Journal articles on the topic 'High grade prostatic intraepithelial neoplasia'

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1

Bostwick, David G., and Junqi Qian. "High-grade prostatic intraepithelial neoplasia." Modern Pathology 17, no. 3 (January 23, 2004): 360–79. http://dx.doi.org/10.1038/modpathol.3800053.

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2

Klink, Joseph C., Ranko Miocinovic, Cristina Magi Galluzzi, and Eric A. Klein. "High-Grade Prostatic Intraepithelial Neoplasia." Korean Journal of Urology 53, no. 5 (2012): 297. http://dx.doi.org/10.4111/kju.2012.53.5.297.

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3

Weiss, Mark A. "High-Grade Prostatic Intraepithelial Neoplasia." Archives of Pathology & Laboratory Medicine 125, no. 3 (March 1, 2001): 440–42. http://dx.doi.org/10.5858/2001-125-0440-hgpin.

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4

Xiao, Guang-Qian, and Pamela D. Unger. "Focal Signet Ring Cell High-Grade Prostatic Intraepithelial Neoplasia on Needle Biopsy." International Journal of Surgical Pathology 25, no. 4 (January 6, 2017): 344–47. http://dx.doi.org/10.1177/1066896916685835.

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Signet ring cell prostatic intraepithelial neoplasia is a rare speculated variant of high-grade prostatic intraepithelial neoplasia (HGPIN). Here, we present a free-standing and isolated signet ring cell HGPIN that was not associated with invasive carcinoma on needle biopsy and demonstrated the existence of this type of HGPIN variant. The differentiation between HGPIN and intraductal carcinoma of prostate is also discussed.
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5

Sakr, W. A., D. J. Grignon, G. P. Haas, K. L. Schomer, L. K. Heilbrun, B. J. Cassin, I. J. Powell, J. A. Montie, J. E. Pontes, and J. D. Crissman. "Epidemology of High Grade Prostatic Intraepithelial Neoplasia." Pathology - Research and Practice 191, no. 9 (September 1995): 838–41. http://dx.doi.org/10.1016/s0344-0338(11)80965-9.

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6

Waters, David J. "High-Grade Prostatic Intraepithelial Neoplasia in Dogs." European Urology 35, no. 5-6 (1999): 456–58. http://dx.doi.org/10.1159/000019878.

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7

Berman, David M., Jiming Yang, and Jonathan I. Epstein. "Foamy Gland High-Grade Prostatic Intraepithelial Neoplasia." American Journal of Surgical Pathology 24, no. 1 (January 2000): 140. http://dx.doi.org/10.1097/00000478-200001000-00018.

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8

Wael Sakr, A., Athanase Billis, Peter Ekman, Timothy Wilt, and David G. Bostwick. "Epidemiology of High-Grade Prostatic Intraepithelial Neoplasia." Scandinavian Journal of Urology and Nephrology 34, no. 205 (January 2000): 11–18. http://dx.doi.org/10.1080/003655900750169275.

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9

Allen, Elizabeth A., David A. Brinker, Domenico Coppola, Jose I. Diaz, and Jonathan I. Epstein. "Multilocular prostatic cystadenoma with high-grade prostatic intraepithelial neoplasia." Urology 61, no. 3 (March 2003): 644. http://dx.doi.org/10.1016/s0090-4295(02)02274-4.

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10

Billis, Athanase, and Luis A. Magna. "Inflammatory Atrophy of the Prostate." Archives of Pathology & Laboratory Medicine 127, no. 7 (July 1, 2003): 840–44. http://dx.doi.org/10.5858/2003-127-840-iaotp.

