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Relevant bibliographies by topics / Prostate Cancer cells Interleukin-6

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Academic literature on the topic 'Prostate Cancer cells Interleukin-6'

Author: Grafiati

Published: 4 June 2021

Last updated: 1 February 2022

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Journal articles on the topic "Prostate Cancer cells Interleukin-6"

1

Li, Desheng, Shanbin Zhang, Minfang Zuo, Xinming Hu та Shuming He. "Interleukin-6, Tumor Necrosis Factor-α Expression Levels in Prostate Cancer Tissues and Their Effects on Epithelial Interstitial Transformation, Migration and Invasion in Prostate Cancer Cells". Journal of Biomaterials and Tissue Engineering 10, № 12 (2020): 1773–79. http://dx.doi.org/10.1166/jbt.2020.2496.

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Background: To investigate the expression of Interleukin-6, Interleukin-6 in prostate cancer tissues and its effect on migration and evasiveness of cancer cells. Material and Methods: The releasing of Interleukin-6, Tumor necrosis factor-α in prostate cancer cells was detected by ELISA method. For prostate cancer cells after knockout, additional Interleukin-6 or Tumor necrosis factor-α induction was given in vitro. After 12 h of culture, the effects of Interleukin-6, Tumor necrosis factor-α on the migration and evasiveness of prostate cancer cells were observed by Western blot method and matrices invasion experiment. Results: The expression of epithelial mesenchymal transition-related proteins, the migration and invasion ability of prostate cancer cells in each gene knockout group were significantly reduced. After induction of inflammatory factors (Interleukin-6 or Tumor necrosis factor-α) in the gene knockout group for 12 h, the expression levels of epithelial mesenchymal transition-related proteins, the migration and aggressiveness of prostate cancer were significantly higher than those after knockout. Conclusion: Interleukin-6 and Tumor necrosis factor-α can induce epithelial mesenchymal transition in LNCaP and PC3 cells, promote cell invasion and metastasis, and provide a new direction for future research.

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Chun, Jae Yeon, Nagalakshmi Nadiminty, Smitha Dutt, et al. "Interleukin-6 Regulates Androgen Synthesis in Prostate Cancer Cells." Clinical Cancer Research 15, no. 15 (2009): 4815–22. http://dx.doi.org/10.1158/1078-0432.ccr-09-0640.

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Cross, N. A., M. Papageorgiou, and C. L. Eaton. "Bone marrow stromal cells promote growth and survival of prostate cancer cells." Biochemical Society Transactions 35, no. 4 (2007): 698–700. http://dx.doi.org/10.1042/bst0350698.

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Prostate cancers frequently metastasize to the skeleton, and it has been hypothesized that this environment selectively supports the growth of these tumours. Specifically there is strong evidence that interactions between tumour cells and BMSCs (bone marrow stromal cells) play a major role in supporting prostate cancer growth and survival in bone. Here, we examine factors shown to be secreted by BMSCs, such as IGFs (insulin-like growth factors) and IL-6 (interleukin 6), shown to promote prostate cancer cell proliferation and to potentially replace the requirement for androgens. In addition we discuss another factor produced by BMSCs, osteoprotegerin, which may promote tumour cell survival by suppressing the biological activity of the pro-apoptotic ligand TRAIL (tumour-necrosis-factor-related apoptosis-inducing ligand).

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Afdal, Afdal, Eryati Darwin, Yanwirasti Yanwirasti, and Rizal Hamid. "The Expression of Transforming Growth Factor Beta-1 and Interleukin-6 on Human Prostate: Prostate Hyperplasia and Prostate Cancer." Open Access Macedonian Journal of Medical Sciences 7, no. 12 (2019): 1905–10. http://dx.doi.org/10.3889/oamjms.2019.548.

