Bibliografías temáticas / Prostate cancer

Literatura académica sobre el tema "Prostate cancer"

Autor: Grafiati

Publicado: 4 de junio de 2021

Última modificación: 31 de julio de 2024

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Artículos de revistas sobre el tema "Prostate cancer"

Lorenzo, Guillermo, Thomas J. R. Hughes, Pablo Dominguez-Frojan, Alessandro Reali y 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, n.º 4 (7 de enero de 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 y 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, n.º 10 (23 de octubre de 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 y Susan E. Waltz. "Abstract 1243: RON receptor signaling enhances prostate cancer metastasis in Hi-Myc mice". Cancer Research 83, n.º 7_Supplement (4 de abril de 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 y Jelena Popadic-Gacesa. "Influence of hormonal therapy on the level of prostate specific antigen in patients with advanced prostatic cancer". Medical review 63, n.º 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 y Irina U. Agoulnik. "Abstract 815: Regulation of p53 by INPP4B and high fat diet in mouse prostate". Cancer Research 82, n.º 12_Supplement (15 de junio de 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, n.º 1 (3 de septiembre de 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. y J. L. MAGANDI. "PROSTATE CANCER". Professional Medical Journal 17, n.º 02 (10 de junio de 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 y Travis J. Jerde. "Expansion of prostate epithelial progenitor cells after inflammation of the mouse prostate". American Journal of Physiology-Renal Physiology 308, n.º 12 (15 de junio de 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 y Dov Kadmon. "Differential Expression of Nuclear Retinoid Receptors in Normal and Malignant Prostates". Journal of Clinical Oncology 18, n.º 1 (1 de enero de 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 y Hirotsugu Uemura. "WS1-3-5 A Prostate Cancer Model by the Prostate Specific Deletion of PTEN(Prostate Cancer)". Japanese Journal of Urology 99, n.º 2 (2008): 149. http://dx.doi.org/10.5980/jpnjurol.99.149_1.

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Tesis sobre el tema "Prostate cancer"

Holt, Jim. "Prostate Cancer". Digital Commons @ East Tennessee State University, 2019. https://dc.etsu.edu/etsu-works/6456.

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Birtle, A. J. "Prostate specific antigen negative prostate cancer". Thesis, University College London (University of London), 2005. http://discovery.ucl.ac.uk/1444634/.

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Prostate specific antigen (PSA) has been used in the diagnosis and monitoring of prostate cancer for almost 20 years. Most men who present with metastatic prostate cancer have markedly elevated serum levels of PSA. However, approximately 1% of cases have serum PSA levels that are much lower than the tumour burden would suggest - so-called "PSA-Negative" tumours. Their diagnosis may be delayed, and management compromised. Little is known about this patient group. The aim of this study was to improve the understanding and management of "PSA-negative" prostate cancer. The clinical history and tissue from 33 patients who presented with treatment-naive metastatic prostate cancer and a serum PSA < 10 ng/ml were included in this study, the largest series so far reported. Clinical and immunohistochemical features were defined and alternative biomarkers investigated. Potential mechanisms underlying PSA-negativity were explored using prostate cancer cell lines and archival tissue. From the clinical case notes review, patients presenting with low serum PSA and metastatic prostate cancer have a similar pattern of disease to men with high PSA prostate cancer. However, response duration to first line hormonal treatment and overall survival were shorter. Immunohistochemistry performed on archival prostatic tissue has shown that the majority of the cancers are positive for PSA, despite low serum levels. The extent of PSA immunostaining is patchy and could be missed on biopsy. PSMA and AR are expressed, however, and represent alternative diagnostic aids. The study indicates that PSMA and PAP should be explored as potential serum biomarkers in this patient group. The androgen receptor (AR) remains expressed in over 90 % of these cases and therefore defects in this pathway are unlikely to explain the low serum PSA levels. Neither loss of heterozygosity nor gene methylation of AR or PSA appear to be mechanisms underlying low serum PSA levels.

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Holt, Jim y Fereshteh Gerayli. "Prostate Cancer Screening". Digital Commons @ East Tennessee State University, 2019. https://dc.etsu.edu/etsu-works/6471.