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Abstract Context.—Recently, prostatic atrophy associated with chronic inflammation has been linked to carcinoma either directly or indirectly by first developing into high-grade prostatic intraepithelial neoplasia. Objective.—The purpose of our study was to test this hypothesis in autopsies. Design.—A step section method was used to cut the posterior lobe in coronal planes at intervals of 0.3 to 0.5 cm in 100 consecutive autopsies of men older than 40 years. Prostatic atrophy was classified as simple, hyperplastic (or postatrophic hyperplasia), and sclerotic and was analyzed for the presence of chronic inflammation. Prostatic atrophy without (group A) and with inflammation (group B) was correlated with the following variables: age, race, histologic (incidental) carcinoma, high-grade prostatic intraepithelial neoplasia, and extent of both these lesions. Results.—Of the 100 prostates examined, 12%, 22% and 66%, respectively, had no atrophy, atrophy without inflammation (group A), and atrophy with inflammation (group B). There was no statistically significant difference between groups A and B for age (P = .55), race (P = .89), presence of histologic (incidental) carcinoma (P = .89), extensive carcinoma (P = .43), presence of high-grade prostatic intraepithelial neoplasia (P = .65), extensive high-grade intraepithelial neoplasia (P = .30), or subtypes of prostatic atrophy. Neither a topographical relation nor a morphologic transition was seen between prostatic atrophy and histologic carcinoma or high-grade intraepithelial neoplasia. Sclerotic atrophy either alone or combined with other subtypes was more frequent in the group with inflammation. A striking morphologic finding was a topographical relation of focal inflammation with sclerotic atrophy in areas with erosion of the epithelium. Conclusions.—Inflammatory prostatic atrophy does not appear to be associated with histologic (incidental) carcinoma or high-grade intraepithelial neoplasia. One possible cause of inflammatory infiltrate associated with prostatic atrophy may be the extravasated prostatic secretions, which were noted in areas of eroded epithelium, a common finding in the sclerotic type of prostatic atrophy.
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11

Yee, David S., Navneet Narula, Ibrahim Ramzy, John Boker, Thomas E. Ahlering, Douglas W. Skarecky, and David K. Ornstein. "Reduced Annexin II Protein Expression in High-Grade Prostatic Intraepithelial Neoplasia and Prostate Cancer." Archives of Pathology & Laboratory Medicine 131, no. 6 (June 1, 2007): 902–8. http://dx.doi.org/10.5858/2007-131-902-raipei.

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Abstract Context.—Annexin II is a calcium-dependent phospholipid-binding protein that plays a role in many cellular functions, including apoptosis, signal transduction, and cellular motility. The protein is strongly expressed in normal prostatic epithelial glands, but its expression in benign prostatic lesions has not been reported. Although commonly underexpressed in prostate cancer, the association of reduced expression with pathologic grade and stage is unknown. Objective.—To compare annexin II expression in benign prostatic lesions with expression in high-grade prostatic intraepithelial neoplasia and prostate cancer, as well as to correlate expression levels with pathologic grade and stage. Design.—A semi-quantitative assessment of annexin II expression was performed in radical prostatectomy specimens from 74 patients and prostate needle core biopsy specimens from 13 patients. Foci with normal prostatic glands, atrophic glands, basal cell hyperplasia, high-grade prostatic intraepithelial neoplasia, and prostatic adenocarcinoma were evaluated. Results.—Annexin II expression was present in more than 50% of glands in most (>85%) samples of benign prostatic epithelium, atrophic glands, and basal cell hyperplasia. In high-grade prostatic intraepithelial neoplasia, annexin II staining was markedly reduced in epithelial cells but not in basal cells. Annexin II was absent or focally present in moderately differentiated adenocarcinoma but was retained in poorly differentiated adenocarcinomas. Conclusions.—Reduced annexin II expression may be a useful diagnostic biomarker to help identify small foci of moderately differentiated adenocarcinoma on needle core biopsy specimens since it is consistently expressed in benign prostatic glands. Re-expression of annexin II in poorly differentiated adenocarcinoma may provide prognostic information.
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12

Bono, A. V., A. V. Bono, R. Montironi, L. Mazzucchelli, and I. Ferrari. "BICALUTAMIDE MONOTHERAPY IN HIGH-GRADE PROSTATIC INTRAEPITHELIAL NEOPLASIA." European Urology Supplements 5, no. 2 (April 2006): 250. http://dx.doi.org/10.1016/s1569-9056(06)60917-2.

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13

Melissari, M. "High grade prostatic intraepithelial neoplasia with squamous differentiation." Journal of Clinical Pathology 59, no. 4 (April 1, 2006): 437–39. http://dx.doi.org/10.1136/jcp.2005.028241.

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14

Prange, W., A. Erbersdobler, P. Hammerer, M. Graefen, S. H. Hautmann, R. E. Hautmann, H. Huland, and R. P. Henke. "High-Grade Prostatic Intraepithelial Neoplasia in Cystoprostatectomy Specimens." European Urology 39, Suppl. 4 (2001): 30–31. http://dx.doi.org/10.1159/000052580.