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BACKGROUND: Prostate hyperplasia and prostate cancer are two of the most common pathological condition of the prostate to be found on male. Both of these diseases share common pathogenesis involving inflammation of prostatic tissues. Chronic inflammation will induce the release of cytokines, followed by cells injury and tissues damage. One of the cytokines that play a role in prostate pathology is IL-6. The inflammation will also induce the releases of anti-inflammatory cytokines such as TGFβ-1.AIM: This study aims to analyse the expression of IL-6 and TGFβ-1, in prostate hyperplasia and prostate cancer. MATERIAL AND METHODS: This is an observational study, using paraffin-embedded tissue samples of prostate hyperplasia and prostate cancer. Samples were obtained from the laboratory of Pathological Anatomy, Faculty of Medicine, Andalas University, Padang, Indonesia. Immunohistochemistry was performed to detect the cytokine expression, and a semiqunatitaves measurement according to Immunoreactive score (IRS) was performed for evaluation. For the TGFβ-1, the stromal expression was also analysed by measurement of the stromal stained area. The correlation of cytokine expression to Gleason index score was also analysed in prostate cancer. RESULTS: The result showed that this study found that TGFβ-1 was detected both in the stromal component as well as epithelial. With the stromal being the dominant site of expression. The stromal TGFβ-1 expression was of significantly higher in prostate hyperplasia compares to prostate cancer (p < 0.05), while the epithelial expression of TGFβ-1 was not found to be significantly different. IL-6 was mostly expressed intracytoplasmic in epithelia. The IL-6 expression was significantly higher in prostate cancer compared to hyperplasia. However, there was no significant correlation to found between IL-6 expression to the Gleason Score among prostate cancers. CONCLUSION: This study concluded that there were differences in expression of both TGFβ-1 and IL-6 between prostate hyperplasia and prostate cancer tissue by immunohistochemistry.

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Feng, Siting, Qizhu Tang, Meng Sun, Jae Yeon Chun, Christopher P. Evans, and Allen C. Gao. "Interleukin-6 increases prostate cancer cells resistance to bicalutamide via TIF2." Molecular Cancer Therapeutics 8, no. 3 (2009): 665–71. http://dx.doi.org/10.1158/1535-7163.mct-08-0823.

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Culig, Zoran, Hannes Steiner, Georg Bartsch, and Alfred Hobisch. "Interleukin-6 regulation of prostate cancer cell growth." Journal of Cellular Biochemistry 95, no. 3 (2005): 497–505. http://dx.doi.org/10.1002/jcb.20477.

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Lin, Yi-Chia, Po-Cheng Liao, Te-Fu Tsai, et al. "Zoledronic Acid Elicits Proinflammatory Cytokine Profile in Osteolytic Prostate Cancer Cells." ISRN Pathology 2014 (April 23, 2014): 1–8. http://dx.doi.org/10.1155/2014/124746.

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Zoledronic acid (ZA), a bisphosphonate used to prevent skeletal fractures in patients with cancers, was demonstrated to induce apoptosis in a number of cancer cells. Our previous study showed that ZA also induces autophagic cell death in metastatic prostate cancer cells. However, the clinical trials using ZA in the treatment of metastatic prostate cancer did not have a longer diseases-free period. Since most of ZA was attracted to the bone after administration, we hypothesized that local prostate cancer cells may evolve prosurvival pathways upon low concentration of ZA treatment. In this study, we investigated the inflammatory effects of ZA on osteolytic PC3 prostate cancer cell, since inflammation was reported to be related to cancer development and survival. Exposure of PC3 cells to various concentrations of ZA resulted in induction of apoptosis and autophagy. The expression of inflammatory biomarkers including interleukin 6 (IL-6), cyclooxygenase-2 (COX-2), and NF-κB was remarkably upregulated in response to ZA treatment in a dose- and time-dependent manner. The production of IL-6 was elevated upon ZA treatment. The antiapoptotic protein Bcl2 was increased with parallel increased level of IL-6. Our data suggest that treatment with low concentrations of ZA enhances the inflammatory profile and may serve as a prosurvival signaling pathway in PC3 cells.

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Deeble, Paul D., Daniel J. Murphy, Sarah J. Parsons, and Michael E. Cox. "Interleukin-6- and Cyclic AMP-Mediated Signaling Potentiates Neuroendocrine Differentiation of LNCaP Prostate Tumor Cells." Molecular and Cellular Biology 21, no. 24 (2001): 8471–82. http://dx.doi.org/10.1128/mcb.21.24.8471-8482.2001.

