Relevant bibliographies by topics / Carcinoma of Prostate

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Academic literature on the topic 'Carcinoma of Prostate'

Author: Grafiati
Published: 4 June 2021
Last updated: 15 February 2022

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Journal articles on the topic "Carcinoma of Prostate"

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Sruogis, Algimantas, Ugnius Mickys, Tadas Petraitis, Edita Kaubrienė, and Feliksas Jankevičius. "Prostatos urotelio karcinoma, diagnozuota atlikus biopsiją. Klinikinis atvejis ir literatūros apžvalga." Lietuvos chirurgija 3, no. 4 (January 1, 2005): 0. http://dx.doi.org/10.15388/lietchirur.2005.4.2303.

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Algimantas Sruogis1, Ugnius Mickys2, Tadas Petraitis1, Edita Kaubrienė3, Feliksas Jankevičius11 Vilniaus universiteto Onkologijos institutoUrologijos skyrius,Santariškių g. 1, LT-08661 VilniusEl paštas: sruogis@loc.lt2 Lietuvos nacionalinis patologijos centras3 Vilniaus universiteto Onkologijos institutoIntervencinės echoskopijos irultragarsinės diagnostikos skyrius Tikslas Nustatyti diagnostinius prostatos urotelio karcinomos kriterijus, diferencijuojant urotelio karcinomą, peraugančią šlapimo pūslės kaklelį ir prostatą, nuo prostatos adenokarcinomos, peraugančios šlapimo pūslę. Atvejis Pacientas, 37 metų, trejus metus gydytas nuo lėtinio prostatito. Prostatos sekrete nustačius atipinių ląstelių, įtarus prostatos vėžį, ligonis nusiųstas į VU Onkologijos institutą. Tyrimo pro tiesiąją žarną, cistoskopijos, rentgenologinio, ultragarso ir serumo žymenų tyrimo duomenimis, diddesnių pokyčių nerasta. Atlikus transuretrinę šlapimo pūslės gleivinės biopsiją (TUR) iš šlapimo pūslės sienelių, kaklelio ir šlaplės prostatinės gleivinės, histologiškai nustatyti normalūs urotelio audiniai. Šlapimo citologinis tyrimas buvo neigiamas. Atlikus transrektalinę prostatos biopsiją, diagnozuotas prostatos urotelio navikas, imunohistochemiškai neigiamas PSA (prostatos specifiniam antigenui) ir teigiamas citokeratinams CK8 ir CK HMW. Pacientui buvo atlikta radikali cistoprostatektomija, pašalinti dubens limfmazgiai ir suformuotas šlapimo nuotėkis į ileum segmentą, išvestą į priekinę pilvo sieną (Brycker būdu). Morfologinė diagnozė – prostatos urotelio karcinoma. Taip pat diagnozuota prostatos adenokarcinoma ir prostatos intraepitelinė neoplazija. Po 15 mėnesių PSA lygis buvo 0,2 ng/ml, jokių ligos progresavimo požymių nepasireiškė. Remiantis šiuo klinikiniu atveju straipsnyje apžvelgiama literatūra, aiškinantis prostatos urotelio karcinomos ir adenokarcinomos skirtumus. Išvados Diagnozuojant prostatos urotelio karcinomą reikia vadovautis tam tikrais kriterijais: 1) prostatos urotelio karcinoma turi būti verifikuota makro-, mikroskopiškai ir imunohistocheminiais metodais, 2) neturėtų būti kitų urotelio karcinomos židinių organizme. Būtent prostatos biopsija leidžia patologui nustatyti tikslią diagnozę prieš operaciją. Imunohistocheminis tyrimas padeda atlikti diferencinę diagnostiką. Po operacijos tiriant pašalintus audinius, diagnozė patikslinama histomorfologiškai, naudojant imunohistocheminius tyrimus, net jei ir labai retai nustatoma prostatos urotelio karcinoma. Reikšminiai žodžiai: prostatos vėžys, urotelio karcinoma, prostatos urotelio karcinoma, prostatos biopsija Prostate urothelial carcinoma diagnosed on prostatic needle biopsy. Case report with literature overview Algimantas Sruogis1, Ugnius Mickys2, Tadas Petraitis1, Edita Kaubrienė3, Feliksas Jankevičius11 Vilnius University Institute of Oncology,Urology Department,Santariškių str. 1,LT-08661 Vilnius, LithuaniaE-mail: sruogis@loc.lt2 Lithuanian National Centre of Pathology3 Vilnius University Institute of Oncology,Radiology Department Objective To establish criteria for the diagnosis of primary urothelial prostate carcinoma after the differential diagnosis including high-grade urothelial carcinoma extending into the bladder neck and prostate versus poorly differentiated prostate adenocarcinoma extending into the bladder. Case report The patient was a 37-year-old man with severe prostatism symptoms, who presented with an atypical seminal vesicles fluid cytological test result. The prostate was also normal by the digital examination, endoscopy, roentgenography, ultrasonography and serum markers. A diagnostic transurethral resection of bladder mucosa, bladder neck specimen revealed normal urothelial tissues. The urine cytological test result was negative. The transrectal biopsy of the prostate revealed an urothelial carcinoma with a negative staining of PSA (prostate-specific antigen) and positive of cytokeratins CK 8 and CK HMW. The patient subsequently underwent radical cystoprostatectomy and pelvic lymphadenectomy with ileal conduit m. Brycker creation. The histological diagnosis was the urothelial carcinoma of the prostate. Also, the prostate showed foci of High Grade PIN and prostate adenocarcinoma. After 15 months the patient has a PSA level of 0.2 ng/mL, no symptoms, no evidence of progression. Based on this case of the urothelial carcinoma of prostate, the literature was reviewed and the morphological differentiation between urothelial carcinoma and adenocarcinoma of the prostate was discussed. Conclusions The diagnostic criteria are the following: (1) the tumor should be a macro-, microscopically and imunohistochemically verified as urothelial carcinoma localized exclusively in the prostate gland; (2) there must be no other primary urothelial carcinoma in the body. These criteria can be readily applied when evaluating surgical resection specimens. With the use of radiologically guided or endoscopically derived biopsies, however, the pathologist is increasingly called upon to make a diagnosis before definitive surgical resection. In these circumstances, the pathologist will often resort to immunostains to help refine the differential diagnosis. Moreover, even when surgical resection specimens are evaluated, immunostains are still used in conjunction with histomorphology to confirm the diagnosis, particularly when a rare entity such as primary urothelial prostate carcinoma is encountered. Keywords: prostate cancer, urothelial carcinoma, prostate urothelial carcinoma, prostatic needle biopsy
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Krušlin, Božo, Lucija Škara, Tonći Vodopić, Borna Vrhovec, Jure Murgić, Goran Štimac, Ana Fröbe, Cvjetko Lež, Monika Ulamec, and Koraljka Gall-Trošelj. "Genetics of Prostate Carcinoma." Acta Medica Academica 50, no. 1 (May 26, 2021): 71. http://dx.doi.org/10.5644/ama2006-124.327.