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15

Haffner, Michael C., and Christopher E. Barbieri. "Shifting Paradigms for High-grade Prostatic Intraepithelial Neoplasia." European Urology 69, no. 5 (May 2016): 831–33. http://dx.doi.org/10.1016/j.eururo.2015.11.020.

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16

Acosta, Andres M., Asma Sharif, John V. Groth, and Andre Kajdacsy-Balla. "Ductal Spread Versus High-Grade Prostatic Intraepithelial Neoplasia." International Journal of Surgical Pathology 24, no. 8 (September 24, 2016): 718–19. http://dx.doi.org/10.1177/1066896916668639.

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17

Argani, Pedram, and Jonathan I. Epstein. "Inverted (Hobnail) High-Grade Prostatic Intraepithelial Neoplasia (PIN)." American Journal of Surgical Pathology 25, no. 12 (December 2001): 1534–39. http://dx.doi.org/10.1097/00000478-200112000-00010.

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18

Bishara, Tarek, Dharam M. Ramnani, and Jonathan I. Epstein. "High-grade Prostatic Intraepithelial Neoplasia on Needle Biopsy." American Journal of Surgical Pathology 28, no. 5 (May 2004): 629–33. http://dx.doi.org/10.1097/00000478-200405000-00010.

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19

Bostwick, David G., Mahul B. Amin, Paul Dundore, William Marsh, and Daniel S. Schultz. "Architectural patterns of high-grade prostatic intraepithelial neoplasia." Human Pathology 24, no. 3 (March 1993): 298–310. http://dx.doi.org/10.1016/0046-8177(93)90041-e.

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20

Steiner, Mitchell S. "High grade prostatic intraepithelial neoplasia is a disease." Current Urology Reports 2, no. 3 (May 2001): 195–98. http://dx.doi.org/10.1007/s11934-001-0078-9.

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21

Ayala, Alberto G., and Jae Y. Ro. "Prostatic Intraepithelial Neoplasia: Recent Advances." Archives of Pathology & Laboratory Medicine 131, no. 8 (August 1, 2007): 1257–66. http://dx.doi.org/10.5858/2007-131-1257-pinra.

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Abstract Context.—There have been 2 putative prostatic cancer precursors, prostatic intraepithelial neoplasia (PIN) and atypical adenomatous hyperplasia (adenosis), but PIN remains as a well-known precancerous condition. Objective.—To describe recent advances in knowledge of PIN and to better define the diagnostic criteria and differential diagnosis of PIN. Data Sources.—Review of the pertinent literature and our experience. Conclusions.—The presence of ductal/acinar epithelial changes including nuclear enlargement, prominent nucleoli, chromatin alterations, and luminal complexity is an easy way to identify the disorder. Four main patterns of high-grade PIN (HGPIN) have been described: tufting, micropapillary, cribriform, and flat. In addition, variants of HGPIN have also been described. Both HGPIN and prostatic carcinoma share an increased incidence and severity with advancing age and with high rates of occurrence in the peripheral zone of the prostate. Furthermore, HGPIN and prostate cancer share genetic and molecular markers as well, with PIN representing an intermediate stage between benign epithelium and invasive carcinoma. The clinical significance of HGPIN is that it identifies patients at risk for prostatic carcinoma. With the increased use of extended biopsy protocols, clinicians are more likely to identify HGPIN and less likely to miss concurrent carcinoma.
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22

Aldaoud, Najla, Amer Hallak, Nour Abdo, Samir Al Bashir, Noor Marji, and Ashley Graboski-Bauer. "Interobserver Variability in the Diagnosis of High-Grade Prostatic Intraepithelial Neoplasia in a Tertiary Hospital in Northern Jordan." Clinical Pathology 13 (January 2020): 2632010X1989847. http://dx.doi.org/10.1177/2632010x19898472.

