Relevant bibliographies by topics / PDGFR

Contents

  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers
  6. Reports

Academic literature on the topic 'PDGFR'

Author: Grafiati
Published: 4 June 2021
Last updated: 2 February 2022

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Journal articles on the topic "PDGFR"

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Lesluyes, Tom, Jean-Yves Blay, Patrick Schoffski, et al. "Expression and prognostic significance of PDGF ligands (A, B, C, and D) and PDGFR (A, B, and L) in soft-tissue sarcomas and GIST." Journal of Clinical Oncology 35, no. 15_suppl (2017): 11067. http://dx.doi.org/10.1200/jco.2017.35.15_suppl.11067.

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11067 Background: Sarcomas are a variety of rare connective tissue cancers. Doxorubicin and olaratumab (Ab against PDGFRA) improved survival in a recent Phase 1/2 study. Besides PDGFRA mutated gastrointestinal stroma tumor (GIST) and dermatofibrosarcoma protuberans, the role of PDGFR and the according ligands in the biology of sarcoma remain unclear. Methods: The expression levels of PDGF (A,B,C,D) and PDGFRs (A,B,L) were studied in a series of 255 sarcoma pts in localized phase using the Agilent 014850 platform. Data are available online (http://atg-sarc.sarcomabcb.org). Histologies were GIST
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Lin, Li-Han, Jiun-Sheng Lin, Cheng-Chieh Yang, Hui-Wen Cheng, Kuo-Wei Chang, and Chung-Ji Liu. "Overexpression of Platelet-Derived Growth Factor and Its Receptor Are Correlated with Oral Tumorigenesis and Poor Prognosis in Oral Squamous Cell Carcinoma." International Journal of Molecular Sciences 21, no. 7 (2020): 2360. http://dx.doi.org/10.3390/ijms21072360.

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Oral squamous cell carcinoma (OSCC) is a cancerous disease with poor prognosis. According to the statistics, the 5-year survival rate has not improved significantly over the past 20 years. The platelet-derived growth factor (PDGF) and its signaling pathway is a key regulator of angiogenesis and tumorigenesis. High level of PDGF and its receptor (PDGFR) have been reported in several types of malignancies. In this study, we investigated the relationship of the molecular expression levels of PDGF and PDGFR with clinicopathological parameters in OSCC. To this end, we measured the mRNA and protein
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Ball, Stephen G., Christopher Bayley, C. Adrian Shuttleworth, and Cay M. Kielty. "Neuropilin-1 regulates platelet-derived growth factor receptor signalling in mesenchymal stem cells." Biochemical Journal 427, no. 1 (2010): 29–40. http://dx.doi.org/10.1042/bj20091512.

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Using human MSCs (mesenchymal stem cells) lacking VEGF (vascular endothelial growth factor) receptors, we show that the pro-angiogenic receptor neuropilin-1 associates with phosphorylated PDGFRs [PDGF (platelet-derived growth factor) receptors], thereby regulating cell signalling, migration, proliferation and network assembly. Neuropilin-1 co-immunoprecipitated and co-localized with phosphorylated PDGFRs in the presence of growth factors. Neuropilin-1 knockdown blocked PDGF-AA-induced PDGFRα phosphorylation and migration, reduced PDGF-BB-induced PDGFRβ activation and migration, blocked VEGF-A
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Gueller, Saskia, Sigal Gery, and H. Phillip Koeffler. "Adaptor Protein Lnk Binds to PDGFRA, PDGFRB and FIP1L1-PDGFRA, but Not to the TEL-PDGFRB Fusion Protein." Blood 110, no. 11 (2007): 2213. http://dx.doi.org/10.1182/blood.v110.11.2213.2213.

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Abstract PDGFRA and PDGFRB (platelet derived growth factor receptors alpha and beta) are frequently expressed on malignant hematopoietic cells and regulate various cellular responses such as development, proliferation, differentiation, cell survival and cellular transformation. Stimulation by either autocrine loops or constitutional activation by chromosomal translocation (i.e. chronic myelomonocytic leukemia [CMML, TEL-PDGFRB] or chronic eosinophilic leukemia [CEL, FIP1L1-PDGFRA]) makes them important factors in development of hematopoietic disorders. Normally, interaction with the ligand PDG
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Kilvaer, Thomas Karsten, Andrej Valkov, Sveinung W. Sorbye, et al. "Platelet-Derived Growth Factors in Non-GIST Soft-Tissue Sarcomas Identify a Subgroup of Patients with Wide Resection Margins and Poor Disease-Specific Survival." Sarcoma 2010 (2010): 1–10. http://dx.doi.org/10.1155/2010/751304.

