Littérature scientifique sur le sujet « Cell survival of prostate cancer cells »
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Articles de revues sur le sujet "Cell survival of prostate cancer cells"
Tindall, Donald J. « S1 Molecular Mechanisms of Prostate Cancer Cell Survival following Androgen Ablative Therapy ». Japanese Journal of Urology 97, no 2 (2006) : 127. http://dx.doi.org/10.5980/jpnjurol.97.127_2.
Texte intégralCross, N. A., M. Papageorgiou et C. L. Eaton. « Bone marrow stromal cells promote growth and survival of prostate cancer cells ». Biochemical Society Transactions 35, no 4 (20 juillet 2007) : 698–700. http://dx.doi.org/10.1042/bst0350698.
Texte intégralKashani, Kilbas, Yerlikaya, Gurkan et Arisan. « Cisplatin and Paclitaxel Modulated the Cell Survival Potential of Prostate Cancer Cells ». Proceedings 40, no 1 (5 janvier 2020) : 42. http://dx.doi.org/10.3390/proceedings2019040042.
Texte intégralLEE, E. C. Y., et M. TENNISWOOD. « PROGRAMMED CELL DEATH AND SURVIVAL PATHWAYS IN PROSTATE CANCER CELLS ». Archives of Andrology 50, no 1 (janvier 2004) : 27–32. http://dx.doi.org/10.1080/01485010490250498.
Texte intégralSalih, T., K. Aziz, S. Thiyagarajan, M. Armour, B. Shanmugam, J. Zeng, S. J. Adam, D. W. Felsher, T. L. DeWeese et P. T. Tran. « Radiosensitization of MYC-overexpressing prostate cancer cells by statins. » Journal of Clinical Oncology 29, no 7_suppl (1 mars 2011) : 26. http://dx.doi.org/10.1200/jco.2011.29.7_suppl.26.
Texte intégralMamouni, Kenza, Georgios Kallifatidis et Bal L. Lokeshwar. « Targeting Mitochondrial Metabolism in Prostate Cancer with Triterpenoids ». International Journal of Molecular Sciences 22, no 5 (28 février 2021) : 2466. http://dx.doi.org/10.3390/ijms22052466.
Texte intégralDariane, Charles, Sylvie Clairefond, Benjamin Péant, Laudine Communal, Zhe Thian, Véronique Ouellet, Dominique Trudel et al. « High Keratin-7 Expression in Benign Peri-Tumoral Prostatic Glands Is Predictive of Bone Metastasis Onset and Prostate Cancer-Specific Mortality ». Cancers 14, no 7 (23 mars 2022) : 1623. http://dx.doi.org/10.3390/cancers14071623.
Texte intégralJähnisch, Hanka, Susanne Füssel, Andrea Kiessling, Rebekka Wehner, Stefan Zastrow, Michael Bachmann, Ernst Peter Rieber, Manfred P. Wirth et Marc Schmitz. « Dendritic Cell-Based Immunotherapy for Prostate Cancer ». Clinical and Developmental Immunology 2010 (2010) : 1–8. http://dx.doi.org/10.1155/2010/517493.
Texte intégralHarris, Koran S., et Bethany A. Kerr. « Prostate Cancer Stem Cell Markers Drive Progression, Therapeutic Resistance, and Bone Metastasis ». Stem Cells International 2017 (2017) : 1–9. http://dx.doi.org/10.1155/2017/8629234.
Texte intégralPulukuri, Sai MuraliKrishna, Christopher S. Gondi, Sajani S. Lakka, Aman Jutla, Norman Estes, Meena Gujrati et Jasti S. Rao. « RNA Interference-directed Knockdown of Urokinase Plasminogen Activator and Urokinase Plasminogen Activator Receptor Inhibits Prostate Cancer Cell Invasion, Survival, and Tumorigenicity in Vivo ». Journal of Biological Chemistry 280, no 43 (26 août 2005) : 36529–40. http://dx.doi.org/10.1074/jbc.m503111200.
Texte intégralThèses sur le sujet "Cell survival of prostate cancer cells"
Wilce, Alice J. « Understanding the function and mechanisms of intestinal cell kinase in the growth and survival of prostate cancer cells ». Thesis, Queensland University of Technology, 2015. https://eprints.qut.edu.au/85439/1/Alice_Wilce_Thesis.pdf.
