Academic literature on the topic 'Prostate adenocarcinoma'

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Journal articles on the topic "Prostate adenocarcinoma"

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Mai, Kien T., Denise C. Landry, and John P. Collins. "Secondary Colonic Adenocarcinoma of the Prostate Histologically Mimicking Prostatic Ductal Adenocarcinoma." Tumori Journal 88, no. 4 (July 2002): 341–44. http://dx.doi.org/10.1177/030089160208800418.

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Purpose To study the clinical presentation and pathological features of secondary colonic adenocarcinoma of the prostate. Materials and methods Six cases of colonic adenocarcinoma extending into the prostate were retrieved from the surgical pathology and autopsy files of the period 1985-1999. Immunostaining for prostatic acid phosphatase (PAP), prostate specific antigen (PSA), cytokeratin 7 (CK7), cytokeratin 20 (CK20) and carcinoembryonic antigen (CEA) was carried out in all cases. Clinical charts were also reviewed. Results Secondary colonic carcinoma spread into the prostatic stroma and along the prostatic ducts. In all four surgical cases, patients with a known history of rectal carcinoma presented with symptoms of urinary obstruction after 12 to 36 months of being free of recurrent or metastatic disease. In three surgical cases the secondary carcinoma involved the prostatic urethra in a form mimicking endometriod carcinoma, which led to an incorrect diagnosis of prostatic endometrioid carcinoma in one case. The tumor cells were immunoreactive to CK20 and CEA and not reactive to CK7, PAP and PSA. Conclusions Colonic carcinoma involving the prostate may mimic prostatic duct carcinoma due to the ductal and urethral involvement. Using a panel of immunostaining and clinical history is helpful in the differential diagnosis.
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Celik, Orcun, Salih Budak, Gokhan Ekin, Ilker Akarken, and Yusuf Ozlem Ilbey. "A case with primary signet ring cell adenocarcinoma of the prostate and review of the literature." Archivio Italiano di Urologia e Andrologia 86, no. 2 (June 30, 2014): 148. http://dx.doi.org/10.4081/aiua.2014.2.148.

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Primary signet cell carcinoma of the prostate is a rare histological variant of prostate malignancies. It is commonly originated from the stomach, colon, pancreas, and less commonly in the bladder. Prognosis of the classical type is worse than the adenocarcinoma of the prostate. Primary signet cell adenocarcinoma is diagnosed by eliminating the adenocarcinomas of other organs such as gastrointestinal tract organs. In this case report, we present a case with primary signet cell adenocarcinoma of the prostate who received docetaxel chemotherapy because of short prostate specific antigen doubling time.
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Yang, Chen, and Peter A. Humphrey. "False-Negative Histopathologic Diagnosis of Prostatic Adenocarcinoma." Archives of Pathology & Laboratory Medicine 144, no. 3 (November 15, 2019): 326–34. http://dx.doi.org/10.5858/arpa.2019-0456-ra.

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Context.— Histopathologic diagnosis of adenocarcinoma of the prostate is based on light-microscopic examination of hematoxylin-eosin–stained tissue sections. Multiple factors, including preanalytic and analytic elements, affect the ability of the pathologist to accurately diagnose prostatic adenocarcinoma. False-negative diagnosis, that is, failure to diagnose prostatic adenocarcinoma, may have serious clinical consequences. It is important to delineate and understand those factors that may affect and cause histopathologic false-negative diagnoses of prostatic adenocarcinoma. Objectives.— To review common factors involved in histopathologic underdiagnosis of prostatic adenocarcinoma, including the following: (1) tissue processing and sectioning artifacts, (2) minimal adenocarcinoma, (3) deceptively benign appearing variants of acinar adenocarcinoma, (4) single cell adenocarcinoma, and (5) treatment effects. Data Sources.— Data sources included published, peer-reviewed literature and personal experiences of the senior author. Conclusions.— Knowledge of the reasons for histopathologic false-negative diagnosis of adenocarcinoma of the prostate is an important component in the diagnostic assessment of prostate tissue sections. Diagnostic awareness of the histomorphologic presentations of small (minimal) adenocarcinoma; deceptively benign appearing variants including atrophic, foamy gland, microcystic, and pseudohyperplastic variants; single cell carcinoma; and treatment effects is critical for establishment of a definitive diagnosis of adenocarcinoma and the prevention of false-negative diagnoses of prostate cancer.
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Murgod, Priyanka Sangappa, Preeti Rajeev Doshi, Amit Ravindra Nisal, and Ravindra Chandrashekar Nimbargi. "Histomorphological Mimickers of benign prostatic lesions with prostatic adenocarcinoma." Journal of Pathology of Nepal 11, no. 1 (March 20, 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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Yee, David S., Navneet Narula, Ibrahim Ramzy, John Boker, Thomas E. Ahlering, Douglas W. Skarecky, and David K. Ornstein. "Reduced Annexin II Protein Expression in High-Grade Prostatic Intraepithelial Neoplasia and Prostate Cancer." Archives of Pathology & Laboratory Medicine 131, no. 6 (June 1, 2007): 902–8. http://dx.doi.org/10.5858/2007-131-902-raipei.

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Abstract Context.—Annexin II is a calcium-dependent phospholipid-binding protein that plays a role in many cellular functions, including apoptosis, signal transduction, and cellular motility. The protein is strongly expressed in normal prostatic epithelial glands, but its expression in benign prostatic lesions has not been reported. Although commonly underexpressed in prostate cancer, the association of reduced expression with pathologic grade and stage is unknown. Objective.—To compare annexin II expression in benign prostatic lesions with expression in high-grade prostatic intraepithelial neoplasia and prostate cancer, as well as to correlate expression levels with pathologic grade and stage. Design.—A semi-quantitative assessment of annexin II expression was performed in radical prostatectomy specimens from 74 patients and prostate needle core biopsy specimens from 13 patients. Foci with normal prostatic glands, atrophic glands, basal cell hyperplasia, high-grade prostatic intraepithelial neoplasia, and prostatic adenocarcinoma were evaluated. Results.—Annexin II expression was present in more than 50% of glands in most (>85%) samples of benign prostatic epithelium, atrophic glands, and basal cell hyperplasia. In high-grade prostatic intraepithelial neoplasia, annexin II staining was markedly reduced in epithelial cells but not in basal cells. Annexin II was absent or focally present in moderately differentiated adenocarcinoma but was retained in poorly differentiated adenocarcinomas. Conclusions.—Reduced annexin II expression may be a useful diagnostic biomarker to help identify small foci of moderately differentiated adenocarcinoma on needle core biopsy specimens since it is consistently expressed in benign prostatic glands. Re-expression of annexin II in poorly differentiated adenocarcinoma may provide prognostic information.
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Rita, Roza, Delyuzar, and Lidya Imelda Laksmi. "Correlation between AgNOR Expression and Ki-67 Expression with Prostate Adenocarcinoma Grading." Majalah Patologi Indonesia 29, no. 3 (September 7, 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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., Abeer, Farah Kalsoom, Anum Malik, Aneela Khwaja, Nusrat Alvi, and Asma Ejaz. "Incidence of Adenocarcinoma with Gleason Grade in Clinically Enlarged Prostate Glands." Pakistan Journal of Medical and Health Sciences 16, no. 2 (February 26, 2022): 313–14. http://dx.doi.org/10.53350/pjmhs22162313.