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Background. Optimal treatment of nongastrointestinal stromal tumor soft-tissue sarcomas (non-GIST STSs) is resection with wide margins. This study investigates the prognostic impact of the angiogenesis-associated platelet-derived growth factors (PDGFs) and their receptors (PDGFRs) in non-GIST STS patients with wide and nonwide resection margins.Method. Tumor samples and clinical data from 249 patients with non-GIST STS were obtained, and tissue microarrays were constructed for each specimen. Immunohistochemistry was used to evaluate the expression of PDGF-A, -B, -C, and -D and PDGFR-αand -β.Re
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Rogers, Madison A., and Katherine A. Fantauzzo. "The emerging complexity of PDGFRs: activation, internalization and signal attenuation." Biochemical Society Transactions 48, no. 3 (2020): 1167–76. http://dx.doi.org/10.1042/bst20200004.

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The platelet-derived growth factor receptor (PDGFR) family of receptor tyrosine kinases allows cells to communicate with the environment to regulate diverse cellular activities. Here, we highlight recent data investigating the structural makeup of individual PDGFRs upon activation, revealing the importance of the whole receptor in the propagation of extracellular ligand binding and dimerization. Furthermore, we review ongoing research demonstrating the significance of receptor internalization and signal attenuation in the regulation of PDGFR activity. Interactions with internalization machiner
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Tsao, Anne S., Nusrat Harun, Junya Fujimoto, et al. "Elevated PDGFRB gene copy number gain as prognostic in resected malignant pleural mesothelioma." Journal of Clinical Oncology 30, no. 15_suppl (2012): 7078. http://dx.doi.org/10.1200/jco.2012.30.15_suppl.7078.

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7078 Background: PDGF/PDGFR pathway has been implicated in malignant pleural mesothelioma (MPM) carcinogenesis. We sought to evaluate the incidence of PDGFRB gene copy number gain (CNG) and PDGFR pathway protein expression by immunohistochemistry (IHC) in the tumor cell cytoplasm, membrane, nucleus, and stroma, and correlate it to patient clinical outcome. Methods: 88 archived tumor blocks from resected MPM with full clinical information were used to perform the analyses. IHC biomarkers for PDGFRα,β and p-PDGFRβ, and fluorescence in situ hybridization were performed for analysis of PDGFRB gene
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Fitter, Stephen, Kate Vandyke, Stan Gronthos, and Andrew C. W. Zannettino. "Suppression of PDGF-induced PI3 kinase activity by imatinib promotes adipogenesis and adiponectin secretion." Journal of Molecular Endocrinology 48, no. 3 (2012): 229–40. http://dx.doi.org/10.1530/jme-12-0003.

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Improved glucose and lipid metabolism is a unique side effect of imatinib therapy in some chronic myeloid leukaemia (CML) patients. We recently reported that plasma levels of adiponectin, an important regulator of insulin sensitivity, are elevated following imatinib therapy in CML patients, which could account for these improved metabolic outcomes. Adiponectin is secreted exclusively from adipocytes, suggesting that imatinib modulates adiponectin levels directly, by transcriptional upregulation of adiponectin in pre-existing adipocytes, and/or indirectly, by stimulating adipogenesis. In this r
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Kanaan, Rana, and Charlie Strange. "Use of multitarget tyrosine kinase inhibitors to attenuate platelet-derived growth factor signalling in lung disease." European Respiratory Review 26, no. 146 (2017): 170061. http://dx.doi.org/10.1183/16000617.0061-2017.