Texte intégralZhang, Xiaomeng. « Significance and molecular basis of Id-1 in regulation of cancer cell survival and invasion ». Click to view the E-thesis via HKUTO, 2007. http://sunzi.lib.hku.hk/hkuto/record/B39325477.
Texte intégralFaysal, Joanne M. « The Effects of Hypoxia with Concomitant Acidosis on Prostate Cancer Cell Survival ». Scholarly Repository, 2010. http://scholarlyrepository.miami.edu/oa_theses/69.
Texte intégralWin, Hla Yee. « Role of protein kinase C-iota in prostate cancer ». [Tampa, Fla.] : University of South Florida, 2008. http://purl.fcla.edu/usf/dc/et/SFE0002322.
Texte intégralZhang, Xiaomeng, et 張效萌. « Significance and molecular basis of Id-1 in regulation of cancer cell survival and invasion ». Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2007. http://hub.hku.hk/bib/B39325477.
Texte intégralSoori, Mehrnoosh. « Neuroendocrine differentiation of prostate cancer cells a survival mechanism during early stages of metastatic colonization of bone / ». Access to citation, abstract and download form provided by ProQuest Information and Learning Company ; downloadable PDF file, 105 p, 2009. http://proquest.umi.com/pqdweb?did=1654490661&sid=6&Fmt=2&clientId=8331&RQT=309&VName=PQD.
Texte intégralEkman, Maria. « The role of Smad7 and TRAF6 in Prostate Cancer Cell Invasion, Migration and Survival ». Doctoral thesis, Uppsala universitet, Ludwiginstitutet för cancerforskning, 2011. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-159150.
Texte intégralArmstrong, Chris. « Inhibition of treatment-induced cell survival signalling enhances radiosensitivity of PTEN-deficient prostate cancer ». Thesis, Queen's University Belfast, 2015. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.680869.
Texte intégralBUSA', ROBERTA. « Role of the RNA-binding protein Sam68 in prostate cancer cell survival and proliferation ». Doctoral thesis, Università degli Studi di Roma "Tor Vergata", 2009. http://hdl.handle.net/2108/908.
Texte intégralProstate carcinoma (PCa) is one of the main causes of death in the western male population. Although initially controlled by anti-androgenic therapies, PCa often evolves to become androgen-insensitive and highly metastatic. A predominant role in the development of androgen-refractoriness is played by the upregulation of signal transduction pathways that allow prostate cancer cells to autonomously produce their own requirements of growth factors and nutrients (Grossmann et al., 2001). The tyrosine kinase Src is frequently activated in advanced human prostate carcinomas and in our laboratory we have observed that its activation correlates with tyrosine phosphorylation of the RNA-binding protein Sam68 (Paronetto et al., 2004), belonging to the STAR family (Signal transduction and RNA metabolism) and involved in RNA metabolism. In the first part of this PhD Thesis, we have investigated the expression and function of Sam68 in human prostate cancer cells. We observed that Sam68 is up-regulated both at protein and mRNA levels in patients affected by PCa. Moreover, it was observed that down-regulation of Sam68 by RNAi in LNCaP prostate cancer cells delayed cell cycle progression, reduced the proliferation rate and sensitized cells to apoptosis induced by DNA-damaging agents. Microarray analyses revealed that a subset of genes involved in proliferation and apoptosis were altered when Sam68 was knocked down in LNCaP cells. Finally, stable cell lines expressing a truncated GFP-Sam68GSG protein, that interacts with endogenous Sam68 affecting its activity, displayed reduced growth rates and higher sensitivity to cisplatin-induced apoptosis, resembling down-regulation of Sam68 by RNAi. Together, these results indicate that Sam68 expression supports prostate cancer cells proliferation and survival to cytotoxic agents (Busà et al., 2007). Stemming from this evidence, we then aimed to investigate the role played by Sam68 in the response to genotoxic drugs such as mitoxantrone (MTX), a topoisomerase II inhibitor.We observed that MTX caused a subcellular re-localization of Sam68 from nucleoplasm to nuclear granules. Co-staining experiments indicated that Sam68-positive nuclear granules are sites of accumulation of several RNA-binding proteins involved in alternative splicing, such