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<p>The aim of this review is to provide a brief overview of some current approaches regarding diagnostics, pathologic features, treatment, and genetics of prostate carcinoma (PCa). Prostate carcinoma is the most common visceral tumor and the second most common cancer-related cause of death in males. Clinical outcomes for patients with localized prostate cancer are excellent, but despite advances in prostate cancer treatments, castrate-resistant prostate cancer and metastatic prostate cancer patients have a poor prognosis. Advanced large-scale genomic studies revealed a large number of genetic alterations in prostate cancer. The meaning of these alterations needs to be validated in the specific prostate cancer molecular subtype context. Along these lines, there is a critical need for establishing genetically engineered mouse models, which would include speckle type BTB/POZ protein and isocitrate Dehydrogenase (NADP (+)) 1 mutant, as well as androgen receptor neuroendocrine subtypes of prostate cancer. Another urgent need is developing highly metastatic prostate cancer models, as only up to 17% of available models dis- play bone metastases and exhibit a less typical neuroendocrine prostate cancer or sarcomatoid carcinoma. Moreover, androgen deprivation and relapse should be mimicked in the genetically engineered mouse models, as androgen independence may yield a better model for metastatic castrate-resistant prostate cancer. The development of such refined animal models should be guid- ed by comparative genomics of primary versus corresponding metastatic tumors. Such an approach will have the potential to illuminate the key genetic events associated with specific molecular prostate cancer subsets and indicate directions for effective therapy.</p><p><strong>Conclusion</strong>. Despite excellent results in the treatment of localized prostatic carcinoma, castrate-resistant prostate can- cer and metastatic prostate cancer have a poor prognosis. Advanced large-scale genomic studies revealed a large number of ge- netic alterations in PCa. Experimental models of prostate carcinoma in genetically modified mice could provide new data about the genetic changes in such cancers and help in developing better animal models for treatment resistant prostate carcinomas.</p>
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Spirovski, M., M. A. Lucic, K. M. Koprivek, D. Kozic, N. M. Prvulovic, M. M. Popov, and D. Jovanovic. "Magnetic resonance imaging and proton magnetic resonance spectroscopy in the diagnosis of prostate carcinoma." Acta chirurgica Iugoslavica 56, no. 4 (2009): 183–87. http://dx.doi.org/10.2298/aci0904183s.