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Platelet-derived growth factors (PDGFs) and their receptors (PDGFRs) play a fundamental role in the embryonic development of the lung. Aberrant PDGF signalling has been documented convincingly in a large variety of pulmonary diseases, including idiopathic pulmonary arterial hypertension, lung cancer and lung fibrosis. Targeting PDGF signalling has been proven to be effective in these diseases. In clinical practice, the most effective way to block PDGF signalling is to inhibit the activity of the intracellular PDGFR kinases. Although the mechanism of action of such drugs is not specific for PDG
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Ren, Wenying, Stephanie W. Watts та Barry L. Fanburg. "Serotonin transporter interacts with the PDGFβ receptor in PDGF-BB-induced signaling and mitogenesis in pulmonary artery smooth muscle cells". American Journal of Physiology-Lung Cellular and Molecular Physiology 300, № 3 (2011): L486—L497. http://dx.doi.org/10.1152/ajplung.00237.2010.

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The serotonin transporter (SERT) and the platelet-derived growth factor receptor (PDGFR) have been implicated in both clinical and experimental pulmonary hypertension (PH) and the facilitation of pulmonary artery smooth muscle cell (PASMC) growth. To gain a better understanding of the possible relationship of these two cell surface molecules we have explored interactions between SERT and PDGFR. We have previously demonstrated that SERT transactivates PDGFRβ in serotonin-stimulated PASMC proliferation. We now provide evidence for a role for SERT in PDGF-BB signaling and PASMC proliferation by u
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Dissertations / Theses on the topic "PDGFR"

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Zhang, Xiao-Qun. "Functional Studies on the PDGFR α gene promoter and effects of autocrine PDGF-A stimulation in vivo". Doctoral thesis, Uppsala universitet, Institutionen för genetik och patologi, 2001. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-1455.

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Platelet-derived growth factor receptor α (PDGFRα) plays an important role during embryogenesis. After implantation, the patterns of expression of Pdgfrα and its ligand Pdgf-A undergo an "autocrine-paracrine transition", in that Pdgf-A becomes expressed in the ectoderm and epithelia, while Pdgfrα is expressed in the adjacent mesenchymal tissue. In human tumors, such as malignant glioma, both PDGF and PDGFRα are overexpressed within the same tissue, indicating that an autocrine PDGF loop is generated in the tumors. This thesis is focused on the in vivo functionality of the PDGFRα gene (PDGFRA)
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Eger, Glenda. "Regulation and Function of MAP Kinases in PDGF Signaling." Doctoral thesis, Uppsala universitet, Ludwiginstitutet för cancerforskning, 2016. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-301057.

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Platelet-derived growth factor (PDGF) is a family of signaling molecules that stimulates cell growth, survival and migration. PDGF is recognized by specific transmembrane proteins, the PDGF receptors, which relay the signals to the cell activating the Mitogen-activated protein (MAP) kinases and other signaling pathways. Aberrant activation of these pathways is frequently detected in cancer. Hence, the study of these processes is essential for identifying potential drug targets or diagnostic markers. In paper I, we identified Receptor Subfamily 4 Group A Member 1 NR4A1 to be regulated by PDGF v
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Pinto, Rodrigo Pozza. "Expressão imunoistoquímica do p16 e do PDGFR-beta no adenocarcinoma gástrico." reponame:Biblioteca Digital de Teses e Dissertações da UFRGS, 2005. http://hdl.handle.net/10183/11082.

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O adenocarcinoma de estômago foi a principal causa de morte por neoplasia maligna no mundo durante grande parte do século XX e atualmente é superado somente pelas neoplasias epiteliais malignas de pulmão. Cerca de 750.000 novos casos são diagnosticados anualmente. Apresenta grande variação geográfica, sendo suas maiores incidências encontradas no Japão, América do Sul, Europa Oriental e Oriente Médio. É duas vezes mais freqüente em homens do que em mulheres; é pouco comum antes dos 40 anos e atinge sua maior incidência por volta da sétima década de vida. No Brasil as estimativas para o ano de
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Ma, Haisha. "Regulation of Platelet-Derived Growth Factor Receptor Signaling and its Targeting in Cancer Therapy." Doctoral thesis, Uppsala universitet, Ludwiginstitutet för cancerforskning, 2015. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-248172.