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Whether to screen for prostate cancer in aging men is a topic that is fairly well researched, but recommendations are controversial, because the evidence supporting any recommendation is equivocal. The evidence clearly does not support routine screening of all average-risk men, but for men aged 55 to 69 years, either not routinely screening, or engaging each man in shared decision making for his individual preference on screening, is reasonable and consistent with the evidence. Many organizations, including the American Cancer Society, have not yet reassessed their guidelines, in response to the US Preventative Services Task Force revised guideline.

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Lexander, Helena. "Protein expression in prostate cancer /". Stockholm, 2006. http://diss.kib.ki.se/2006/91-7140-617-4/.

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Lundberg, Kajsa. "On immunotherapy against prostate cancer". Stockholm : Karolinska institutet, 2010. http://diss.kib.ki.se/2010/978-91-7409-805-1/.

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Wirth, Manfred P. y Michael Fröhner. "Adjuvant Hormonal Treatment for Prostate Cancer: The Bicalutamide Early Prostate Cancer Program". Saechsische Landesbibliothek- Staats- und Universitaetsbibliothek Dresden, 2014. http://nbn-resolving.de/urn:nbn:de:bsz:14-qucosa-133551.

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Adjuvant hormonal therapy has been demonstrated to be able to delay disease progression in nonmetastatic prostate cancer. To date, however, a favorable impact on survival has only been demonstrated in lymph-node-positive disease and in external-beam radiotherapy series with locally advanced and probably mainly micrometastatic tumors. The Bicalutamide Early Prostate Cancer Program is the largest study under way to define the role of adjuvant treatment in early prostate cancer and identify subgroups of patients likely to benefit from immediate hormonal therapy. At the time of the most recently published analysis, the risk of objective clinical progression was significantly reduced in the bicalutamide arm (hazards ratio 0.58, 95% confidence interval 0.51–0.66, p < 0.0001). However, further maturation of data is needed to see whether this difference will lead to a survival advantage
Dieser Beitrag ist mit Zustimmung des Rechteinhabers aufgrund einer (DFG-geförderten) Allianz- bzw. Nationallizenz frei zugänglich

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Wirth, Manfred P. y Michael Fröhner. "Adjuvant Hormonal Treatment for Prostate Cancer: The Bicalutamide Early Prostate Cancer Program". Karger, 2003. https://tud.qucosa.de/id/qucosa%3A27515.

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Adjuvant hormonal therapy has been demonstrated to be able to delay disease progression in nonmetastatic prostate cancer. To date, however, a favorable impact on survival has only been demonstrated in lymph-node-positive disease and in external-beam radiotherapy series with locally advanced and probably mainly micrometastatic tumors. The Bicalutamide Early Prostate Cancer Program is the largest study under way to define the role of adjuvant treatment in early prostate cancer and identify subgroups of patients likely to benefit from immediate hormonal therapy. At the time of the most recently published analysis, the risk of objective clinical progression was significantly reduced in the bicalutamide arm (hazards ratio 0.58, 95% confidence interval 0.51–0.66, p < 0.0001). However, further maturation of data is needed to see whether this difference will lead to a survival advantage.
Dieser Beitrag ist mit Zustimmung des Rechteinhabers aufgrund einer (DFG-geförderten) Allianz- bzw. Nationallizenz frei zugänglich.

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Storey, Dawn J. "Fatigue and prostate cancer". Thesis, University of Edinburgh, 2008. http://hdl.handle.net/1842/29383.

