review

Introducción: Las biopsias prostáticas (BP) de repetición, ante la persistencia de la sospecha de cáncer de próstata (CP), son frecuentes y su rendimiento bajo. En el contexto de una BP negativa existe un escenario microscópico (EM), que definimos como el conjunto de lesiones no neoplásicas identificable. La existencia de algunas de estas lesiones incrementa el riesgo de detección de CP en BP sucesivas, mientras que otras parecen tener un efecto protector. El objetivo de esta revisión sistemática es identificar el conjunto de lesiones que puede formar parte del EM de una BP negativa y analizar la evidencia actual de su asociación con el riesgo de detección de CP en BP sucesivas. Adquisición de la evidencia: Dos revisores independientes realizaron una búsqueda bibliográfica en Medline, Embase y Central Cochrane, con los términos de búsqueda: small acinar proliferation or ASAP or prostatic intraepithelial neoplasia or HGPIN or adjacent small atypical glands or pinatyp or atrophy or proliferative inflammatory atrophy or pia or prostatic inflammation or prostatitis and prostate cancer. Se identificaron 1.015 referencias y siguiendo los principios de la declaración PRISMA y de selección PICO, se identificaron 57 artículos originales válidos para esta revisión. Síntesis de la evidencia: La proliferación acinar atípica de célula pequeña se asocia a una tasa de detección de CP en BP sucesivas que oscila entre el 32 y 48%. La neoplasia intraepitelial prostática de alto grado (HGPIN) se asocia a CP entre el 13 y 42%, siendo su multifocalidad la que define el incremento en el riesgo de detección. La atrofia prostática, la atrofia proliferativa inflamatoria y la infamación prostática parecen tener un efecto protector sobre la detección de CP en BP sucesivas. Por otra parte, el riesgo de detección de CP en varones con HGPIN multifocal se reduce significativamente si coexiste atrofia proliferativa inflamatoria. Conclusiones: El EM de una BP negativa puede estar compuesto por las lesiones de proliferación acinar atípica de célula pequeña, HGPIN, atrofia prostática, atrofia proliferativa inflamatoria e infamación prostática ya que todas parecen estar asociadas al riesgo de detección de CP en BP sucesivas. Esta revisión nos permite generar la hipótesis de que el EM de una BP negativa puede ser de utilidad en la decisión indicar BP de repetición

Introduction: In cases of persistent suspicion of prostate cancer (PC), repeat prostate biopsies (PB) are frequently performed in spite of their low yield. In the context of a negative PB, there is a microscopic scenario (MS), which we define as the group of recognizable non-neoplastic lesions. While some of these lesions seem to have a protective effect, the existence of others increases the risk of PC detection in posterior PB. The objective of this systematic review is to identify the lesions that may belong to the MS of a negative PB and analyse the current evidence of their association with the risk of detecting PC in subsequent PBs. Evidence acquisition: Two independent reviewers conducted a literature search on Medline, Embase and Central Cochrane with the following search terms: small acinar proliferation, ASAP, prostatic intraepithelial neoplasia, HGPIN, adjacent small atypical glands, pinatyp, atrophy, proliferative inflammatory atrophy, pia, prostatic inflammation, prostatitis and prostate cancer. 1,015 references were first identified, and 57 original articles were included in the study, following the PRISMA declaration and the PICO selection principles. Evidence synthesis: Atypical small acinar proliferation is associated with PC detection in repeat PB with rates ranging between 32 and 48%. High-grade prostatic intraepithelial neoplasia (HGPIN) is related to PC in 13 to 42% of cases. Studies show that HGPIN, when multifocal, is a significant independent risk factor for PC. Prostatic atrophy, inflammatory proliferative atrophy and prostatic inflammation seem to act as protective factors on the detection of PC in repeat PB. On the other hand, the risk of PC detection reduces significantly in male patients with multifocal HGPIN and coexistent PIA. Conclusions: The MS of a negative PB may include atypical small acinar proliferation, HGPIN, prostatic atrophy, inflammatory proliferative atrophy and prostatic inflammation lesions, since they all seem to be associated with the risk of PC detection in repeat PB. This review has led us to create the hypothesis that the MS of a negative PB might be a valuable and useful tool when considering repeat PB

Could pollen extract in association with vitamins be favorable in the reduction of chronic prostatic inflammation? A case-series analysis.

The aim of the present case-series analysis was to assess the safety and efficacy of pollen extract in association with vitamins in order to reduce the chronic prostatic inflammation in patients with class IV chronic prostatitis (CP). Nineteen non-consecutive patients performed a prostate biopsy for a suspect of prostate cancer. The biopsy histopathological examination showed a class IV CP, in presence of mild/moderate/high degree of inflammation, in association with an extensive (multiple biopsy sites, i.e., ≥ 3) high-grade prostatic intraepithelial neoplasia PIN (HGPIN) and/or atypical small acinar proliferation (ASAP). According to EAU Prostate Cancer Guidelines prostate biopsy was repeated after 6 months, because of the presence of extensive HGPIN or ASAP. Oral administration of pollen extract in association with vitamins (two capsules every 24 h) was prescribed until the repeat biopsy. Repeat biopsy histopathological examination showed, in 13 patients (68.4%), a lower degree of inflammation (absent/mild/moderate).