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Prostate intraepithelial neoplasia is described as a precursor lesion to prostatic adenocarcinoma. High-grade prostate intraepithelial neoplasia (HGPIN) is classified as both grade 2 and 3 prostate intraepithelial neoplasia due to inconsistency between pathologists’ findings. In our study, we assessed the interobserver variability in the diagnosis of HGPIN among genitourinary and nongenitourinary pathologists. All cases with prostate adenocarcinoma diagnosis on needle core biopsy, radical prostatectomy, and transurethral resection of prostate (TURP) between the years 2005 and 2014 were included. In total, 191 prostate cancer cases were included: 109 needle core biopsies, 45 radical prostatectomies, and 37 TURP. All were independently reviewed by 2 urologic pathologists for the presence of HGPIN. High-grade prostate intraepithelial neoplasia was diagnosed in 65 cases (34%), among which the lesion was recognized by the reporting pathologists in 36 (55%) of the cases and was missed in 29 (45%) of the cases with a κ coefficient of 0.53. There was a moderate interobserver agreement in the diagnosis of HGPIN. Consultation with genitourinary pathologist can improve HGPIN diagnosis.
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23

Pradhan, SV, and P. Sharan. "Prostatic intraepithelial neoplasia- the story evolves." Journal of Pathology of Nepal 6, no. 12 (September 24, 2016): 1028–33. http://dx.doi.org/10.3126/jpn.v6i12.16258.

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Prostatic intraepithelial neoplasia is preneoplastic lesion described from early of this 20th century. PIN includes a spectrum of features ranging from low grade to high grade neoplasia. The studies are focused on their influence to predict the occurence of prostatic carcinoma. This review analyses the various development in the identification and differentiation of PIN and their clinical implication.
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24

Tomlins, Scott A., Nallasivam Palanisamy, Javed Siddiqui, Arul M. Chinnaiyan, and Lakshmi P. Kunju. "Antibody-Based Detection of ERG Rearrangements in Prostate Core Biopsies, Including Diagnostically Challenging Cases: ERG Staining in Prostate Core Biopsies." Archives of Pathology & Laboratory Medicine 136, no. 8 (August 1, 2012): 935–46. http://dx.doi.org/10.5858/arpa.2011-0424-oa.

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Context.—Fusions of androgen-regulated genes and v-ets erythroblastosis virus E26 oncogene homolog (avian) (ERG) occur in approximately 50% of prostate cancers, encoding a truncated ERG product. In prostatectomy specimens, ERG rearrangements are greater than 99% specific for prostate cancer or high-grade prostatic intraepithelial neoplasia adjacent to ERG-rearranged prostate cancer by fluorescence in situ hybridization and immunohistochemistry. Objective.—To evaluate ERG staining by immunohistochemistry on needle biopsies, including diagnostically challenging cases. Design.—Biopsies from a retrospective cohort (n = 111) enriched in cores requiring diagnostic immunohistochemistry and a prospective cohort from all cases during 3 months (n = 311) were stained with an anti-ERG antibody (clone EPR3864). Results.—Among evaluable cores (n = 418), ERG staining was confined to cancerous epithelium (71 of 160 cores; 44%), high-grade prostatic intraepithelial neoplasia (12 of 68 cores; 18%), and atypical foci (3 of 28 cores; 11%), with staining in only 2 of 162 cores (1%) diagnosed as benign. The ERG was expressed in about 5 morphologically benign glands across 418 cores and was uniformly expressed by all cancerous glands in 70 of 71 cores (99%). Conclusions.—ERG staining is more prostate cancer–specific than α-methylacyl-coenzyme A racemase, and staining in an atypical focus supports a diagnosis of cancer if high-grade prostatic intraepithelial neoplasia can be excluded. Thus, ERG staining shows utility in diagnostically challenging biopsies and may be useful in molecularly subtyping prostate cancer and in stratifying isolated high-grade prostatic intraepithelial neoplasia by risk of subsequent cancer.
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25

Morikawa, T., A. Goto, K. Tomita, Y. Tsurumaki, S. Ota, T. Kitamura, and M. Fukayama. "Recurrent prostatic stromal sarcoma with massive high-grade prostatic intraepithelial neoplasia." Journal of Clinical Pathology 60, no. 3 (May 26, 2006): 330–32. http://dx.doi.org/10.1136/jcp.2006.039032.

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26

Humphrey, P. A., and P. E. Swanson. "Immunoreactive p53 Protein in High-Grade Prostatic Intraepithelial Neoplasia." Pathology - Research and Practice 191, no. 9 (September 1995): 881–87. http://dx.doi.org/10.1016/s0344-0338(11)80972-6.