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ABSTRACT Neuroendocrine (NE) differentiation in prostatic adenocarcinomas has been reported to be an early marker for development of androgen independence. Secretion of mitogenic peptides from nondividing NE cells is thought to contribute to a more aggressive disease by promoting the proliferation of surrounding tumor cells. We undertook studies to determine whether the prostate cancer cell line LNCaP could be induced to acquire NE characteristics by treatment with agents that are found in the complex environment in which progression of prostate cancer towards androgen independence occurs. We found that cotreatment of LNCaP cells with agents that signal through cyclic AMP-dependent protein kinase (PKA), such as epinephrine and forskolin, and with the cytokine interleukin-6 (IL-6) promoted the acquisition of an NE morphological phenotype above that seen with single agents. Convergent IL-6 and PKA signaling also resulted in potentiated mitogen-activated protein kinase (MAPK) activation without affecting the level of signal transducer and activator of transcription or PKA activation observed with these agents alone. Cotreatment with epinephrine and IL-6 synergistically increased c-fos transcription as well as transcription from the β4 nicotinic acetylcholine receptor subunit promoter. Potentiated transcription from these elements was shown to be dependent on the MAPK pathway. Most importantly, cotreatment with PKA activators and IL-6 resulted in increased secretion of mitogenic neuropeptides. These results indicate that PKA and IL-6 signaling participates in gene transcriptional changes that reflect acquisition of an NE phenotype by LNCaP cells and suggest that similar signaling mechanisms, particularly at sites of metastasis, may be responsible for the increased NE content of many advanced prostate carcinomas.

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Tsui, Ke-Hung, Kang-Shuo Chang, Hsin-Ching Sung та ін. "Mucosa-Associated Lymphoid Tissue 1 Is an Oncogene Inducing Cell Proliferation, Invasion, and Tumor Growth via the Upregulation of NF-κB Activity in Human Prostate Carcinoma Cells". Biomedicines 9, № 3 (2021): 250. http://dx.doi.org/10.3390/biomedicines9030250.

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Prostate cancer is one of the most common seen malignancies and the leading cause of cancer-related death among men. Given the importance of early diagnosis and treatment, it is worth to identify a potential novel therapeutic target for prostate cancer. Mucosa-associated lymphoid tissue 1 (MALT1) is a novel gene involved in nuclear factor κB (NF-κB) signal transduction by acting as an adaptor protein and paracaspase, with an essential role in inflammation and tumorigenesis in many cancers. This study investigated the functions and the potential regulatory mechanisms of MALT1 in the human prostate cancer cells. We found that MALT1 is abundant in prostate cancer tissues. MALT1 facilitated NF-κB subunits (p50 and p65) nuclear translocation to induce gene expression of interleukin 6 (IL-6) and C-X-C motif chemokine 5 (CXCL5) in prostate carcinoma cells. MALT1 promoted cell proliferation, invasion, and tumor growth in vitro and in vivo. MALT1 enhanced NF-κB activity in prostate carcinoma cells; moreover, NF-κB induced MALT1 expression determined by reporter and immunoblot assays, implying there is a positive feedback loop between MALT1 and NF-κB. In conclusion, MALT1 is a NF-κB-induced oncogene in the human prostate carcinoma cells.

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Zheng, Xiaoli, and Jin Chu. "Up-regulation of interleukin-33 serum levels in metastatic prostate cancer." American Journal of BioMedicine 4, no. 1 (2016): 56–70. http://dx.doi.org/10.18081/2333-5106/016-56-70.

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Prostate cancer is one of the most frequent cancers worldwide. IL-33 is the most recently described member of the IL-1 family of cytokines and is a ligand for the ST2 receptor. IL-33 is expressed intracellularly predominantly by stromal cells such as endothelial and epithelial cells as well as smooth muscle cells and fibroblasts and it is involved in the pathogenesis of different inflammatory process. The present study was undertaken to evaluate the prognostic significance of the serum levels IL-33 in patients with prostate cancer Ninety-five patients with prostate cancer, ages 59–88 years (71.2 ± 0.34 years), were examined in the present study, the exclusion criteria were presence of autoimmune diseases and none were under any treatment for prostate cancer at the time of examination. The diagnosis of prostate cancer was confirmed by needle biopsy or by C. Blood for the measurement of serum IL-33 was collected into nonheparinized tubes. Prognostic significance of tumor on disease-specific survival was assessed using univariate and multivariate Cox’s proportional hazards model analyses. Serum IL-33 levels were significantly higher in patients with metastatic prostate cancer than in patients with stage B and stage C prostate cancer, and univariate analysis demonstrated that IL-33 was associated with a poor prognosis in metastatic prostate cancer patients. These results indicate that the serum IL-33 level may be associated with the prognosis of patients with prostate cancer.