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Methods: Four studies were conducted: Study A, was a pilot study which examined fatigue over 3 months after different treatments for localised prostate cancer (radiotherapy, brachytherapy and androgen deprivation, n=45). Study B focussed on fatigue over 12 months after brachytherapy (n=51). Two cross sectional postal surveys explored fatigue in recurrence free prostate cancer survivors (Study C, n=443) and hormone controlled prostate cancer (Study D, n=198). Throughout, fatigue was assessed using the Brief Fatigue Inventory and a case definition of clinically significant fatigue (CSF) was also constructed and applied in Studies A and B. Results: Study A found CSF increased after treatment but returned to baseline 3 months after radiotherapy, whereas it appeared to be prolonged after brachytherapy. CSF was not associated with C reactive protein or interleukin-6. Study B found CSF increased between baseline and 1 month after brachytherapy (6 vs.29%, p=0.001) and was higher than the non-cancer comparison group (29 vs. 4% p=0.001). CSF returned towards baseline levels of 6 months. There were no baseline predictors of developing CSF. Study C found 29% of recurrence free prostate cancer survivors had fatigue after radiotherapy or radical prostatectomy (33 vs. 22% p=0.024) but it was not independently associated with treatment received after controlling for other factors 43% of men with hormone controlled prostate cancer had fatigue in Study D. Conclusions: Fatigue is an important symptom in men treated for prostate cancer but resolves within months of brachytherapy. Almost one third of recurrence free survivors have fatigue but it does not appear to be related to the type of treatment received. Fatigue is most prevalent in men with hormone controlled prostate cancer.

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Hendrickx, Wouter R. L. "Selenium and prostate cancer". Thesis, University of East Anglia, 2012. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.588614.

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Prostate cancer is the second most common diagnosed cancer and the third most common cause of death related to cancer among men in developed countries. Several epidemiological studies, prospective cohort studies and animal tumour models state an inverse relationship between selenium status and cancer incidence. Se- methylselenocysteine (SeMSC), present in garlic, onions, leeks and broccoli, has been shown to be the most effective anti-carcinogenic selenium form in animal models. The aim of the work presented in this thesis was to investigate the influence of selenium compounds (Se-methylselenocysteine and selenomethionine) on prostate cancer progression and metastasis using various human cell lines (LNCaP, OU145 and PC3). Standard 20 gel and SILAC (stable isotope labelling with amino acids in cell culture) proteomics were used, in combination with mass spectrometry, to identify selenium- responsive proteins. IMPOH2, GPI, EZR and RGS10 were validated by western blot, while POIA3 and 00X5 showed a selenium response under serum depleted conditions. Some proteins require more scrutinizing (galectin-1, XRCC5, TAGLN2, 00X5 and FLT) as conflicting results were obtained during validation. Preliminary analysis using 20 gel proteomics revealed galectin-1 to be selenium-responsive in PNT1A cells, although this could not be confirmed by Western blot or an in-house ELlSA. Previously, it has been shown that SeMSC decreased the expression of collagen I and increased that of collagen IV and collagen VI. A LNCaP 3D gel suspension model was developed to allow further investigation of extracellular matrix components using fluorescence microscopy. In addition, the effect of selenium exposure on the migration and invasion of PC3 cells was investigated using a transwell kinetic assay and revealed a dose response increase, especially under low baseline selenium concentrations. In order to optimize future selenium in vitro projects the dynamics of several selenium biomarkers were investigated using different conditions, enabling better comparison between cell lines and/or selenium compounds.

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Grönberg, Henrik. "Prostate cancer : epidemiological studies". Doctoral thesis, Umeå universitet, Onkologi, 1995. http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-96894.

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Prostate cancer is a large and increasing medical problem both in Sweden and in the rest of the developed world, with about 300.000 new cases diagnosed world wide annually. Despite the high incidence of this disease, little is known about the aetiology of prostate cancer. The aim of this study was to try to understand more about the natural history and to find possible a etiological risk factors for this tumour. In a population based study of prostate cancer cases in northern Sweden it was found that the large increase in prostate cancer during the last two decades was mainly caused by well (Gl) and moderately (G2) differentiated tumours. However, the incidence of poorly differentiated (G3) tumours remained unchanged. The introduction of new diagnostic methods is the most plausible explanation for the increase of these low grade tumours. The relative survival in prostate cancer was found to be independent of patient age at diagnosis, indicating that tumour proliferation and the aggressiveness of this disease is equal in all ages. However, due to the increasing occurrence of concurrent diseases with growing age the number of lost years caused by prostate cancer decreases dramatically in older age groups. The overall cause specific mortality for prostate cancer was found to be around 50%. In accordance with most other cancer tumours, the annual mortality rate decreased with longer survival also for prostate cancer patients. In a study from the Swedish Twin Register it was found that the proband concordance rates for prostate cancer were 4,5 time greater among monozygotic compared to dizygotic twins. In a large nation-wide cohort study of men who had a father with prostate cancer, the overall standardised incidence ratio (SIR) was 1.70 for prostate cancer. Younger age at diagnosis among the fathers were associated with an increased risk among sons. This cohort study and the twin study indicates that both inherited and familial factors are of importance in a subgroup of prostate cancer patients. In a prospective case-control study, both a high body mass index (BMI) and a high food intake were found to be independent risk factors for prostate cancer. Both BMI and a high food intake might be indicators of a high fat diet, which so far is the most consistent exogenous risk factor for prostate cancer. The use of tobacco or alcoholic beverages were not associated with prostate cancer risk.

