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Lorenzo, Guillermo, Thomas J. R. Hughes, Pablo Dominguez-Frojan, Alessandro Reali i Hector Gomez. "Computer simulations suggest that prostate enlargement due to benign prostatic hyperplasia mechanically impedes prostate cancer growth". Proceedings of the National Academy of Sciences 116, nr 4 (7.01.2019): 1152–61. http://dx.doi.org/10.1073/pnas.1815735116.
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Prostate cancer and benign prostatic hyperplasia are common genitourinary diseases in aging men. Both pathologies may coexist and share numerous similarities, which have suggested several connections or some interplay between them. However, solid evidence confirming their existence is lacking. Recent studies on extensive series of prostatectomy specimens have shown that tumors originating in larger prostates present favorable pathological features. Hence, large prostates may exert a protective effect against prostate cancer. In this work, we propose a mechanical explanation for this phenomenon. The mechanical stress fields that originate as tumors enlarge have been shown to slow down their dynamics. Benign prostatic hyperplasia contributes to these mechanical stress fields, hence further restraining prostate cancer growth. We derived a tissue-scale, patient-specific mechanically coupled mathematical model to qualitatively investigate the mechanical interaction of prostate cancer and benign prostatic hyperplasia. This model was calibrated by studying the deformation caused by each disease independently. Our simulations show that a history of benign prostatic hyperplasia creates mechanical stress fields in the prostate that impede prostatic tumor growth and limit its invasiveness. The technology presented herein may assist physicians in the clinical management of benign prostate hyperplasia and prostate cancer by predicting pathological outcomes on a tissue-scale, patient-specific basis.
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Patrick Opoku Maison, Douglas Arthur, Alvin Asante-Asamani i Patrick Kafui Akakpo. "An Analysis of Prostate Biopsy Results at the Cape Coast Teaching Hospital, Ghana". International Journal of Medical Science and Clinical Invention 9, nr 10 (23.10.2022): 6281–85. http://dx.doi.org/10.18535/ijmsci/v9i10.03.
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Introduction: Prostate cancer is the commonly diagnosed male cancer worldwide. The best technique for the diagnosis of prostate cancer is prostate biopsy. Transrectal ultrasound (TRUS)-guided biopsy of the prostate enhances early diagnosis of prostate cancers. Objective: The aim of the study is to describe the clinical and pathological characteristics of Prostate cancers as seen at the Cape Coast Teaching Hospital Materials and Methods: A total of 62 patients who underwent TRUS-guided prostatic biopsy over a period of 3 years (January 2019- December 2021) participated in the study. Their data were analyzed retrospectively using the archives of the pathology department of the Cape Coast Teaching Hospital. Results: Of the 62 patients who underwent TRUS-guided prostrate biopsy from January 2019 to December 2021, their mean age was 68.3 with an age range of 34-89 years. 67.7% had adenocarcinoma of the prostate, 1.6% had spindle cell cancer, 24.2% had benign prostate hyperplasia and 6.5% had chronic prostatitis. Conclusion: The indications for prostate biopsy in our center detect more patients with prostate cancer than other prostate pathologies. The serum PSA significantly correlated with the Gleason grade.
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Jones, Angelle D., Carissa Lester i Susan E. Waltz. "Abstract 1243: RON receptor signaling enhances prostate cancer metastasis in Hi-Myc mice". Cancer Research 83, nr 7_Supplement (4.04.2023): 1243. http://dx.doi.org/10.1158/1538-7445.am2023-1243.
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Abstract Prostate cancer (PCa) is the second leading cause of cancer mortality among men globally. Death from PCa is typically due to the lack of effective treatments for advanced forms of prostate cancers including castration-resistant prostate cancer (CRPC) and metastatic prostate cancers (mPCa). Distantly metastasized cancers drop the 5-year survival rate from 98% to 30%. Understanding the intrinsic and extrinsic mechanisms that lead to the development of these advanced prostate cancers could improve treatment options. The RON receptor tyrosine kinase is a cell surface receptor, which is activated by growth factor ligands (HGFL or Gas6), which binding promotes several cancer phenotypes in various cancers including prostate cancer. Our laboratory has shown that RON is overexpressed in 86% of primary and 100% of metastatic human prostate cancers compared to normal prostate tissue. Additionally, we have shown that RON overexpression in the prostates of mice can induce Prostatic intraepithelial neoplasia (PIN) lesions, adenocarcinoma, and increases several cancer phenotypes including proliferation, cell survival, metastasis, and increased recruitment of tumor-associated macrophages. However, we have yet to explore the effect of RON on prostate cancer metastasis. We hypothesize that RON expression enhances metastasis by promoting an increase in the amount of disseminating prostate cancer cells. To test this hypothesis, the Hi-Myc mouse model has been employed. The MYC gene is one of the most dysregulated genes in prostate cancers and Myc expression has been detected in the early stages of prostate cancer development, PIN lesion, and all later stages of prostate cancer. Additionally, the Hi-Myc model is clinically relevant as prostate tumor development in this model is similar to that in humans in regard to progression from PIN lesions to adenocarcinoma. From the Hi-Myc model, we have generated two additional genetic modifications within prostate epithelial cells: 1) Hi-Myc mice with prostate-specific RON overexpression (OE) and 2) Hi-Myc mice with prostate-specific RON loss (ΔEpi). In this study we report that a lack of prostate RON expression diminishes adenocarcinoma development and metastasis within the Hi-Myc mouse model. Moreover, RON overexpression promotes the development of metastatic adenocarcinoma that was not observed in the prostates from Hi-Myc control mice. These studies suggest that RON expression supports the advancement of primary tumors to metastatic prostate cancer within the Hi-Myc mouse models. Therefore, future directions include determining the signaling pathways driven by RON that promotes this metastatic phenotype in both castration-sensitive and resistant tumors. Citation Format: Angelle D. Jones, Carissa Lester, Susan E. Waltz. RON receptor signaling enhances prostate cancer metastasis in Hi-Myc mice [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2023; Part 1 (Regular and Invited Abstracts); 2023 Apr 14-19; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2023;83(7_Suppl):Abstract nr 1243.
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Vojinov, Sasa, Goran Marusic, Ivan Levakov i Jelena Popadic-Gacesa. "Influence of hormonal therapy on the level of prostate specific antigen in patients with advanced prostatic cancer". Medical review 63, nr 7-8 (2010): 479–82. http://dx.doi.org/10.2298/mpns1008479v.
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% Karcinomi prostate % Antagonisti androgena % Kastracija % Testosteron % Luteinizirajuci hormone AB Introduction. The aim of this study was to investigate the influence of androgen blockades on prostate specific antigen (PSA) values in patients with locally advanced and metastatic prostatic cancer. Material and methods. The research was conducted on 60 patients. The group of 45 patients with prostatic cancer was divided into 3 subgroups, based on the type of the applied treatment protocol (15 patients on monotherapy with luteinizing hormone-releasing hormone agonists, 15 patients on total androgen blockade and 15 patients on monotherapy with antiandrogen). The control group consisted of 15 patients with benign prostatic hyperplasia. For all patients, the values of testosteron, luteinizing hormone and prostate specific antigen were monitored before as well as after 3 and 6 months during the treatment protocol. Results. All types of the applied treatment protocols in the therapy of prostatic cancer decreased the values of prostate specific antigen significantly The application of total androgen blockade and monotherapy with luteinizing hormone-releasing hormone agonists decreased the levels of prostate specific antigen significantly in comparison with monotherapy with antiandrogen. Conclusion. Although prostate specific antigen is not a prostatic cancer specific parameter, the dynamics of its decrease during the therapy of androgen blockade represents a significant marker of the therapy effect. Cilj rada je bio da se ispita uticaj androgenih blokada na vrednosti prostata specificnog antigena kod bolesnika sa lokalno uznapredovalim i metastatskim karcinomom prostate. Ispitivani uzorak se sastojao od 60 bolesnika. Grupa od 45 bolesnika sa karcinomom prostate bila je podeljena na tri podgrupe, u zavisnosti od primenjenog terapijskog protokola (15 bolesnika na monoterapiji agonistima luteinizirajuceg rilizing hormona, 15 bolesnika na totalnoj androgenoj blokadi i 15 bolesnika na monoterapiji antindrogenom). Kontrolnu grupu cinilo je 15 pacijenata sa benignom hiperplazijom prostate. Svim pacijentima su pracene vrednosti testosterona, luteinizirajuceg hormona i prostata specificnog antigena neposredno pre, kao i tri, to jest sest meseci nakon uvodjenja odgovarajuceg protokola. Sve tri vrste primenjenih terapijskih protokola u lecenju karcinoma prostate statisticki su znatno snizavale vrednosti prostata specificnog antigena u odnosu na pocetne vrednosti. Primena totalne androgene blokade i monoterapije agonistima luteinizirajuceg rilizing hormona dovela je do statisticki znatnog snizenja vrednosti prostata specificnog antigena u poredjenju sa monoterapijom antiandrogenom. Iako prostata specificni antigen nije specifican marker za karcinom prostate, dinamika njegove promene u toku androgene blokade predstavlja bitan pokazatelj terapijskog efekta.
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Ceyhan, Yasemin, Manqi Zhang i Irina U. Agoulnik. "Abstract 815: Regulation of p53 by INPP4B and high fat diet in mouse prostate". Cancer Research 82, nr 12_Supplement (15.06.2022): 815. http://dx.doi.org/10.1158/1538-7445.am2022-815.
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Abstract Obesity is one of the risk factors for prostate neoplasia development, however the underlying molecular mechanisms that link obesity and prostate cancer remain elusive. The roles of AR, p53, EZH2, INPP4B, and PTEN are implicated in prostate cancer etiology. Androgen receptor (AR) signaling interacts functionally with PTEN, INPP4B, EZH2, and p53 signaling in prostate epithelium, and its transcriptional activity is reprogrammed by changes in the levels of these proteins during prostate cancer progression. Phosphatase and tensin homolog (PTEN) and Inositol Polyphosphate 4-Phosphatase Type-II B (INPP4B) are dual specificity phosphatases which are tumor suppressors in prostate cancer and are lost in nearly half of advanced castration resistant prostate cancers (CRPC). p53 is also a tumor suppressor gene that is frequently inactivated in prostate cancers. Enhancer of Zeste 2 (EZH2) is an epigenetic silencer that increases methylation of histone H3 on K27 and K9 residues and acts as an oncogene in CRPC. We have previously shown that INPP4B inhibits the Akt and PKC signaling pathways, which are activated in obesity. Using an Inpp4b-deficient mouse model, we showed that three-month-old Inpp4b-/- males developed prostatic intraepithelial neoplasia (PIN) when fed a high fat diet (HFD). While the AR protein levels were not altered, the transcriptional activity of AR was reduced in the prostates of Inpp4b-/- males. Furthermore, the prostates of HFD-fed Inpp4b-/- males exhibited increased expression of pro-inflammatory cytokines and macrophage infiltration. It was previously reported that indolent nature of the prostate neoplasia, which is caused by prostate specific Pten knockout, is due to the compensatory increase in other tumor suppressor proteins, such as p53, SMAD4, and PML. Concomitant with Pten, knockout of these individual tumor suppressors led to drastic acceleration of prostate neoplasia. Similar to prostates of Pten-/- mice, p53 levels increased in Inpp4b-/- males fed a low fat diet (LFD). Unlike males fed LFD, p53 protein levels decreased in HFD fed Inpp4b-/- mice, consistent with the development of PIN in this group. EZH2 levels as well as the levels of its targets, H3K27me3 and H3K9me2, decreased in ventral prostates of the Inpp4b-/- males and that decrease was exacerbated by the HFD. Similar to our mouse model, we observed significant positive correlation between the INPP4B and EZH2 expression in the prostates of healthy men and prostate cancer patients. In summary, we showed that loss of INPP4B synergizes with the HFD in reprogramming AR activity, reduction of EZH2 levels, and increases inflammation. Importantly, HFD reverses compensatory increase in p53 protein levels in prostates of Inpp4b-/- males. These alterations contribute to the development of PIN in the prostates of HFD-fed Inpp4b-/- males. Citation Format: Yasemin Ceyhan, Manqi Zhang, Irina U. Agoulnik. Regulation of p53 by INPP4B and high fat diet in mouse prostate [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2022; 2022 Apr 8-13. Philadelphia (PA): AACR; Cancer Res 2022;82(12_Suppl):Abstract nr 815.
