Relevant bibliographies by topics / Tyrosine Kinase (RTK) Pathway

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

Academic literature on the topic 'Tyrosine Kinase (RTK) Pathway'

Author: Grafiati
Published: 4 June 2021
Last updated: 6 September 2023

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Journal articles on the topic "Tyrosine Kinase (RTK) Pathway"

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Fraser, Jane, Ainara G. Cabodevilla, Joanne Simpson, and Noor Gammoh. "Interplay of autophagy, receptor tyrosine kinase signalling and endocytic trafficking." Essays in Biochemistry 61, no. 6 (2017): 597–607. http://dx.doi.org/10.1042/ebc20170091.

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Vesicular trafficking events play key roles in the compartmentalization and proper sorting of cellular components. These events have crucial roles in sensing external signals, regulating protein activities and stimulating cell growth or death decisions. Although mutations in vesicle trafficking players are not direct drivers of cellular transformation, their activities are important in facilitating oncogenic pathways. One such pathway is the sensing of external stimuli and signalling through receptor tyrosine kinases (RTKs). The regulation of RTK activity by the endocytic pathway has been exte
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Li, X., L. Wheldon, and J. K. Heath. "Sprouty: a controversial role in receptor tyrosine kinase signalling pathways." Biochemical Society Transactions 31, no. 6 (2003): 1445–46. http://dx.doi.org/10.1042/bst0311445.

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Sprouty was first identified in Drosophila as a novel antagonist of the fibroblast growth factor signalling pathway. Sprouty proteins comprise a big family, members of which are characterized by a cysteine-rich domain which confers inhibitory activity, whereas differences in the N-terminal region may be responsible for functional divergence. The role of Sprouty in RTK (receptor tyrosine kinase) signalling pathways is still controversial. Sprouty may negatively or positively regulate RTK signalling via differential interaction with different signalling molecules, and hence exert different mecha
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Myers, Andrea Pomrehn, Laura B. Corson, Janet Rossant, and Julie C. Baker. "Characterization of Mouse Rsk4 as an Inhibitor of Fibroblast Growth Factor-RAS-Extracellular Signal-Regulated Kinase Signaling." Molecular and Cellular Biology 24, no. 10 (2004): 4255–66. http://dx.doi.org/10.1128/mcb.24.10.4255-4266.2004.

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ABSTRACT Receptor tyrosine kinase (RTK) signals regulate the specification of a varied array of tissue types by utilizing distinct modules of proteins to elicit diverse effects. The RSK proteins are part of the RTK signal transduction pathway and are thought to relay these signals by acting downstream of extracellular signal-regulated kinase (ERK). In this study we report the identification of ribosomal S6 kinase 4 (Rsk4) as an inhibitor of RTK signals. Among the RSK proteins, RTK inhibition is specific to RSK4 and, in accordance, is dependent upon a region of the RSK4 protein that is divergen
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He, Fang, Cong Chang, Bowen Liu, et al. "Copper (II) Ions Activate Ligand-Independent Receptor Tyrosine Kinase (RTK) Signaling Pathway." BioMed Research International 2019 (May 14, 2019): 1–8. http://dx.doi.org/10.1155/2019/4158415.

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Receptor tyrosine kinase (RTK) is activated by its natural ligand, mediating multiple essential biological processes. Copper (II) ions are bioactive ions and are crucial in the regulation of cell signaling pathway. However, the crosstalk between copper (II) ions and RTK-mediated cellular signaling remains unclear. Herein, we reported the effect of copper (II) ions on the ligand-independent RTK cellular signaling pathway. Our results indicate that both EGFR and MET signaling were activated by copper (II) in the absence of the corresponding ligands, EGF and HGF, respectively. Consequently, coppe
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Mamer, Spencer B., Alexandra A. Palasz, and P. I. Imoukhuede. "Mapping Tyrosine Kinase Receptor Dimerization to Receptor Expression and Ligand Affinities." Processes 7, no. 5 (2019): 288. http://dx.doi.org/10.3390/pr7050288.