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Background: Prostatic cancer is the 2nd most common malignancy in men. The understanding of incidence of malignancy along with Gleason grading of tumor is significant that led the development of investigations for early detection and prompt treatment of patients Aims: The aim of this study is to determine the incidence of malignancies with Gleason grade in patients with clinically enlarge prostate glands. Materials and Methods: This is a descriptive cross sectional study conducted in Rahbar medical and dental college from 100 patients with clinically enlarge prostate glands from January 2018 to December 2020. Results: A total 100 prostatic biopsies were examined histologically from January 2018 to December 2020. Out of 100 biopsies 12(12%) cases were diagnosed as adenocarcinoma and 88 (88%) were benign lesions. The age of patients ranges from 52 to 95 years with mean age of patients was 73.5 years. Majority (41.66 %) of adenocarcinomas reported as Gleason grade group 5. In 16.66 % cases the malignancy was incidental as clinically there was no any suspicion of carcinoma. Perineural invasion was noted in 66.66% of adenocarcinomas, and in 16.66% of cases lymphovascular invasion was reported, that correlates with higher grade of tumor. Conclusion: Majority of the tumor diagnosed were in grade group 4 that shows increased death rate. Prostate cancer is continue to rise and screening of every patient with enlarge prostate should be done for early detection of malignancy. Keywords: prostate gland, adenocarcinoma, Gleason grade
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Okidi, Ronald, Cyprian Opira, Vanusa Da Consolação Sambo, Caroline Achola, and 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, no. 3 (October 7, 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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Karia, Kunjal Mukesh, and Mrinal Kishor Mallya. "Clinicopathological correlation of p53 expression in benign prostatic hyperplasia and prostate adenocarcinoma." Indian Journal of Pathology and Oncology 9, no. 1 (February 15, 2022): 60–64. http://dx.doi.org/10.18231/j.ijpo.2022.015.

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Prostate adenocarcinoma is the 6 most common carcinoma in men worldwide. It is usually a cancer of the elderly age group. Benign prostatic hyperplasia is a common cause of urinary incontinence and urine flow symptoms, usually seen in the middle along with elderly age group. In this study we have evaluated the expression of p53 immunohistochemistry (IHC) in prostate adenocarcinoma with benign prostatic hyperplasia along with its diagnostic, treatment and prognostic implications.: 1. Assessment of clinical and biochemical parameters in patients with benign prostatic hyperplasia (BPH) and prostate adenocarcinoma. 2. To assess p53(IHC) expression in benign prostatic hyperplasia and prostate adenocarcinoma : The study population comprised of a subset of patients who came to Ramaiah hospital, Bangalore from May 2018 till June 2019, for treatment regarding prostate related symptoms. The clinicodemographic data was collected and prostate biopsies were taken for which histopathological assessment was done. A total of 60 cases comprising of 30 cases of BPH and 30 cases of prostatic adenocarcinoma was subjected to p53 immunohistochemistry. The results were tabulated and statistically analyzed for significance.The present prospective study was conducted on 60 patients with 30 cases (50%) of BPH and 30 cases (50%) of prostatic adenocarcinoma. Based on the tumor differentiation there was 1 case (3.3%) of well differentiated carcinoma, 18 cases(60%) of moderately differentiated carcinoma and 11cases (36.6%) of poorly differentiated carcinomas. We observed an inverse relationship between p53 expression and histological grade. All poorly differentiated carcinoma had higher p53(>50% expression). There was statistically significant difference in expression of p53 between cases of BPH and carcinoma prostate, indicated by P value of <0.05. Among prostate carcinomas p53 had higher expression on those cases with Gleason score 9 and 10.: P53 expression directly correlates with Gleason score, while inversely correlating with tumor differentiation of prostate carcinoma cases. The expression of p53 is low in BPH as compared to that of prostate cancers. Hence it can be used as a good diagnostic and prognostic marker in prostate carcinoma.
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Engki Aditya, Didit Pramudhito, Aspitriani, and Legiran. "Comparison of Androgen Receptor Expression in Patients with Benign Prostate Hyperplasia and Adenocarcinoma Prostate." Sriwijaya Journal of Surgery 5, no. 2 (October 11, 2022): 502–8. http://dx.doi.org/10.37275/sjs.v5i2.75.

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Introduction: Benign prostate hyperplasia is a proliferation of stromal cells and epithelial cells which results an enlargement of the prostate gland and can cause obstruction of the urinary tract. Adenocarcinoma prostate is an invasive carcinoma consisting of a neoplasm of prostate epithelial cells with secretory cell differentiation. Abnormal growth of the prostate gland like benign lesions and malignant lesions are generally affected by androgen receptor (AR). The aim of this research is to analyse the comparison of AR expression in benign prostate hyperplasia and adenocarcinoma prostate. Methods: The design of this research is analiytical study with cross sectional approach. The samples are 18 cases of benign prostate hyperplasia and 20 cases of adenocarcinoma prostate. The samples are observed only once and at a time. Results: The average age of the adenocarcinoma prostate case was 63.95 ± 12.03 years (age range 33-84 years) while in the benign prostate hyperplasia case, the average age was 66.78 ± 9.49 (age range 54–89 years). There are no different about the expression of AR in benign prostate hyperplasia and adenocarcinoma prostate used Allred scores. There was a weak and negative correlation between Gleason score and AR expression in the adenocarcinoma prostate case group (p=0.237). Conclusion: There are no differences related to the expression of AR between the case of adenocarcinoma prostate and benign prostatic hyperplasia.
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Dissertations / Theses on the topic "Prostate adenocarcinoma"

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Noronha, Marcelo Ramos. "Adenocarcinoma da próstata = estudo de fatores clinicopatológicos preditivos de progressão bioquímica (PSA) pós-prostatectomia radical." [s.n.], 2010. http://repositorio.unicamp.br/jspui/handle/REPOSIP/310489.