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Overactivity of platelet-derived growth factor receptor (PDGFR) is a frequent event in many types of solid tumors. Therefore, it is of great importance to uncover the mechanisms that regulate PDGF/PDGFR signalling, to develop efficient inhibitors targeting this pathway. The first step of downregulation of PDGFR activity upon ligand binding is internalization; thus we investigated how endocytosis pathways affect PDGFR signaling. We showed that in Ras-transformed fibroblasts, the internalization of PDGFR is shifted from the routine clathrin-dependent endocytosis to macropinocytosis, which result
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Urie, Birdget K. "Evaluation of Expression and Function of VEGFR2, PDGFRα, PDGFRβ, KIT, and RET in Canine Apocrine Gland of the Anal Sac Adenocarcinoma and Thyroid Carcinoma". The Ohio State University, 2012. http://rave.ohiolink.edu/etdc/view?acc_num=osu1337702663.

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Veevers, Jennifer. "Mesenchymal stromal cell migration is regulated by fibronectin through integrin-mediated activation of PDGFR-β". Thesis, University of Manchester, 2010. https://www.research.manchester.ac.uk/portal/en/theses/mesenchymal-stromal-cell-migration-is-regulated-by-fibronectin-through-integrinmediated-activation-of-pdgfr(cc992a74-a9f3-4f3d-8687-f59230a58d1a).html.

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Human adult mesenchymal stem cells (MSCs) derived from bone marrow have the capacity to self-renew and to differentiate into a variety of cells and tissues. They can leave their niche to migrate to remote tissues where they play a critical role in angiogenesis, wound repair and tissue regeneration. A major goal in adult stem cell research is to define how MSC fate is controlled by the pericellular extracellular matrix (ECM) and soluble factors that largely constitute their tissue-specific niches. Defining crucial regulatory signals that control the fate and function of MSCs in vitro will contr
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Arndt, Philipp Friedrich David [Verfasser]. "MiR-34a regulates Migration of Mouse Lung Fibroblasts by modulating PDGFR signalling / Philipp Friedrich David Arndt." Gieߟen : Universitätsbibliothek, 2020. http://d-nb.info/1224970470/34.

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CARRON, CLEMENCE. "Etude fonctionnelle de la proteine tel et des onco-proteines derivees tel-pdgfr et tel-jak2." Paris 6, 1999. http://www.theses.fr/1999PA066554.

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Les regulateurs transcriptionnels de la famille ets participent a divers processus oncogeniques chez l'homme. Ils sont impliques sous forme de proteines de fusion issues de translocations chromosomiques specifiques. Tel appartient a la famille ets. Tel est remanie dans plusieurs leucemies humaines. Dans ces remaniements chromosomiques, tel est fusionne a differents partenaires (pdgfr, abl, jak2, tkc, aml1). Le plus souvent, c'est la partie 5 de tel qui est fusionnee a la portion 3 des genes partenaires. Cette region de tel code, notamment, un domaine conserve entre certaines proteines ets, le
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Arndt, Philipp [Verfasser]. "MiR-34a regulates Migration of Mouse Lung Fibroblasts by modulating PDGFR signalling / Philipp Friedrich David Arndt." Gieߟen : Universitätsbibliothek, 2020. http://d-nb.info/1224970470/34.

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Fierros, Juancarlos. "PLATELET DERIVED GROWTH FACTOR RECEPTOR B (PDGFRB) EXPRESSING CELLS DURING ZEBRAFISH CORONARY VESSEL DEVELOPMENT." CSUSB ScholarWorks, 2017. https://scholarworks.lib.csusb.edu/etd/567.

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Coronary heart disease is a prevalent issue in developed countries throughout the world. It can have crippling effects on the quality of life and even lead to mortality, in the case of myocardial infarction. Part of the problem is the lack of a robust regenerative response in mammals after injury. Zebrafish have an amazing ability to regenerate after injury, and studies have demonstrated that the regenerative response recapitulates embryonic development. Our lab previously reported the first analysis of coronary vessel development in zebrafish and demonstrated that coronary endothelial cells u
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Books on the topic "PDGFR"

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Guinivan, Phyllis. Platelet-derived growth factor (PDGF). U.S. Dept. of Health and Human Services, Public Health Service, National Institutes of Health, National Cancer Institute, International Cancer Research Data Bank, 1988.

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Herbertson, Alexandra Lenore. The rat bone marrow stromal cell osteogenic system: Characterization of subpopulations, fractionation and effects of PDGF. University of Toronto, Faculty of Dentistry], 1998.