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Purpose: To estimate the diagnostic possibilities of magnetic resonance imaging (MRI) techniques and threedimensional multivoxel proton magnetic resonance spectroscopy (MRS) in patients with clinical suspicion of prostate carcinoma. Materials and methods: 36 patients suspected to have prostate carcinoma underwent MRI with dynamic contrast enhanced study and MRS at 1.5T MRI unit using a pelvic phased array coil. MRI and MRS results were correlated with pathohystological findings after radical prostatectomy and standard biopsy with 12 or 24 cores or guided biopsy. Results: Out of 44 detected prostate carcinomas, 38 (86.36%) demonstrated low T2W signal intensity while pathognomonic contrast enhancement has been detected in 40 (91%) carcinomas. MRS showed (Cho+Cr)/Ci ratio mean value of 3.52 in carcinoma, and 0.14 in normal prostatic tissue (p<0,01). Conclusion: MR techniques, both nonenhanced and contrast enhanced when combined with MRS can provide reliable diagnostic results in the evaluation of prostate carcinoma even by use of pelvic phased array coil at 1.5T unit.
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Robinson, Brian, Cristina Magi-Galluzzi, and Ming Zhou. "Intraductal Carcinoma of the Prostate." Archives of Pathology & Laboratory Medicine 136, no. 4 (April 1, 2012): 418–25. http://dx.doi.org/10.5858/arpa.2011-0519-ra.

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Context.—Intraductal carcinoma of the prostate (IDC-P) is a distinct clinicopathologic entity, characterized by an expansile proliferation of secretory cells within prostatic ducts and acini that demonstrate marked architectural and cytologic atypia. Intraductal carcinoma of the prostate is strongly associated with high-grade and high-volume, invasive prostate cancer and a poorer prognosis than cases without IDC-P. Objective.—To review the historic perspectives, pathologic and genetic features, diagnostic criteria and differential diagnoses, and the clinical significance of IDC-P. Data Sources.—Relevant studies indexed in PubMed. Conclusions.—It is critical to recognize IDC-P, especially in prostate biopsies in which the clinical implications of IDC-P are greatest. Morphologic criteria have been proposed to distinguish IDC-P from several other lesions with similar histologic appearance such as high-grade prostatic intraepithelial neoplasia, invasive cribriform prostate cancer, and urothelial carcinoma involving the prostate. Intraductal carcinoma of the prostate is an uncommon finding in prostate biopsies, and it is even rarer as an isolated finding without concomitant prostate cancer in biopsies. However, patients with isolated IDC-P in biopsies are recommended for either definitive treatment or immediate repeat biopsy.
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Billis, Athanase, and Luis A. Magna. "Prostate Elastosis." Archives of Pathology & Laboratory Medicine 124, no. 9 (September 1, 2000): 1306–9. http://dx.doi.org/10.5858/2000-124-1306-pe.

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Abstract Background.—Elastosis of the prostate may be seen on needle biopsy and radical prostatectomy specimens, but its significance is unknown. Prostatic atrophy (or postatrophic hyperplasia) is one of the most frequent mimics of prostatic adenocarcinoma. Objective.—To observe the frequent occurrence of elastosis of the prostate stroma in areas of postatrophic hyperplasia. Design.—A step-section method was used to cut the posterior lobe (or peripheral zone) in coronal planes at intervals of 0.3 to 0.5 cm in 100 consecutive autopsy specimens of men older than 40 years. Elastosis was detected because of a basophilic tinge of the stroma on hematoxylin-eosin stain and confirmed using elastic fiber stains. Presence of elastosis correlated with the following variables: age, prostatic atrophy (simple, hyperplastic, or sclerotic), local arteriosclerosis, histologic carcinoma, high-grade prostatic intraepithelial neoplasia, benign or malignant nephrosclerosis, generalized atherosclerosis, nodular prostatic hyperplasia, and acute inflammation. For statistics, a stepwise linear regression method adjusted for age was used. Results and Conclusions.—Elastosis was found in 65 of the prostates examined and was significantly more frequent with increasing age (P &lt; .001), prostatic atrophy (P &lt; .001), and local arteriosclerosis (P &lt; .02). There was no significant relation to histologic carcinoma, high-grade prostatic intraepithelial neoplasia, benign or malignant nephrosclerosis, generalized atherosclerosis, nodular prostatic hyperplasia, and acute inflammation. The correlation with local arteriosclerosis favors a possible role of ischemia to its etiopathogenesis. The absence of correlation to neoplastic and preneoplastic lesions and the striking spatial relationship of elastosis to prostatic atrophy (or postatrophic hyperplasia) add a new microscopic feature for the diagnosis of this latter lesion, helping in the differential diagnosis with prostate adenocarcinoma.
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Mneimneh, Wadad S., Konstantinos Linos, Paras Shah, Timothy A. Jennings, Hugh Fisher, and Tipu Nazeer. "Micropapillary Carcinoma: New Variant of Prostatic Acinar Adenocarcinoma." Archives of Pathology & Laboratory Medicine 136, no. 11 (November 1, 2012): 1447–50. http://dx.doi.org/10.5858/arpa.2011-0359-cr.