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Orientadores: Luciana Rodrigues de Meirelles, Athanase Billis
Dissertação (mestrado) - Universidade Estadual de Campinas, Faculdade de Ciências Médicas
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Resumo: O adenocarcinoma de próstata é a segunda neoplasia maligna que afeta homens, sendo precedida somente pelo cancer de pele. A prostatectomia radical continua sendo a mais aceita estratégia terapêutica para os casos confinado a próstata. Alguns achados clinicopatológicos em pacientes submetidos a prostatectomia radical são controvertidos como tendo valor preditivo de progressão bioquímica pós-cirurgia. O monitoramento da progressão da moléstia pós-prostatectomia radical é feito através de dosagem do PSA sérico cujo aumento pode significar recidiva local e/ou metástases. O valor de corte do PSA sérico indicando progressão é variável entre os autores. Há uma recomendação recente da Associação Americana de Urologia para que este valor seja ?0,2ng/mL com um segundo valor >0,2ng/mL. Não está estabelecido se pacientes mais jovens ou de raça negra mostram taxa de recidiva bioquímica maior. O PSA pré-operatório é um dado de grande importância preditiva, mas não está estabelecido a validade da estratificação dos valores em 3 categorias: 4-10ng/mL, 10-20ng/mL e >20ng/mL. Margens cirúrgicas comprometidas no espécime cirúrgico estão na categoria I (valor preditivo comprovado). É controvertido se a contagem final de Gleason 3+4=7 é semelhante ou não a 4+3=7 como fator preditivo de progressão bioquímica pós-prostatectomia radical. O estudo foi retrospectivo e os dados foram coletados dos prontuários médicos de 300 pacientes submetidos consecutivamente à prostatectomia radical no Hospital de Clínicas da Universidade Estadual de Campinas, no período de janeiro de 1997 a maio de 2007. O objetivo principal do trabalho foi avaliar a progressão bioquímica (PSA) pós prostatectomia radical de acordo com: raça, idade, margens cirúrgicas comprometidas, invasão microscópica do colo vesical, contagem final de Gleason, extensão do tumor, estádio patológico e PSA pré-operatório. Os dados obtidos foram analisados estatisticamente utilizando-se o teste de Mann-Whitney, o produto limite de Kaplan-Meier utilizando-se o teste do log-rank para comparação entre os grupos e o método de Cox para avaliar risco do tempo de progressão bioquímica (PSA) pós-prostatectomia radical. O nível de significância considerado para rejeição da hipótese nula foi p<0,05 bicaudal. Os resultados mais importantes neste trabalho foram: diferença estatisticamente significante quanto ao tempo de progressão bioquímica de pacientes com PSA pré-operatório ?10ng/mL, margens cirúrgicas comprometidas, invasão microscópica do colo vesical, Gleason 4+3=7, tumores mais extensos e tumores não confinados à próstata. Não houve associação da idade e raça com progressão bioquímica. Em análise univariada, os fatores preditivos significantes do tempo e risco de progressão pós-prostatectomia radical foram o PSA pré-operatório, as margens cirúrgicas positivas, a invasão das vesículas seminais, a invasão microscópica do colo vesical e o Gleason 4+3=7. Em análise multivariada, somente PSA pré-operatório, margens positivas e invasão das vesículas seminais mostraram-se fatores preditivos independentes do tempo e risco de progressão bioquímica pós-prostatectomia radical
Abstract: Adenocarcinoma of the prostate is the second malignancy that affects men, being preceded only by skin cancer. Radical prostatectomy remains the most widely accepted treatment strategy for cases confined to the prostate. Some clinical and pathological findings in patients undergoing radical prostatectomy are at issue as having predictive value of biochemical progression after surgery. The monitoring of disease progression after radical prostatectomy is done by measuring concentrations of PSA which can mean increased local recurrence and/or metastases. The cutoff of PSA indicating progression varies among authors. There is a recent recommendation of the American Urological Association that this value is ?0.2ng/mL with a second value >0.2ng/mL. It has not been established whether younger or black patients show higher rate of biochemical recurrence. The preoperative PSA is an important predictive factor for biochemical recurrence, but it has not been established the validity of the stratification of values in three categories: 4-10ng/mL, 10-20ng/mL, and >20ng/mL. Positive surgical margins in the surgical specimen are in category I (proven predictive value). It is controversial whether the final Gleason score 3+4=7 is similar or not to 4+3=7 as a predictor of biochemical progression after radical prostatectomy. The study was based on 300 whole-mount consecutive radical prostatectomies. The aim of this study was to analyse the risk and time for biochemical progression after surgery, according to race, age, positive surgical margins, bladder neck invasion, Gleason score, tumor extension, pathological stage and serum PSA preoperative levels. Time to biochemical progression-free outcome was compared using the Kaplan-Meier product-limit analysis using the log-rank to compare the groups. To assess individual variables for risk and time to biochemical progression, we created a univariate Cox proportional hazards model, and to assess the influence of several variables simultaneously, we developed a final multivariate Cox proportional hazards model of the statistically significant covariates. The most important results were: There was a significant association to time of progression of patients with preoperative PSA ?10ng/mL, positive surgical margins, microscopic invasion of the bladder neck, Gleason 4+3=7, more extensive tumors and non confined tumors. No association of race and age to biochemical progression following radical prostatectomy. On univariate analysis, the significant predictive variables for risk and time to biochemical progression were: preoperative PSA, positive surgical margins, seminal vesicle invasion, microscopic invasion of the bladder neck, and Gleason 4+3=7. On multivariate analysis, only positive surgical margins and seminal vesicle invasion were independent predictive variables
Mestrado
Anatomia Patologica
Mestre em Ciências Médicas
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Silva, Elcio Dias 1951. "Margens cirurgicas na prostatectomia radical : comparação entre cirurgia retropubica e laparoscopica." [s.n.], 2006. http://repositorio.unicamp.br/jspui/handle/REPOSIP/312194.