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Dissertations / Theses on the topic "Prostate Cancer cells Interleukin-6"

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Asbagh, Layka Abbasi Doymaz Fuat. "Investigating the role of zoledronic acid on interleukin-6 cytokine expression in prostate cancer cell lines/." [s.l.]: [s.n.], 2006. http://library.iyte.edu.tr/tezlerengelli/master/biyoteknoloji/T000552.pdf.

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Palmer, Jodie. "The IL-6 type cytokine family in prostate cancer." Monash University, Centre for Functional Genomics and Human Disease, 2003. http://arrow.monash.edu.au/hdl/1959.1/9441.

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Sanford, Daniel C. "C/EBP delta expression and function in prostate cancer biology." Columbus, Ohio : Ohio State University, 2006. http://rave.ohiolink.edu/etdc/view?acc%5Fnum=osu1141421403.

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MacManus, Christopher Francis. "Characterisation of Interleukin-8 signalling in prostate cancer cells : implications for disease progression." Thesis, Queen's University Belfast, 2005. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.426688.

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Kroon, Paula. "Importance of the IL-6/STAT3 signalling pathway in prostate cancer stem cells." Thesis, University of York, 2012. http://etheses.whiterose.ac.uk/3714/.

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Prostate cancer is the most diagnosed cancer in men in the Western world. Currently, most treatments are directed towards an androgen receptor-expressing cell, which encompasses the majority of prostate tumours. Unfortunately, the tumour recurs in the majority of patients. This recurrence is thought to arise due to the presence of a rare population of prostate cancer stem cells. These cells are also hypothesized to be responsible for tumour initiation, maintenance, recurrence and metastasis. It is therefore important to develop novel therapies to target these tumour-initiating cells. Interleukin-6 (IL-6) is a pro-inflammatory cytokine, which is involved in the regulation of a multitude of cellular functions, including proliferation, apoptosis, and differentiation. IL-6 and the associated JAK-STAT signalling pathway have been implicated in the development and progression of a variety of tumours, including prostate cancer. In this study we have demonstrated that these stem-like cells, selected from primary prostate cancer cultures have elevated IL-6 levels and express the IL-6 receptor, suggesting that these cells are constitutively active. Targeting IL-6, and downstream activation of STAT3, resulted in a significant decrease in colony forming ability of these stem-like cells. Moreover, treatment with a small molecule inhibitor of STAT3 resulted in a modest inhibition of tumour growth, with a significant increase in the proportion of CD24+ luminal cells. Whilst the impact on established tumours was modest, LLL12 abolished tumour initiation, suggesting that activation of STAT3, through IL-6, is important for the maintenance of the undifferentiated stem-like cells within prostate tumours. Targeting the JAK-STAT signalling pathway in this cell population might result in a more durable response to current standard of care therapies.

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Soori, 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.

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Basel, Dennis [Verfasser]. "Antagonizing autocrine Interleukin-6 receptor signaling inhibits prostate cancer growth in bone / Dennis Basel." Berlin : Medizinische Fakultät Charité - Universitätsmedizin Berlin, 2018. http://d-nb.info/1170876900/34.

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O'Brien, John D. "The Effect of Small Organic Compounds on Triple Negative Breast Cancer Cells." Ohio University / OhioLINK, 2012. http://rave.ohiolink.edu/etdc/view?acc_num=ohiou1344436677.

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Dang, David. "LYSOPHOSPHATIDIC ACID IS A MEDIATOR OF INTERLEUKIN-6 PRODUCTION IN OVARIAN CANCER CELLS." VCU Scholars Compass, 2009. http://scholarscompass.vcu.edu/etd/1907.