as SR proteins like SC35 and ASF/SF2, and TIA-1 and hnRNP A1, involved in cellular stress responses to various stimuli (Guil et al., 2006). Sam68 also accumulated in cytoplasmic granules that were also co-stained with hnRNP A1 and TIA-1, suggesting that these structures are the well described cytoplasmic stress granules (SGs). These data strongly suggest that Sam68 is part of a RNA-mediated stress response of the cell. Thus, we have begun to investigate whether changes in subcellular localization of Sam68 induced by genotoxic drugs affect alternative splicing of Sam68 target mRNAs, such as CD44 (Matter et al., 2002). Preliminary experiments have shown that MTX treatment in PC3 cells induces changes in alternative splicing of CD44 pre-mRNA. In particular, inclusion of variable exons v5 and v6, known to be regulated by Sam68 (Matter et al., 2002; Cheng and Sharp, 2006), was stimulated. We are current extending these studies to determine whether downregulation of Sam68 by RNAi affects these modifications of CD44 alternative splicing caused by MTX Since Sam68 is known to link signal transduction pathways to RNA metabolism (Lukong and Richard, 2003), we asked whether changes in Sam68 subcellular localization induced by MTX are determined by activation of specific signal transduction pathways. Our data show that although MTX triggers activation of DNA damage pathway, through ATM kinase, and stress-induced MAPKs p38 and JNK1/2 pathways, specific inhibition of these pathways did not affect the subcellular relocalization of Sam68. Thus, it is possible that direct changes in the chromatin structure or function trigger the observed accumulation of Sam68 and splicing factors in nuclear granules. Finally, a set of observations performed during our studies implicate Sam68 in nucleolar functions. In a co-immunoprecipitation experiment aimed at the identification of Sam68-interacting proteins in LNCaP cells we found Nucleolin, a nucleolar protein involved in rRNA metabolism (Rickards et al., 2007). This interaction has been confirmed and mapped to the carboxyterminal region of Sam68 by in vitro studies. Moreover, a RNA-protein co-immunoprecipitation experiment revealed that Sam68 binds 18S rRNA These observations lead us to investigate whether Sam68 plays a role in rRNA metabolism. First, we observed by FISH analysis, and then confermed by real time PCR, that downregulation of Sam68 caused a significant increase in the levels of pre-rRNA compared with control siRNA treated cells. Moreover, ChIP assays aimed at determining the site of the association of Sam68 with rDNA in PC3 cells revealed that Sam68 binds the 18S rRNA coding region. Thus, the results presented herein strongly suggest a novel role of Sam68 in the regulation of pre-rRNA maturation. Our current studies are aimed at investigating this hypothesis further. References: Busà R, Paronetto MP, Farini D, Pierantozzi E, Botti F, Angelini DF, Attisani F, Vespasiani G, Sette C., Oncogene 2007 26(30):4372-82. Cheng C, Sharp PA. (2006). Regulation of CD44 alternative splicing by SRm160 and its potential role in tumor cell invasion. Mol Cell Biol. 26(1):362-70. Grossmann ME, Tindall DJ (2001). Androgen receptor signaling in androgen-refractory prostate cancer. J Natl Cancer Inst. 93:1687-97; Guil S, Long JC, Cáceres JF. (2006). hnRNP A1 relocalization to the stress granules reflects a role in the stress response. Mol Cell Biol. 26(15):5744-58. Lukong KE, Richard S (2003). Sam68, the KH domain-containing superSTAR. Bioch. Biophys. Acta 1653: 73-86. Matter N, Herrlich P, Konig H (2002). Signal-dependent regulation of splicing via phosphorylation of Sam68. Nature 420:691-695. Paronetto MP, Farini D, Sammarco I, Maturo G, Vespasiani G, Geremia R et al (2004). Expression of a truncated form of the c-Kit tyrosine kinase receptor and activation of Src kinase in human prostatic cancer. Am. J. Path. 164:1243-1251; Rickards B, Flint SJ, Cole MD, LeRoy G. (2007). Nucleolin is required for RNA polymerase I transcription in vivo. Mol Cell Biol. 27(3):937-48.
Eng, Grace Tzi Ai. « An investigation of the effect of some stable nitroxide antioxidants in prostate cancer cells ». Thesis, Queensland University of Technology, 2015. https://eprints.qut.edu.au/82982/4/Grace_Eng_Thesis.pdf.