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Orientador: Ubirajara Ferreira
Dissertação (mestrado) - Universidade Estadual de Campinas, Faculdade de Ciências Médicas
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Resumo: Introdução: margem cirúrgica comprometida ou positiva é definida como tumor estendendo-se na superfície de corte do cirurgião. A porcentagem deste evento, resultante de incisão capsular, varia de 1,3 a 71 % (EPSTEIN, 2001). O objetivo deste estudo é comparar o comprometimento das margens cirúrgicas nas prostatectomias radicais realizadas por via retropúbica e laparoscópica, em dois serviços de referência no Brasil. Pacientes e Métodos: foram analisados os exames anátomo-patológjcos de 179 pacientes submetidos a prostatecomia radical por adenocarcinoma de próstata, 89 por via retropúbica e 90 por via laparoscópica. Critérios de inclusão: pacientes com PSA (antígeno específico da próstata) igual ou menor que 15 ng/ml (nanogramas por mililitro) e Gleason igual ou menor que 7 na biópsia prostática, estádio clínico máximo T2. Resultados: houve comprometimento de margem cirúrgica em 41,57 % dos pacientes submetidos à PRR (prostatectomia radical retropúbica), distribuídos da seguinte maneira: 34,21 % nos estádios pT2 (7,69 % no pT2a, zero no pT2b e 40,98 % no pT2c) e 84,61% nos estádios pT3 (77,77 % no pT3a e 100 % no pT3b). Nos pacientes submetidos a PRL (prostatectomia radical laparoscópica) houve margens cirúrgicas positivas em 24,44 % dos pacientes, distribuídos da seguinte maneira: 20,98 % nos estádios pT2 (11,11 % no pT2a, 27,27 % no pT2b e 21,31 % no pT2c) e 55,55 % nos estádios pT3 (zero % no pT3a e 62,50 % no pT3b). Conclusão: nas amostras analisadas, a proporção de margem cirúrgica positiva foi maior nas prostatectomias radicais realizadas pela via retropúbica do que pela laparoscópica (p= 0,023), em dois serviços de referência nas respectivas técnicas, no Brasil. No entanto, o fato das cirurgias retropúbicas serem realizadas por médicos residentes, em instituição de ensino, e as laparoscópicas realizadas por um único cirurgião experiente, e os exames anátomo-patológicos realizados por técnicas e patologistas distintos, não permite a generalização dos resultados. Maior número de pacientes em estudo prospectivo e randomizado seria necessário para uma melhor comparação entre os grupos
Abstract: Introduction: Compromised or positive surgical margin is defined as a tumor extending at the surgeon cutting surface. A percentage from this event, resulted from capsular incision, varies from 1.3 to 71% (EPSTEIN, 2001). The goal of this study is to compare the compromising of surgical margins at the radical prostatectomies performed through both retropubic and laparoscopic way, in two reference medical services in Brazil. Patients and Methods: pathological examinations were analyzed from 179 patients who underwent to radical prostatectomy by prostate adenocarcinoma, 89 patients by retropubic and 90 patients by laparoscopic way. Inclusion criteria: patients with PSA (prostate specific antigen) equal or less than 15 ng/ml (nanograms by miiiliter) and Gleason score equal or less than 7 at the prostate biopsy, maximum clinical T2 stage. Results: There has been compromising of the surgical margin in 41,57% of the patients who underwent to RRP (radical retropubic prostatectomy), distributed in the following way: 34,21% at pT2 stage (7,69% at pT2a, 0% at pT2b and 40,98% at pT2c) and 84,61% at pT3 (77,77% at pT3a and 100% at pT3b) stage. In the patients who had undergone to LRP (Laparoscopic Radical Prostatectomy), there have been positive surgical margins in 24,44% of the patients as following: 20,98% at pT2 stage (11,11% at pT2a. 27,27% at pT2b and 21,31% at pT2c stage) and 55,55% at pT3 stage (0% at pT3a and 62,50% at pT3b) Conclusion: At the analyzed samples, the proportion of positive surgical margin was greater at the radical prostatectomy performed by retropubic route than by laparocospic one (p=0,023), in two reference medical services using the respective techniques in Brazil. However, the fact that the retropubic surgeries were performed by resident doctors, in teaching school-hospital institution, while the laparoscopic ones were performed by a single expert surgeon and that the pathological examinations were performed by both distinct techniques and pathologists, the result generalization is not allowed. A greater number of patients in a randomized and prospective study would be necessary for a better comparison between the groups
Mestrado
Cirurgia
Mestre em Cirurgia
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Singh, Paras B. "Risk factor analyses for adenocarcinoma of the human prostate." Thesis, Lancaster University, 2011. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.538609.

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Baca, Sylvan Charles. "The landscape of somatic mutations in primary prostate adenocarcinoma." Thesis, Harvard University, 2013. http://dissertations.umi.com/gsas.harvard:10824.

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Prostate cancer is the second leading cause of cancer deaths among men. Targeted analyses of DNA from prostate cancers have identified recurrent somatic alterations that promote tumor growth and survival. Only recently, however, has the comprehensive analysis of cancer genomes become possible due to rapid advances in DNA sequencing technology.
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Pisani, Carla. "Study of the effects induced by high doses per fraction in radiotherapy: correlations between biological and clinical parameters – the case of intraoperative irradiation of prostate adenocarcinoma." Doctoral thesis, Università del Piemonte Orientale, 2021. http://hdl.handle.net/11579/128008.

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Brasil, Antonio Augusto Azevedo Vital. "Atrofia prostática em espécimes de prostatectomia radical = há relação topográfica com neoplasia intraepitelial prostática alto grau e adenocarcinoma?" [s.n.], 2010. http://repositorio.unicamp.br/jspui/handle/REPOSIP/308454.

