Prostate cancer cell-stromal cell crosstalk via FGFR1 mediates antitumor activity of dovitinib in bone metastases

Bone is the most common site of prostate cancer (PCa) progression to a therapy-resistant, lethal phenotype. We found that blockade of fibroblast growth factor receptors (FGFRs) with the receptor tyrosine kinase inhibitor dovitinib has clinical activity in a subset of men with castration-resistant PC...

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Autor principal: Wan, X.
Otros Autores: Corn, P.G, Yang, J., Palanisamy, N., Starbuck, M.W, Efstathiou, E., Li-Ning Tapia, E.M, Zurita, A.J, Aparicio, A., Ravoori, M.K, Vazquez, E.S, Robinson, D.R, Wu, Y.-M, Cao, X., Iyer, M.K, McKeehan, W., Kundra, V., Wang, F., Troncoso, P., Chinnaiyan, A.M, Logothetis, C.J, Navone, N.M
Formato: Capítulo de libro
Lenguaje:Inglés
Publicado: American Association for the Advancement of Science 2014
Acceso en línea:Registro en Scopus
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Aporte de:Registro referencial: Solicitar el recurso aquí
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024 7 |2 scopus  |a 2-s2.0-84907289340 
024 7 |2 cas  |a dovitinib, 804551-71-1, 915769-50-5; fibroblast growth factor, 62031-54-3; fibroblast growth factor 2, 106096-93-9; 4-amino-5-fluoro-3-(5-(4-methylpiperazin-1-yl)-1H-benzimidazol-2-yl)quinolin-2(1H)-one; Antineoplastic Agents; Benzimidazoles; Fibroblast Growth Factor 2; Quinolones; Receptor, Fibroblast Growth Factor, Type 1 
040 |a Scopus  |b spa  |c AR-BaUEN  |d AR-BaUEN 
100 1 |a Wan, X. 
245 1 0 |a Prostate cancer cell-stromal cell crosstalk via FGFR1 mediates antitumor activity of dovitinib in bone metastases 
260 |b American Association for the Advancement of Science  |c 2014 
270 1 0 |m Navone, N.M.; Department of Genitourinary Medical Oncology, David H. Koch Center for Applied Research of Genitourinary Cancers, University of Texas MD Anderson Cancer CenterUnited States 
506 |2 openaire  |e Política editorial 
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504 |a Memarzadeh, S., Xin, L., Mulholland, D.J., Mansukhani, A., Wu, H., Teitell, M.A., Witte, O.N., Enhanced paracrine FGF10 expression promotes formation of multifocal prostate adenocarcinoma and an increase in epithelial androgen receptor (2007) Cancer Cell, 12, pp. 572-585 
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504 |a Valta, M.P., Tuomela, J., Bjartell, A., Valve, E., Väänänen, H.K., Härkönen, P., FGF-8 is involved in bone metastasis of prostate cancer (2008) Int. J. Cancer, 123, pp. 22-31 
504 |a Li, Z.G., Mathew, P., Yang, J., Starbuck, M.W., Zurita, A.J., Liu, J., Sikes, C., Navone, N.M., Androgen receptor-negative human prostate cancer cells induce osteogenesis in mice through FGF9-mediated mechanisms (2008) J. Clin. Invest., 118, pp. 2697-2710 
504 |a Yang, J., Fizazi, K., Peleg, S., Sikes, C.R., Raymond, A.K., Jamal, N., Hu, M., Navone, N.M., Prostate cancer cells induce osteoblast differentiation through a Cbfa1-dependent pathway (2001) Cancer Res., 61, pp. 5652-5659 
504 |a Roychowdhury, S., Iyer, M.K., Robinson, D.R., Lonigro, R.J., Wu, Y.M., Cao, X., Kalyana-Sundaram, S., Chinnaiyan, A.M., Personalized oncology through integrative high-throughput sequencing: A pilot study (2011) Sci. Transl. Med., 3, p. 111ra121 
504 |a Martin, A., David, V., Quarles, L.D., Regulation and function of the FGF23/klotho endocrine pathways (2012) Physiol. Rev., 92, pp. 131-155 