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Suresh, Kishanrao. "Prostate health in India (BPH & Prostate Cancer)". Archives of Cancer Science and Therapy 6, nr 1 (3.09.2022): 009–17. http://dx.doi.org/10.29328/journal.acst.1001028.
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The prostate gland, found only in men, is an extremely important organ of the reproductive system, but it is not taken care of adequately, leading to prostate inflammation and benign hypertrophy or even cancer. Benign prostate enlargement compresses urine flow through the urethra, leading to uncomfortable urinary symptoms. Hyperplasia increases the risk of bladder stones, urinary tract infections, and kidney problems. In India prevalence of Benign Prostrate Hyperplasia (BPH) is around 50% of men by the age of 60 years. Studies suggest that benign prostatic hyperplasia is a result of the disproportion between oestrogen & testosterone. A higher proportion of oestrogen within the prostate boosts the growth of prostate cells. The management of BPH is streamlined in recent times and the majority are on medical treatment. Prostate cancers are one of the cancers showing a significant increase in incidence along with mouth and kidney and lung cancers among the male population. With an estimated population of 1400 million and about 98 million males over 50 years of age in mid-2022 and the average life expectancy increasing 68.4 years, has a bearing on the changing incidence and pattern of prostate cancer in the current decade in India. Based on the five population-based cancer registries in 2009-10, the age-adjusted annual incidence rates per lakh population of prostate cancers were highest in Delhi (10.2) followed by Bengaluru (8.7), Mumbai (7.3), Chennai (7) and Bhopal (6.1). Cancer can co-exist with BPH. Prostate cancer management is still in the development stage with a 5-year life expectancy of around 64%. The prostate is the second leading site of cancer among males in large Indian cities like Delhi, Kolkata, Pune, and Thiruvananthapuram, and the third leading site of cancer in cities like Bangalore and Mumbai. Despite the limitations of diagnosis, the annual cancer incidence rate ranges from 5.0-9.1 per 100,000/year, as compared to the rates in the United States and other developed countries of 110 &180 for whites and blacks respectively. This article is a review of Prostate health in India based on a personal observation of around 183 cases by the author in the last 10 years. Materials & methods: This is an observational study report of three cohorts of men across the country. The sample was of people encountering the author. The sample included i) 69 septuagenarians plus ii) 30 senior citizens aged 60 - 70 years and iii) 84 men in 40 – 60 - year age groups over the last decade. The data source was sharing annual check-up reports or consultation report in person for seeking 2nd opinion. A minimum of 2 consultations, first when diagnosed and the recent between July 2021 to June 2022.
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MWAKYOMA, H. A., i J. L. MAGANDI. "PROSTATE CANCER". Professional Medical Journal 17, nr 02 (10.06.2010): 235–40. http://dx.doi.org/10.29309/tpmj/2010.17.02.2351.
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Objectives: To correlate histopathological grades of prostate cancer by Gleason’s scoring system and pretreatment PSA levels in patients with prostate cancer. Study Design: A prospective longitudinal study. Setting: Muhimbili National Hospital in the Departments of Histopathology and Morbid anatomy, Surgery and Biochemistry. Study Period: 15 months (from November 2006 to March 2008). Patients and Methods: Tissues were obtained from 131 cases of Transurethral Trucut biopsy and were formalin fixed and paraffin-embedded for diagnosis. The prostatic tumours were diagnosed and assigned Gleason’s histopathological grades and scores using Haematoxylin and Eosin (H&E) stained sections. Blood for PSA assay was analyzed by a method based on the immunoradiometric principle in which two monoclonal antibodies are directed against two different epitopes of PSA molecule. Results: During the period of study, 113 patients were diagnosed to have carcinoma of the prostate. The mean age at diagnosis was 68 years. The predominant histological type was adenocarcinoma (99.1%). The majority (45.1%) had moderately differentiated adenocarcinoma. Sixty one percent (61%) of patients had Gleason’s score of 5-7 and 81.5% of patients had significant elevation of pretreatment PSA of > 20.0 ng/ml. There was a positive correlation between Gleason’s score and pretreatment PSA levels in patients with Prostate cancer (r = +0.6) and was statistically significant (P< 0.05). Conclusions: It is known that the intermediate (5-7) Gleason’s score prostatic cancers are highly unpredictable in their clinical aggressiveness. This limitation is of particular importance as the majority of the tumours (76%) in our study fell into this intermediate category. Thus, predicting the biological potential of the majority of prostatic cancers in asymptomatic patients based upon histology alone is problematic. The combination of pretreatment PSA levels which correlated well with Gleason’s score in our study will be helpful in planning the choice of therapy in most patients with prostatic cancer in order to improve the prognosis.
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Wang, Liang, Marloes Zoetemelk, Brahmananda R. Chitteti, Timothy L. Ratliff, Jason D. Myers, Edward F. Srour, Hal Broxmeyer i Travis J. Jerde. "Expansion of prostate epithelial progenitor cells after inflammation of the mouse prostate". American Journal of Physiology-Renal Physiology 308, nr 12 (15.06.2015): F1421—F1430. http://dx.doi.org/10.1152/ajprenal.00488.2014.
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Prostatic inflammation is a nearly ubiquitous pathological feature observed in specimens from benign prostate hyperplasia and prostate cancer patients. The microenvironment of the inflamed prostate is highly reactive, and epithelial hyperplasia is a hallmark feature of inflamed prostates. How inflammation orchestrates epithelial proliferation as part of its repair and recovery action is not well understood. Here, we report that a novel epithelial progenitor cell population is induced to expand during inflammation. We used sphere culture assays, immunofluorescence, and flow cytometry to show that this population is increased in bacterially induced inflamed mouse prostates relative to naïve control prostates. We confirmed from previous reports that this population exclusively possesses the ability to regrow entire prostatic structures from single cell culture using renal grafts. In addition, putative progenitor cells harvested from inflamed animals have greater aggregation capacity than those isolated from naïve control prostates. Expansion of this critical cell population requires IL-1 signaling, as IL-1 receptor 1-null mice exhibit inflammation similar to wild-type inflamed animals but exhibit significantly reduced progenitor cell proliferation and hyperplasia. These data demonstrate that inflammation promotes hyperplasia in the mouse prostatic epithelium by inducing the expansion of a selected epithelial progenitor cell population in an IL-1 receptor-dependent manner. These findings may have significant impact on our understanding of how inflammation promotes proliferative diseases such as benign prostatic hyperplasia and prostate cancer, both of which depend on expansion of cells that exhibit a progenitor-like nature.
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Lotan, Yair, Xiao C. Xu, Moshe Shalev, Reuben Lotan, Russell Williams, Thomas M. Wheeler, Timothy C. Thompson i Dov Kadmon. "Differential Expression of Nuclear Retinoid Receptors in Normal and Malignant Prostates". Journal of Clinical Oncology 18, nr 1 (1.01.2000): 116. http://dx.doi.org/10.1200/jco.2000.18.1.116.
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PURPOSE: To determine (1) whether nuclear retinoic acid receptors (RARs) and retinoid X receptors (RXRs) are differentially expressed in normal and in cancerous human prostate tissues and (2) whether oral fenretinide therapy impacts the expression of these receptors in prostate cancer. PATIENTS AND METHODS: In situ hybridization with antisense riboprobes was used to probe for RAR and RXR transcripts in prostate tissues in a two-phased study: (1) expression of retinoid receptors in eight normal prostates was compared with their expression in 10 randomly picked radical prostatectomy specimens (group A); (2) expression of retinoid receptors was determined in 22 radical prostatectomy specimens from participants in a clinical study (group B). Twelve patients received oral fenretinide 200 mg/d, and 10 received placebo pills for 28 days before surgery. RESULTS: RARα, RARγ, RXRα, and RXRγ mRNAs were detected in most normal and cancerous prostates. In group A, RARβ mRNA was expressed in only four of 10 malignant prostates but was present in seven of eight benign prostates (P = .05). RXRβ mRNA was expressed in four of eight benign prostates and in zero of 10 malignant prostates (P = .023). In group B prostates, RARβ and RXRβ mRNAs were markedly reduced in all cancers and in the adjacent, nonmalignant tissue. There were no differences between receptor expression in the fenretinide-treated group and the placebo group. CONCLUSION: RARβ and RXRβ mRNAs are selectively lost in both prostate cancer and adjacent morphologically normal prostatic tissue, supporting the concept of a field of carcinogenesis. One month of oral fenretinide (200 mg/d) did not influence the expression of retinoid receptors in prostate cancer.
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Tomioka, Atsushi, Motoyoshi Tanaka, Satoshi Anai, Tomohiro Ikeda, Keiji Shimada, Marco Velasco, Keigo Saito, Yoshihiko Hirao i Hirotsugu Uemura. "WS1-3-5 A Prostate Cancer Model by the Prostate Specific Deletion of PTEN(Prostate Cancer)". Japanese Journal of Urology 99, nr 2 (2008): 149. http://dx.doi.org/10.5980/jpnjurol.99.149_1.
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Sun, Feng, He-ge Chen, Wei Li, Xi Yang, Xin Wang, Richeng Jiang, Zhiyong Guo i in. "Androgen Receptor Splice Variant AR3 Promotes Prostate Cancer via Modulating Expression of Autocrine/Paracrine Factors". Journal of Biological Chemistry 289, nr 3 (2.12.2013): 1529–39. http://dx.doi.org/10.1074/jbc.m113.492140.
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Deregulation of androgen receptor (AR) splice variants has been implicated to play a role in prostate cancer development and progression. To understand their functions in prostate, we established a transgenic mouse model (AR3Tg) with targeted expression of the constitutively active and androgen-independent AR splice variant AR3 (a.k.a. AR-V7) in prostate epithelium. We found that overexpression of AR3 modulates expression of a number of tumor-promoting autocrine/paracrine growth factors (including Tgfβ2 and Igf1) and expands prostatic progenitor cell population, leading to development of prostatic intraepithelial neoplasia. In addition, we showed that some epithelial-mesenchymal transition-associated genes are up-regulated in AR3Tg prostates, suggesting that AR3 may antagonize AR activity and halt the differentiation process driven by AR and androgen. This notion is supported by our observations that the number of Ck5+/Ck8+ intermediate cells is increased in AR3Tg prostates after castration, and expression of AR3 transgene in these intermediate cells compromises prostate epithelium regeneration upon androgen replacement. Our results demonstrate that AR3 is a driver of prostate cancer, at least in part, through modulating multiple tumor-promoting autocrine/paracrine factors.