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Libros sobre el tema "Prostate cancer"

K, Oh William y Logue John, eds. Prostate cancer. Edinburgh: Mosby Elsevier, 2007.

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S, Ernstoff Marc, Heaney John A y Peschel Richard E, eds. Prostate cancer. Malden, Mass: Blackwell Science, 1998.

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A, Dawson Nancy y Vogelzang Nicholas, eds. Prostate cancer. New York, USA: Wiley-Liss, 1994.

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P, Karr James, Yamanaka Hidetoshi y Tokyo Symposium on Prostate Cancer (2nd : 1987), eds. Prostate cancer. New York: Elsevier, 1989.

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Mason, Malcolm. Prostate Cancer. Oxford: Oxford University Press, 2003.

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Chung, Leland W. K., William B. Isaacs y Jonathan W. Simons. Prostate Cancer. New Jersey: Humana Press, 2000. http://dx.doi.org/10.1385/1592590098.

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Sotelo, René, Juan Arriaga, Raed A. Azhar y Inderbir S. Gill, eds. Prostate Cancer. Cham: Springer International Publishing, 2015. http://dx.doi.org/10.1007/978-3-319-05600-5.

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Pestell, Richard G., Marja T. Nevalainen y Michael Milken, eds. Prostate Cancer. Totowa, NJ: Humana Press, 2008. http://dx.doi.org/10.1007/978-1-60327-079-3.

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Tindall, Donald J., ed. Prostate Cancer. New York, NY: Springer New York, 2013. http://dx.doi.org/10.1007/978-1-4614-6828-8.

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Hricak, Hedvig y Peter Scardino, eds. Prostate Cancer. Cambridge: Cambridge University Press, 2008. http://dx.doi.org/10.1017/cbo9780511551994.

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Capítulos de libros sobre el tema "Prostate cancer"

Marshall, James R. y David P. Wood. "Prostate". En Cancer Precursors, 333–43. New York, NY: Springer New York, 2002. http://dx.doi.org/10.1007/0-387-21605-7_21.

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Muniyan, Sakthivel, Yu-Wei Chou, Shou-Qiang Ou-Yang y Ming-Fong Lin. "Human Prostatic Acid Phosphatase in Prostate Carcinogenesis". En Prostate Cancer, 323–48. New York, NY: Springer New York, 2013. http://dx.doi.org/10.1007/978-1-4614-6828-8_12.

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Sotelo, René, Camilo Andrés Giedelman Cuevas, Juan Arriaga, Ylbia Madrid de Roosen, Hernán Alonso Aponte Varón, Vanda Daniela López Günther, Anthony Laurence Zietman, José Luis Gaona Morales, Carlos Sucre Márquez y Eudo José Herrera Morillo. "Prostate Cancer". En Prostate Cancer, 73–165. Cham: Springer International Publishing, 2014. http://dx.doi.org/10.1007/978-3-319-05600-5_7.

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Tsuji, Hiroshi, Hitoshi Ishikawa y Takuma Nomiya. "Prostate Cancer". En Carbon-Ion Radiotherapy, 231–39. Tokyo: Springer Japan, 2013. http://dx.doi.org/10.1007/978-4-431-54457-9_27.