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A micropapillary variant of prostatic acinar adenocarcinoma has not been reported in the literature. Herein, we report a case of a 50-year-old patient who presented with an elevated prostate-specific antigen concentration and was subsequently diagnosed with prostatic acinar adenocarcinoma on biopsy. Radical prostatectomy specimen revealed prostatic carcinoma with Gleason score 4 + 5 = 9/10, with micropapillary component constituting 80% of tumor volume. Immunohistochemical studies of the prostate carcinoma showed a homogeneously positive prostate-specific antigen and α-methylacyl-CoA racemase, high-molecular-weight cytokeratin, and p63 protein cocktail pattern of staining in both micropapillary and conventional components. Pelvic lymph nodes were negative for metastatic disease. In contrast to the aggressive behavior of micropapillary carcinomas of other organs, the disease in our patient has thus far followed a more benign course, with low stage on presentation and a 2-year follow-up free of disease. However, prognostic correlation should be established on large series in order to assign this variant to a grade category within the Gleason scheme.
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Tonini, G., R. Rosini, A. Teppa, V. Aulenti, F. Kalantary, M. Tosana, D. Bianchi, and F. Zorzi. "Adenoid cystic/basal cell carcinoma of the prostate: case report." Urologia Journal 75, no. 4 (October 2008): 245–48. http://dx.doi.org/10.1177/039156030807500409.

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Although most prostate carcinomas belong to the conventional acinar type, unusual variants have been reported. The adenoid cystic/basal cell carcinoma of the prostate is a rare tumor with distinctive histopathologic features. There are quite few publications in the literature concerning the diagnosis, treatment, and prognosis of this neoplasm. Methods. A 71-year-old man had an increased PSA value (5.11 ng/dL); the prostatic biopsy examination was positive for adenoid cystic/basal cell carcinoma. For this reason we proceeded with radical prostatectomy. The histology examination showed an acinar conventional carcinoma and adenoid cystic/basal cell carcinoma. At eight months the patient did not show any recurrence. Conclusions. Various histologic and immunohistochemical features are helpful in recognizing the adenoid cystic/basal cell carcinoma of the prostate. Clinically, the only difference from a conventional adenocarcinoma is that the PSA value is usually normal or only slightly increased. This tumor has a biological potential that can result in metastases in some cases; the current treatment consists primarily in the surgical resection. A close, long-term follow-up is strongly recommended.
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Smith, D. C., J. A. Tucker, and D. L. Trump. "Hypercalcemia and neuroendocrine carcinoma of the prostate: a report of three cases and a review of the literature." Journal of Clinical Oncology 10, no. 3 (March 1992): 499–505. http://dx.doi.org/10.1200/jco.1992.10.3.499.

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PURPOSE Hypercalcemia is a rare complication of prostate cancer, and no definite association with any histologic subtype of prostatic malignancy has been documented. We have recently seen three patients who developed hypercalcemia in the setting of prostate cancer. All had neuroendocrine carcinoma of the prostate (NCPs), which prompted an exploration of the potential association of hypercalcemia with NCP. DESIGN An extensive review of literature published in the English-language was conducted to identify cases of hypercalcemia associated with prostate cancer and well-documented cases of NCP. RESULTS We found 17 reported cases of hypercalcemia clearly associated with prostate cancer and a total of 61 cases of well-documented NCP. Including our cases, 11 of the 20 reported cases of hypercalcemia associated with prostate carcinoma were in patients with neuroendocrine carcinomas. CONCLUSION Hypercalcemia in the setting of prostate cancer should prompt a search for unusual histologies.
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(MD Radiology), Dr Mohammed Ameer Ali Khan Afrose MBBS. "MRI in Diagnosis of Prostate Carcinoma." Journal of Medical Science And clinical Research 05, no. 03 (March 14, 2017): 18676–84. http://dx.doi.org/10.18535/jmscr/v5i3.67.

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He, Lin, Christopher Metter, Vitaly Margulis, and Payal Kapur. "A Review Leveraging a Rare and Unusual Case of Basal Cell Carcinoma of the Prostate." Case Reports in Pathology 2021 (May 4, 2021): 1–8. http://dx.doi.org/10.1155/2021/5520581.