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Lysophosphatidic acid (LPA) is a naturally occurring bioactive lysophospholipid that mediates a broad range of cellular processes such as cell proliferation, survival, migration and invasion. LPA also plays a potential role in human oncogenesis as suggested by elevated expression of its receptors and its producing enzymes in malignant tissues. In the current study, we demonstrated that LPA is a potent mediator of interleukin-6 (IL-6) production in ovarian cancer. IL-6 is a pleiotropic cytokine which is thought to be an important mediator of ovarian cancer development and progression. Here, we demonstrated that IL-6 levels are indeed increased in the plasma of ovarian cancer patients as compared to normal women. The IL-6 concentrations in ascites of ovarian cancer patients are even higher than those present in the plasma samples. These results suggest that increased IL-6 are expressed and secreted by ovarian cancer cells, forming a gradient from the ascites to the blood. Ovarian cancer cells indeed produce IL-6 in culture. However, when these cells are starved in serum-free medium, they cease producing IL-6, suggesting that IL-6 is not constitutively expressed, but rather in response to exogenous factors present in serum. We showed that IL-6 expression is not driven by peptide growth factors such as insulin-like growth factor I or epidermal growth factor. Instead, IL-6 expression is most potently induced by the lysophospholipid growth factor LPA. Treatment of ovarian cancer cells with LPA leads to transcriptional activation of the IL-6 gene promoter through activation of the NF-kB and C/EBP transcription factors. LPA also induces tyrosine phosphorylation and activation of Stat-3, a well known intracellular effector of IL-6. However, blockade of IL-6 with a neutralizing antibody only slightly reduced Stat-3 phosphorylation in response to LPA, suggesting that LPA may induce Stat-3 directly or through secondary mediators other than IL-6. Together, these studies demonstrate the role of LPA in regulation of IL-6 production and the underlying mechanism in ovarian cancer.

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Champa, Zachary J. "Modulation of IL-6 and IL-8 Expression in Ovarian Cancer Cells by a Small OrganicCompound." Ohio University / OhioLINK, 2016. http://rave.ohiolink.edu/etdc/view?acc_num=ohiou1460987166.

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Book chapters on the topic "Prostate Cancer cells Interleukin-6"

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Culig, Zoran. "Interleukin-6 Function and Targeting in Prostate Cancer." In Advances in Experimental Medicine and Biology. Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-55617-4_1.

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Culig, Zoran. "Androgen-Independent Induction of Androgen-Responsive Genes by Interleukin-6 Regulation." In Androgen-Responsive Genes in Prostate Cancer. Springer New York, 2013. http://dx.doi.org/10.1007/978-1-4614-6182-1_11.

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Savary, C. A., and Eva Lotzová. "Down-Regulation of Human Bone Marrow Cells and Their Progenitors by IL-2-Activated Lymphocytes." In Interleukin-2 and Killer Cells in Cancer. CRC Press, 2018. http://dx.doi.org/10.1201/9781351073790-6.

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J., Nicholas. "Interleukin-6 in the Breast Tumor Microenvironment." In Breast Cancer - Focusing Tumor Microenvironment, Stem cells and Metastasis. InTech, 2011. http://dx.doi.org/10.5772/21947.

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"Targeting Interleukin-6 for the Treatment of Castration-Resistant Prostate Cancer." In Cutting Edge Therapies for Cancer in the 21st Century, edited by Sonia Godoy-Tundidor, Sucharitha Balasubramaniam, Ana Romero- Weaver, and Zoran Culig. BENTHAM SCIENCE PUBLISHERS, 2014. http://dx.doi.org/10.2174/9781608058808114010011.

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Morello, Matteo, Gustavo E. Ayala, Fabiana Rosati, et al. "Loss of Caveolin-1 Increases Tumor Cell Migration, Is Predictive of Disease-Free Survival, and Induces Steroidogenesis in Prostate-Derived Fibroblasts." In TRANSLATIONAL - Steroidal Regulation of Breast & Prostate Cancer. The Endocrine Society, 2011. http://dx.doi.org/10.1210/endo-meetings.2011.part1.or7.or06-6.

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RUBENSTEIN, M., P. D. GUINAN, M. W. SHAW, and R. J. ABLIN. "Altered Helper-T, Suppressor-T Cell Representation in Those with Advanced Stage Prostatic Cancer." In Protides of the Biological Fluids. Elsevier, 1985. http://dx.doi.org/10.1016/b978-0-08-031739-7.50222-6.

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Conference papers on the topic "Prostate Cancer cells Interleukin-6"

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Chun, Yae Yeon, Nagalakshmi Nadiminty, Wei Lou, et al. "Abstract 1727: Interleukin-6 and intracrine androgens in prostate cancer cells." 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.am10-1727.