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Mottet, Nicolas y Jean-Pierre Droz. "Prostate Cancer". En Cancer and Aging Handbook, 315–33. Hoboken, NJ, USA: John Wiley & Sons, Inc., 2013. http://dx.doi.org/10.1002/9781118312513.ch21.

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Haseman, M. K. y N. L. Reed. "Prostate Cancer". En Nuclear Oncology, 83–102. Berlin, Heidelberg: Springer Berlin Heidelberg, 1999. http://dx.doi.org/10.1007/978-3-642-58643-9_5.

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Garcia, Michael A., Eric K. Hansen y Mack Roach. "Prostate Cancer". En Handbook of Evidence-Based Radiation Oncology, 559–603. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-62642-0_26.

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Böhmer, Dirk. "Prostate Cancer". En Target Volume Definition in Radiation Oncology, 291–300. Berlin, Heidelberg: Springer Berlin Heidelberg, 2015. http://dx.doi.org/10.1007/978-3-662-45934-8_14.

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Granov, Anatoliy, Leonid Tiutin y Thomas Schwarz. "Prostate Cancer". En Positron Emission Tomography, 163–74. Berlin, Heidelberg: Springer Berlin Heidelberg, 2011. http://dx.doi.org/10.1007/978-3-642-21120-1_14.

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Smith, David C. y Donald L. Trump. "Prostate Cancer". En Geriatric Medicine, 305–15. New York, NY: Springer New York, 1997. http://dx.doi.org/10.1007/978-1-4757-2705-0_23.

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Actas de conferencias sobre el tema "Prostate cancer"

Maheswari, M., S. Meera, R. Sharmikha Sree y R. A. Kalpana. "Prostate Cancer Discernment". En 2020 International Conference on Power, Energy, Control and Transmission Systems (ICPECTS). IEEE, 2020. http://dx.doi.org/10.1109/icpects49113.2020.9337027.

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Chernorotov, Vladimir Alekseyevich, Victor Sergeyevich Kostenich y Roman Romanovich Zvegintsev. "LANDMARKS AND MODERN APPROACHES IN PROSTATE CANCER DIAGNOSIS". En Themed collection of papers from Foreign international scientific conference «Joint innovation - joint development». Part 2. by HNRI «National development» in cooperation with PS of UA. October 2023. - Harbin (China). Crossref, 2024. http://dx.doi.org/10.37539/231024.2023.39.48.008.

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The article describes the main landmarks of prostate cancer diagnostics development. Current morbidity and mortality rates in the Russian Federation and the world are given, the tendencies of prostate cancer morbidity increase are noted. The authors of the article have done the work on systematisation and characterisation of modern diagnostic methods with their critical evaluation.

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Tse, Zion Tsz Ho, Sheng Xu, Alexander Squires, Yue Chen, Reza Seifabadi, Harsh Agrawal, Peter Pinto, Peter Choyke y Bradford Wood. "Robot for MRI-Guided Prostate Cancer Focal Laser Ablation". En 2017 Design of Medical Devices Conference. American Society of Mechanical Engineers, 2017. http://dx.doi.org/10.1115/dmd2017-3511.

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Prostate cancer is the most common cancer among males, leading to approximately 27,000 deaths in the United States [1]. Focal laser ablation (FLA) has been shown to be a promising approach for prostate cancer treatment with the advantage of efficiently ablating the cancer cells while inflicting less damage on the surrounding tissues. In current FLA procedures, a rigid template — with holes spacing of 5mm — guides the FLA catheter to the target position. Drawbacks of the conventional approach for catheter targeting are 1) limited degrees of freedom (DoF) and 2) a low insertion resolution. In addition, the targeting capability of the rigid template is compromised when the pubic arch or nerve bundles intersect the catheter trajectory. We hypothesized that a compact design of an MRI-conditional robot with two active planar DoFs, one passive rotation DoF, and remote catheter insertion capacities could enhance the clinical workflow required for MRI-guided FLA prostate procedures.