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Basal cell carcinoma (BCC) is a rare nonacinar variant of prostatic carcinoma. In spite of prostatic acinar adenocarcinoma being one of the most common carcinomas in prostate, <100 prostatic BCC cases have been reported to date. Adenoid cystic/cribriform histology has been described in varying proportions to occur in prostatic BCC and is reported to be associated with aggressive behavior and high risk of metastasis. Herein, we present a case of prostatic BCC with adenoid cystic morphology, comprehensively describe its immunohistochemical and MYB/MYBL1 gene rearrangement findings, discuss its differential diagnosis, and review the literature of this rare entity.
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Dissertations / Theses on the topic "Carcinoma of Prostate"

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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
Made available in DSpace on 2018-08-16T20:47:04Z (GMT). No. of bitstreams: 1 Brasil_AntonioAugustoAzevedoVital_M.pdf: 4698841 bytes, checksum: 5d8edbe0e4ce7ce977504d4197f2f985 (MD5) Previous issue date: 2010
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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Herrera, Maria Lourdes C. "The expression of various growth factors in the normal human prostate, benign prostatic hyperplasia, and prostate carcinoma." Thesis, Hong Kong : University of Hong Kong, 1996. http://sunzi.lib.hku.hk/hkuto/record.jsp?B1754628X.

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Chang, Ching-Jey George. "Prostate, benign hypertrophy and prostatic carcinoma - a study of cell biology of prostate and chemotherapy for prostatic hypertrophy and prostatic cancer /." The Ohio State University, 1994. http://rave.ohiolink.edu/etdc/view?acc_num=osu1487856906256116.

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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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Hellawell, Giles. "The IGF1R in human prostate cancer." Thesis, University of Oxford, 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.249458.

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Roulson, Jo-An. "Bone marrow endothelial transmigration of prostate carcinoma cells." Thesis, University of Manchester, 2008. https://www.research.manchester.ac.uk/portal/en/theses/bone-marrow-endothelial-transmigration-of-prostate-carcinoma-cells(997acbf2-bbbc-455b-bb84-b439ffb9f839).html.

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Haq, Mahmudul. "Host-tumor interactions in skeletal metastasis of prostate carcinoma." Thesis, McGill University, 1992. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=56996.

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Approximately 70% of patients with prostatic cancer develop bone metastases. Metastatic prostate adenocarcinomas are associated with high mortality rates and represent a leading cause of cancer-related deaths among males. To study the host-tumor interactions underlying the predilection of prostate cancer cells for skeletal bone, an experimental model was developed using rat Dunning carcinoma Mat-LyLu cells. Inoculations of these cells into the left ventricle of the heart led to the development of spinal metastases in 100% of inoculated animals. A subline of Mat-LyLu (Mat-LyLu-B5) was subsequently selected through sequential inoculation of bone marrow derived carcinoma cells into the left ventricle of the heart and was found to have an increased metastatic potential compared to the parental line. The possible role of tumor cell adhesion to host cells in the process of bone marrow colonization was then investigated in vitro using the metastatic line and primary cultures of rat bone marrow-derived stromal cells. It was found that the adhesion of the metastatic Mat-LyLu cells to a bone marrow stromal cell culture highly enriched for endothelial cells (BMEC) was significantly higher than the adhesion to other bone-derived cells including non-endothelial BM stromal cells (3x) and osteoblasts (1.4x). It was also significantly higher than the adhesion to rat fibroblasts (5.5x) and to hepatic endothelial cells (7x). The results suggest that the adhesion of prostate carcinoma cells to the bone marrow endothelium may play a role in their metastasis to bone.
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Weaver, Jennifer. "Development of an in vitro model for investigating the properties of human prostate epithelial cells and prostatic carcinoma cells /." St Andrews, 2008. http://hdl.handle.net/10023/755.

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Amiry, Naeem. "Investigating the role of TFF1 in mammary and prostate carcinoma." Thesis, University of Auckland, 2011. http://hdl.handle.net/2292/6480.

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Trefoil Factor-1 (TFF1) belongs to the family of trefoil factor peptides. Trefoil factors protect the gastrointestinal tract against mucosal injury. Trefoil peptides are upregulated and secreted in an autocrine and paracrine fashion in response to gastrointestinal injury. They facilitate cell migration and prevent anoikis. TFF1 is also expressed in various tissues and regulated by multiple cellular processes. Several studies have also demonstrated increased expression of TFF1 in a high percentage of mammary and prostate carcinoma cases. However, the functional role of autocrine TFF1 in mammary and prostate carcinoma has not been previously elucidated. Herein, I demonstrate that forced expression of TFF1 in mammary carcinoma cells resulted in increased total cell number as a consequence of increased cell proliferation and survival. Forced expression of TFF1 enhanced anchorage-independent growth and promoted scattered cell morphology with increased cell migration and invasion. Moreover, forced expression of TFF1 increased tumor size in xenograft models. Conversely, depletion of TFF1 by RNA interference (RNAi) in mammary carcinoma cells significantly reduced anchorageindependent growth and migration. Furthermore, neutralization of secreted TFF1 protein by polyclonal antibody decreased mammary carcinoma cell viability in vitro and resulted in regression of mammary carcinoma xenografts. In prostate carcinoma cell lines utilized herein, I demonstrate that forced expression of TFF1 did not affect proliferation and anchorage-independent growth. However, forced expression of TFF1 enhanced prostate carcinoma cell migration and invasion. Additionally, functional inhibition of TFF1 by RNAi or polyclonal antibody abrogated prostate carcinoma cell invasion. I have therefore demonstrated that TFF1 possesses oncogenic functions in mammary carcinoma cells and enhances prostate carcinoma cell invasion. Functional antagonism of TFF1 can therefore be considered as a novel therapeutic strategy for mammary carcinoma.
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Tran, Nhan Le. "Molecular characterization of cadherin expression and function in prostate carcinoma." Diss., The University of Arizona, 2002. http://hdl.handle.net/10150/279962.