Texte intégralLivres sur le sujet "Cell survival of prostate cancer cells"
Meridith, Alan T. Handbook of prostate cancer cell research : Growth, signalling, and survival. New York : Nova Biomedical Books, 2009.
Trouver le texte intégralT, Meridith Alan, dir. Handbook of prostate cancer cell research : Growth, signalling, and survival. Hauppauge, NY : Nova Science, 2009.
Trouver le texte intégralHandbook of prostate cancer cell research : Growth, signalling, and survival. New York : Nova Biomedical Books, 2009.
Trouver le texte intégralSardinian International Meeting on Modulating Factors in Multistage Chemical Carcinogenesis (5th 1989 Cagliari, Italy). Chemical carcinogenesis 2 : Modulating factors. New York : Plenum Press, 1991.
Trouver le texte intégralClarke, Noel W. Metastatic disease in prostate cancer. Sous la direction de James W. F. Catto. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199659579.003.0068.
Texte intégralMeridith, Alan T. Handbook of Prostate Cancer Cell Research : Growth, Signalling and Surviva. Nova Science Publishers, Incorporated, 2009.
Trouver le texte intégralGrant, Warren, et Martin Scott-Brown. Prevention of cancer. Sous la direction de Patrick Davey et David Sprigings. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199568741.003.0350.
Texte intégralEisen, Tim. The patient with renal cell cancer. Sous la direction de Giuseppe Remuzzi. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0172.
Texte intégralFarghaly, Samir A. Adoptive Cell Immunotherapy for Epithelial Ovarian Cancer. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190248208.003.0005.
Texte intégral(Editor), A. Columbano, F. Feo (Editor), P. Pani (Editor) et R. Pascale (Editor), dir. Chemical Carcinogenesis, Volume 2 : Modulating Factors. Plenum Press, 1991.
Trouver le texte intégralChapitres de livres sur le sujet "Cell survival of prostate cancer cells"
Buczek, Magdalena E., Jerome C. Edwards et Tarik Regad. « Prostate Cancer and Prostate Cancer Stem Cells ». Dans Principles of Stem Cell Biology and Cancer, 193–212. Chichester, UK : John Wiley & Sons, Ltd, 2015. http://dx.doi.org/10.1002/9781118670613.ch10.
Texte intégralBadeaux, Mark A., et Dean G. Tang. « Prostate Cancer Cell Heterogeneity and Prostate Cancer Stem Cells ». Dans Cancer Stem Cells, 183–91. Hoboken, NJ : John Wiley & Sons, 2014. http://dx.doi.org/10.1002/9781118356203.ch14.
Texte intégralMoscatelli, David, et E. Lynette Wilson. « The Prostate Stem Cell Niche ». Dans Stem Cells and Prostate Cancer, 91–109. New York, NY : Springer New York, 2013. http://dx.doi.org/10.1007/978-1-4614-6498-3_6.
Texte intégralLiu, Qingxin, Yun Zhang, Danielle Jernigan et Alessandro Fatatis. « Survival and Growth of Prostate Cancer Cells in the Bone : Role of the Alpha-Receptor for Platelet-Derived Growth Factor in Supporting Early Metastatic Foci ». Dans Signaling Pathways and Molecular Mediators in Metastasis, 261–75. Dordrecht : Springer Netherlands, 2011. http://dx.doi.org/10.1007/978-94-007-2558-4_11.
Texte intégralChanda, Diptiman, et Selvarangan Ponnazhagan. « Mesenchymal Stem Cells in Prostate Cancer ». Dans Stem Cell Therapeutics for Cancer, 171–85. Hoboken, NJ : John Wiley & Sons, Inc, 2013. http://dx.doi.org/10.1002/9781118660423.ch13.
Texte intégralJoshi, Molishree U., Courtney K. von Bergen et Scott D. Cramer. « Targeting the Prostate Stem Cell for Chemoprevention ». Dans Stem Cells and Prostate Cancer, 127–48. New York, NY : Springer New York, 2013. http://dx.doi.org/10.1007/978-1-4614-6498-3_8.