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27

Humphrey, Peter A. "High Grade Prostatic Intraepithelial Neoplasia in Prostate Needle Biopsy." Journal of Urology 189, no. 1 (January 2013): 315–16. http://dx.doi.org/10.1016/j.juro.2012.10.036.

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28

Allina, D. O., Yu Yu Andreeva, L. E. Zavalishina, T. V. Kekeeva, and G. A. Frank. "High-grade prostatic intraepithelial neoplasia: State-of-the-art." Arkhiv patologii 77, no. 1 (2015): 69. http://dx.doi.org/10.17116/patol201577169-.

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29

Reyes, Adriana O., Paul E. Swanson, Joseph M. Carbone, and Peter A. Humphrey. "Unusual Histologic Types of High-Grade Prostatic Intraepithelial Neoplasia." American Journal of Surgical Pathology 21, no. 10 (October 1997): 1215–22. http://dx.doi.org/10.1097/00000478-199710000-00013.

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30

Eminaga, Okyaz, Fabian Woetzel, Jochen Fries, Susanne Neiss, Michaela Heitmann, Udo Engelmann, Axel Heidenreich, and Ute Warnecke-Eberz. "miRNA expression profiles in high-grade prostatic intraepithelial neoplasia." Journal of Clinical Oncology 34, no. 2_suppl (January 10, 2016): 45. http://dx.doi.org/10.1200/jco.2016.34.2_suppl.45.

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45 Background: High-grade prostatic intraepithelial neoplasia (HGPIN) is widely believed to be a precursor of prostate cancer (PCa). However, little is known about the expression of miRNAs variations in HGPIN compared to normal tissues and PCa. Methods: The expression data of 1054 miRNAs from TCGA were applied to identify relevant miRNAs associated with tumor progression (i.e., miR-98-5p, miR-183-5p, 345-5p, miR-143 miR-210-3p and miR-378-3p). miRNA were isolated by miRNeasy FFPE kit (Qiagen, Hilden, Germany) from paraffin-embedded tissues (FFPE) of prostate specimens with PCa, HGPIN and normal tissues. Early-stage PCa was defined as PCa with pT2 tumor stage, Gleason score <=7a (3+4) and PSA level <10 ng/ml. Quantitative miRNA expression data were acquired and analyzed using a real-time TaqMan-based PCR with the ABI Prism 7900HT (Life Technologies, Darmstadt, Germany). ANOVA analysis were performed to evaluate the expression of miRNAs between HGPIN, Normal and PCa tissues. All statistical analysis was performed using SPSS (IBM, Armonk, USA). P values were adjusted using the false discovery rate for multiple comparisons. The small nuclear U6 RNA was used as an endogenous control. Results: The expression of miR-143-3p, miR-210-3p and miR-345-5p and miR-98-5-p were varied between normal tissue, HGPIN and early-stage PCa. Interestingly, decrease in expression of miR-143.-3p, miR-98-5p and miR-210-3p was associated with tumor development (Normal tissues > HGPIN > early-stage PCa) (FDR<0.001). Furthermore, overexpression of miR-345-5p was observed in normal tissues compared to HGPIN and early-stage PCa, which both showed similar expression level of miR-345-5p. No significant differences in expression of miR-375, miR-183-5p and miR-378-3p were observed between HGPIN and PCa. These miRNAs were interacted with genes related to HIF-1 signaling pathway, p53 signaling pathway, androgen receptor signaling pathway, intrinsic apoptotic signaling pathway, RNA transcription, homologous recombination and non-homologous end-joining. Conclusions: HGPIN shows an altered expression of miRNAs interact with genes related to hypoxia, androgen receptor signaling pathway, cell cycle and epigenetic regulation.
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31

Moul, Judd W., and Mark Frydenberg. "Isolated high grade prostatic intraepithelial neoplasia may not predict future prostatic malignancy." Evidence-based Oncology 3, no. 4 (December 2002): 187–88. http://dx.doi.org/10.1054/ebon.2002.0041.

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32

Billis, Athanase, and Luis A. Magna. "Prostate Elastosis." Archives of Pathology & Laboratory Medicine 124, no. 9 (September 1, 2000): 1306–9. http://dx.doi.org/10.5858/2000-124-1306-pe.