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Orientadores: Athanase Billis, Luciana Rodrigues de Meirelles
Dissertação (mestrado) - Universidade Estadual de Campinas, Faculdade de Ciências Médicas
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Resumo: A relação entre a atrofia inflamatória com a neoplasia intraepitelial alto grau e o carcinoma, é controversa. Tem sido sugerida uma relação topográfica e que o epitélio proliferativo da atrofia inflamatória possa progredir para neoplasia intraepitelial prostática alto grau (NIPAG) e/ou carcinoma (CA). O propósito do nosso estudo foi analisar em espécimes de prostatectomia radical uma possível relação topográfica entre estas lesões. Um total de 3186 quadrantes pertencentes a 100 prostatectomias radicais completamente representadas, foi analisado. Determinou-se a frequência de quadrantes mostrando: somente atrofia inflamatória (AI), AI+CA, AI+NIPAG, ou AI+NIPAG+CA. A extensão e a distância entre as lesões foram avaliadas através de um método semiquantitativo de contagem de pontos previamente descrito. Também foram analisados focos de atrofia completa ou parcial sem inflamação. Os métodos estatísticos empregados foram os testes de Kruskal-Wallis e Mann-Whitney, e o coeficiente de correlação de Spearman. A média dos quadrantes exibindo somente AI, AI+CA, AI+NIPAG, e AI+NIPAG+CA foi 3.29, 2.51, 0.77, e 0.44; e a amplitude (0-21), (0-11), (0-6), (0-4), respectivamente (p<0.01). A maioria dos focos de AI estavam a uma distância >5mm dos focos de NIPAG e CA. Não houve correlação significativa entre a extensão da AI (p= 0.64, r= 0.05) com a extensão da NIPAG. Houve uma significativa correlação negativa entre a extensão da AI (p=0.01, r=-0.27) com a extensão do CA. Resultados similares foram encontrados considerando focos de atrofia com ou sem inflamação. Focos de atrofia parcial não evidenciaram inflamação crônica inespecífica. Nosso estudo não evidenciou associação topográfica significativa entre AI, NIPAG e/ou CA
Abstract: It is controversial whether there is any relationship of proliferative inflammatory atrophy (PIA) to high-grade prostatic intraepithelial neoplasia (HGPIN) and cancer (CA). It has been suggested a topographic relation and a potential of the proliferative epithelium in PIA to progress to HGPIN and/or CA. The aim of this study was to analyze in radical prostatectomies a possible topographic relation of the lesions. A total of 3186 quadrants from 100 whole-mount consecutive surgical specimens was examined. The frequency of quadrants showing: only PIA, PIA+CA, PIA+HGPIN, or PIA+HGPIN+CA was determined. Extent and distance between the lesions were evaluated by a semiquantitative point-count method previously described. We also studied foci with partial or complete atrophy without inflammation. The statistical methods included the Kruskal-Wallis and the Mann-Whitney tests and the Spearman correlation coefficient. The mean (range) of quadrants showing only PIA, PIA+CA, PIA+HGPIN, and PIA+HGPIN+CA was 3.29 (0-21), 2.51 (0-11), 0.77 (0-6), and 0.44 (0-4), respectively (p<0.01). Most of the foci of PIA were significantly located in a distance >5mm than <5mm from HGPIN or CA. There was no significant correlation between extent of PIA (p=0.64, r=0.05) with extent of HGPIN. There was a significant negative correlation of extent of PIA (p=0.01, r=-0.27) with extent of CA. Similar results were found considering foci either with or without inflammation. Chronic inespecific inflammation was not seen in foci of partial atrophy. A topographic relation of PIA to HGPIN and/or CA was not supported by our study
Mestrado
Anatomia Patologica
Mestre em Ciências Médicas
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Pearcy, Richard Malcolm. "Measurement of individualised quality of life in patients with prostatic adenocarcinoma." Thesis, University of Bristol, 2003. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.288289.

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Harper, Curt E. "Prostate cancer chemoprevention with genistein and resveratrol in models of spontaneously developing prostate cancer." Thesis, Birmingham, Ala. : University of Alabama at Birmingham, 2007. https://www.mhsl.uab.edu/dt/2007p/harper.pdf.

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Reggio, Ernesto. ""Tratamento percutâneo do adenocarcinoma de próstata por crioablação"." Universidade de São Paulo, 2006. http://www.teses.usp.br/teses/disponiveis/5/5153/tde-12042006-135835/.

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Diversas são as formas de tratamento do câncer de próstata, com resultados oncológicos e complicações variadas . A crioablação foi proposta nos anos 60 e com a evolução dos métodos de imagem a técnica ressurgiu; 44 pacientes, divididos em 3 grupos (portadores de tumor de alto risco, tumores de baixo risco e falha de tratamento após radioterapia) foram submetidos a crioterapia por via percutânea transperineal. Sobrevida livre de doença foi de 87% no grupo baixo risco, 34% no grupo alto risco e 58% no grupo de resgate após falha de radioterapia. A complicação mais freqüente foi disfunção erétil (94,5%); obstrução infravesical ocorreu em 9 pacientes (20,4%); 6 pacientes (13,6%) apresentaram algum grau de incontinência urinária. Não houve nenhum caso de fístula uretroretal ou mortalidade relacionada ao procedimento
There are several treatments for prostate cancer with an assorted oncologic results and complications. Cryoablation was proposed in the 60 and the improvement of radiological techniques allowed the perineal percutaneous treatment; 44 patients divided into three groups (high risk tumors, low risk tumors and patients with recurrent prostate cancer following radiotherapy) were submitted to perineal percutaneous prostate cryoablation. Biochemical-free survival was 87% in low risk group, 34% in the high-risk group and 58% in salvage cryoablation. Erectile dysfunction was the most frequent complication (94,5%); Infravesical obstruction occurred in 20,4% of the patients and six (13,6%) developed urinary incontinence. There were no urethrorectal fistulae or mortality related to the procedure
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Pereira, Renan Augusto. "Expressão de ciclina D1 em adenocarcinoma de próstata utilizando a técnica de imunohistoquímica." Universidade de São Paulo, 2013. http://www.teses.usp.br/teses/disponiveis/17/17143/tde-11062013-075728/.