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Tribian, L. S., M. Lennartz, N. C. Blessin, S. Kind, F. Viehweger, A. Menz, E. Burandt i in. "Diagnostic role and prognostic impact of PSAP immunohistochemistry: A tissue microarray study on 31,358 cancer tissues from 127 different tumor types". American Journal of Clinical Pathology 160, Supplement_1 (1.11.2023): S47—S48. http://dx.doi.org/10.1093/ajcp/aqad150.107.
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Abstract Introduction/Objective Prostatic specific acid phosphatase (PSAP) protein is produced in prostate epithelial cells and it is used as an immunohistochemical marker for prostate cancer. However, studies have reported PSAP expression to occur in various other tumor entities as well. Methods/Case Report Prostatic specific acid phosphatase (PSAP) protein is produced in prostate epithelial cells and it is used as an immunohistochemical marker for prostate cancer. However, studies have reported PSAP expression to occur in various other tumor entities as well. Results (if a Case Study enter NA) In prostate cancer, PSAP staining was seen in 100% of Gleason 3 + 3, 95.5% Gleason 4 + 4, 93.8% recurrent prostate cancer under androgen deprivation therapy, 91.0% Gleason 5 + 5 and 31.2% small cell neuroendocrine prostate cancer. Reduced PSAP staining was strongly linked to high pT stage, high Gleason grade, lymph node metastasis, early PSA-recurrence (p<0.0001 each),high androgen receptor expression and TMPRSS2:ERG fusions. In multivariate analyses, low PSAP expression was able to predict PSA recurrence independent of pre- and postoperative prognostic markers in ERG negative cancers. In extra-prostatic cancers, PSAP immunostaining was only seen in 3 of 94 (3.2%) neuroendocrine tumors of the pancreas and in 1 of 129 (0.8%) diffuse type gastric adenocarcinomas. Conclusion A positive PSAP immunostaining is highly specific for prostate cancer and reduced PSAP expression is associated with an aggressive prostate cancer phenotype. The independent association of reduced PSAP expression with poor prognosis in ERG negative prostate cancer makes PSAP measurement a candidate marker for prognostic multiparameter panels for prostate cancer.
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Mehta, Pritesh, Michela Antonelli, Saurabh Singh, Natalia Grondecka, Edward W. Johnston, Hashim U. Ahmed, Mark Emberton, Shonit Punwani i Sébastien Ourselin. "AutoProstate: Towards Automated Reporting of Prostate MRI for Prostate Cancer Assessment Using Deep Learning". Cancers 13, nr 23 (6.12.2021): 6138. http://dx.doi.org/10.3390/cancers13236138.
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Multiparametric magnetic resonance imaging (mpMRI) of the prostate is used by radiologists to identify, score, and stage abnormalities that may correspond to clinically significant prostate cancer (CSPCa). Automatic assessment of prostate mpMRI using artificial intelligence algorithms may facilitate a reduction in missed cancers and unnecessary biopsies, an increase in inter-observer agreement between radiologists, and an improvement in reporting quality. In this work, we introduce AutoProstate, a deep learning-powered framework for automatic MRI-based prostate cancer assessment. AutoProstate comprises of three modules: Zone-Segmenter, CSPCa-Segmenter, and Report-Generator. Zone-Segmenter segments the prostatic zones on T2-weighted imaging, CSPCa-Segmenter detects and segments CSPCa lesions using biparametric MRI, and Report-Generator generates an automatic web-based report containing four sections: Patient Details, Prostate Size and PSA Density, Clinically Significant Lesion Candidates, and Findings Summary. In our experiment, AutoProstate was trained using the publicly available PROSTATEx dataset, and externally validated using the PICTURE dataset. Moreover, the performance of AutoProstate was compared to the performance of an experienced radiologist who prospectively read PICTURE dataset cases. In comparison to the radiologist, AutoProstate showed statistically significant improvements in prostate volume and prostate-specific antigen density estimation. Furthermore, AutoProstate matched the CSPCa lesion detection sensitivity of the radiologist, which is paramount, but produced more false positive detections.
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Sanjay Kalra, Nitin Kapoor i Saurabh Arora. "Diabetes and the prostate". Journal of the Pakistan Medical Association 73, nr 12 (28.11.2023): 2491–92. http://dx.doi.org/10.47391/jpma.23-101.
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Here we discuss the interactions between prostatic health and diabetes. Diabetes may be associated with changes in prostatic anatomy, physiology, clinical morbidity, and clinical outcomes. Certain glucose-lowering drugs may impact prostatic health, and some prostato-tropic medications can influence glycaemic control. One should be vigilant for symptoms and signs of prostate health in diabetes. Keywords: benign prostatic hyperplasia, erectile dysfunction, male gonad, male reproductive health, metformin, prostatic cancer, SGLT2i.
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Basavaraj, Dr Rashmi G. S., i Dr Ravikumar Malladad. "Association of serum prostate-specific antigen with Complete Blood Counts in patients with prostatic cancer". Tropical Journal of Pathology and Microbiology 7, nr 4 (31.08.2021): 162–69. http://dx.doi.org/10.17511/jopm.2021.i04.02.
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Background: Prostate cancer is the second most common cancer and one of the most leadingcauses of death in men worldwide. The prostate-specific antigen (PSA) as a screening methodshowed that there has been a slight decrease in prostate cancer mortality. Effective biomarkers inscreening and diagnosis would be beneficial for avoiding unnecessary operations. The predictive andprognostic value of complete blood count (CBC) has been manifested by recent studies. We aimed todetermine the association of serum PSA with Complete blood counts in patients with prostate cancer.Method: The present study included 100 subjects, 50 patients diagnosed with new prostate cancerand 50 patients with prostate cancer. All the was undertaken in the central diagnostic laboratory atVIMS and RC. Blood samples were collected from all the subjects after taken permission from theinstitutional ethics committee and consent form. The haemoglobin, RBCs, MCV, MCHC, RDW will beanalysed by using laboratory standard methods (Beckman coulter LH-780) and The serum PSAlevels are estimated by commercially available kits based on enzyme-linked immunosorbent assay(ELISA). Results: In the present study found significantly elevated levels of a prostate specificantigen in both groups of prostatic cancer patients. The reduced levels of hemoglobin, red bloodcells, platelets, neutrophils were observed in prostatic cancer patients when compared to newlydiagnosed prostate cancer patients. The PSA levels were negatively correlated with total bloodcounts. Conclusion: This study suggests that the elevated levels of prostate specific antigen wereuseful for diagnosis and prognosis of prostatic cancers, along with the monitoring of complete bloodcount may be useful for the treatment of patients with prostatic cancers.
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Pascal, Laura E., Khalid Z. Masoodi, June Liu, Xiaonan Qiu, Qiong Song, Yujuan Wang, Yachen Zang i in. "Conditional deletion of ELL2 induces murine prostate intraepithelial neoplasia". Journal of Endocrinology 235, nr 2 (listopad 2017): 123–36. http://dx.doi.org/10.1530/joe-17-0112.
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Elongation factor, RNA polymerase II, 2 (ELL2) is an RNA Pol II elongation factor with functional properties similar to ELL that can interact with the prostate tumor suppressor EAF2. In the prostate, ELL2 is an androgen response gene that is upregulated in benign prostatic hyperplasia (BPH). We recently showed that ELL2 loss could enhance prostate cancer cell proliferation and migration, and that ELL2 gene expression was downregulated in high Gleason score prostate cancer specimens. Here, prostate-specific deletion of ELL2 in a mouse model revealed a potential role for ELL2 as a prostate tumor suppressor in vivo. Ell2-knockout mice exhibited prostatic defects including increased epithelial proliferation, vascularity and PIN lesions similar to the previously determined prostate phenotype in Eaf2-knockout mice. Microarray analysis of prostates from Ell2-knockout and wild-type mice on a C57BL/6J background at age 3 months and qPCR validation at 17 months of age revealed a number of differentially expressed genes associated with proliferation, cellular motility and epithelial and neural differentiation. OncoPrint analysis identified combined downregulation or deletion in prostate adenocarcinoma cases from the Cancer Genome Atlas (TCGA) data portal. These results suggest that ELL2 and its pathway genes likely play an important role in the development and progression of prostate cancer.
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Iguchi, Taro, Ching Wang, Tatsuya Nakatani i Gabriel Haas. "WS1-3-6 Is Oxidative Stress Associated with Prostate Cancer Risk?(Prostate Cancer)". Japanese Journal of Urology 99, nr 2 (2008): 149. http://dx.doi.org/10.5980/jpnjurol.99.149_2.
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Song, Liankun, Vyvyan Nguyen, Shan Xu, Jana Yamak, Kia Arabzadehkaffash, Ali Fazelpour, Merci Mino, Matthew Tippin, Shuang Meng i Xiaolin Zi. "Abstract 1: Transcriptional profiling of prostatic Skp2 knock-in mouse model and development of the associated prostate organoids for testing Skp2 targeting agents". Cancer Research 82, nr 12_Supplement (15.06.2022): 1. http://dx.doi.org/10.1158/1538-7445.am2022-1.
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Abstract S-phase kinase associated protein 2 (Skp2) is a promising drug target as studies have demonstrated that Skp2 is required for spontaneous tumor development that occurs in the retinoblastoma protein (pRb), Pten, or p53 deficient mice. We, therefore, aim to establish CRISPR human Skp2 (hSkp2) knock-in in the prostates of mice to study the molecular profiling features in prostate carcinogenesis. Prostate weights increased in transgenic mice and overexpression of hSkp2 induced prostatic lesions including hyperplasia, mouse prostate intraepithelial neoplasia (mPIN), and carcinoma, which suggested the initial role of hSkp2 in early prostate carcinogenesis. RNAseq results revealed Myl3 and Ctgf as the top down-expressed and up-expressed genes respectively in hSkp2 mice prostates. Gene set enrichment analysis (GSEA) demonstrated the significant upregulations of ribosome and proteasome pathways which had similar alterations in the human prostate cancer dataset with Skp2 overexpression, suggesting the potential role of ribosome biogenesis in prostate tumorigenesis and for drug development. In addition, Skp2 organoids derived from transgenic mice prostates were being developed for convenient and efficient screening of specific Skp2 inhibitors. Flavokawain A (FKA) and Skp2 inhibitor C1 both selectively decreased the viability and altered the morphologies of hSkp2 organoids, meanwhile FKA exhibited less toxicity on wild-type organoids. Citation Format: Liankun Song, Vyvyan Nguyen, Shan Xu, Jana Yamak, Kia Arabzadehkaffash, Ali Fazelpour, Merci Mino, Matthew Tippin, Shuang Meng, Xiaolin Zi. Transcriptional profiling of prostatic Skp2 knock-in mouse model and development of the associated prostate organoids for testing Skp2 targeting agents [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2022; 2022 Apr 8-13. Philadelphia (PA): AACR; Cancer Res 2022;82(12_Suppl):Abstract nr 1.
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Parnes, Howard L., Ian M. Thompson i Leslie G. Ford. "Prevention of Hormone-Related Cancers: Prostate Cancer". Journal of Clinical Oncology 23, nr 2 (10.01.2005): 368–77. http://dx.doi.org/10.1200/jco.2005.08.027.