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Dehghani, Hossein, Shihao Zhang, Pankaj Kulkarni, Pradipta Biswas, Leslie Simms y Sang-Eun Song. "Design and Simulation of Robotic Needle Guide for Transperineal Prostate Biopsy". En 2018 Design of Medical Devices Conference. American Society of Mechanical Engineers, 2018. http://dx.doi.org/10.1115/dmd2018-6867.

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Prostate cancer is the third leading cause of cancer-related death for males in the United States [1]. Over three million Americans with prostate cancer were reported in 2016 [2] marking the prostate cancer as the most prevalent cancer among males in the US. In 2016, 180,890 new cases and 26,120 deaths were reported [1]. The prostate is a male reproductive gland located in the pelvis and surrounded by the rectum posteriorly and the bladder superiorly.

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Satish, Pranav, Alex Freeman, Daniel Kelly, Alex Kirkham, Clement Orczyk, Benjamin Simpson, Francesco Giganti, Hayley Whitaker, Mark Emberton y Joseph Norris. "Prostate cancer topography and tumour conspicuity on multiparametric magnetic resonance imaging: A systematic review and meta-analysis". En VIRTUAL ACADEMIC SURGERY CONFERENCE 2021. Cambridge Medicine Journal, 2021. http://dx.doi.org/10.7244/cmj.2021.04.001.2.

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Introduction The implications of tumour location on mpMRI conspicuity are not fully understood. Identifying topographical correlates that influence conspicuity may improve outcomes. Here, we present the first systematic review and meta-analysis describing the effect of tumour location on prostate cancer conspicuity on mpMRI. Methods Medline, PubMed, EMBASE and Cochrane databases were systematically searched and results were assessed as per the PRISMA statement. Differential tumour conspicuity on mpMRI was compared between cancers in the peripheral zone (PZ), transitional zone (TZ), base, apex, anterior and posterior. Meta-analysis was conducted to compare diagnostic odds ratios (DOR) of mpMRI detection for tumours in the PZ and TZ. PROSPERO registration: CRD42021228087. Results Thematic synthesis showed apical and basal tumours had reduced conspicuity compared to mid-gland tumours. Cancer in the TZ demonstrated increased conspicuity on T2-weighted imaging, whilst PZ cancers had higher conspicuity on diffusion-weighted and dynamic contrast enhancement imaging. mpMRI had better diagnostic accuracy for PZ lesions, albeit higher specificity for TZ lesions. Meta-analysis showed an increased DOR for PZ tumours (OR: 7.206 [95% CI: 4.991;10.403], compared to TZ (OR: 5.310 [95% CI: 3.082; 9.151]). However, the test for subgroup differences was not significant (p = 0.2743). Conclusions Cancer in the apex or base of the prostate may be less conspicuous than mid-gland tumours. Similarly, TZ cancer appears to have reduced conspicuity compared to PZ cancer, however, meta-analysis did not show a significant difference between DOR. Future larger studies with prospective datasets are required to clarify the relationship between tumour position and conspicuity.

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Arioua, Khalil. "CD16A and CD16B mRNA levels as a potential immunological marker in prostate cancer". En Наука России: Цели и задачи. Наука России, 2021. http://dx.doi.org/10.18411/sr-05-12-2021-06.