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Abstract Background.—Elastosis of the prostate may be seen on needle biopsy and radical prostatectomy specimens, but its significance is unknown. Prostatic atrophy (or postatrophic hyperplasia) is one of the most frequent mimics of prostatic adenocarcinoma. Objective.—To observe the frequent occurrence of elastosis of the prostate stroma in areas of postatrophic hyperplasia. Design.—A step-section method was used to cut the posterior lobe (or peripheral zone) in coronal planes at intervals of 0.3 to 0.5 cm in 100 consecutive autopsy specimens of men older than 40 years. Elastosis was detected because of a basophilic tinge of the stroma on hematoxylin-eosin stain and confirmed using elastic fiber stains. Presence of elastosis correlated with the following variables: age, prostatic atrophy (simple, hyperplastic, or sclerotic), local arteriosclerosis, histologic carcinoma, high-grade prostatic intraepithelial neoplasia, benign or malignant nephrosclerosis, generalized atherosclerosis, nodular prostatic hyperplasia, and acute inflammation. For statistics, a stepwise linear regression method adjusted for age was used. Results and Conclusions.—Elastosis was found in 65 of the prostates examined and was significantly more frequent with increasing age (P &lt; .001), prostatic atrophy (P &lt; .001), and local arteriosclerosis (P &lt; .02). There was no significant relation to histologic carcinoma, high-grade prostatic intraepithelial neoplasia, benign or malignant nephrosclerosis, generalized atherosclerosis, nodular prostatic hyperplasia, and acute inflammation. The correlation with local arteriosclerosis favors a possible role of ischemia to its etiopathogenesis. The absence of correlation to neoplastic and preneoplastic lesions and the striking spatial relationship of elastosis to prostatic atrophy (or postatrophic hyperplasia) add a new microscopic feature for the diagnosis of this latter lesion, helping in the differential diagnosis with prostate adenocarcinoma.
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33

Jankovic-Velickovic, Ljubinka, Biljana Djordjevic, Gorana Rancic, and Goran Marjanovic. "Expression of nuclear Ki-67 antigen in prostatic high grade intraepithelial neoplasia and prostatic carcinoma." Vojnosanitetski pregled 64, no. 5 (2007): 325–30. http://dx.doi.org/10.2298/vsp0705325j.

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Background/Aim. Prostatic intraepithelial high grade neoplasia (PINHG) is accepted as preneoplastic lesion in prostatic carcinoma. One of the fundamental events in early oncogenesis is the disruption of proliferative activity. One of the numerous regulatory proteins is Ki-67 expressed in all proliferating cells. Index Ki-67 is considered to have prognostic significance. The aim of the study was to compare the level of proliferation in hyperplastic epithelium, prostatic carcinoma (Gleason score > 6) and PINHG. Methods. Micromorphological examination was done in 85 patients. Pathohistological analysis was performed on standard histologic specimens with the estimation of Gleason score and the presence of PINHG in its surroundings. Nuclear proliferative activity was analyzed immunohistochemically in 19 cases, using a monoclonal anti-Ki-67 antibody. Results. PINHG was found in prostatic carcinoma surrounding in 30% of the patients. In hyperplastic epithelia Ki-67 proliferative activity was 1,08, in PINHG 2,25 (p < 0,05), while in prostatic cancer, Ki-67 index was 17,64. Proliferative activity in prostatic carcinoma was significantly higher than in PINHG (p < 0,001) and hyperplasia (p < 0,001). Conclusion. This study confirmed that high grade PIN lesion predominately appears in the surrounding of poor or moderately differentiated prostate carcinoma, and that it represents progressive disorder of proliferation in preneoplastic and neoplastic prostatic epithelium. .
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34

Meng, Maxwell V., Katsuto Shinohara, and Gary D. Grossfeld. "Significance of high-grade prostatic intraepithelial neoplasia on prostate biopsy." Urologic Oncology: Seminars and Original Investigations 21, no. 2 (March 2003): 145–51. http://dx.doi.org/10.1016/s1078-1439(03)00009-7.

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35

&NA;. "The nonsteroidal SERM* toremifene** reduces high-grade prostatic intraepithelial neoplasia." Inpharma Weekly &NA;, no. 1394 (July 2003): 13. http://dx.doi.org/10.2165/00128413-200313940-00027.