Texte intégralUlkus, Lindsey, Min Wu et Scott D. Cramer. « Stem Cell Models for Functional Validation of Prostate Cancer Genes ». Dans Stem Cells and Prostate Cancer, 149–73. New York, NY : Springer New York, 2013. http://dx.doi.org/10.1007/978-1-4614-6498-3_9.
Texte intégralKlein, Sandra, Fiona M. Frame et Norman J. Maitland. « Therapy Resistance in Prostate Cancer : A Stem Cell Perspective ». Dans Stem Cells : Current Challenges and New Directions, 279–300. New York, NY : Springer New York, 2013. http://dx.doi.org/10.1007/978-1-4614-8066-2_13.
Texte intégralChang, Woochul, Byeong-Wook Song et Ki-Chul Hwang. « Mesenchymal Stem Cell Survival in Infarcted Myocardium : Adhesion and Anti-death Signals ». Dans Stem Cells and Cancer Stem Cells, Volume 10, 35–43. Dordrecht : Springer Netherlands, 2013. http://dx.doi.org/10.1007/978-94-007-6262-6_4.
Texte intégralIchikawa, T., Y. Furuya, K. Akakura et J. Shimazaki. « Growth-Stimulating Effect of Growth Factor(s) from Androgen Independent Tumor Cells (CS 2-Cell) on Androgen Responsive Tumor Cells (SC 115-Cell) ». Dans Molecular and Cellular Biology of Prostate Cancer, 279. Boston, MA : Springer US, 1991. http://dx.doi.org/10.1007/978-1-4615-3704-5_29.
Texte intégralActes de conférences sur le sujet "Cell survival of prostate cancer cells"
Su, Fengmin, Yiming Fan, He Xu, Nannan Zhao, Yangbo Deng, Yulong Ji et Hongbin Ma. « Ultra-High Speed Vitrification of Prostate Cancer Cells Based on Thin Film Evaporation ». Dans ASME 2019 6th International Conference on Micro/Nanoscale Heat and Mass Transfer. American Society of Mechanical Engineers, 2019. http://dx.doi.org/10.1115/mnhmt2019-3910.
Texte intégralChetram, Mahandranauth A., Danaya A. Bethea, Taylor J. Stowers et Cimona V. Hinton. « Abstract 538 : ROS differentially regulates prostate cancer cell survival ». Dans 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.am2012-538.
Texte intégralKreutz, Fernando T. « Abstract A029 : Cell-based cancer immunotherapy using tumor presenting cells : A phase II trial with local advance prostate cancer patients ». Dans Abstracts : CRI-CIMT-EATI-AACR Inaugural International Cancer Immunotherapy Conference : Translating Science into Survival ; September 16-19, 2015 ; New York, NY. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/2326-6074.cricimteatiaacr15-a029.
Texte intégralChang, Megan, Micaela Morgado, Viral Patel, Michael Gwede, Mary Cindy Farach-Carson et Nikki Delk. « Abstract B15 : Bone marrow stromal cell-secreted inflammatory cytokines promote treatment resistance and survival of prostate cancer cells ». Dans Abstracts : AACR Special Conference on Cellular Heterogeneity in the Tumor Microenvironment ; February 26 — March 1, 2014 ; San Diego, CA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1538-7445.chtme14-b15.
Texte intégralNiture, Suresh, Malathi Ramalinga, Habib Kedir et Deepak Kumar. « Abstract 2342 : TNFAIP8 promotes prostate cancer cell survival by modulating autophagy ». Dans 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.am2017-2342.
Texte intégralBaraket, David, Jing Zhang, Theresa Barberi, Alan D. Friedman et Ido Paz-Priel. « Abstract 841 : The role of C/EBPβ in prostate cancer cell survival. » Dans Proceedings : AACR 104th Annual Meeting 2013 ; Apr 6-10, 2013 ; Washington, DC. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1538-7445.am2013-841.
Texte intégralToo, Catherine K. L., Lynn N. Thomas et Jennifer Merrimen. « Abstract 86 : Prolactin and testosterone induction of carboxypeptidase-D to promote cell survival is greater in prostate cancer cells than benign prostate cells, and their synergistic action in prostate cancer cells is effectively blocked by receptor antagonists Δ1-9-G129R and flutamide. » Dans Proceedings : AACR 104th Annual Meeting 2013 ; Apr 6-10, 2013 ; Washington, DC. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1538-7445.am2013-86.