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The epithelial cytoarchitecture and function in the prostate gland are maintained in part by the E-cadherin/catenin complex. In human prostate adenocarcinoma, an association between the loss of E-cadherin, increased Gleason score, and extracapsular dissemination has been observed. Further characterizations of human prostate carcinoma cell lines show loss of E-cadherin and expression of N-cadherin in poorly differentiated prostate carcinoma cell lines. N-cadherin expression correlates with an invasive phenotype in cancer cells and mediates the interactions between malignant tumor cells and N-cadherin expressing cells, such as prostate stromal fibroblasts. Additionally, N-cadherin-mediated intercellular adhesions generate a compensatory mechanism that promotes anchorage-independent growth and suppresses apoptosis through a phosphatidylinositol 3-kinase/Akt/protein kinase B survival pathway. Activated Akt results in the phosphorylation of two downstream substrates, Bad and CREB, to regulate Bcl-2 protein stability and bcl-2 transcription, respectively. Under serum deprivation, N-cadherin intercellular adhesion stimulates a 4-fold increase in bcl-2 mRNA expression resulting in a 3.5-fold increase in Bcl-2 protein expression, while the cellular level of proapoptotic protein Bax remains constant. Following N-cadherin homophilic adhesion the phosphatidylinositol 3-kinase p85 subunit is found in immunoprecipitates of the N-cadherin/catenin complex. The recruitment of phosphatidylinositol 3-kinase is dependent on both N-cadherin homophilic adhesion and N-cadherin binding to an intact actin cytoskeleton. These results suggest that the association of the N-cadherin/catenin complex with the actin cytoskeleton acts as a scaffold to localize the activation of phosphatidylinositol 3-kinase/Akt signaling pathway at adherens junctions. The identification of outside-in signal transduction mediated by N-cadherin adhesion provides new information on anti-apoptotic cell-cell adhesion mechanisms enhancing the activity of the phosphatidylinositol 3-kinase/Akt cell survival pathway in metastatic prostate carcinoma. Collectively, these observations indicate that alterations in cadherin expression play a role in prostate cancer progression that may have a profound affect on metastatic cell survival.
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Books on the topic "Carcinoma of Prostate"

1

M, Bolla, Rambeaud J. J, and Vincent François, eds. Local prostatic carcinoma. Basel: Karger, 1994.

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Petrovich, Zbigniew, Luc Baert, and Luther W. Brady, eds. Carcinoma of the Prostate. Berlin, Heidelberg: Springer Berlin Heidelberg, 1996. http://dx.doi.org/10.1007/978-3-642-60956-5.

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Altwein, Jens E., Peter Faul, and Wolfgang Schneider, eds. Incidental Carcinoma of the Prostate. Berlin, Heidelberg: Springer Berlin Heidelberg, 1991. http://dx.doi.org/10.1007/978-3-642-76129-4.

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service), SpringerLink (Online, ed. General Methods and Overviews, Lung Carcinoma and Prostate Carcinoma. Dordrecht: Springer Netherlands, 2008.

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Hayat, M. A., ed. General Methods and Overviews, Lung Carcinoma and Prostate Carcinoma. Dordrecht: Springer Netherlands, 2008. http://dx.doi.org/10.1007/978-1-4020-8442-3.

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Hayat, M. A. Handbook of Immunohistochemistry and in Situ Hybridization of Human Carcinomas: Molecular Pathology, Colorectal Carcinoma, and Prostate Carcinoma. Burlington: Elsevier, 2005.

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Wernert, Nicholas. Immunhistochemie der Prostata und des Prostatakarzinoms: Neue Aspekte der Histogenese = Immunohistochemistry of the prostate and prostate carcinoma : new aspects of histogenesis. Stuttgart: Fischer, 1991.