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36

Mai, K. T., H. M. Yazdi, E. Belanger, W. A. Stinson, I. Cagiannos, and C. Morash. "High grade prostatic intraepithelial neoplasia involving small ducts and acini." Histopathology 46, no. 4 (April 2005): 475–77. http://dx.doi.org/10.1111/j.1365-2559.2005.02011.x.

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37

Godoy, G., and S. S. Taneja. "Contemporary clinical management of isolated high-grade prostatic intraepithelial neoplasia." Prostate Cancer and Prostatic Diseases 11, no. 1 (October 2, 2007): 20–31. http://dx.doi.org/10.1038/sj.pcan.4501014.

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38

Schlesinger, Cory, David G. Bostwick, and Kenneth A. Iczkowski. "High-Grade Prostatic Intraepithelial Neoplasia and Atypical Small Acinar Proliferation." American Journal of Surgical Pathology 29, no. 9 (September 2005): 1201–7. http://dx.doi.org/10.1097/01.pas.0000168178.48535.0d.

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39

Steiner, Mitchell S. "High-grade prostatic intraepithelial neoplasia and prostate cancer risk reduction." World Journal of Urology 21, no. 1 (February 21, 2003): 15–20. http://dx.doi.org/10.1007/s00345-002-0313-0.

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40

Weinstein, Michael H., and Jonathan I. Epstein. "Significance of high-grade prostatic intraepithelial neoplasia on needle biopsy." Human Pathology 24, no. 6 (June 1993): 624–29. http://dx.doi.org/10.1016/0046-8177(93)90242-9.

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41

Krasnyak, S. S. "Pathogenetic therapy of benign prostatic hyperplasia and prostatic intraepithelial neoplasia." Experimental and Сlinical Urology 13, no. 4 (October 30, 2020): 66–74. http://dx.doi.org/10.29188/2222-8543-2020-13-4-66-74.

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Introduction. Benign prostatic hyperplasia (BPH) is a neoplasm and clinically occurred by progressive enlargement of the prostate. However, prostate neoplasm can also be malignant, which is come out from high-grade prostatic intraepithelial neoplasia (PIN). It is a proven precancerous condition. Purpose. Тo evaluate the data published on September and October 2020 on the prevalence, pathogenesis of BPH and PIN and methods of their treatment. Materials and methods. The search results in scientific databases PubMed, MEDLINE, Embase were analyzed for the queries «BPH», «PIN», «epidemiology of BPH», «pathogenesis», «treatment of PIN». Results. BPH is a very common disease in the elderly population. The pathogenesis of BPH includes age, genetics or hormones disorders, growth factors, inflammation, and lifestyle factors. PIN is the only common precursor of prostatic cancer. The main treatment methods are 5α-reductase inhibitors, phosphodiesterase-5 inhibitors, and surgical methods. In addition, plant active molecules are also widely used in the treatment of BPH and PIN. Conclusions. While 5α-reductase and phosphodiesterase-5 inhibitors treatment, as well as surgical methods have a lot of adverse events and complications, a unique herbal complex Gardaprost was developed, which suppresses hyperplasia of prostate. Curcumin, genistein and epigalocatechin-3- gallate, which are part of the preparation, form a safe agent aimed at combating the growth of the prostate gland in BPH, and also has a significant effect in the prevention of exacerbations of chronic prostatitis and malignancy in patients with PIN.
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42

Hameed, Omar, and Peter A. Humphrey. "Stratified epithelium in prostatic adenocarcinoma: a mimic of high-grade prostatic intraepithelial neoplasia." Modern Pathology 19, no. 7 (April 7, 2006): 899–906. http://dx.doi.org/10.1038/modpathol.3800601.

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43

Zweig, J. I. "Eradication of prostatic high grade intraepithelial neoplasia: Hypothesis and clinical proof." Journal of Clinical Oncology 25, no. 18_suppl (June 20, 2007): 1534. http://dx.doi.org/10.1200/jco.2007.25.18_suppl.1534.