Texte intégralTanaka, Mai, Samantha S. Dykes et Dietmar W. Siemann. « Abstract 2507 : Axl suppression inhibits cell migration, invasion and survival in breast and prostate cancer cell lines ». Dans Proceedings : AACR Annual Meeting 2018 ; April 14-18, 2018 ; Chicago, IL. American Association for Cancer Research, 2018. http://dx.doi.org/10.1158/1538-7445.am2018-2507.
Texte intégralLiang, Yayun, Benford Mafuvadze, Xiaoqin Zou, Cynthia Besch-Williford et Salman M. Hyder. « Abstract 5422 : Inhibition of oxidosqualene cyclase blocks proliferation and survival of prostate cancer cells ». Dans Proceedings : AACR 106th Annual Meeting 2015 ; April 18-22, 2015 ; Philadelphia, PA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1538-7445.am2015-5422.
Texte intégralGoulart, Ana Emilia, Luciana B. Ferreira, Paula Priscilla de Freitas, Nadia Batoreu, MARTIN H. BONAMINO et Etel Rodrigues Pereira Gimba. « Abstract 163 : Investigation of molecular mechanisms by which PCA3 modulates prostate cancer cell survival ». Dans Proceedings : AACR 106th Annual Meeting 2015 ; April 18-22, 2015 ; Philadelphia, PA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1538-7445.am2015-163.
Texte intégralRapports d'organisations sur le sujet "Cell survival of prostate cancer cells"
McCarthy, James B., et Eva Turley. Hyaluronan Tumor Cell Interactions in Prostate Cancer Growth and Survival. Fort Belvoir, VA : Defense Technical Information Center, décembre 2009. http://dx.doi.org/10.21236/ada525644.
Texte intégralMcCarthy, James B., et Eva Turley. Hyaluronan Tumor Cell Interactions in Prostate Cancer Growth and Survival. Fort Belvoir, VA : Defense Technical Information Center, décembre 2006. http://dx.doi.org/10.21236/ada470057.
Texte intégralElledge, Stephen. Identification of Genes Required for the Survival of Prostate Cancer Cells. Fort Belvoir, VA : Defense Technical Information Center, juin 2011. http://dx.doi.org/10.21236/ada547231.
Texte intégralElledge, Stephen J. Identificaton of Genes Required for the Survival of Prostate Cancer Cells. Fort Belvoir, VA : Defense Technical Information Center, juin 2010. http://dx.doi.org/10.21236/ada552841.
Texte intégralKnudsen, Beatrice S. Control of Prostate Cancer Cell Growth and Survival by the Extracellular Matrix. Fort Belvoir, VA : Defense Technical Information Center, juillet 1999. http://dx.doi.org/10.21236/ada371208.
Texte intégralHuang, Wen-Chin. A Novel Anti-Beta2-Microglobulin Antibody Inhibition of Androgen Receptor Expression, Survival, and Progression in Prostate Cancer Cells. Fort Belvoir, VA : Defense Technical Information Center, mai 2010. http://dx.doi.org/10.21236/ada545568.
Texte intégralHuang, Wen-Chin. A Novel Anti-Beta2-Microglobulin Antibody Inhibition of Androgen Receptor Expression, Survival, and Progression in Prostate Cancer Cells. Fort Belvoir, VA : Defense Technical Information Center, janvier 2012. http://dx.doi.org/10.21236/ada561161.
Texte intégralBrooks, James D. Single Cell Characterization of Prostate Cancer-Circulating Tumor Cells. Fort Belvoir, VA : Defense Technical Information Center, septembre 2013. http://dx.doi.org/10.21236/ada596639.
Texte intégralBrooks, James B. Single Cell Characterization of Prostate Cancer Circulating Tumor Cells. Fort Belvoir, VA : Defense Technical Information Center, août 2011. http://dx.doi.org/10.21236/ada550987.
Texte intégralPizzo, Salvatore, et Robin E. Bachelder. Targeting Prostate Cancer Stemlike Cells through Cell Surface-Expressed GRP78. Fort Belvoir, VA : Defense Technical Information Center, octobre 2014. http://dx.doi.org/10.21236/ada613546.
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