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Androgens are known to play an important role in normal prostate development, benign prostatic hyperplasia, established prostate cancer, and in prostate carcinogenesis. However, despite convincing experimental and clinical evidence, the epidemiologic data correlating sex steroid levels with disease risk is inconsistent. More recent work has focused on studies of polymorphisms in germ-line DNA in an effort to develop polygenic models of prostate cancer susceptibility and prognosis. Such models have the potential to aid in the selection of men for specific chemopreventive interventions and to help determine which men with localized prostate cancer are most likely to benefit from aggressive therapy. In this review, we will provide a brief summary of androgen metabolic pathways followed by an assessment of the epidemiology literature addressing the relationship between androgens and prostate cancer. Finally, we will address the two major questions that have arisen in response to the recently published results from the Prostate Cancer Prevention Trial: Who are the best candidates for finasteride chemoprevention, and what are the clinical implications of the high prevalence of prostate cancer that was detected in men with prostate-specific antigen levels in the so-called “normal” range?
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Yucel, Cem, i Salih Budak. "Association between large prostate calculi and prostate cancer". Archivio Italiano di Urologia e Andrologia 90, nr 3 (30.09.2018): 181–83. http://dx.doi.org/10.4081/aiua.2018.3.181.
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Objective: We investigated the relationship between large prostate calculi and prostate cancer (PCa) risk. Materials and methods: The medical records of 340 patients who received a prostate biopsy at our institution between January 2015 and August 2016 were reviewed retrospectively. Of the patients, 82 had large prostatic calculi visualised by transrectal ultrasonography and 88 did not or had scarce prostatic calculi. We divided these patients into two groups: patients with large prostatic calculi (group 1) and patients without prostatic calculi (group 2). These groups were compared according to age, total prostate specific antigen (PSA) level, prostate volume, and final pathological diagnosis.Results: The mean age of all patients was 61.4 ± 6.2 years, the mean total PSA was 12.3 ± 17.4 ng/mL, the mean prostate volume was 41.7 ± 17.6 mL, and the overall cancer detection rate was 31.5%. The cancer detection rates were 41.3% and 22.6% in groups 1 and 2, respectively (p = 0.018). No significant differences in mean age, mean total PSA, or mean prostate volume were observed between the groups. Conclusions: In the present study, large prostatic calculi were associated with PCa. However, more study is needed to examine the relationship between large prostatic calculi and PCa in more detail. The effects of particularly large prostate calculi in the development of PCa will be a necessary focus of future research.
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Okidi, Ronald, Cyprian Opira, Vanusa Da Consolação Sambo, Caroline Achola i David Martin Ogwang. "Prostate hyperplasia in St Mary’s Hospital Lacor: utility of prostate specific antigen in screening for prostate malignancy". African Health Sciences 20, nr 3 (7.10.2020): 1259–63. http://dx.doi.org/10.4314/ahs.v20i3.30.
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Introduction: Prostate cancer is the second commonest cancer in men worldwide. At present, every patient with lower urinary tract symptoms (LUTS) in St. Mary’s Hospital Lacor is undergoing prostate biopsy regardless of the prostate specific antigen (PSA) level. We sought to determine the association between PSA and malignant prostate histology.
Methods: This was a retrospective study. Data on age, PSA, prostate volume and prostate histology reported between Jan 2012 and Dec 2019 were retrieved from St. Mary’s Hospital Lacor archive and analyzed using STATA SE/13.0.
Results: Records of 97 patients with LUTS was analyzed. The median (range) age of the patients was 71 (43-100) years. Median (range) of prostate volume was 91.8 (8.0-360.0) cc. Overall, PSA ranged from 0.21 to 399.2 ng/ml. Prostate histology showed 3.1% acinar adenocarcinoma, 24.7% adenocarcinoma and 72.2% benign prostatic hyperplasia. The median PSA amongst pa- tients with malignant and non-malignant prostates were 15.8 ng/ml and 6.07 ng/ml respectively. Serum PSA level was signifi- cantly higher in patients with malignant prostate histology (Difference of mean= 9.7; p=0.001).
Conclusion: Patients with LUTS and PSA levels of 15ng/ml or more were more likely to have malignant prostate histology.
Keywords: Prostate specific antigen; Prostate cancer.
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Bronte, Vincenzo, Tihana Kasic, Giorgia Gri, Keti Gallana, Giovanna Borsellino, Ilaria Marigo, Luca Battistini i in. "Boosting antitumor responses of T lymphocytes infiltrating human prostate cancers". Journal of Experimental Medicine 201, nr 8 (11.04.2005): 1257–68. http://dx.doi.org/10.1084/jem.20042028.
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Immunotherapy may provide valid alternative therapy for patients with hormone-refractory metastatic prostate cancer. However, if the tumor environment exerts a suppressive action on antigen-specific tumor-infiltrating lymphocytes (TIL), immunotherapy will achieve little, if any, success. In this study, we analyzed the modulation of TIL responses by the tumor environment using collagen gel matrix–supported organ cultures of human prostate carcinomas. Our results indicate that human prostatic adenocarcinomas are infiltrated by terminally differentiated cytotoxic T lymphocytes that are, however, in an unresponsive status. We demonstrate the presence of high levels of nitrotyrosines in prostatic TIL, suggesting a local production of peroxynitrites. By inhibiting the activity of arginase and nitric oxide synthase, key enzymes of L-arginine metabolism that are highly expressed in malignant but not in normal prostates, reduced tyrosine nitration and restoration of TIL responsiveness to tumor were achieved. The metabolic control exerted by the tumor on TIL function was confirmed in a transgenic mouse prostate model, which exhibits similarities with human prostate cancer. These results identify a novel and dominant mechanism by which cancers induce immunosuppression in situ and suggest novel strategies for tumor immunotherapy.
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Corrêa, Lívia L., Giovanna A. Balarini Lima, Helena B. de Melo Paiva, Cíntia M. dos Santos Silva, Suzana A. Cavallieri, Luiz Carlos D. de Miranda i Mônica R. Gadelha. "Prostate cancer and acromegaly". Arquivos Brasileiros de Endocrinologia & Metabologia 53, nr 8 (listopad 2009): 963–68. http://dx.doi.org/10.1590/s0004-27302009000800009.
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Acromegalic patients have an increased prevalence of prostatic disorders compared to age-matched healthy subjects. Increased size of the whole prostate or the transitional zone, together with an elevated incidence of other structural changes, such as nodules, cysts, and calcifications, have been reported. Prostate enlargement in young acromegalic patients with low testosterone levels due to central hypogonadism supports the hypothesis that chronic GH and IGF-I excess cause prostate hyperplasia. The relationship between prostatic carcinoma and acromegaly is, until now, only circumstantial. Long-term follow-up of these patients is necessary since epidemiologic studies showed association between serum IGF-I levels in the upper normal limit and prostate cancer in the general population. This review approaches prostate diseases in patients with acromegaly.
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Viehweger, F., M. Lennartz, N. C. Blessin, D. Dum, E. Burandt, G. Sauter, R. Simon i in. "Prostein expression in human tumors: A tissue microarray study on 19,202 tumors". American Journal of Clinical Pathology 160, Supplement_1 (1.11.2023): S45. http://dx.doi.org/10.1093/ajcp/aqad150.101.
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Abstract Introduction/Objective Prostein (P501S), also termed solute carrier family 45 member 3 (SLC45A3) is an androgen regulated protein which is preferentially expressed in prostate epithelial cells. Because of its frequent expression in prostate cancer, prostein was suggested a diagnostic prostate cancer marker. Methods/Case Report In order to comprehensively assess the diagnostic utility of prostein immunohistochemistry, a tissue microarray containing 19,202 samples from 152 different tumor types and subtypes as well as 608 samples of 76 different normal tissue types was analyzed by immunohistochemistry. Results (if a Case Study enter NA) Prostein immunostaining was typically cytoplasmic, granular and perinuclear and predominated in prostate cancer. Prostein positivity was seen in 96.7% of 419 prostate cancers including 78.3% with a strong staining. In 12,233 extra-prostatic tumors, prostein positivity was observed in 9.8% of cases but only 0.4% had a strong staining. Extra-prostatic prostein positive tumors were 50 different tumor categories, 12 of which included at least one strongly positive case. Extra-prostatic tumors with highest rates of prostein positivity included salivary gland tumors (7.6%-44.4%), neuroendocrine neoplasms (15.8%-44.4%), adenocarcinomas of the gastrointestinal tract (7.3%-14.8%), biliopancreatic adenocarcinomas (3.6%-38.7%), hepatocellular carcinomas (8.1%), and adenocarcinomas of other organs (up to 21%). Conclusion In summary, our data provide a comprehensive overview on prostein expression in human cancers. Prostein is a highly sensitive prostate cancer marker occurring in >96% of prostate cancers. Because prostein can also be expressed in various other tumor entities, labeling of a tumor mass as a prostate cancer should not be based on prostein positivity alone.
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Rita, Roza, Delyuzar i Lidya Imelda Laksmi. "Correlation between AgNOR Expression and Ki-67 Expression with Prostate Adenocarcinoma Grading". Majalah Patologi Indonesia 29, nr 3 (7.09.2020): 145–50. http://dx.doi.org/10.55816/mpi.v29i3.446.
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BackgroundProstate cancer is the second most common cancer and fifth most common cancer cause of death in males. Tissue biopsy is a goldstandard examination to diagnose prostate cancer. One of the hallmarks of cancer is increased activity of cell proliferation. Thisactivity can be detected with Ki-67 and AgNOR (Argyrophilic nucleolar organizing region). The aim of this study is to analyzedcorrelation between AgNOR and Ki-67 expression in grading of prostated adenocarcinoma.MethodsThis analytic cross-sectional study was held in Laboratory of Anatomical Pathology of Medical Faculty of USU/ RSUP H. AdamMalik Medan. Thirty paraffin blocks diagnosed with prostate adenocarcinoma were stained with H&E and p63 immunohistochemistrythen evaluated based on Gleason’s histopathological grading and stained with Agnor and Ki 67.ResultsAgNOR expression yang diperoleh pada grading adenokarsinoma prostat group 1, 2, 3, 4, dan 5 berturut-turut adalah 43; 32,40(±14,54); 64,29 (±28,2); 59,5 (±28,32); 69,22 (±29,26). Ekspresi Ki-67 pada setiap grading adenokarsinoma prostat group 1, 2, 3, 4,dan 5 secara berurutan adalah 43; 32,4 (±14,53); 64,29 (±28,2), 59,5 (±28,31); 69,22 (±29,26). Statistical analyses showed thatthere was no significantly correlation between grading of prostate adenocarcinoma and AgNOR expression (p=0.065), and Ki-67expression (p=0.18). Nevertheless, a significantly correlation between KI-67 expression and grading of prostate adenocarcinomawas found (p=0.34).ConclusionKi-67 could be used as prognostic indicator for prostate adenocarcinoma.
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Rahman, Md Tahminur, i ATM Mowladad Chowdhury. "Prostate Cancer". Anwer Khan Modern Medical College Journal 7, nr 2 (18.02.2017): 36–44. http://dx.doi.org/10.3329/akmmcj.v7i2.31644.