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O câncer de próstata é o tumor maligno mais freqüente nos homens com idade superior a 50 anos, excetuando-se os tumores cutâneos. No Brasil estima-se para o ano de 2012 cerca de 60.180 casos novos deste tipo de neoplasia. Os marcadores tumorais permitem fazer o rastreamento do câncer, o diagnóstico diferencial entre uma neoplasia benigna e maligna, a avaliação de prognóstico e o acompanhamento terapêutico, assim como a detecção da recidiva tumoral. Dentre estes marcadores tumorais, tem-se dado muito atenção para as proteínas que mediam e participam da progressão do ciclo celular. A ciclina D1 é uma proteína nuclear de vida curta que é destruída pela via da ubiquitina ATP dependente, e está envolvida na transição celular da fase do ciclo G1 (repouso) para a fase S (síntese) tanto em células normais como em células neoplásicas. A super expressão de ciclina D1 remove a regulação normal do ciclo celular causando proliferação celular descontrolada, um crescimento anormal dos tecidos e a transformação para um fenótipo neoplásico, atuando como oncogene. No presente trabalho foi estudado a expressão de ciclina D1 em adenocarcinomas de próstata, tendo como objetivo avaliar a relação desta proteína com parâmetros epidemiológicos, clínicos e histopatológicos. Adicionalmente também foi feita comparação de escore de Gleason e lateralidade tumoral entre biópsias prostáticas com agulha e de prostatectomias radicais. No ensaio para ciclina D1 foram analisados 85 casos através de imunoistoquímica (IHQ) de material proveniente de prostatectomias radicais diagnosticados com adenocarcinoma de próstata entre os anos de 2005 e 2010 em nosso serviço. O método de avaliação se utilizou de microscopia ótica comum e contagem semi-quantitativa, comparado-se a expressão com achados clínicos, epidemiológicos e histopatológicos utilizando-se Teste T de Fisher, Qui Quadrado, Mann-Whitney, Curva ROC e correlação de Spearman. Os resultados demonstraram correlação positiva de ciclina D1 com escore de Gleason (p<0,05), com volume prostático (p=0,01) e uma tendência a correlação positiva com invasão perineural (p=0,07). Não houve correlação estatística entre ciclina D1 e o aumento de PSA, assim como outros achados histopatológicos. As biópsias prostáticas com agulha apresentaram subestimação em 40% dos casos para escore de Gleason e de 62,3% dos casos para lateralidade tumoral quando comparadas a prostatectomia radical. Já que as taxas de subestimação de escore de Gleason e lateralidade tumoral são relativamente altas e visto a urgência em se padronizar novos biomarcadores para o câncer prostático, sugerimos que ciclina D1 pode ser utilizada como biomarcador em patologia cirúrgica da próstata auxiliando numa gradação histológica mais precisa em biópsias com agulha colaborando para melhor vigilância e escolha terapêutica.
Prostate cancer is the most common malignant tumor in men older than 50 years, except for skin tumors. In Brazil it is estimated for the year 2012 about 60,180 new cases of this type of neoplasm. Tumor markers allow to cancer screening, differential diagnosis between a benign and malignant, assessment of prognosis and therapeutic monitoring, and detection of tumor recurrence. Among these tumor markers, has been given much attention for proteins that mediate and participate in cell cycle progression. Cyclin D1 is a short-lived nuclear protein that is destroyed by the ATP ubiquitin dependent pathway, and is involved in the transition of cell cycle G1 phase (resting) to the S phase (synthesis) cells both in normal and neoplastic cells. The overexpression of cyclin D1 removes the normal regulation of cell cycle causing uncontrolled cell proliferation, abnormal growth of tissues and transformation to a neoplastic phenotype, acting as an oncogene. In the present work we studied the expression of cyclin D1 in prostate adenocarcinomas, and to evaluate the relationship of this protein with epidemiologic factors, clinical and histopathological features. Additionally comparison was also made of Gleason score and laterality between tumor biopsies and prostate needle radical prostatectomies. In the assay for cyclin D1 were 85 cases analyzed by immunohistochemistry (IHC) of material from radical prostatectomies diagnosed with prostate adenocarcinoma between the years 2005 and 2010 at our institution. The evaluation method utilized were light microscopy and semi-quantitative score, comparing the cyclin D1 expression with clinical, epidemiological and histopathological features using Fisher\'s exact test, chi square test, Mann-Whitney test, ROC curve and Spearman correlation. The results showed a positive correlation of cyclin D1 with Gleason score (p <0.05), prostate volume (p = 0.01) and a trend toward positive correlation with perineural invasion (p = 0.07). There was no statistical correlation between cyclin D1 and increased PSA, as well as other histopathologic features. Prostate needle biopsies showed underestimation in 40% of cases for Gleason score and 62.3% of cases for tumor laterality when compared to radical prostatectomy. Since the rates of underestimation of Gleason score and tumor laterality are relatively high and the urgency to standardize new biomarkers for prostate cancer, we suggest that cyclin D1 may be used as biomarkers in surgical pathology of the prostate assisting more accurate histological grading in needle biopsies and collaborating for better surveillance and therapeutic choice.
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Books on the topic "Prostate adenocarcinoma"

1

Bruce, Andrew W., and John Trachtenberg, eds. Adenocarcinoma of the Prostate. London: Springer London, 1987. http://dx.doi.org/10.1007/978-1-4471-1398-0.

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Alers, J. C. Interphase cytogenetics of prostatic adenocarcinoma: (interfase cytogenetica van het adenocarcinoom van de prostaat). Delft: Eburon, 1997.

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Schmid, Hans-Peter. The clinically organ-confined adenocarcinoma of the prostate. Heidelberg: Steinkopff, 1994. http://dx.doi.org/10.1007/978-3-642-85430-9.

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The Gleason grading system: A complete guide for pathologists and clinicians. Philadelphia: Wolters Kluwer/Lippincott Williams & Wilkins Health, 2013.

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1925-, Bruce Andrew W., and Trachtenberg John 1949-, eds. Adenocarcinoma of the prostate. London: Springer-Verlag, 1987.

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Bruce, Andrew W., and John Trachtenberg. Adenocarcinoma of the Prostate. Springer, 2012.

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Bruce, Andrew W., and John Trachtenberg. Adenocarcinoma of the Prostate. Springer, 2011.

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(Editor), Anthony V. D'Amico, and Gerald E. Hanks (Editor), eds. Radiotherapeutic Management of Prostate Adenocarcinoma. A Hodder Arnold Publication, 1999.

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The Clinically Organ-Confined Adenocarcinoma of the Prostate: Natural History, Selection Criteria for Radical Prostatectomy and Prognostic Factors Bas (Forstschritte Der Urologie Und Nephrologie). Springer, 1996.

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Schmid, Hans-Peter. Clinically Organ-Confined Adenocarcinoma of the Prostate: Natural History, Selection Criteria for Radical Prostatectomy and Prognostic Factors Based on Long-Term Follow-up. Steinkopff, Dietrich, 2012.