504 |a Wöhrle, S., Bonny, O., Beluch, N., Gaulis, S., Stamm, C., Scheibler, M., Müller, M., Graus-Porta, D., FGF receptors control vitamin D and phosphate homeostasis by mediating renal FGF-23 signaling and regulating FGF-23 expression in bone (2011) J. Bone Miner. Res., 26, pp. 2486-2497 
504 |a Kim, K.B., Chesney, J., Robinson, D., Gardner, H., Shi, M.M., Kirkwood, J.M., Phase I/II and pharmacodynamic study of dovitinib (TKI258), an inhibitor of fibroblast growth factor receptors and VEGF receptors, in patients with advanced melanoma (2011) Clin. Cancer Res., 17, pp. 7451-7461 
504 |a Angevin, E., Lopez-Martin, J., Lin, C.C., Gschwend, J.E., Harzstark, A., Castellano, D., Soria, J.C., Escudier, B., Phase I study of dovitinib (TKI258), an oral FGFR, VEGFR, and PDGFR inhibitor, in advanced or metastatic renal cell carcinoma (2013) Clin. Cancer Res., 19, pp. 1257-1268 
504 |a Antonarakis, E.S., Carducci, M.A., Targeting angiogenesis for the treatment of prostate cancer (2012) Expert Opin. Ther. Targets, 16, pp. 365-376 
504 |a Murakami, M., Simons, M., Fibroblast growth factor regulation of neovascularization (2008) Curr. Opin. Hematol., 15, pp. 215-220 
504 |a O'Connor, J.P., Jackson, A., Parker, G.J., Roberts, C., Jayson, G.C., Dynamic contrast-enhanced MRI in clinical trials of antivascular therapies (2012) Nat. Rev. Clin. Oncol., 9, pp. 167-177 
504 |a Murukesh, N., Dive, C., Jayson, G.C., Biomarkers of angiogenesis and their role in the development of VEGF inhibitors (2010) Br. J. Cancer, 102, pp. 8-18 
504 |a Jacob, A.L., Smith, C., Partanen, J., Ornitz, D.M., Fibroblast growth factor receptor 1 signaling in the osteo-chondrogenic cell lineage regulates sequential steps of osteoblast maturation (2006) Dev. Biol., 296, pp. 315-328 
504 |a Casanovas, O., Hicklin, D.J., Bergers, G., Hanahan, D., Drug resistance by evasion of antiangiogenic targeting of VEGF signaling in late-stage pancreatic islet tumors (2005) Cancer Cell, 8, pp. 299-309 
504 |a Kerbel, R.S., Therapeutic implications of intrinsic or induced angiogenic growth factor redundancy in tumors revealed (2005) Cancer Cell, 8, pp. 269-271 
504 |a Dror Michaelson, M., Regan, M.M., Oh, W.K., Kaufman, D.S., Olivier, K., Michaelson, S.Z., Spicer, B., Smith, M.R., Phase II study of sunitinib in men with advanced prostate cancer (2009) Ann. Oncol., 20, pp. 913-920 
504 |a Navone, N.M., Olive, M., Ozen, M., Davis, R., Troncoso, P., Tu, S.M., Johnston, D., Logothetis, C.J., Establishment of two human prostate cancer cell lines derived from a single bone metastasis (1997) Clin. Cancer Res., 3, pp. 2493-2500 
504 |a Efstathiou, E., Titus, M., Tsavachidou, D., Tzelepi, V., Wen, S., Hoang, A., Molina, A., Logothetis, C.J., Effects of abiraterone acetate on androgen signaling in castrate-resistant prostate cancer in bone (2012) J. Clin. Oncol., 30, pp. 637-643 
504 |a Lonigro, R.J., Grasso, C.S., Robinson, D.R., Jing, X., Wu, Y.M., Cao, X., Quist, M.J., Chinnaiyan, A.M., Detection of somatic copy number alterations in cancer using targeted exome capture sequencing (2011) Neoplasia, 13, pp. 1019-1025 
504 |a Robinson, D.R., Wu, Y.M., Kalyana-Sundaram, S., Cao, X., Lonigro, R.J., Sung, Y.S., Chen, C.L., Chinnaiyan, A.M., Identification of recurrent NAB2-STAT6 gene fusions in solitary fibrous tumor by integrative sequencing (2013) Nat. Genet., 45, pp. 180-185 