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Prostate cancer is the number one cancer by incidence in males of increasing age & second by mortality throughout the world. Many known etiological factors are associated with increased risk of prostatic carcinoma including male hormone & its active metabolites, genetic predisposition (BRCA2, inherited polymorphism of some transcription factors), racial difference, environmental factors, food habits etc, Recently an association of importance has been given to molecular level changes; inflammatory cytokines, trace elements like zinc with prostate cancer. Diagnostic modalities & treatment facilities are important for better management & giving improved quality of life to the patients. The present review article highlights some of these findings on prostate cancer namely genetic factors, Highfatty diet, Hormone, medication, sexual activity, inflammatory cytokines, trace element zinc, PSA. These will lead to in hand better understanding of the pathophysiology of prostate cancer.Anwer Khan Modern Medical College Journal Vol. 7, No. 2: Jul 2016, P 36-44
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Das, Dweepanita, Kirk Wojno i Michael J. Imperiale. "BK Virus as a Cofactor in the Etiology of Prostate Cancer in Its Early Stages". Journal of Virology 82, nr 6 (26.12.2007): 2705–14. http://dx.doi.org/10.1128/jvi.02461-07.
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ABSTRACT Prostate cancer has been projected to cause almost 10% of all male cancer deaths in the United States in 2007. The incidence of mutations in the tumor suppressor genes Rb1 and p53, especially in the early stages of the disease, is low compared to those for other cancers. This has led to the hypothesis that a human virus such as BK virus (BKV), which establishes a persistent subclinical infection in the urinary tract and encodes oncoproteins that interfere with these tumor suppressor pathways, is involved. Previously, we detected BKV DNA in the epithelial cells of benign and proliferative inflammatory atrophy ducts of cancerous prostate specimens. In the present report, we demonstrate that BKV is present at a much lower frequency in noncancerous prostates. Additionally, in normal prostates, T-antigen (TAg) expression is observed only in specimens harboring proliferative inflammatory atrophy and prostatic intraepithelial neoplasia. We further demonstrate that the p53 gene from atrophic cells expressing TAg is wild type, whereas tumor cells expressing detectable nuclear p53 contain a mix of wild-type and mutant p53 genes, suggesting that TAg may inactivate p53 in the atrophic cells. Our results point toward a role for BKV in early prostate cancer progression.
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Zhang, Manqi, Yasemin Ceyhan, Shenglin Mei, Taghreed Hirz, David B. Sykes i Irina U. Agoulnik. "Regulation of EZH2 Expression by INPP4B in Normal Prostate and Primary Prostate Cancer". Cancers 15, nr 22 (15.11.2023): 5418. http://dx.doi.org/10.3390/cancers15225418.
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The phosphatases INPP4B and PTEN are tumor suppressors that are lost in nearly half of advanced metastatic cancers. The loss of PTEN in prostate epithelium initially leads to an upregulation of several tumor suppressors that slow the progression of prostate cancer in mouse models. We tested whether the loss of INPP4B elicits a similar compensatory response in prostate tissue and whether this response is distinct from the one caused by the loss of PTEN. Knockdown of INPP4B but not PTEN in human prostate cancer cell lines caused a decrease in EZH2 expression. In Inpp4b−/− mouse prostate epithelium, EZH2 levels were decreased, as were methylation levels of histone H3. In contrast, Ezh2 levels were increased in the prostates of Pten−/− male mice. Contrary to PTEN, there was a positive correlation between INPP4B and EZH2 expression in normal human prostates and early-stage prostate tumors. Analysis of single-cell transcriptomic data demonstrated that a subset of EZH2-positive cells expresses INPP4B or PTEN, but rarely both, consistent with their opposing correlation with EZH2 expression. Unlike PTEN, INPP4B did not affect the levels of SMAD4 protein expression or Pml mRNA expression. Like PTEN, p53 protein expression and phosphorylation of Akt in Inpp4b−/− murine prostates were elevated. Taken together, the loss of INPP4B in the prostate leads to overlapping and distinct changes in tumor suppressor and oncogenic downstream signaling.
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Hall, M., D. D. Mickey, A. S. Wenger i L. M. Silverman. "Adenylate kinase: an oncodevelopmental marker in an animal model for human prostatic cancer." Clinical Chemistry 31, nr 10 (1.10.1985): 1689–91. http://dx.doi.org/10.1093/clinchem/31.10.1689.
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Abstract Data are presented demonstrating that adenylate kinase (AK; EC 2.7.4.3) is an oncodevelopmental enzyme in the prostate of Copenhagen rats. We selected the Dunning tumor (dorsal rat prostate) as a model system because it most nearly approximates the human pathology. Four sublines of the tumor (R3327-H, R3327-AT, MAT Lu, and MAT LyLu) were studied. The tumor sublines were maintained as solid tumors in syngeneic rats and as monolayers in tissue culture. AK activity appeared in conjunction with malignant transformation of the dorsal prostate. We also determined the normal developmental enzyme pattern: AK was present in prostates of newborns, but was undetectable in prostates of adults. However, AK increased after castration. Therefore, we propose AK as a potential oncofetal tumor marker in prostatic cancer.
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Yılmaz, Sercan, Mehmet Yılmaz, Serdar Yalcın, Engin Kaya, Eymen Gazel, Halil Cagrı Aybal, Hakan Özdemir, Mehmet Yorubulut, Ali Yusuf Oner i Lutfi Tunc. "Basic factors predicting prostate cancer in Prostate Imaging Reporting and Data System-3 lesions". Yeni Üroloji Dergisi 16, nr 16-2 (29.06.2021): 184–89. http://dx.doi.org/10.33719/yud.2021;16-2-850090.
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Objective: We aimed to investigate the role of the digital rectal examination, PSA density, regional location of the lesion and prostate size in predicting prostate cancer in Prostate Imaging and Data Reporting System (PI-RADS)-3 lesions. Material and Methods: A total of 236 patients with multiparametric MRI performed for clinical suspicion of prostate cancer and reported PI-RADS-3 enrolled between January 2016 and July 2019 in this retrospective study. The datas were extracted from the hospital’s electronic records, patient files and outpatient clinic records. Multiparametric MRI was performed patients to whom have elevated PSA level and/or suspicious digital rectal examination. Patients diagnosed with and without prostate cancer were compared in terms of age, PSA, PSA density, prostate size, pathological results, lesion localization and DRE findings. Results: One hundred thirty- independent predictor seven patients with an initial score of PI-RADS-3 were subjected to further analysis. Prostat cancer detection rate in overall and clinically significant prostate cancer detection rate was 26.2% and 4.3%, respectively. There was a significant difference regarding DRE findings (p=0.001) and PZ location of the lesion (p=0.005) between PCa and no PCa groups. Digital rectal examination (p=0.001) was an independent predictor of prostate cancer in multivariate logistic regression analysis. Conclusion: Digital rectal examination is a practical and important parameter in clarifying the suspicion of prostate cancer in PI-RADS-3 lesions. Keywords: prostatic neoplasms, digital rectal examination, multiparametric magnetic resonance imaging, image guided biopsy
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Kuriyama, Manabu. "Prostate-Specific Antigen in Prostate Cancer". International Journal of Biological Markers 1, nr 2 (maj 1986): 67–76. http://dx.doi.org/10.1177/172460088600100202.
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Prostate-specific antigen (PA) has been evaluated clinically as a tumor marker of prostate cancer with the use of enzyme immunoassay (EIA). For serodetection of prostate cancer, PA was assayed in a total of 1,109 sera. From mean ± 3 S.D. of normal controls, upper cut-off values in males were decided as 2.5 and 1.2 ng/ml in Americans and Japanese, respectively. Serum PA values in prostate cancer patients were positive in 78% of Americans and 62% of Japanese. However, in benign prostatic hypertrophy (BPH) cases, a high false positive rate of 41% was observed in Americans. Simultaneous assays of serum PA and PAP showed high sensitivity and specificity in the detection of prostate cancer. This antigen could be used, as well as PAP, for monitoring prostate cancer patients. Furthermore, serum PA levels prior to treatment may express to some degree the malignant potential of the cancer. These results suggest that PA may be useful as a tumor marker of prostate cancer.
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Nomani, Beenish Hussain, i Mohiuddin Alamgir. "Diagnostic Utility Of Various Biomarkers For Prostate Cancer: A Review". Journal of Bahria University Medical and Dental College 09, nr 02 (5.03.2019): 151–55. http://dx.doi.org/10.51985/jbumdc2019015.
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Prostate carcinoma is one of the most widespread occurring cancers in males and is the second most common cause of cancer related mortality in men around the world. The therapeutic success rate for prostate cancer can be greatly improved if the disease is detected at an early stage. Therefore, a successful therapy depends immensely on the clinical indicators (biomarkers) for early diagnosis and progression of the disease, as well as the prognosis after the clinical intervention. Despite of its limitations, prostate biopsy is the “gold standard” for diagnosis of prostatic carcinoma. Beyond the shadow of doubt, the advent of PSA level has marked a new era for the efficient screening of prostatic lesions, but PSA alone cannot be considered as an authentic tool for diagnosis. Therefore, the use of new imaging techniques and molecular markers are of great importance for an accurate diagnosis of prostate cancer. Recent advances in molecular techniques have provided new tools facilitating the discovery of new biomarkers for prostate cancer. The aim of this review is to examine the current status of prostate cancer biomarkers, with special focus the on their diagnostic utility and therefore determine a panel of two or three markers for the prompt diagnosis of prostatic carcinoma.
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Mackinnon, A. Craig, Benjamin C. Yan, Loren J. Joseph i Hikmat A. Al-Ahmadie. "Molecular Biology Underlying the Clinical Heterogeneity of Prostate Cancer: An Update". Archives of Pathology & Laboratory Medicine 133, nr 7 (1.07.2009): 1033–40. http://dx.doi.org/10.5858/133.7.1033.
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Abstract Context.—Recent studies have uncovered a number of possible mechanisms by which prostate cancers can become resistant to systemic androgen deprivation, most involving androgen-independent reactivation of the androgen receptor. Genome-wide expression analysis with microarrays has identified a wide array of genes that are differentially expressed in metastatic prostate cancers compared to primary nonrecurrent tumors. Recently, recurrent gene fusions between TMPRSS2 and ETS family genes have been identified and extensively studied for their role in prostatic carcinoma. Objective.—To review the recent developments in the molecular biology of prostate cancer, including those pertaining to the androgen receptor and the newly identified TMPRSS2-related translocations. Data Sources.—Literature review and personal experience. Conclusions.—Prostatic adenocarcinoma is a heterogeneous group of neoplasms with a broad spectrum of pathologic and molecular characteristics and clinical behaviors. Numerous mechanisms contribute to the development of resistance to androgen ablation therapy, resulting in ligand-independent reactivation of the androgen receptor, including amplification, mutation, phosphorylation, and activation of coreceptors. Multiple translocations of members of the ETS oncogene family are present in approximately half of clinically localized prostate cancers. TMPRSS2:ERG gene rearrangement appears to be an early event in prostate cancer and is not observed in benign or hyperplastic prostatic epithelium. Duplication of TMPRSS2:ERG appears to predict a worse prognosis. The relationship between TMPRSS2:ERG gene rearrangement and other morphologic and prognostic parameters of prostate cancer is still unclear.
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Mukendi, Alain Mwamba, Eunice Van Den Berg, Sugeshnee Pather i Rushen Siva Padayachee. "Metachronous or synchronous male breast and prostate cancers a duality to lookout for." F1000Research 7 (20.11.2018): 1825. http://dx.doi.org/10.12688/f1000research.16997.1.