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Introduction and purpose Understanding the movement of immune cells in prostate cancer is the best solution for development antitumor therapy. In our study, we will evaluate level mRNA CD16А (FCGR3A) and mRNA CD16B (FCGR3B) in patients diagnosing benign hyperplasia and patients diagnosing prostate cancer (Pc). Materials and methods In the study, we analyzed 240 samples of mRNA, 49 was the blood of healthy donors, 37 was the blood of prostate cancer patients and 62 tumors of prostate, 37 were blood of hyperplasia and 55 was tissue of hyperplasia, all patients treated in the Hospital 33 (Niznhy Novgord, Russia). The relative level of mRNA in peripheral blood and tumors was determined by the method of reverse transcription-polymerase chain reaction in real time. Results In the peripheral blood of patients with prostate cancer and patients with hyperplasia, the level of mRNA FCGR3A and FCGR3B was statistically significantly lower than in healthy individuals. The normalization of the CD16 level in the blood of healthy donors was higher The relative level of mRNA FCGR3A, FCGR3B was the highest in patients with Prostate antigen specific (PSA) from 10Ng/ml to 20Ng/ml. The higher level mRNA FCGR3A and FCGR3B was for patients with higher testosterone ≥8mmol/L. also a higher level of FCGR3A, FCGR3B was found in patients diagnosed with an adenopathy:, a higher size prostate and a higher Gleason Scores. The results of Classification based on the degree of differentiation shows that the level of mRNA FCGR3A and FCGR3B in patients with medium differentiation was higher and statistically significant than in patient with lower differentiation. Conclusion. The Changes in the mRNA level of genes encoding CD16A (FCGR3A) and CD16B (FCGR3A) was detected in blood and tumor samples. The results indicate the potential use of these indicators as monitoring immunological markers in hyperplasia and prostate cancer.

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Bauer, John J., Jianchao Zeng, Wei Zhang, Isabell A. Sesterhenn, Robert Dean, Judd W. Moul y Seong K. Mun. "Simulated prostate biopsy: prostate cancer distribution and clinical correlation". En Medical Imaging 2000, editado por Seong K. Mun. SPIE, 2000. http://dx.doi.org/10.1117/12.383030.

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Liang, Haipeng, Wanli Zuo, Dimitri Kessler, Tristan Barrett y Zion Tsz Ho Tse. "MRI-Guided Robotic Prostate Biopsy". En THE HAMLYN SYMPOSIUM ON MEDICAL ROBOTICS. The Hamlyn Centre, Imperial College London London, UK, 2023. http://dx.doi.org/10.31256/hsmr2023.6.

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Prostate cancer is one of the most common malignancies and the second leading cause of cancer death in men [1]. Approximately 52,300 new cases of prostate cancer are detected in the UK every year, that’s more than 140 every day. Magnetic resonance imaging (MRI) has been widely used in the diagnosis of prostate cancer, as it can offer high-resolution tissue imaging at arbitrary orientations and monitor therapeutic agents, surgical tools, and tissue properties. Therefore, a robot - under the guidance of MRI - can target the tumor regions with high accuracy to obtain the biopsy samples for diagnosis, thus reducing unnecessary gland punctures and maximizing the utility of a minimally invasive system. However, as MR scanners require a strong magnetic field, ferromagnetic materials are precluded as they can cause a hazard to the device and patients, and paramagnetic materials can generate their own magnetic field which will distort the image quality. As a result, MR-safe actuators are required to power the robot. Plus, due to the limited size of the MR bores, the robot operating inside should be as compact as possible [2]. In this paper, a robotic system for MRI-guided prostate biopsy is proposed. Comparing with the existing designs, it has a compact size, with the workspace covering the whole prostate. The use of pneumatically powered actuators can avoid the influence of electromagnetic interference. The working principle, mathematical model, and mechanism design are presented. The needle insertion experiment under an MR environment was conducted.

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Kosari, Farhad, John C. Cheville, Cristiane M. Ida, R. Jeffrey Karnes, Alexey A. Leontovich, Thomas J. Sebo, Sibel Erdogan, Stephen J. Murphy y George Vasmatzis. "Abstract 3008: Shared gene expression alterations in prostate cancer and histologically benign prostate from patients with prostate cancer". En Proceedings: AACR 103rd Annual Meeting 2012‐‐ Mar 31‐Apr 4, 2012; Chicago, IL. American Association for Cancer Research, 2012. http://dx.doi.org/10.1158/1538-7445.am2012-3008.

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Vickers, Sofia Lage, Juan Antonio Bizzotto, Alejandra Paez, Javier Cotignola, Carlos Scorticati, Osvaldo Mazza, Pia Valacco, Geraldine Gueron y Elba Vazquez. "Abstract A058: Integrative prostate cancer tissue proteomics dissects clear and distinct proteomes for human prostate cancer and benign prostatic hyperplasia". En Abstracts: AACR Special Conference: Prostate Cancer: Advances in Basic, Translational, and Clinical Research; December 2-5, 2017; Orlando, Florida. American Association for Cancer Research, 2018. http://dx.doi.org/10.1158/1538-7445.prca2017-a058.