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1534 Background: Recently normal prostate tissue has been found to contain a high concentration of retinoid X receptors (RXRs), they are found in the highest concentrations in ectodermal tissue. Loss of these receptors is associated with prostatic intraepithelial neoplasia (PIN), and can be present in patients with a normal PSA. There are 115,000 cases of high grade PIN discovered yearly in the United States.The drug bexarotene used to treat cutaneous T cell lymphoma (CTCL). The compound is not a true retinoid in structure, perusal of the structure reveals two aromatic rings one of which contains a carboxy group which would make one anticipate strong hydrogen bonding when it undergoes binding to the RXRs as if it were a retinoid, resulting in “up regulation” of the tissue with increase in differentiation to normal tissue. Based upon this it was felt that it would be fruitful to try bexarotene in High Grade PIN. Method: The diagnosis was based upon 12 biopsies which were done in conjunction with ultrasound localization of the biopsy site, with careful recording of there anatomical position. The patient was started on bexarotene 225 mg per day. The drug was given as a single dose once daily; this dose is 40% of the dose normally used to treat CTCL. The drug was administered for 30 doses During the period of therapy the patient was on Atorvastin T4 total was within the normal range. Results: Four weeks following the last dose of bexarotene the prostate was rebiopsied with 12 biopsies taken. Six of the biopsies were taken from the putative area, the rest in an enlarging target like pattern. The repeat biopsy was negative for the presence of PIN. 14 months later 12 more biopsies were obtained using the same technique, these repeat biopsies were also found to be negative; ie. 24 negative biopsies over 14 months. It is unlikely that the previously involved area was missed. Conclusion: If a mechanism of action were to be formulated, the induction of and increase in RXRs in normal prostate cells would be reasonable. Cells that undergo the formation of PIN, strong hydrogen bonding and inability of those cells to produce more receptors could result in apoptosis. Undoubtedly further study is required to evaluate the effect of this drug in high grade PIN. No significant financial relationships to disclose.
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Leite, Katia R. M. "Why do we keep reporting high-grade prostatic intraepithelial neoplasia (HGPIN)?" International braz j urol 42, no. 2 (April 2016): 180–82. http://dx.doi.org/10.1590/s1677-5538.ibju.2016.02.02.

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45

Swanson, Gregory P., A. Taylor Kingman, Courtney N. Shaver, Yolanda Munoz Maldonado, and T. Phillip Reilly. "High Grade Prostatic Intraepithelial Neoplasia and the Risk of Prostate Cancer." Open Journal of Urology 08, no. 03 (2018): 67–76. http://dx.doi.org/10.4236/oju.2018.83008.

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46

Bostwick, David G., Junqi Qian, and Kenneth Frankel. "The Incidence of High Grade Prostatic Intraepithelial Neoplasia in Needle Biopsies." Journal of Urology 154, no. 5 (November 1995): 1791–94. http://dx.doi.org/10.1016/s0022-5347(01)66785-5.

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Martinez, Fernando, and Daniel Cowan. "Clear Cell Cribriform Hyperplasia Associated with High-Grade Prostatic Intraepithelial Neoplasia." Pathology Case Reviews 8, no. 2 (March 2003): 74–77. http://dx.doi.org/10.1097/01.pcr.0000054876.23431.12.

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Prange, Wilhelm, Andreas Erbersdobler, Peter Hammerer, Markus Graefen, Stefan H. Hautmann, Richard E. Hautmann, Hartwig Huland, and Rolf-P. Henke. "Significance of high-grade prostatic intraepithelial neoplasia in needle biopsy specimens." Urology 57, no. 3 (March 2001): 486–90. http://dx.doi.org/10.1016/s0090-4295(00)01010-4.

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Trabzonlu, Levent, Ibrahim Kulac, Qizhi Zheng, Jessica L. Hicks, Michael C. Haffner, William G. Nelson, Karen S. Sfanos, et al. "Molecular Pathology of High-Grade Prostatic Intraepithelial Neoplasia: Challenges and Opportunities." Cold Spring Harbor Perspectives in Medicine 9, no. 4 (August 6, 2018): a030403. http://dx.doi.org/10.1101/cshperspect.a030403.

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ÖZNUR, MELTEM, SEVIM BAYKAL KOCA, PELIN YILDIZ, BURAK BAHADIR, and KEMAL BEHZATOĞLU. "Inverted (hobnail) high-grade prostatic intraepithelial neoplasia and invasive inverted pattern." Oncology Letters 10, no. 4 (August 10, 2015): 2395–99. http://dx.doi.org/10.3892/ol.2015.3584.

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