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Introduction: Breast cancer is well known as the stereotypical women's cancer, and prostate cancer represents the well-known stereotypical male counterpart. While prostate cancer carries the potential to metastasize to the breast, the synchronous or metachronous co-occurrence of primary breast and primary prostate cancers is quite unusual. Prostate cancer in men of African descent may have its own behavior with regards to its relationship with male breast cancer. Case presentation: Case 1: A 64 year old male presented to Chris Hani Baragwanath Hospital (CHBAH) with a 2 years history of a painless left breast lump. A core biopsy was confirmed breast carcinoma. Tamoxifen was started but, due to disease progression, he underwent left modified radical mastectomy followed by chemotherapy. Prostate biopsy was done for raised Prostate Specific Antigen (PSA) and suspicious prostate on digital rectal examination. A prostatic adenocarcinoma was subsequently diagnosed with bone metastasis on bone scan. He was started on Androgen deprivation therapy and followed up every 3 months. Case 2: A 68 year old male presented to CHBAH with a 1 year history of a painless right breast lump. A core biopsy confirmed breast cancer. Tamoxifen was started, followed by right modified radical mastectomy and chemotherapy for disease progression. A raised PSA and suspicious prostate on digital rectal examination prompted a prostate biopsy revealing a prostatic adenocarcinoma. Bone scan was negative for metastasis. He is currently on 3 monthly Androgen deprivation therapy and awaiting radiation. Conclusion: This clinical practice article not only presents this exceptionally rare duality but highlights that both cancers can coexist either as sporadic conditions, or as a result of genetic mutations. Thus, we suggest that men with prostate cancer be screened clinically, biochemically and genetically for breast cancer and vice versa.
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Mukendi, Alain Mwamba, Eunice Van Den Berg, Sugeshnee Pather i Rushen Siva Padayachee. "Metachronous or synchronous male breast and prostate cancers a duality to lookout for." F1000Research 7 (26.02.2019): 1825. http://dx.doi.org/10.12688/f1000research.16997.2.
Pełny tekst źródłaStreszczenie:
Introduction: Breast cancer is well known as the stereotypical women's cancer, and prostate cancer represents the well-known stereotypical male counterpart. While prostate cancer carries the potential to metastasize to the breast, the synchronous or metachronous co-occurrence of primary breast and primary prostate cancers is quite unusual. Prostate cancer in men of African descent may have its own behaviour with regards to its relationship with male breast cancer. Case presentation: Case 1: A 64 year old male presented to Chris Hani Baragwanath Hospital (CHBAH) with a 2 years history of a painless left breast lump. A core biopsy was done and confirmed breast carcinoma. Tamoxifen was started but, due to disease progression, he underwent left modified radical mastectomy followed by chemotherapy. Prostate biopsy was done for raised Prostate Specific Antigen (PSA) and suspicious prostate on digital rectal examination. A prostatic adenocarcinoma was subsequently diagnosed with bone metastases on bone scan. He was started on Androgen deprivation therapy and followed up every 3 months. Case 2: A 68 year old male presented to CHBAH with a 1 year history of a painless right breast lump. A core biopsy confirmed breast cancer. Tamoxifen was started, followed by right modified radical mastectomy and chemotherapy for disease progression. A raised PSA and suspicious prostate on digital rectal examination prompted a prostate biopsy revealing a prostatic adenocarcinoma. Bone scan was negative for metastasis. He is currently on 3 monthly Androgen deprivation therapy and awaiting radiation. Conclusion: This clinical practice article not only presents this exceptionally rare duality but highlights that both cancers can coexist either as sporadic conditions, or as a result of genetic mutations. Thus, we suggest that men with prostate cancer be screened clinically, biochemically and genetically for breast cancer and vice versa.
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Rahman, Mohammad Mukhlesur, Muhammad Mahmud Alam, Mohammad Ohiduzzaman Khan, Mohammad Rezaul Karim i Md Sajid Hasan. "Frequency of Prostate Cancer Among the Prostatic Tissue Samples- Collected From Different Tertiary Level Hospital in Dhaka City". Bangladesh Journal of Urology 21, nr 2 (21.10.2020): 88–92. http://dx.doi.org/10.3329/bju.v21i2.49864.
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Background: Prostate cancer is the development of cancer in the prostate, a gland in the male reproductive system. The cancer cells may spread from the prostate to other area of the body, particularly the bones and lymph nodes. It may initially cause no symptoms. A disease known as benign prostatic hyperplasiamay produce similar symptoms.
Objective: To identify the frequency of prostate cancer in prostatic tissue submitted for histopathological examination in selected hospital of Dhaka City.
Method: This analytical observational study consists of review of 3914 histopathological reports of prostatic specimen examined in 13 selected tertiary level hospitals in Dhaka city. This study was carried out from January 2007 to December 2009 (three years). All data were compiled, analyzed and appropriate statistical tests were done to make inference.
Results: During the study period, among the 2914 histopathological specimen of prostatic tissue, 637(about 16%) cases were diagnosed as prostate cancer (including PIN), 3221 (about 82%) cases were benign prostatic hyperplasia, 53 (1 .35%) were chronic prostatitis and the remaining 3 cases were other rare disease e.g. lipid storage disease etc. Among the prostate cancer, most common was prostatic adenocarcinoma (about 95%); about 3% was Prostatic Intraepithelial Neoplasia (PIN), 1% squamous cell carcinoma arid I % are primary Transtiona1 cell carcinoma (TCC). Most of the patients diagnosed with prostate cancers are of advanced age - between 70 to 80 years (53.46%), and the second peak age is 60- 70 years (34.57 %). Of the prostate cancer cases 8.78% were well differentiated, 34.84% were moderately differentiated and 64.36% were poorly differentiated. The ratio between benign and malignant prostatic disease was about 5:1. Though all the prostatic diseases are common in elderly people, benign prostatic disease occurs more commonly: in younger patients than the prostate cancer.
Conclusion: From this study it is evident that the burden of prostate cancer is still low in our context. But the disease seems to be increasing in recent years mainly due to increasing number of aged population. So in near future, the burden of the disease will be increasing throughout the world including our country. Prostate cancer is a slow growing tumor. It has a very sensitive tumor marker (PSA) also. Early diagnosis and proper management certainly improves the prognosis of the disease. There is a screening program for early diagnosis of the disease though it is relatively a costly program. Screening should be considered in persons who have a strong family history of prostate cancer. Every urologist, health policy makers should be aware of the burden of the disease and appropriate planning, necessary manpower & skill development, resource allocation should be made to combat the situation efficiently.
Bangladesh Journal of Urology, Vol. 21, No. 2, July 2018 p.88-92
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Sadiq, Sarah, Abdul Khaliq Naveed, Palvasha Waheed, Fatima Qaiser i Shoaib N. Hashmi. "PROSTATE AND BREAST CANCER". Professional Medical Journal 25, nr 05 (10.05.2018): 703–8. http://dx.doi.org/10.29309/tpmj/2018.25.05.312.
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Background: CK2, a serine/threonine, protein kinase, targets over and above300 substrates including c-Myc. CK2 expression is elevated in human cancers includingbreast cancer and prostate cancer. c-Myc protooncogene expression is also up-regulated inthese cancers. Objectives: To evaluate the co expression and correlation of CK2 and c-Mycin prostate cancer as compared to their correlation in breast cancer. Study Design: Crosssectional analytical study. Setting: Army Medical College and AFIP, Duration: Two years.Methods: A retrospective study of immunohistochemical analysis, approved by Armed ForcesInstitute of Pathology Ethical Committee. Paraffin embedded tissues of diagnosed prostatecancer, 30 in number, 30 cases of Benign Prostatic Hypertrophy (BPH) and 30 cases of breastadenocarcinoma, were included in the study. We stained tissue sections for CK2 and c-Mycand measured staining intensity for each protein expression. Data analysis was done by SPSSversion 20. Pearson correlation coefficient was used for correlating the expression of bothproteins. P-value was calculated. Results: A strong correlation of CK2 with c-Myc was seen inprostate cancer tissue, in comparison to BPH. There was a very significant correlation presentbetween CK2 and c-Myc, especially in invasive cases of breast cancer. Conclusion: CK2 andc-Myc expressions are highly and significantly correlated in prostate cancer and breast cancerespecially in invasive cases. CK2 has influence over c-Myc and both can be used for forecastingthe cancer phenotype and aggression of disease.
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Tribian, Laura Sophie, Maximilian Lennartz, Doris Höflmayer, Noémi de Wispelaere, Sebastian Dwertmann Rico, Clara von Bargen, Simon Kind i in. "Diagnostic Role and Prognostic Impact of PSAP Immunohistochemistry: A Tissue Microarray Study on 31,358 Cancer Tissues". Diagnostics 13, nr 20 (18.10.2023): 3242. http://dx.doi.org/10.3390/diagnostics13203242.
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Prostate-specific acid phosphatase (PSAP) is a marker for prostate cancer. To assess the specificity and prognostic impact of PSAP, 14,137 samples from 127 different tumor (sub)types, 17,747 prostate cancers, and 76 different normal tissue types were analyzed via immunohistochemistry in a tissue microarray format. In normal tissues, PSAP staining was limited to the prostate epithelial cells. In prostate cancers, PSAP was seen in 100% of Gleason 3 + 3, 95.5% of Gleason 4 + 4, 93.8% of recurrent cancer under androgen deprivation therapy, 91.0% of Gleason 5 + 5, and 31.2% of small cell neuroendocrine cancer. In non-prostatic tumors, PSAP immunostaining was only found in 3.2% of pancreatic neuroendocrine tumors and in 0.8% of diffuse-type gastric adenocarcinomas. In prostate cancer, reduced PSAP staining was strongly linked to an advanced pT stage, a high classical and quantitative Gleason score, lymph node metastasis, high pre-operative PSA levels, early PSA recurrence (p < 0.0001 each), high androgen receptor expression, and TMPRSS2:ERG fusions. A low level of PSAP expression was linked to PSA recurrence independent of pre- and postoperative prognostic markers in ERG-negative cancers. Positive PSAP immunostaining is highly specific for prostate cancer. Reduced PSAP expression is associated with aggressive prostate cancers. These findings make PSAP a candidate marker for prognostic multiparameter panels in ERG-negative prostate cancers.
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Pan, Bin, Yunlin Ye, Haiping Liu, Jianli Zhen, Hongmei Zhou, Yutong Li, Lijun Qu, Youke Wu, Chuanrong Zeng i Weifeng Zhong. "URG11 Regulates Prostate Cancer Cell Proliferation, Migration, and Invasion". BioMed Research International 2018 (31.05.2018): 1–10. http://dx.doi.org/10.1155/2018/4060728.