504 |a Han, B., Mehra, R., Dhanasekaran, S.M., Yu, J., Menon, A., Lonigro, R.J., Wang, X., Chinnaiyan, A.M., A fluorescence in situ hybridization screen for E26 transformation-specific aberrations: Identification of DDX5-ETV4 fusion protein in prostate cancer (2008) Cancer Res., 68, pp. 7629-7637 
504 |a Yang, D., Han, L., Kundra, V., Exogenous gene expression in tumors: Noninvasive quantification with functional and anatomic imaging in a mouse model (2005) Radiology, 235, pp. 950-958 
504 |a Mathew, P., Thall, P.F., Bucana, C.D., Oh, W.K., Morris, M.J., Jones, D.M., Johnson, M.M., Logothetis, C.J., Platelet-derived growth factor receptor inhibition and chemotherapy for castration-resistant prostate cancer with bone metastases (2007) Clin. Cancer Res., 13, pp. 5816-5824 
504 |a Efstathiou, E., Titus, M., Tsavachidou, D., Tzelepi, V., Wen, S., Hoang, A., Molina, A., Logothetis, C.J., Effects of abiraterone acetate on androgen signaling in castrate-resistant prostate cancer in bone (2012) J. Clin. Oncol., 30, pp. 637-643 
504 |a Zurita, A.J., Jonasch, E., Wang, X., Khajavi, M., Yan, S., Du, D.Z., Xu, L., Heymach, J.V., A cytokine and angiogenic factor (CAF) analysis in plasma for selection of sorafenib therapy in patients with metastatic renal cell carcinoma (2012) Ann. Oncol., 23, pp. 46-52 
520 3 |a Bone is the most common site of prostate cancer (PCa) progression to a therapy-resistant, lethal phenotype. We found that blockade of fibroblast growth factor receptors (FGFRs) with the receptor tyrosine kinase inhibitor dovitinib has clinical activity in a subset of men with castration-resistant PCa and bone metastases. Our integrated analyses suggest that FGF signaling mediates a positive feedback loop between PCa cells and bone cells and that blockade of FGFR1 in osteoblasts partially mediates the antitumor activity of dovitinib by improving bone quality and by blocking PCa cell-bone cell interaction. These findings account for clinical observations such as reductions in lesion size and intensity on bone scans, lymph node size, and tumor-specific symptoms without proportional declines in serum prostate-specific antigen concentration. Our findings suggest that targeting FGFR has therapeutic activity in advanced PCa and provide direction for the development of therapies with FGFR inhibitors. © 2014, American Association for the Advancement of Science. All rights reserved.  |l eng 
536 |a Detalles de la financiación: National Institutes of Health, NIH, CA96824 
536 |a Detalles de la financiación: Prostate Cancer Foundation, PCF 
593 |a Department of Genitourinary Medical Oncology, David H. Koch Center for Applied Research of Genitourinary Cancers, University of Texas MD Anderson Cancer Center, Houston, TX 77030, United States 
593 |a Michigan Center for Translational Pathology, University of Michigan, Ann Arbor, MI 48109, United States 
593 |a Rolanette and Berdon Lawrence Bone Disease Program of Texas, Houston, TX 77030, United States 
593 |a University of Athens Greece School of Medicine, Athens, 11528, Greece 
593 |a Department of Cancer Systems Imaging, University of Texas MD Anderson Cancer Center, Houston, TX 77030, United States 
593 |a Department of Biological Chemistry, University of Buenos Aires-National Research Council of Argentina (CONICET-IQUIBICEN), Ciudad Autonoma de Buenos Aires, C1428EGA, Argentina 
593 |a Center for Cancer and Stem Cell Biology, IBT-Texas AandM Health Science Center, Houston, TX 77030, United States 