Histomorphological study of prostatic adenocarcinoma and its mimics.

CONTEXT: Prostate adenocarcinoma (PC) is one of the common cancers in India and world over. Numerous prostatic, nonprostatic lesions, and normal structures can be very similar to adenocarcinoma. A pathologist's awareness of the benign mimics is important for the diagnosis of PC. AIM: The aim of this study was to determine the prevalence, clinical, and histopathological features of PC, and its common mimics, and to study the criteria for their distinction from PC. MATERIALS AND METHODS: A prospective study of histopathological features of radical prostatectomy and transurethral resection of the prostate specimens, sent to the department of pathology in a medical college, for a period of 2 years was done. A brief clinical history followed by a clinical examination, including per-rectal findings and serum prostate-specific antigen (PSA) levels, was noted. RESULTS: After excluding all the cases of benign hyperplasia of prostate without any associated findings, 50 cases of operated surgical specimens of prostate were studied. PC was the most frequent diagnosis in 28 patients of 50 cases (56.0%). Basal cell hyperplasia formed the predominant mimic (26.0%), followed by prostatic intraepithelial neoplasia (8%), prostate atrophy (4%), clear-cell cribriform hyperplasia(4%),, and one case of atypical adenomatous hyperplasia (2%). Serum PSA was >4 ng/mL in all the cases of PC. In three of the mimics, PSA was >4 ng/mL and in the rest it was <4 ng/mL. Immunohistochemistry (IHC) was not applied in our study. CONCLUSION: Biopsy still remains a gold standard for diagnosis of PC and its mimics. All the lesions in the above study were diagnosed on routine hematoxylin and eosin staining. IHC is useful especially for lesions in the grey zone but not in routine histopathological study and should not be used as a screening test but should be applied in specific selected cases only.

Comparison of prostatic adenocarcinoma Gleason 5 and intraductal carcinoma of the prostate with tumor necrosis. A morphometric study.

Intraductal carcinoma of the prostate(IDCP) is defined as a solid or cribriform neoplastic growth confined to ducts and acini, with preservation of the basal cell layer. Since IDCP can often present tumor necrosis (TN), it should be distinguished from Gleason 5 (GP5) invasive adenocarcinoma for staging and clinical purposes. In the present study we reviewed 344 radical prostatectomies performed at our institution and selected all cases with either >5% GP5 or IDCP for assessment of TN on histology slides (n = 59). A total of 19 cases with TN were identified, and morphology, size, location, and histoarchitecture of the lesions with TN were recorded. Subsequently, the corresponding sections were stained with a basal cell immunomarker (P63), and lesions with TN were assigned to IDCP or invasive carcinoma GP5 for comparison. Our results show that a branched shape and size 501-1000 µm are more common in IDCP, while a size >1000 µm and location within 1 mm of the periprostatic soft tissue are significantly more prevalent in invasive adenocarcinoma GP5. These features, however, usually cannot be assessed in core biopsies. In this setting, the utilization of immunohistochemistry is warranted to differentiate IDCP and GP5 with necrosis.

The impact of metformin use on the risk of prostate cancer after prostate biopsy in patients with high grade intraepithelial neoplasia

ABSTRACT Purpose We report our experience on metformin use in diabetic patients and its impact on prostate cancer (PCa) after a high-grade prostatic intraepithelial neoplasia (HGPIN) diagnosis. Materials and Methods We retrospectively analyzed 551 patients with a diagnosis of HGPIN without PCa in a first prostate biopsy. The cohort of the study consisted of 456 nondiabetic subjects, and 95 diabetic patients. Among the patients with diabetes 44 were treated with metformin, and 51 with other antidiabetic drugs. A transrectal ultrasound prostate biopsy scheme with 22 cores was carried out 4-6 months after the first diagnosis of HGPIN. Results Among 195 (35.4%) patients with cancer, there were statistically significant differences in terms of PCa detection (p<0.001), Gleason score distribution (p<0.001), and number of positive biopsy cores (p<0.002) between metformin users and non-users. Metformin use was associated with a decreased risk of PCa compared with neveruse (p<0.001). Moreover, increasing duration of metformin assumption (≥2 years) was associated with decreasing incidence of PCa and higher Gleason score ≥7 compared with assumption <2 years. Conclusions This preliminary experience suggests that metformin use may have some beneficial effects in patients with diabetes and HGPIN; metformin should not be overlooked in these patients because it is neither new nor expensive.

The impact of metformin use on the risk of prostate cancer after prostate biopsy in patients with high grade intraepithelial neoplasia.