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Book chapters on the topic "Prostate adenocarcinoma"

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Sundar, Gangadhara, Stephanie Ming Young, Eric Ting, Bingcheng Wu, Min En Nga, and Shantha Amrith. "Prostate Adenocarcinoma." In Ocular Adnexal Lesions, 297–99. Singapore: Springer Singapore, 2019. http://dx.doi.org/10.1007/978-981-13-3798-7_57.

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Gorovets, Daniel, Brandon S. Imber, Neil Desai, and Michael J. Zelefsky. "Prostate Adenocarcinoma." In Practical Guides in Radiation Oncology, 313–23. Cham: Springer International Publishing, 2022. http://dx.doi.org/10.1007/978-3-030-99590-4_25.

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Desai, Neil, and Michael Zelefksy. "Prostate Adenocarcinoma." In Target Volume Delineation and Field Setup, 213–25. Berlin, Heidelberg: Springer Berlin Heidelberg, 2012. http://dx.doi.org/10.1007/978-3-642-28860-9_24.

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Desai, Neil B., and Michael J. Zelefsky. "Prostate Adenocarcinoma." In Target Volume Delineation for Conformal and Intensity-Modulated Radiation Therapy, 361–75. Cham: Springer International Publishing, 2014. http://dx.doi.org/10.1007/174_2014_988.

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Bosland, Maarten C. "Adenocarcinoma, Prostate, Rat." In Genital System, 252–60. Berlin, Heidelberg: Springer Berlin Heidelberg, 1987. http://dx.doi.org/10.1007/978-3-642-72550-0_38.

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Alfonsi, Ugolino, Anna Ventriglia, Riccardo Manfredi, and Roberto Pozzi Mucelli. "Adenocarcinoma of the Prostate." In MRI of the Female and Male Pelvis, 183–228. Cham: Springer International Publishing, 2014. http://dx.doi.org/10.1007/978-3-319-09659-9_8.

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Hasson, Brian F., Charlie Ma, Lu Wang, David E. Wazer, Jay E. Reiff, Jay E. Reiff, Brandon J. Fisher, et al. "Adenocarcinoma of the Prostate." In Encyclopedia of Radiation Oncology, 5. Berlin, Heidelberg: Springer Berlin Heidelberg, 2013. http://dx.doi.org/10.1007/978-3-540-85516-3_1009.

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Skoog, Lambert, and Edneia Miyki Tani. "Prostate Adenocarcinoma, Cytological Findings." In Encyclopedia of Pathology, 425–27. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-33286-4_965.

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Shah, Rajal B., and Ming Zhou. "Histologic Variants of Acinar Adenocarcinoma, Ductal Adenocarcinoma, Neuroendocrine Tumors, and Other Carcinomas." In Prostate Biopsy Interpretation, 69–95. Cham: Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-030-13601-7_6.

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Wong, Ching Yee Oliver, and Dafang Wu. "Case 37: Metastatic Prostate Adenocarcinoma." In Phenotypic Oncology PET, 121–22. Cham: Springer International Publishing, 2022. http://dx.doi.org/10.1007/978-3-031-09737-9_37.

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Conference papers on the topic "Prostate adenocarcinoma"

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Hsu, L., N. Yee, K. Eng, and J. Betancourt. "An Unusual Diagnosis of Metastatic Prostate Adenocarcinoma." In American Thoracic Society 2020 International Conference, May 15-20, 2020 - Philadelphia, PA. American Thoracic Society, 2020. http://dx.doi.org/10.1164/ajrccm-conference.2020.201.1_meetingabstracts.a5794.

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Peswani, Disha L., Aditya Mathker, Dheerendra Kashyap, Karim Bensalah, Altug Tuncel, Wareef Kabbani, Jeffrey Cadeddu, Jung Hun Oh, Jean Gao, and Hanli Liu. "Feasibility of Detecting Prostate Adenocarcinoma Using Optical Reflectance Spectroscopy." In Biomedical Optics. Washington, D.C.: OSA, 2008. http://dx.doi.org/10.1364/biomed.2008.btuf44.

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Ramos, Rodrigo, Jorge Cutigi, Cynthia Ferreira, Adriane Evangelista, and Adenilso Simão. "Analyzing different cancer mutation data sets from breast invasive carcinoma (BRCA), lung adenocarcinoma (LUAD), and prostate adenocarcinoma (PRAD)." In Anais Principais do Simpósio Brasileiro de Computação Aplicada à Saúde. Sociedade Brasileira de Computação - SBC, 2020. http://dx.doi.org/10.5753/sbcas.2020.11500.

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With the advancements of next-generation sequencing (NGS) technologies, a massive volume of genetic data has been generated. It makes possible the study of complex disease by computational approaches. In the context of cancer, there is a huge variety of mutation data in public databases. However, it is not feasible to use all available data in every analysis; thus, a data subset must be selected. This work is aiming to investigate and understand the mutational characteristics presented in different cancer mutation data sets of the same type of cancer. To achieve this goal, exploration and visualization of cancer mutation data were performed. Several analyses are presented for three common types of cancer: 1) Breast Invasive Carcinoma (BRCA); 2) Lung Adenocarcinoma (LUAD); and Prostate Adenocarcinoma (PRAD). For each cancer type, three distinct data sets were analyzed in order to understand if there are significant differences or similarities among them. The analyses show that BRCA and LUAD have evidence of similarity among their data sets, while PRAD is likely heterogeneous.
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Gargan, P. E., and V. A. Ploplis. "IDENTIFICATION AND PURIFICATION OF AN INHIBITOR TO PLASMINOGEN ACTIVATORS FROM PROSTATE ADENOCARCINOMA CELLS." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643192.