593 |a Department of Diagnostic Radiology, University of Texas MD Anderson Cancer Center, Houston, TX 77030, United States 
593 |a Department of Pathology, University of Texas MD Anderson Cancer Center, Houston, TX 77030, United States 
690 1 0 |a DOVITINIB 
690 1 0 |a FIBROBLAST GROWTH FACTOR 
690 1 0 |a FIBROBLAST GROWTH FACTOR RECEPTOR 1 
690 1 0 |a PROSTATE SPECIFIC ANTIGEN 
690 1 0 |a 4-AMINO-5-FLUORO-3-(5-(4-METHYLPIPERAZIN-1-YL)-1H-BENZIMIDAZOL-2-YL)QUINOLIN-2(1H)-ONE 
690 1 0 |a ANTINEOPLASTIC AGENT 
690 1 0 |a BENZIMIDAZOLE DERIVATIVE 
690 1 0 |a FIBROBLAST GROWTH FACTOR 2 
690 1 0 |a FIBROBLAST GROWTH FACTOR RECEPTOR 1 
690 1 0 |a QUINOLONE DERIVATIVE 
690 1 0 |a ANIMAL EXPERIMENT 
690 1 0 |a ANIMAL MODEL 
690 1 0 |a ANTIANGIOGENIC ACTIVITY 
690 1 0 |a ANTINEOPLASTIC ACTIVITY 
690 1 0 |a ARTICLE 
690 1 0 |a BONE METASTASIS 
690 1 0 |a BONE QUALITY 
690 1 0 |a BONE SCINTISCANNING 
690 1 0 |a CANCER CELL 
690 1 0 |a CASTRATION RESISTANT PROSTATE CANCER 
690 1 0 |a CELL INTERACTION 
690 1 0 |a CONTROLLED STUDY 
690 1 0 |a DRUG MEGADOSE 
690 1 0 |a DRUG TARGETING 
690 1 0 |a HUMAN 
690 1 0 |a HUMAN CELL 
690 1 0 |a LOW DRUG DOSE 
690 1 0 |a LYMPH NODE 
690 1 0 |a LYMPH NODE SIZE 
690 1 0 |a MOLECULAR INTERACTION 
690 1 0 |a MOUSE 
690 1 0 |a MUSCULOSKELETAL SYSTEM PARAMETERS 
690 1 0 |a NONHUMAN 
690 1 0 |a OSTEOBLAST 
690 1 0 |a POSITIVE FEEDBACK 
690 1 0 |a PROSTATE CANCER 
690 1 0 |a PROTEIN BLOOD LEVEL 
690 1 0 |a PROTEIN EXPRESSION 
690 1 0 |a RECEPTOR BLOCKING 
690 1 0 |a SIGNAL TRANSDUCTION 
690 1 0 |a STROMA CELL 
690 1 0 |a TUMOR MICROENVIRONMENT 
690 1 0 |a TUMOR VOLUME 
690 1 0 |a ANIMAL 
690 1 0 |a APOPTOSIS 
690 1 0 |a BONE 
690 1 0 |a BONE NEOPLASMS 
690 1 0 |a DISEASE MODEL 
690 1 0 |a DRUG EFFECTS 
690 1 0 |a DRUG SCREENING 
690 1 0 |a GENE EXPRESSION REGULATION 
690 1 0 |a GENETICS 
690 1 0 |a MALE 
690 1 0 |a METABOLISM 
690 1 0 |a NEOVASCULARIZATION, PATHOLOGIC 
690 1 0 |a PATHOLOGY 
690 1 0 |a PROSTATIC NEOPLASMS 
690 1 0 |a SECONDARY 
690 1 0 |a STROMA CELL 
690 1 0 |a TUMOR CELL LINE 
690 1 0 |a VASCULARIZATION 
690 1 0 |a ANIMALS 
690 1 0 |a ANTINEOPLASTIC AGENTS 
690 1 0 |a APOPTOSIS 
690 1 0 |a BENZIMIDAZOLES 
690 1 0 |a BONE AND BONES 
690 1 0 |a BONE NEOPLASMS 
690 1 0 |a CELL LINE, TUMOR 
690 1 0 |a DISEASE MODELS, ANIMAL 
690 1 0 |a FIBROBLAST GROWTH FACTOR 2 
690 1 0 |a GENE EXPRESSION REGULATION, NEOPLASTIC 
690 1 0 |a HUMANS 
690 1 0 |a MALE 
690 1 0 |a MICE 
690 1 0 |a NEOVASCULARIZATION, PATHOLOGIC 
690 1 0 |a OSTEOBLASTS 
690 1 0 |a PROSTATIC NEOPLASMS 
690 1 0 |a PROSTATIC NEOPLASMS, CASTRATION-RESISTANT 
690 1 0 |a QUINOLONES 
690 1 0 |a RECEPTOR, FIBROBLAST GROWTH FACTOR, TYPE 1 
690 1 0 |a SIGNAL TRANSDUCTION 
690 1 0 |a STROMAL CELLS 
690 1 0 |a TUMOR MICROENVIRONMENT 
690 1 0 |a XENOGRAFT MODEL ANTITUMOR ASSAYS 
700 1 |a Corn, P.G. 
700 1 |a Yang, J. 
700 1 |a Palanisamy, N. 
700 1 |a Starbuck, M.W. 
700 1 |a Efstathiou, E. 
700 1 |a Li-Ning Tapia, E.M. 
700 1 |a Zurita, A.J. 
700 1 |a Aparicio, A. 
700 1 |a Ravoori, M.K. 
700 1 |a Vazquez, E.S. 
700 1 |a Robinson, D.R. 
700 1 |a Wu, Y.-M. 
700 1 |a Cao, X. 
700 1 |a Iyer, M.K. 
700 1 |a McKeehan, W. 
700 1 |a Kundra, V. 
700 1 |a Wang, F. 
700 1 |a Troncoso, P. 
700 1 |a Chinnaiyan, A.M. 
700 1 |a Logothetis, C.J. 
700 1 |a Navone, N.M. 
773 0 |d American Association for the Advancement of Science, 2014  |g v. 6  |k n. 252  |p Sci. Transl. Med.  |x 19466234  |t Science Translational Medicine 
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