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Wu, Kongming, Ke Chen, Kevin Li, Jennifer D. Wu, and Richard G. Pestell. "Abstract A21: DACH1 blocks prostate cancer cell growth and interleukin-6 signaling." In Abstracts: Second AACR International Conference on Frontiers in Basic Cancer Research--Sep 14-18, 2011; San Francisco, CA. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/1538-7445.fbcr11-a21.

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McNeel, Douglas, Marcella Fasso, Laura Johnson, et al. "Abstract 2837: Combined targeting of antigens expressed in prostate cancer and prostate stem cells using Listeria-based cancer vaccines for the treatment of prostate cancer." In 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.am2013-2837.

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Shigemura, Katsumi, Wen-chin Haung, Haiyen Zhau, et al. "Abstract 521: Active sonic hedgehog signaling between androgen independent human prostate cancer cells and normal/benign but not cancer-associated prostate stromal 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.am2011-521.

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Goksel, Gamze, Ayhan Bilir, Ruchan Uslu, Hakan Akbulut, Ummu Guven, and Gulperi Oktem. "Abstract 4072: Wnt1 gene expression alters heterogeneous population of prostate cancer cells; decreased expression pattern observed in CD133+/CD44+prostate cancer stem cells." In 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.am2013-4072.

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Yamamura, Soichiro, Takeshi Chiyomaru, Shinichiro Fukuhara, et al. "Abstract 5340: MicroRNA-720 promotes cell proliferation and invasion in prostate cancer cells." In 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.am2013-5340.

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Kulik, George A., Sazzad Hassan, Yelena Karpova, and Vitaliy Baurin. "Abstract SY04-01: Behavioral stress protects prostate cancer cells from apoptosis." 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-sy04-01.

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Dong, Xeusen, Liangliang Liu, Ning Xie, Shihua Sun, and Stephen R. Plymate. "Abstract 4082: Mechanisms of androgen receptor splicing in prostate cancer cells." In 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.am2013-4082.

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Wang, Jo-Hsin, Pei-Chi Li, Li-Chiung Lin, Fu-Ning Hsu, Mei-Chih Chen, and Ho Lin. "Abstract 2120: Cdk5 involves in interleukin-6 induces AR activation through phosphorylation of serine 727 Stat3 and serine 81 AR in prostate cancer cells." In Proceedings: AACR Annual Meeting 2014; April 5-9, 2014; San Diego, CA. American Association for Cancer Research, 2014. http://dx.doi.org/10.1158/1538-7445.am2014-2120.

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Too, Catherine K. L., Lynn N. Thomas та 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." У 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.

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Reports on the topic "Prostate Cancer cells Interleukin-6"

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Keller, Evan T. Interleukin-6 and Prostate Cancer Progression. Defense Technical Information Center, 2001. http://dx.doi.org/10.21236/ada398242.

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Keller, Evan T. Interleukin-6 and Prostate Cancer Progression. Defense Technical Information Center, 2002. http://dx.doi.org/10.21236/ada407280.

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Keller, Evan T. Interleukin-6 and Prostate Cancer Progression. Defense Technical Information Center, 2003. http://dx.doi.org/10.21236/ada418080.

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Knudsen, Beatrice S. Hepatocyte Growth Factor and Interleukin-6 in Prostate Cancer Bone Metastasis. Defense Technical Information Center, 2005. http://dx.doi.org/10.21236/ada435856.

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Knudesen, Beatrice S. Hepatocyte Growth Factor and Interleukin-6 in Prostate Cancer Bone Metastasis. Defense Technical Information Center, 2003. http://dx.doi.org/10.21236/ada416620.

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Knudsen, Beatrice S. Hepatocyte Growth Factor and Interleukin-6 in Prostate Cancer Bone Metastasis. Defense Technical Information Center, 2006. http://dx.doi.org/10.21236/ada467982.

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Knudsen, Beatrice S. Hepatocyte Growth Factor and Interleukin-6 in Prostate Cancer Bone Metastasis. Defense Technical Information Center, 2004. http://dx.doi.org/10.21236/ada428439.

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Redvers, Richard P. The Role of Interleukin-6/GP130 Signaling in Prostate Cancer Progression and Its Contribution to Bone Metastasis Morbidity. Defense Technical Information Center, 2007. http://dx.doi.org/10.21236/ada469521.

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