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The rat prostate adencarcinoma cell line (PA-III), derived from qerm-free Lobund Wistar rats has served as a unique model for prostatic cancer. The supernatant from confluent cultures of the cell line was shown by zymographic analysis to contain three molecular forms of plasminogen activator. One of the activators was characterized in a previous study and has been classified as a tissue type plasminogen activator(Mr=30,000). In the same study the activator with a Mr=45,000 was shown to be of the urokinase class. The high molecular weight(Mr=120, 000) activator, which has not been described previously, was identified as a complex between the tissue plasminogen activator and an inhibitor. Dissociation of the activator and its inhibitor was achieved by incubation of the complex with ammonium hydroxide (1.5M) in the presence of NaDodGO4 (2%). Treatment with NaDodSO4 alone did not dissociate the complex but did however enhance its fibrinolytic activity, suggesting disruption of hydropnotic interactions leading to exposure of the activators active site.A scheme for the purification of the two plasminogen activators, the activator-inhibitor complex, and the free inhibitor was developed. The various components were purified approximately 1000 fold by hydrophobic interaction chromatography on Phenyl-Sepharose, affinity chromatography on Con A Sepharose and by gel filtration on Sephacryl S-200. The purified inhibitor was capable of inhibiting the fibrinolytic activity of both the urokinase type and tissue type plasminogen activators produced by the PAIII cells.
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Laksmi, Lidya Imelda, and T. Ibnu Alferraly. "Immunohistochemistry Expression of Ki-67 in Nodular Hyperplasia, Prostatic Intraepithelial Neoplasia and Adenocarcinoma Prostate." In International Conference of Science, Technology, Engineering, Environmental and Ramification Researches. SCITEPRESS - Science and Technology Publications, 2018. http://dx.doi.org/10.5220/0010098308840886.

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Cho, Han Jin, Ji Hee Kim, and Jung Han Yoon Park. "Abstract 609: Benzyl isothiocyanate inhibits prostate cancer development in the transgenic adenocarcinoma mouse prostate model." In 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.am2012-609.

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Cho, Han Jin, So Young Park, Eun Ji Kim, and Jung Han Yoon Park. "Abstract 2876: 3,3’-Diindolylmethane inhibits prostate cancer development in the transgenic adenocarcinoma mouse prostate model." In Proceedings: AACR 101st Annual Meeting 2010‐‐ Apr 17‐21, 2010; Washington, DC. American Association for Cancer Research, 2010. http://dx.doi.org/10.1158/1538-7445.am10-2876.

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Yang, Xu, Wang Hong, Guocan Wang, Anna Liu, Maarten c. Bosland, and Chung s. Yang. "Abstract 5247: δ-Tocopherol inhibits the development of prostate adenocarcinoma in prostate specific Pten-/- mice." In Proceedings: AACR Annual Meeting 2017; April 1-5, 2017; Washington, DC. American Association for Cancer Research, 2017. http://dx.doi.org/10.1158/1538-7445.am2017-5247.

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Popescu, Nirvana, Mircea Ivanescu, Mircea Nitulescu, Decebal Popescu, Cristian Vladu, Razvan M. Plesea, and Iancu E. Plesea. "On the Hölder Evaluation of the Prostate Adenocarcinoma Cellular Architecture." In 2020 24th International Conference on System Theory, Control and Computing (ICSTCC). IEEE, 2020. http://dx.doi.org/10.1109/icstcc50638.2020.9259745.

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Krishnan, Anand, Shubham Dwivedi, Maricris Bautista, and Tauqeer Iftikhar. "Abstract LB077: Adrenergic signaling induces neuroendocrine differentiation of prostate adenocarcinoma cells." In Proceedings: AACR Annual Meeting 2021; April 10-15, 2021 and May 17-21, 2021; Philadelphia, PA. American Association for Cancer Research, 2021. http://dx.doi.org/10.1158/1538-7445.am2021-lb077.

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Reports on the topic "Prostate adenocarcinoma"

1

Morey, Shannon R. Examination of the Role of DNA Methylation Changes in Prostate Cancer Using the Transgenic Adenocarcinoma of Mouse Prostate (TRAMP) Model. Fort Belvoir, VA: Defense Technical Information Center, March 2008. http://dx.doi.org/10.21236/ada483443.

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Kinney, Shannon R. Examination of the Role of DNA Methylation Changes in Prostate Cancer using the Transgenic Adenocarcinoma of Mouse Prostate (TRAMP) Model. Fort Belvoir, VA: Defense Technical Information Center, March 2009. http://dx.doi.org/10.21236/ada502739.

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Morey Kinney, Shannon R. Examination of the Role of DNA Methylation Changes in Prostate Cancer using the Transgenic Adenocarcinoma of Mouse Prostate (TRAMP) Model. Fort Belvoir, VA: Defense Technical Information Center, March 2010. http://dx.doi.org/10.21236/ada525616.

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Jaffray, David A. An On-Line Tomographic Guidance System for Dose Escalation in Radiotherapy for Adenocarcinoma of the Prostate. Fort Belvoir, VA: Defense Technical Information Center, August 2001. http://dx.doi.org/10.21236/ada402385.

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Eng, Charis E. Genetic Alterations in Epithelial and Stromal Compartments of Prostate Adenocarcinomas. Fort Belvoir, VA: Defense Technical Information Center, January 2005. http://dx.doi.org/10.21236/ada433975.

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Eng, Charis. Genetic Alterations in Epithelial and Stromal Compartments of Prostate Adenocarcinomas. Fort Belvoir, VA: Defense Technical Information Center, January 2004. http://dx.doi.org/10.21236/ada423023.

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Eng, Charis. Genetic Alterations in Epithelial and Stromal Compartments of Prostate Adenocarcinomas. Fort Belvoir, VA: Defense Technical Information Center, January 2006. http://dx.doi.org/10.21236/ada477315.

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Kotula, Leszek, Jiliu Xu, Jill A. Macoska, Piotr Kozlowski, and Magdalena Martinka. The Role of Human Spectrin SH3 Domain Binding Protein 1 (HSSH3BPl) in Prostatic Adenocarcinoma. Fort Belvoir, VA: Defense Technical Information Center, September 2004. http://dx.doi.org/10.21236/ada430579.

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Kotula, Leszek, Jiliu XU, Jill A. Macoska, Piotr Kozlowski, and Magdalena Martinka. The Role of Human Spectrin SH3 Domain Binding Protein 1 (HSSH3BP1) in Prostatic Adenocarcinoma. Fort Belvoir, VA: Defense Technical Information Center, September 2002. http://dx.doi.org/10.21236/ada411959.

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Kotula, Leszek, Jiliu Xu, Jill A. Macoska, Piotr Kozlowski, Magdalena Martinka, and Edward C. Jones. The Role of Human Spectrin SH3 Domain Binding Protein 1 (HSSH3BP1) in Prostatic Adenocarcinoma. Fort Belvoir, VA: Defense Technical Information Center, September 2003. http://dx.doi.org/10.21236/ada419543.

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