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Tyrosine kinase receptor (RTK) ligation and dimerization is a key mechanism for translating external cell stimuli into internal signaling events. This process is critical to several key cell and physiological processes, such as in angiogenesis and embryogenesis, among others. While modulating RTK activation is a promising therapeutic target, RTK signaling axes have been shown to involve complicated interactions between ligands and receptors both within and across different protein families. In angiogenesis, for example, several signaling protein families, including vascular endothelial growth
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Fabian, JR, DK Morrison, and IO Daar. "Requirement for Raf and MAP kinase function during the meiotic maturation of Xenopus oocytes." Journal of Cell Biology 122, no. 3 (1993): 645–52. http://dx.doi.org/10.1083/jcb.122.3.645.

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The role of Raf and MAPK (mitogen-activated protein kinase) during the maturation of Xenopus oocytes was investigated. Treatment of oocytes with progesterone resulted in a shift in the electrophoretic mobility of Raf at the onset of germinal vesicle breakdown (GVBD), which was coincident with the activation of MAPK. Expression of a kinase-defective mutant of the human Raf-1 protein (KD-RAF) inhibited progesterone-mediated MAPK activation. MAPK activation was also inhibited by KD-Raf in oocytes expressing signal transducers of the receptor tyrosine kinase (RTK) pathway, including an activated t
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Taruno, Akiyuki, Naomi Niisato, and Yoshinori Marunaka. "Hypotonicity stimulates renal epithelial sodium transport by activating JNK via receptor tyrosine kinases." American Journal of Physiology-Renal Physiology 293, no. 1 (2007): F128—F138. http://dx.doi.org/10.1152/ajprenal.00011.2007.

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We previously reported that hypotonic stress stimulated transepithelial Na+ transport via a pathway dependent on protein tyrosine kinase (PTK; Niisato N, Van Driessche W, Liu M, Marunaka Y. J Membr Biol 175: 63–77, 2000). However, it is still unknown what type of PTK mediates this stimulation. In the present study, we investigated the role of receptor tyrosine kinase (RTK) in the hypotonic stimulation of Na+ transport. In renal epithelial A6 cells, we observed inhibitory effects of AG1478 [an inhibitor of the EGF receptor (EGFR)] and AG1296 [an inhibitor of the PDGF receptor (PDGFR)] on both t
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Smith, Rachel K., Pamela M. Carroll, John D. Allard, and Michael A. Simon. "MASK, a large ankyrin repeat and KH domain-containing protein involved inDrosophilareceptor tyrosine kinase signaling." Development 129, no. 1 (2002): 71–82. http://dx.doi.org/10.1242/dev.129.1.71.

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The receptor tyrosine kinases Sevenless (SEV) and the Epidermal growth factor receptor (EGFR) are required for the proper development of the Drosophila eye. The protein tyrosine phosphatase Corkscrew (CSW) is a common component of many RTK signaling pathways, and is required for signaling downstream of SEV and EGFR. In order to identify additional components of these signaling pathways, mutations that enhanced the phenotype of a dominant negative form of Corkscrew were isolated. This genetic screen identified the novel signaling molecule MASK, a large protein that contains two blocks of ankyri
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Liu, Zhi, Peng Hou, Meiju Ji, et al. "Highly Prevalent Genetic Alterations in Receptor Tyrosine Kinases and Phosphatidylinositol 3-Kinase/Akt and Mitogen-Activated Protein Kinase Pathways in Anaplastic and Follicular Thyroid Cancers." Journal of Clinical Endocrinology & Metabolism 93, no. 8 (2008): 3106–16. http://dx.doi.org/10.1210/jc.2008-0273.

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Abstract Context: Genetic alterations in receptor tyrosine kinases (RTKs) and phosphatidylinositol 3-kinase (PI3K)/Akt and MAPK pathways have not been fully defined in anaplastic and follicular thyroid cancers [anaplastic thyroid cancer (ATC), follicular thyroid cancer (FTC)]. Objective: The objective of the study was to explore a wide-range genetic basis for the involvement of these pathways in ATC. Design: We examined mutations and copy number gains of a large panel of genes in these pathways and corresponding phosphorylation of ERK (p-ERK) and Akt. Results: We found frequent copy gains of R
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Gonzalez-Magaldi, Monica, Jacqueline M. McCabe, Haley N. Cartwright, Ningze Sun, and Daniel J. Leahy. "Conserved roles for receptor tyrosine kinase extracellular regions in regulating receptor and pathway activity." Biochemical Journal 477, no. 21 (2020): 4207–20. http://dx.doi.org/10.1042/bcj20200702.