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Frohmüller, H. G. W. 1928- and Wirth Manfred P, eds. Uro-oncology: Current status and future trends : proceedings of a Uro-Oncological Workshop, held in Würzburg, Federal Republic of Germany, June 22-25, 1988. New York: Wiley-Liss, 1990.

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Molecular Pathology, Colorectal Carcinoma, and Prostate Carcinoma. Elsevier, 2002. http://dx.doi.org/10.1016/s1874-5784(02)x8001-5.

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E, Altwein Jens, Faul Peter, and Schneider W. 1937-, eds. Incidental carcinoma of the prostate. Berlin: Springer-Verlag, 1991.

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Book chapters on the topic "Carcinoma of Prostate"

1

Denis, L. J., P. A. Catton, M. K. Gospodarowicz, G. P. Murphy, P. O. Hedlund, and F. K. Mostofi. "Prostate Carcinoma." In Prognostic Factors in Cancer, 216–23. Berlin, Heidelberg: Springer Berlin Heidelberg, 1995. http://dx.doi.org/10.1007/978-3-642-79395-0_24.

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Allen, Derek C. "Prostate Carcinoma." In Histopathology Reporting, 335–50. London: Springer London, 2013. http://dx.doi.org/10.1007/978-1-4471-5263-7_31.

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Ansell, I. D. "Prostate — Carcinoma." In Atlas of Male Reproductive Pathology, 61–64. Dordrecht: Springer Netherlands, 1985. http://dx.doi.org/10.1007/978-94-009-4868-6_13.

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Johnson, David Y., Shilpi Wadhwa, and Frank E. Johnson. "Prostate Carcinoma." In Patient Surveillance After Cancer Treatment, 399–401. Totowa, NJ: Humana Press, 2012. http://dx.doi.org/10.1007/978-1-60327-969-7_80.

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O’Rourke, Declan. "Prostate Carcinoma." In Histopathology Reporting, 377–93. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-27828-1_31.

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Allen, Derek C. "Prostate Carcinoma." In Histopathology Reporting, 291–300. London: Springer London, 2000. http://dx.doi.org/10.1007/978-1-4471-3671-2_31.

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Carey, Brendan M. "Imaging Localised Prostate Carcinoma." In Interstitial Prostate Brachytherapy, 33–62. Berlin, Heidelberg: Springer Berlin Heidelberg, 2013. http://dx.doi.org/10.1007/978-3-642-36499-0_3.

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Kirkels, W. J. "Screening for Prostate Cancer." In Carcinoma of the Prostate, 21–26. Berlin, Heidelberg: Springer Berlin Heidelberg, 1996. http://dx.doi.org/10.1007/978-3-642-60956-5_3.

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Van De Voorde, W. M. "Pathology of Prostatic Carcinoma." In Carcinoma of the Prostate, 27–50. Berlin, Heidelberg: Springer Berlin Heidelberg, 1996. http://dx.doi.org/10.1007/978-3-642-60956-5_4.

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Bagshaw, M. A., R. S. Cox, and S. L. Hancock. "External Beam Radiotherapy for Localized Prostatic Cancer at Stanford: Update at the 38th Year." In Carcinoma of the Prostate, 243–58. Berlin, Heidelberg: Springer Berlin Heidelberg, 1996. http://dx.doi.org/10.1007/978-3-642-60956-5_17.

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Conference papers on the topic "Carcinoma of Prostate"

1

Vargas López, Julián David, Nicolás Toro-García, Juan Bernardo Gomez Mendoza, Paula Andrea Toro-Castaño, Rafael Pava-Marín, and Álex Enrique Pava-Ripoll. "Histopathology color image processing in prostate carcinoma." In 15th International Symposium on Medical Information Processing and Analysis, edited by Jorge Brieva, Eduardo Romero, and Natasha Lepore. SPIE, 2020. http://dx.doi.org/10.1117/12.2542359.

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Yıldız, Pınar, Sariha Buyukluoglu, and Mesut Bayraktaroğlu. "Bilateral chylothorax due to gastric carcinoma and metastatic prostate carcinoma: Case reports." In ERS International Congress 2019 abstracts. European Respiratory Society, 2019. http://dx.doi.org/10.1183/13993003.congress-2019.pa2020.

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Wu, Lisa Y., Tiancheng Liu, Bernard Vanwie, William C. Davis, and Clifford E. Berkman. "Abstract A20: Molecular Detection of Prostate-Specific Membrane Antigen in Canine Prostate Carcinoma Cells." In Proceedings: AACR Special Conference on Chemical Systems Biology: Assembling and Interrogating Computational Models of the Cancer Cell by Chemical Perturbations--Jun 27-30, 2012; Boston, MA. American Association for Cancer Research, 2012. http://dx.doi.org/10.1158/1538-7445.csb12-a20.