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Zhang, Xiao-Qun. Functional Studies on the Pdgfra Gene Promoter & Effects of Autocrine Pdgf-A Stimulation in Vivo. Uppsala Universitet, 2001.

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Andrae, Johanna. Pdgf in Cerebellar Development & Tumorigenesis. Uppsala Universitet, 2001.

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Uhrbom, Lene. Roles of Pink4A and Pdgf-B in Glioma. Uppsala Universitet, 1999.

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Dasgupta, Bhaskar. Polymyalgia rheumatica. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199642489.003.0134.

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This chapter reviews advances in pathogenesis; European League Against Rheumatism/American College of Rheumatology (EULAR/ACR) classification criteria with clinical, laboratory, and ultrasound criteria for classification as polymyalgia rheumatica (PMR); the heterogeneity and overlap between PMR, inflammatory arthritis, and large-vessel vasculitis as illustrated by representative cases; recent guidelines on early and correct recognition, investigations, and management of PMR; the scope of disease-modifying agents; socio-economic impact, outcomes, and patient experience in PMR. It also discusses
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Book chapters on the topic "PDGFR"

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Chitu, Violeta, Cristina I. Caescu, E. Richard Stanley, Johan Lennartsson, Lars Rönnstrand, and Carl-Henrik Heldin. "The PDGFR Receptor Family." In Receptor Tyrosine Kinases: Family and Subfamilies. Springer International Publishing, 2015. http://dx.doi.org/10.1007/978-3-319-11888-8_10.

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Srivani, Gowru, Shipra Reddy Bethi, Sheik Aliya, Afroz Alam, and Ganji Purnachandra Nagaraju. "VEGFR and PDGFR Targeting in Pancreatic Cancer." In Role of Tyrosine Kinases in Gastrointestinal Malignancies. Springer Singapore, 2018. http://dx.doi.org/10.1007/978-981-13-1486-5_7.

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Bastien, A. J. "VEGFR and PDGFR: Their Targeting in Liver Cancer." In Role of Tyrosine Kinases in Gastrointestinal Malignancies. Springer Singapore, 2018. http://dx.doi.org/10.1007/978-981-13-1486-5_9.

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Kim, Cheorl-Ho. "GM3-HGFR, FGFR, and PDGFR Cancer Cell Behavior and IGF-1R in Diabetic Wound Healing." In GM3 Signaling. Springer Singapore, 2020. http://dx.doi.org/10.1007/978-981-15-5652-4_17.

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Choi, Nahyun, Jung-Hun Moon, and Jong-Hyuk Sung. "PDGF." In Encyclopedia of Signaling Molecules. Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-67199-4_101813.

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Heldin, Carl-Henrik. "PDGF." In Cancer Therapeutic Targets. Springer New York, 2017. http://dx.doi.org/10.1007/978-1-4419-0717-2_16.

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Choi, Nahyun, Jung-Hun Moon, and Jong-Hyuk Sung. "PDGF." In Encyclopedia of Signaling Molecules. Springer New York, 2016. http://dx.doi.org/10.1007/978-1-4614-6438-9_101813-1.

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Heldin, Carl-Henrik. "PDGF." In Cancer Therapeutic Targets. Springer New York, 2014. http://dx.doi.org/10.1007/978-1-4614-6613-0_16-3.

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Kern, A., H. Görgens, S. Krüger, et al. "PDGFRA-overexpression is associated with a favourable prognosis after resection of primary gastrointestinal stromal tumors — an analysis of mutation and expression status of KIT and PDGFR-alpha in 109 resected patients." In Deutsche Gesellschaft für Chirurgie. Springer Berlin Heidelberg, 2009. http://dx.doi.org/10.1007/978-3-642-00625-8_43.

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Löffler, Helmut, and Torsten Haferlach. "Myeloische und lymphatische Neoplasien mit Eosinophilie und Anomalien von PDGFRA, PDGFRB oder FGFR1." In Hämatologische Erkrankungen. Springer Berlin Heidelberg, 2013. http://dx.doi.org/10.1007/978-3-642-29535-5_9.

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Conference papers on the topic "PDGFR"

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Wang, Fengfei, Annie Moseman, Matthew Doucette, et al. "Abstract 288: PDGFR alpha and PDGFR beta differentially regulate cell proliferation and migration/invasion in medulloblastoma 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.am10-288.