PURPOSE: We report our experience on metformin use in diabetic patients and its impact on prostate cancer (PCa) after a high-grade prostatic intraepithelial neoplasia (HGPIN) diagnosis. MATERIALS AND METHODS: We retrospectively analyzed 551 patients with a diagnosis of HGPIN without PCa in a first prostate biopsy. The cohort of the study consisted of 456 nondiabetic subjects, and 95 diabetic patients. Among the patients with diabetes 44 were treated with metformin, and 51 with other antidiabetic drugs. A transrectal ultrasound prostate biopsy scheme with 22 cores was carried out 4-6 months after the first diagnosis of HGPIN. RESULTS: Among 195 (35.4%) patients with cancer, there were statistically significant differences in terms of PCa detection (p<0.001), Gleason score distribution (p<0.001), and number of positive biopsy cores (pv0.002) between metformin users and non-users. Metformin use was associated with a decreased risk of PCa compared with neveruse (p<0.001). Moreover, increasing duration of metformin assumption (≥2 years) was associated with decreasing incidence of PCa and higher Gleason score ≥7 compared with assumption <2 years. CONCLUSIONS: This preliminary experience suggests that metformin use may have some beneficial effects in patients with diabetes and HGPIN; metformin should not be overlooked in these patients because it is neither new nor expensive.

Impact of the Pathologist on Prostate Biopsy Diagnosis and Immunohistochemical Stain Usage Within a Single Institution.

OBJECTIVES: To determine whether pathologists in a tertiary care institution vary in diagnosis and immunohistochemical stain usage in prostate biopsy specimens. METHODS: Men who underwent prostate needle biopsies between 2008 and 2013 were included. RESULTS: In total, 1,777 prostate biopsy specimens diagnosed by nine pathologists showed variation in diagnostic reporting (atypical small acinar proliferation, 2.0%-8.0%; high-grade prostatic intraepithelial neoplasia, 2.0%-8.5%; nonneoplastic, 30.2%-48.3%; adenocarcinoma, 46.2%-55.3%; P < .001). Variation in Gleason scoring was observed (P < .001), with the 4 + 3 = 7 category having the greatest variability (6.9%-30.3%). A blinded review from the most outlying pathologist in this category revealed 45% grading discrepancies. The mean number of immunostains performed per case (0.3-1.2) differed between pathologists (P < .001), and one pathologist used immunostains at twice the rate of the remaining cohort. CONCLUSIONS: Case pathologist significantly affects prostate biopsy diagnosis and immunohistochemical workup. We recommend evaluation for outlying practice patterns to provide consistent and efficient patient care.

Incidence of Clinically Significant Prostate Cancer After a Diagnosis of Atypical Small Acinar Proliferation, High-grade Prostatic Intraepithelial Neoplasia, or Benign Tissue.

OBJECTIVE: To assess the incidence of clinically significant and insignificant prostate cancer after an initial biopsy that revealed either atypical small acinar proliferation (ASAP), high-grade prostatic intraepithelial neoplasia (HGPIN), or benign tissue. MATERIALS AND METHODS: We retrospectively identified patients diagnosed with ASAP, HGPIN, or benign tissue who had a repeat prostate biopsy within 1 year of diagnosis during 1987-2015. We compared the incidence of any prostate cancer and clinically significant prostate cancer (based on Gleason score, prostate-specific antigen (PSA), number of positive cores, and core volume) for each diagnostic group. RESULTS: A total of 17,016 biopsies were performed in 12,817 patients during 1987-2015. Among the 615 patients who had a repeat biopsy within 1 year of their first, 261 (42.4%), 208 (33.8%), and 146 (23.8%) had ASAP, HGPIN, or benign tissue on the initial biopsy, respectively. The second biopsy demonstrated significant differences in prostate cancer detection rates between these 3 groups (34.1%, 20.2%, and 15.8%, respectively; P <.001), with cancer detected significantly more often in the ASAP group relative to other groups (P <.001 vs benign and P = .001 vs HGPIN). The rates of clinically significant prostate cancer did not differ between groups (8.0%, 6.7%, and 4.1%, respectively, P = .31). CONCLUSION: On repeat biopsy, rates of clinically significant prostate cancer did not differ between patients initially diagnosed with ASAP, HGPIN, or benign tissue. Elevated rates of prostate cancer after a diagnosis of ASAP appear to be largely due to differences in the rate of clinically insignificant disease.

Interpathologist concordance in the histological diagnosis of focal prostatic atrophy lesions, acute and chronic prostatitis, PIN, and prostate cancer.

Epidemiological and biological evidence indicates a causal relationship between the presence of proliferative atrophic lesions and the development of prostatic intraepithelial neoplasia (PIN) and prostate cancer. The presence of inflammatory and atrophic lesions of the prostate is widely underestimated and they are not generally mentioned in pathology reports. We performed a histopathological concordance study among eight genitourinary specialists and seven generalist pathologists, using 116 histological slides of prostate lesions, including proliferative atrophic lesions, PIN, and cancer. The overall agreement between all possible pairs of reviewers was 80% for prostate cancer, 67% for PIN, and 49% for proliferative atrophic lesions. When using as gold standard the assessment of a single genitourinary pathologist, the mean agreement percentage increased to 97% for prostate cancer, 92% for PIN, and 72% for proliferative atrophic lesions.