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Jiang, Hongmei, Man-Tzu Wang, and Daotai Nie. "Abstract LB-292: NANOG promotes chemoresistance in prostate carcinoma cells." 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-lb-292.

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Gangar, Subhash Chander, Gagan Deep, and Rajesh Agarwal. "Abstract 5661: Silibinin inhibits advanced human prostate carcinoma-induced osteoclastogenesis." 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.am10-5661.

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Nolte, A., JP Klußmann, and R. Lang-Roth. "Metastasis of a prostate carcinoma as a differential diagnosis in dysphonia." In Abstract- und Posterband – 90. Jahresversammlung der Deutschen Gesellschaft für HNO-Heilkunde, Kopf- und Hals-Chirurgie e.V., Bonn – Digitalisierung in der HNO-Heilkunde. Georg Thieme Verlag KG, 2019. http://dx.doi.org/10.1055/s-0039-1686613.

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Shieh, Felice, Laura Lavery, Chitai T. Chu, Rebecca Richards-Kortum, Andrew D. Ellington, and Brian A. Korgel. "Semiconductor nanocrystal-aptamer bioconjugate probes for specific prostate carcinoma cell targeting." In Biomedical Optics 2005, edited by Alexander N. Cartwright and Marek Osinski. SPIE, 2005. http://dx.doi.org/10.1117/12.597249.

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Silveira, Jr., Landulfo, Kátia Ramos M. Leite, Miguel Srougi, Fabrício L. Silveira, Marcos Tadeu T. Pacheco, and Carlos A. Pasqualucci. "Could Raman spectroscopy discriminate the biochemical alterations among prostate carcinoma and benign prostate tissues? An in vitro study." In SPIE BiOS. SPIE, 2012. http://dx.doi.org/10.1117/12.910437.

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Morris, Brandon L., Talearia Young, and Cynthia M. van Golen. "Abstract 2924: IGF-IR inibition induces MAPK signaling in prostate carcinoma cells." In Proceedings: AACR 102nd Annual Meeting 2011‐‐ Apr 2‐6, 2011; Orlando, FL. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/1538-7445.am2011-2924.

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Bauer, Markus, Sebastian Zürner, Markus Kreuz, Dominik Otto, Georg Popp, and Ulf-Dietrich Braumann. "Histological grading of the prostate carcinoma using deep learning: an unsupervised approach." In Digital and Computational Pathology, edited by John E. Tomaszewski and Aaron D. Ward. SPIE, 2021. http://dx.doi.org/10.1117/12.2581043.

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Reports on the topic "Carcinoma of Prostate"

1

McCarthy, James B. Hyaluronan Biosynthesis in Prostate Carcinoma. Fort Belvoir, VA: Defense Technical Information Center, January 2003. http://dx.doi.org/10.21236/ada415957.

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McCarthy, James B. Hyaluronan Biosynthesis in Prostate Carcinoma. Fort Belvoir, VA: Defense Technical Information Center, January 2004. http://dx.doi.org/10.21236/ada427815.

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McCarthy, James B. Hyaluronan Biosynthesis in Prostate Carcinoma. Fort Belvoir, VA: Defense Technical Information Center, January 2007. http://dx.doi.org/10.21236/ada470599.

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Xiang, Rong. Novel Combination Therapy for Prostate Carcinoma. Fort Belvoir, VA: Defense Technical Information Center, February 2003. http://dx.doi.org/10.21236/ada417972.

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Xiang, Rong. Novel Combination Therapy for Prostate Carcinoma. Fort Belvoir, VA: Defense Technical Information Center, February 2005. http://dx.doi.org/10.21236/ada435053.

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Xiang, Rong. Novel Combination Therapy for Prostate Carcinoma. Fort Belvoir, VA: Defense Technical Information Center, February 2004. http://dx.doi.org/10.21236/ada423719.

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Lotan, Tamara L. Molecular Profiling of Intraductal Carcinoma of the Prostate. Fort Belvoir, VA: Defense Technical Information Center, October 2014. http://dx.doi.org/10.21236/ada613285.

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Shareef, Mohammed M., Biju Isaac, Sakhi Philip, Thirupandiyur Udayakumar, and Alan Pollack. AKT in Differential miRNA Processing in Prostate Carcinoma. Fort Belvoir, VA: Defense Technical Information Center, September 2013. http://dx.doi.org/10.21236/ada593281.

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James, Ralph, and Michael Furey. Development of Compact Gamma Camera for Detection of Prostate Carcinoma. Office of Scientific and Technical Information (OSTI), July 2013. http://dx.doi.org/10.2172/1095507.

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Roselli, Charles E. Effect of Saw Palmetto on the Development and Progression of Prostate Carcinoma in TRAMP Mice. Fort Belvoir, VA: Defense Technical Information Center, April 2006. http://dx.doi.org/10.21236/ada451378.

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