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Liu, Qing, Guanglin Wu, Kai Xu, Jack A. Roth, and Lin Ji. "Abstract 706: FUS1-mediated tumor suppression by inhibiting PDGF/ PDGFR signaling pathway in human lung cancer." 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.am10-706.

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Najy, Abdo J., Allen Saliganan, Daniel Bonfil та Hyeong‐Reh C. Kim. "Abstract B10: A novel mechanism of prostate cancer metastasis through the PDGF D/β‐PDGFR axis". У Abstracts: First AACR International Conference on Frontiers in Basic Cancer Research--Oct 8–11, 2009; Boston MA. American Association for Cancer Research, 2009. http://dx.doi.org/10.1158/0008-5472.fbcr09-b10.

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Simakajornboon, Narong, Erik Olsen, and Polporn Appiwattanasawee. "Ventilatory Response To Hypoxia In PDGFR (+/-) Mice Pups." In American Thoracic Society 2010 International Conference, May 14-19, 2010 • New Orleans. American Thoracic Society, 2010. http://dx.doi.org/10.1164/ajrccm-conference.2010.181.1_meetingabstracts.a4202.

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Karoor, Vijaya, Masahiko Oka, Sandra J. Walchak, York E. Miller, and Edward C. Dempsey. "Neprilysin Regulates PASMC Phenotype And PDGFR Signaling In Mice." In American Thoracic Society 2010 International Conference, May 14-19, 2010 • New Orleans. American Thoracic Society, 2010. http://dx.doi.org/10.1164/ajrccm-conference.2010.181.1_meetingabstracts.a1171.

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Peyton, Michael, Preeti Chaudhary, Abhijit Ramachandran та John Minna. "Abstract 3601: CP-868,596, a highly potent and selective PDGFR TKI inhibits growth of PDGFRα-driven lung cancer cells". У 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.am2011-3601.

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Benezra, Miriam, Dolores Hambardzumyan, Oula Penate-Medina, et al. "Abstract LB-299: F-dasatinib inhibits glioma cell proliferation and alters expression of PDGFR signaling pathway intermediates in PDGFR-overexpressing glioma models." 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-lb-299.

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Huber, L., C. Aderhold, N. Rotter та B. Kramer. "Die Auswirkung von Tyrosinkinaseinhibitoren auf die PDGF-AA/BB und PDGFR-α/β-Expression in HPV-positiven und –negativen Plattenepithelkarzinomzellen". У Abstract- und Posterband – 91. Jahresversammlung der Deutschen Gesellschaft für HNO-Heilkunde, Kopf- und Hals-Chirurgie e.V., Bonn – Welche Qualität macht den Unterschied. © Georg Thieme Verlag KG, 2020. http://dx.doi.org/10.1055/s-0040-1711599.

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Hosoi, Fumihito, Hiromi Yokoi, Daisuke Nameki, et al. "Abstract B1: Antitumor activity of TSU-68 in PDGF-BB overexpressing U-87MG xenograft model: contribution of PDGFR blocking action." In Abstracts: AACR-NCI-EORTC International Conference: Molecular Targets and Cancer Therapeutics--Nov 12-16, 2011; San Francisco, CA. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/1535-7163.targ-11-b1.

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Wroblewski, Tadeusz, Philip D. Tatman, Anthony Fringuello, et al. "Inhibition of PDGFR May Be a Viable Treatment Option for Meningiomas." In 30th Annual Meeting North American Skull Base Society. Georg Thieme Verlag KG, 2020. http://dx.doi.org/10.1055/s-0040-1702356.

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Reports on the topic "PDGFR"

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Fatatis, Alessandro. Antibody-Mediated Targeting of Alpha PDGF Receptor to Inhibit the Progression of Skeletal Micro-Metastases. Defense Technical Information Center, 2012. http://dx.doi.org/10.21236/ada570817.

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Redwine, Jeffrey M. The In Vivo PDGF Response During Remyelination in Mouse Spinal Cord Following Murine Hepatitis Virus Strain AS9-Induced Transient Demyelination. Defense Technical Information Center, 1998. http://dx.doi.org/10.21236/ad1012058.

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