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Upregulated gene 11 (URG11), a new gene upregulated by hepatitis B virus X protein, is involved in the development and progression of several tumors, including liver, stomach, lung, and colon cancers. However, the role of URG11 in prostate cancer remains yet to be elucidated. By determined expression in human prostate cancer tissues, URG11 was found significantly upregulated and positively correlated with the severity of prostate cancer, compared with that in benign prostatic hyperplasia tissues. Further, the mRNA and protein levels of URG11 were significantly upregulated in human prostate cancer cell lines (DU145, PC3, and LNCaP), compared with human prostate epithelial cell line (RWPE-1). Moreover, by the application of siRNA against URG11, the proliferation, migration, and invasion of prostate cancer cells were markedly inhibited. Genetic knockdown of URG11 also induced cell cycle arrest at G1/S phase, induced apoptosis, and decreased the expression level of β-catenin in prostate cancer cells. Overexpression of URG11 promoted the expression of β-catenin, the growth, the migration, and invasion ability of prostate cancer cells. Taken together, this study reveals that URG11 is critical for the proliferation, migration, and invasion in prostate cancer cells, providing the evidence of URG11 to be a novel potential therapeutic target of prostate cancer.
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Qureshi, Salman Manzoor, Muhammad Ali Sohail, Mujeeb ur Rehman Sahito i Aijaz Hussain Memon. "To determine the frequency of prostate malignancy in patients with clinically benign prostate". Professional Medical Journal 26, nr 08 (10.08.2019): 1289–95. http://dx.doi.org/10.29309/tpmj/2019.26.08.3871.
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To see the frequency of prostatic malignancy in patients presenting with clinically benign prostate. Study Design: Descriptive case series. Setting: Department of Urology at Peoples University of Medical and Health Sciences for Women / Hospital Nawabshah. Period: Fifteen Months, From October 2016 to December 2017. Materials and Methods: A total of 100 patients who presented with the clinically benign prostate in Urology OPD were enrolled. All concern data regarding Age, mode of presentation (lower urinary tract symptoms with IPSS score/ Acute retention of urine), comorbid, clinical examination findings, pre voided and post-void residual urine determination (on ultrasonography) were entered. The laboratory investigation includes complete blood count, urea, creatinine, random blood sugar (RBS), urine DR and CS, coagulation profile were performed before TURP.TURP performed under spinal anesthesia. After TURP the prostatic tissue chips were sent for histopathology as a routine. Data was analyzed through SPSS Version 20.0. Results: The average age of males was 71.38± 7.19 yrs. Most of the patients with (IPSS 20-35) BPH have lower urinary tract symptoms (both obstructive and irritative). DRE was done in all patients to estimate the size of the prostrate, it was varying from grade 1 enlarged n= 27(27%), grade 2 enlarged n= 36(36%), to grade 3 enlarged in n=37(37%). There were 3 (3%) cases reported to have prostate cancer, with findings confirmed by biopsy of TURP Specimen. There was no mortality seen in our study. The clinical presentation of patients, grades of enlargements on DRE and IPSS however, demonstrated no correlation. Conclusion: BPH is more common between 60-80yrs. When patient undergo TURP or open prostatectomy, every specimen should be sent for biopsy because prostate cancer is only confirmed by biopsy, so that prostate cancer is detected early Radiology & PSA values are supportive in their role but are not true diagnostic. Prostatic cancer is a significant morbid condition, so effective measures should be taken to detect prostatic cancer, so that patient can be properly treated according to the stage.
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Murgod, Priyanka Sangappa, Preeti Rajeev Doshi, Amit Ravindra Nisal i Ravindra Chandrashekar Nimbargi. "Histomorphological Mimickers of benign prostatic lesions with prostatic adenocarcinoma". Journal of Pathology of Nepal 11, nr 1 (20.03.2021): 1859–63. http://dx.doi.org/10.3126/jpn.v10i2.29009.
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Background: The prostate is a walnut-sized organ that surrounds the urethra. More than 99% of prostate cancers are prostatic adenocarcinoma. It is the second most commonly occurring cancer in men and the fourth most commonly occurring cancer in India and all over the world. Numerous lesion of the prostate are very similar to prostate cancer, hence awareness is very important. This study aimed to determine the histopathological features of prostate adenocarcinoma and its common mimickers.Materials and Methods: A retrospective study of histopathological features of radical prostatectomy and transurethral resection of the prostate specimens, sent to the department of pathology for a period of one year. A brief clinical history and serum prostate-specific antigen levels were noted.Results: The surgical specimens of 303 cases of prostatic diseases were studied. Benign prostatic hyperplasia was the most frequent diagnosis in 192 patients followed by Prostate adenocarcinoma seen in 80 patients. Prostatic intraepithelial neoplasia formed the predominant mimicker (5.9%), followed by basal cell hyperplasia (3.0%). Serum prostate-specific antigen was seen in the range of 1.73 - 100 ng/ml in the cases of adenocarcinoma. In the mimics, prostate-specific antigen was in the range of 1.2- 18ng/ml.Conclusions: Biopsy remains a gold standard for the diagnosis of adenocarcinoma and its mimickers. The lesions in this study were diagnosed on hematoxylin and eosin staining.
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Xuan, Qiang, Xiaoli Yang, Linjian Mo, Fengyu Huang, Youhong Pang, Min Qin, Zhiqiang Chen, Min He, Qi Wang i Zeng-Nan Mo. "Expression of the Serine Protease Kallikrein 7 and Its Inhibitor Antileukoprotease Is Decreased in Prostate Cancer". Archives of Pathology & Laboratory Medicine 132, nr 11 (1.11.2008): 1796–801. http://dx.doi.org/10.5858/132.11.1796.
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Abstract Context.—Kallikreins are a subgroup of serine proteases with diverse physiologic functions. It has been confirmed that kallikrein 7 (KLK7) is differentially expressed in ovarian and breast cancer. Antileukoprotease (ALP) has been shown to be a specific inhibitor of human kallikrein 7 (hK7). Antileukoprotease overexpression is commonly associated with aggressive, high-risk, or metastatic cancer originating from various organs. Objective.—To investigate the expression and potential role of hK7 and its inhibitor ALP in prostate cancer. Design.—The mRNA expression of KLK7 and ALP transcript in benign prostate epithelial cells and prostate cancers was evaluated by semiquantitative reverse transcription–polymerase chain reaction. We examined hK7 and ALP protein expression by immunohistochemistry in 20 normal prostate tissues, 50 benign prostatic hyperplasia tissues, and 103 prostate cancers. Western blot examination showed protein expression of hK7 and ALP in benign prostate epithelial cells and prostate cancer cell lines. Results.—Semiquantitative polymerase chain reaction examination revealed that the mRNA level of KLK7 and ALP was significantly decreased in prostate cancers compared with that in benign prostate epithelial cells (P < .001). Immunohistochemical expression of hK7 was observed in prostate epithelial cells, whereas little or no staining was observed in prostate cancer. Western blot analysis revealed that hK7 and ALP were decreased in malignant prostate epithelium. Conclusions.—Like hK7, ALP is down-regulated in prostate cancers, which begs the question of whether it remains an effective inhibitor of hK7 or whether it is discordant in time or space and is ineffective as an inhibitor of hK7. The function of KLK7 and ALP in prostate cancer should be further studied.
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Lara, Primo N., Andreas M. Heilmann, Julia A. Elvin, Mamta Parikh, Ralph de Vere White, Regina Gandour-Edwards, Christopher P. Evans i in. "TMPRSS2-ERG Fusions Unexpectedly Identified in Men Initially Diagnosed With Nonprostatic Malignancies". JCO Precision Oncology, nr 1 (listopad 2017): 1–6. http://dx.doi.org/10.1200/po.17.00065.
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Purpose TMPRSS2-ERG gene fusions are frequently found in prostate cancer and are pathognomonic for prostatic origin. In a series of cancer cases assayed with comprehensive genomic profiling (CGP) in the course of clinical care, we reviewed the frequency of TMPRSS2-ERG fusions in patient tumors of various histologic subtypes. Methods Frequency of TMPRSS2-ERG fusions was determined in CGPs from 64,263 cancer cases submitted to Foundation Medicine to assess genomic alterations suggesting benefit from targeted therapy. Genomic results are presented from an index case of prostate cancer that underwent evolution from adenocarcinoma to pure squamous cell carcinoma. Results TMPRSS2-ERG fusions were identified for 0.86% of male patients (250 of 29,030) and not found for female patients (none of 35,233). TMPRSS2-ERG fusions were detected in six tumors classified as squamous carcinoma, five of which were of unknown primary site. The index case is a patient with a large, left retrovesical mass diagnosed as squamous carcinoma by morphologic examination and a history of Gleason score 9 prostate cancer with prior prostatectomy and salvage radiation therapy. TMPRSS2-ERG was detected by genomic profiling in the squamous cell tumor, the primary adenocarcinoma of the prostate, and in a metachronous prostatic adenocarcinoma metastasis. On the basis of these results, the patient received androgen deprivation therapy. A phylogenetic tree demonstrating clonal and histopathologic evolution of prostate cancer in the index patient was constructed. Conclusion In this large CGP dataset, TMPRSS2-ERG fusion was seen in approximately 30% of prostate cancers regardless of histologic type; on occasion, the fusion was detected in advanced cancers not initially carrying a diagnosis of prostate carcinoma. CGP of advanced cancers in men may reveal prostatic origin by detection of the pathognomonic TMPRSS2-ERG fusion gene.
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Nash, GF, KJ Turner, T. Hickish, J. Smith, M. Chand i BJ Moran. "Interactions in the aetiology, presentation and management of synchronous and metachronous adenocarcinoma of the prostate and rectum". Annals of The Royal College of Surgeons of England 94, nr 7 (październik 2012): 456–62. http://dx.doi.org/10.1308/003588412x13373405384611.
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Adenocarcinoma of the prostate and rectum are common male pelvic cancers and may present synchronously or metachronously and, due to their anatomic proximity. The treatment of rectal or prostate cancer (in particular surgery and/or radiotherapy) may alter the presentation, incidence and management should a metachronous tumour develop. This review focuses on the interaction between prostatic and rectal cancer diagnosis and management. We have restricted the scope of this large topic to general considerations, management of rectal cancer after prostate cancer treatment and vice versa, management of synchronous disease and cancer follow-up issues.
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Elo, Teresa, Lan Yu, Eeva Valve, Sari Mäkelä i Pirkko Härkönen. "Deficiency of ERβ and prostate tumorigenesis in FGF8b transgenic mice". Endocrine-Related Cancer 21, nr 4 (17.06.2014): 677–90. http://dx.doi.org/10.1530/erc-13-0480.
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Estrogens contribute to the development and growth of the prostate and are implicated in prostate tumorigenesis. In their target tissues, estrogens mediate their effects via estrogen receptor α (ERα (ESR1)) and β (ERβ (ESR2)). Hyperplasia and decreased differentiation of epithelial cells in the prostate have been reported in ERβ knockout (BERKO) mice. Herein, we studied the effect of ERβ deficiency on prostate tumorigenesis by crossing BERKOFVB mice with prostate-targeted human fibroblast growth factor 8b transgenic (FGF8b-Tg) mice. Consistent with results described in our previous report, the prostates of 1-year-old FGF8b-Tg mice displayed stromal aberrations, prostatic intraepithelial neoplasia (mPIN) lesions, inflammation, and occasionally cancer. The prostates of BERKOFVB mice exhibited mild epithelial hypercellularity and inflammation. The prostate phenotypes of FGF8b-Tg-BERKOFVB mice closely resembled those of FGF8b-Tg mice. However, mucinous metaplasia, indicated by Goblet-like cells in the epithelium, was significantly more frequent in the prostates of FGF8b-Tg-BERKOFVB mice when compared with FGF8b-Tg mice. Furthermore, compared with FGF8b-Tg mice, there was a tendency for increased frequency of inflammation but milder hyperplasias in the prostate stroma of FGF8b-Tg-BERKOFVB mice. The expression levels of mRNAs for FGF8b-regulated genes including osteopontin (Spp1), connective tissue growth factor (Ctgf), fibroblast growth factor receptors (Fgfrs), and steroid hormone receptors and cytokines were similar in the prostates of FGF8b-Tg and FGF8b-Tg-BERKOFVB mice. Our results indicate that ERβ plays a role in the differentiation of the prostatic epithelium and, potentially, in the defensive mechanism required for protection against inflammation but do not support a direct tumor-suppressive function of ERβ in the prostate of FGF8b-Tg mice.