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Informes sobre el tema "Prostate cancer"

Cooney, Kathleen A. Prostate Cancer Aggressiveness Genes in Hereditary Prostate Cancer. Fort Belvoir, VA: Defense Technical Information Center, marzo de 2005. http://dx.doi.org/10.21236/ada446359.

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Cooney, Kathleen A. y Colin Duckett. Prostate Cancer Aggressiveness Genes in Hereditary Prostate Cancer. Fort Belvoir, VA: Defense Technical Information Center, marzo de 2006. http://dx.doi.org/10.21236/ada455279.

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Cooney, Kathleen. Prostate Cancer Aggressiveness Gene in Hereditary Prostate Cancer. Fort Belvoir, VA: Defense Technical Information Center, marzo de 2007. http://dx.doi.org/10.21236/ada472110.

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Navone, Nora M. Osteoblast-Prostate Cancer Cell Interaction in Prostate Cancer Bone. Fort Belvoir, VA: Defense Technical Information Center, febrero de 2000. http://dx.doi.org/10.21236/ada391088.

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Heidari, Afshin, Aida Kazemi, Parisa Najjari, Kamran Dalvandi, Hamidreza Sadeghsalehi, Parinaz Onikzeh y Hadi Zamanian. Comparing Urinary and Sexual Complications of Robot-Assisted Radical Prostatectomy and Laparoscopic Radical Prostatectomy in Prostate Cancer: a Systematic Review and Meta-Analysis Protocol. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, octubre de 2021. http://dx.doi.org/10.37766/inplasy2021.10.0068.

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Review question / Objective: The aims of this study are: 1. To compare urinary complications of robot-assisted radical prostatectomy(RARP) and laparoscopic radical prostatectomy(LRP) in patients with prostate cancer; 2. To compare sexual complications of RARP and LRP in patients with prostate cancer. Condition being studied: Prostate cancer is one of the most prevalent types of cancer; according to 2018 statistics, prostate cancer was responsible for 7.1% of all cancer in men. The primary intervention in such patients is radical prostatectomy surgery (RP), which could be performed in different methods in patients that cancer has not spread beyond the prostate gland or has not spread much. One of the most common types of RP is laparoscopic radical prostatectomy. There are several techniques for performing RP; two are Conventional Laparoscopic Radical Prostatectomy (LRP) and Robot-Assisted Radical Prostatectomy (RARP). Sexual and urinary difficulties can occur in prostate cancer patients due to cancer itself or the treatment. Like any treatment option and surgery, radical prostatectomy can carry risks, like urinary(e.g., incontinency) and sexual complications(e.g., Impotence). In this review, we compared urinary and sexual complications of LRP and RARP.

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Purnell, Jonathan. Imaging Prostatic Lipids to Distinguish Aggressive Prostate Cancer. Fort Belvoir, VA: Defense Technical Information Center, septiembre de 2014. http://dx.doi.org/10.21236/ada609940.

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Shannon, Jackilen. Imaging Prostatic Lipids to Distinguish Aggressive Prostate Cancer. Fort Belvoir, VA: Defense Technical Information Center, septiembre de 2014. http://dx.doi.org/10.21236/ada612470.

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Shannon, Jackilen. Imaging Prostatic Lipids to Distinguish Aggressive Prostate Cancer. Fort Belvoir, VA: Defense Technical Information Center, septiembre de 2013. http://dx.doi.org/10.21236/ada594175.

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Purnell, Jonathan. Imaging Prostatic Lipids to Distinguish Aggressive Prostate Cancer. Fort Belvoir, VA: Defense Technical Information Center, septiembre de 2015. http://dx.doi.org/10.21236/ada626329.

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Marcelli, Marco. Apoptosis in Prostate Cancer. Fort Belvoir, VA: Defense Technical Information Center, abril de 2001. http://dx.doi.org/10.21236/ada398042.

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