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Li, Lin, Siyuan Cheng i Xiuping Yu. "The expression of PKM1 and PKM2 in benign and cancerous prostatic tissues." Journal of Clinical Oncology 41, nr 16_suppl (1.06.2023): e17058-e17058. http://dx.doi.org/10.1200/jco.2023.41.16_suppl.e17058.
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e17058 Background: Prostate cancer (PCa) is the most diagnosed cancers in American men. After androgen deprivation therapy (ADT) fails, there is an increase in the aggressive neuroendocrine (NE) phenotype. Currently, there is no effective treatment for NE prostate cancer (NEPC). The metabolic reprogramming, one of the cancer hallmarks, regulates PCa progression and therapy resistance. However, the energy metabolism in NEPC has not been well studied yet. Pyruvate kinase (PK), catalyzing the final step of glycolysis, has PKM1, PKM2, PKL and PKR four isoforms. PKL and PKR are expressed in the liver and erythrocytes, respectively. Alternative splicing of PKM results in two isoforms, PKM1 and PKM2, which are expressed in most tissues. In prostate adenocarcinoma, loss of PKM1 promotes PCa progression whereas loss of PKM2 suppresses tumor growth. However, the expression pattern of PKM1 and PKM2 in NEPCa remains largely unknown. Methods: Immunofluorescence (IF), immunohistochemistry (IHC), Western blot and RT-qPCR were conducted to examine the expression of PKM1 and PKM2 in both murine and human prostatic tissues. The bioinformatics analysis was done using the publicly available RNA-Seq data obtained from the cBioportal, the Cancer Genome Atlas (TCGA), and the Cancer Cell Line Encyclopedia websites (CCLE). Results: TRAMP is a widely used PCa mouse model. TRAMP mice develop prostatic intraepithelial neoplasia (PIN) and the tumors progress into NEPC following castration. We found that PKM1 expression was detected in normal prostate but not in the PIN lesions. In the TRAMP NEPC tumors, PKM1 expression was detected in the NE areas but not in the adjacent PIN lesions. Compared with the adjacent PIN, NEPC cells displayed lower PKM2 expression. Further, we examined the expression of PKM1 and PKM2 in human prostatic tissues including benign prostatic hyperplasia (BPH), low-grade adenocarcinomas (AdPCa), high-grade AdPCa, and NEPC. We found that in BPH, basal epithelial cells express both PKM1 and PKM2. In PCa, PKM1 was robustly expressed in the stromal cells but its expression was absent in the cancer cells in majority of the specimens examined except a small number of samples where low level of PKM1 was detected in the cancer cells. However, PKM1 expression was detected in 9 out of 12 NEPC samples and colocalized with NE marker chromogranin A. This co-expression was also detected in the NE cells scattered on the prostate adenocarcinoma tissues. As for PKM2, its expression was detected in all the samples examined. However, different from previous report, PKM2 expression levels did not correlate with cancer grade in this cohort. Conclusions: PKM1 is expressed in the basal epithelial cells of benign prostates, a small subset of prostate adenocarcinomas, and 75% NEPC tumors. PKM2 is expressed throughout prostate development, in both benign and cancerous prostate. However, PKM2 expression does not correlate with tumor grade.
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Shen, Wenhao, Hang Dong, Haoran Tang, Yue Zhang, Shidong Jia i Yang Luo. "Diagnosis of prostate cancer using cell-free DNA methylation profiles from expressed prostatic secretions." Journal of Clinical Oncology 41, nr 6_suppl (20.02.2023): 389. http://dx.doi.org/10.1200/jco.2023.41.6_suppl.389.
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389 Background: Urinary and seminal cell-free DNA (cfDNA) have been recognized as promising biomarkers of prostate cancer. DNA methylation signal in tumor is increasingly used as tumor diagnosis and longitudinal monitoring indicator. However, the clinical utility of cfDNA from expressed prostatic secretions (EPS) remains unknown. Methods: The prospective study includes 50 prostate cancer (PC) patients and equivalent benign prostatic hyperplasia (BPH) patients, where EPS samples were collected after the prostatic massage of each patient. Cell-free DNA from EPS was extracted and treated by PredicineEPIC, a liquid biopsy comprehensive DNA methylation assay. The study developed integrated bioinformatic algorithms to profile the genome-wide epigenomic characteristics and investigate tumor-specific methylation patterns. Results: The initial exploratory cohort included 5 PC and 11 BPH cases. PredicineEPIC whole-genome DNA methylation of EPS identified over 300 differentially methylated regions (DMRs). Prostate cancers were distinguished from the BPH group by an unsupervised clustering method, suggesting that the identified DMRs embody the specific profiles of malignant tumors. Additionally, this study detected genome-wide copy number variation burden (CNB) in parallel. A risk model was built for cancer risk assessment based on methylation and CNB characteristics. Conclusions: This study demonstrated the feasibility of methylation profiling of cfDNA in EPS in prostate cancer. This non-invasive liquid biopsy approach could sensitively navigate prostate cancer from benign prostatic hyperplasia, suggesting future direction of methylation-based liquid biopsy in detecting prostate cancer.
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Moretti, M., A. Cichero, P. Pittaluga, M. Varaldo, Aldo V. Bono i Aldo V. Bono. "Prostate-specific Antigen and Prostate Cancer: How can We Improve Specificity and Predictive Power of the Marker?" Urologia Journal 59, nr 4 (sierpień 1992): 52–55. http://dx.doi.org/10.1177/039156039205900414.
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PSA is commonly used in diagnosing prostate cancer but it lacks both specificity and sensitivity; PSA values rise in benign prostatic affections and up to 30% prostate cancers show normal PSA values. Preliminary reports indicate that PSA DENSITY (PSAD), i.e. PSA/prostate-volume ratio, can improve specificity of PSA in diagnosing prostate cancer. We considered PSAD in 55 patients of 160 observed for prostatism: all of them underwent digital rectal examination, transrectal ultrasound and multiple biopsies of the gland. We found cancer in 19 patients (PSAD ranging from 0.17 to 1.77, with a mean value of 0.45), 26 prostatic hyperplasia (PSAD from 0.003 to 0.75, with a mean of 0.13), 6 dysplasia (PSAD from 0.07 to 0.30, with a mean of 0.19). In our experience PSAD > 0.17 or mean value > 0.45 indicate cancer in the absence of significant digital rectal examination and ultrasound findings or normal and borderline PSA values.
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Hammer, Steven J., Daniel W. Good, Paul Scanlan, Javier Palacio-Torralba, Simon Phipps, Grant D. Stewart, Will Shu, Yuhang Chen, S. Alan McNeill i Robert L. Reuben. "Quantitative mechanical assessment of the whole prostate gland ex vivo using dynamic instrumented palpation". Proceedings of the Institution of Mechanical Engineers, Part H: Journal of Engineering in Medicine 231, nr 12 (30.09.2017): 1081–100. http://dx.doi.org/10.1177/0954411917734257.
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An instrumented palpation sensor, designed for measuring the dynamic modulus of tissue in vivo, has been developed and trialled on ex vivo whole prostate glands. The sensor consists of a flexible membrane sensor/actuator with an embedded strain gauge and is actuated using a dynamically varying airflow at frequencies of 1 and 5 Hz. The device was calibrated using an indentation stiffness measurement rig and gelatine samples with a range of static modulus similar to that reported in the literature for prostate tissue. The glands were removed from patients with diagnosed prostate cancer scheduled for radical prostatectomy, and the stiffness was measured within 30 min of surgical removal. Each prostate was later examined histologically in a column immediately below each indentation point and graded into one of the four groups; normal, benign prostatic hyperplasia, cancerous and mixed cancer and benign prostatic hyperplasia. In total, 11 prostates were assessed using multiple point probing, and the complex modulus at 1 and 5 Hz was calculated on a point-by-point basis. The device yielded values of quasi-static modulus of 15 ± 0.5 kPa and dynamic modulus of 20 ± 0.5 kPa for whole prostates, and a sensitivity of up to 80% with slightly lower specificity was achieved on diagnosis of prostate cancer using a combination of mechanical measures. This assessment did not take into account some obvious factors such as edge effects, overlap and clinical significance of the cancer, all of which would improve performance. The device, as currently configured, is immediately deployable in vivo. A number of improvements are also identified which could improve the sensitivity and specificity in future embodiments of the probe.
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Zhang, JJ Haijing, Marlo Nicolas, Aimalie Hardaway, Kelsey Bohn, Daniel Hettel, Eric A. Klein i Nima Sharifi. "3βHSD1 immunohistochemistry and HSD3B1 genotype in prostate cancer." Journal of Clinical Oncology 37, nr 7_suppl (1.03.2019): 277. http://dx.doi.org/10.1200/jco.2019.37.7_suppl.277.
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277 Background: 3β-hydroxysteroid dehydrogenase (3βHSD1), encoded by HSD3B1, catalyzes intratumoral androgen synthesis from adrenal precursors. The HSD3B1(1245A>C) germline variant encodes a more stable enzyme that promotes increased DHT synthesis and more rapid clinical progression in men treated with androgen deprivation therapy (ADT). 3βHSD1 localization and expression in prostate tissue has not been rigorously characterized. We hypothesized that HSD3B1 homozygous variant genotype is associated with elevated 3βHSD1 immunoreactivity compared with wild-type (WT) genotype. Methods: In a pilot study, HSD3B1 genotypes were obtained from prostatectomy tissues of 30 patients with prostate cancer (10 WT, 10 heterozygous, and 10 homozygous variant). Following prostatectomy, tumor tissue with adjacent benign prostate was formalin-fixed and paraffin-embedded. Immunostaining for 3βHSD1 using a validated mouse monoclonal antibody was performed. Human placenta was used as a positive control. Immunostaining patterns and histology was qualitatively assessed by a GU pathologist. Immunoreactivity was quantitatively assessed using ImagePro7. Results: Qualitative IHC scoring localizes 3βHSD1 to epithelial cells in prostatic glands and urothelium, with faint muscle and stromal staining. 3βHSD1 was immunoreactive in 100% of prostates in both benign and malignant regions. When stratified by HSD3B1 genotype, the mean density/intensity was significantly greater for HSD3B1 homozygous variant prostate (670.10u) compared to heterozygous (174.69u) and WT (176.19u) (p=0.044). (Density/Intensity) per square micron demonstrated higher mean values for homozygous variant (35.79)> heterozygous (28.67) >WT (22.56) (p=0.52). Conclusions: These pilot data demonstrate differential tissue expression of 3βHSD1 according to HSD3B1 genotype: importantly, homozygous variant HSD3B1 (1245A>C) specimen showed the most robust 3βHSD1 expression compared to heterozygous and WT prostates. These results explore the potential for 3βHSD1 as a prostate biomarker to predict aggressive disease.