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Receptor Tyrosine Kinases (RTKs) comprise a diverse group of cell-surface receptors that mediate key signaling events during animal development and are frequently activated in cancer. We show here that deletion of the extracellular regions of 10 RTKs representing 7 RTK classes or their substitution with the dimeric immunoglobulin Fc region results in constitutive receptor phosphorylation but fails to result in phosphorylation of downstream signaling effectors Erk or Akt. Conversely, substitution of RTK extracellular regions with the extracellular region of the Epidermal Growth Factor Receptor
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Dissertations / Theses on the topic "Tyrosine Kinase (RTK) Pathway"

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Peterson, Cornelia WM. "Insulin Stimulates Protein Synthesis via RTK-Induction of the Akt-s6k Pathway in Human and Canine Corneal Cells." The Ohio State University, 2019. http://rave.ohiolink.edu/etdc/view?acc_num=osu1555070124329814.

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Koytiger, Grigoriy. "A Systematic Experimental and Computational Approach to Investigating Phosphotyrosine Signaling Networks." Thesis, Harvard University, 2013. http://dissertations.umi.com/gsas.harvard:10943.

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Mutation and over-expression of Receptor Tyrosine Kinases (RTKs) or the proteins they regulate serve as oncogenic drivers in diverse cancers. RTKs catalyze the transfer of phosphate from ATP to the hydroxyl group on tyrosine. The proximal stretch of amino acids including this post translational modification is then able to be recognized by SH2 and PTB domains. Chapter 1 details our work to better understand RTK signaling and its link to oncogenesis using protein microarrays to systematically and quantitatively measure interactions between virtually every SH2 or PTB domain encoded in the human
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Ahier, Arnaud. "Etude des Récepteurs Tyrosine Kinase du parasite helminthe Schistosoma mansoni - Découverte des Venus Kinase Récepteurs, une nouvelle famille de RTK." Phd thesis, Université du Droit et de la Santé - Lille II, 2008. http://tel.archives-ouvertes.fr/tel-00348172.

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La schistosomiase constitue un problème majeur de santé publique dans de nombreux pays émergents d'Afrique, d'Amérique Latine et d'Asie du Sud Est, causant près de 300 000 décès par an. Cette maladie est due au schistosome qui est un ver parasite possédant un cycle de vie complexe. A ce jour une seule drogue est utilisée en monothérapie, le praziquantel ou PZQ, pour lutter contre cette maladie. En raison d'apparitions de résistances au PZQ, il devient nécessaire de rechercher de nouvelles cibles thérapeutiques contre le ver. Au cours de ma thèse je me suis penché sur l'utilisation potentielle
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Ahier, Arnaud Dissous-Lempereur Colette. "Etude des Récepteurs Tyrosine Kinase du parasite helminthe Schistosoma mansoni découverte des Récepteurs Venus Kinase, une nouvelle famille de RTK /." [S.l.] : [s.n.], 2008. http://tel.archives-ouvertes.fr/tel-00348172/fr.

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Reproduction de : Thèse de doctorat : Parasitologie - Biologie moléculaire : Lille 2 : 2008.<br>Résumé en français et en anglais. RTK = Récepteurs Tyrosine Kinase. Titre provenant de l'écran-titre. Bibliogr. p. 104-118.
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Saharinen, Pipsa. "Signaling through the Jak-Stat pathway : regulation of tyrosine kinase activity." Helsinki : University of Helsinki, 2002. http://ethesis.helsinki.fi/julkaisut/mat/bioti/vk/saharinen/.

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Rivera, Reyes Brenda Mariola. "Regulation of the TCR signaling pathway." Connect to text online, 2006. http://rave.ohiolink.edu/etdc/view?acc%5Fnum=case1132588714.

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Edling, Charlotte. "Receptor tyrosine kinase c-Kit signalling in hematopoietic progenitor cells." Doctoral thesis, Umeå : Umeå University, 2006. http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-888.

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Gouzi, Jean. "Le récepteur à activité tyrosine kinase ALK : voies de signalisation et rôle dans la différenciation neuronale." Paris 6, 2006. http://www.theses.fr/2006PA066115.

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Hurlbut, Gregory Donald. "Notch and RTK signaling : transcriptional output and signal integration." Paris 11, 2007. http://www.theses.fr/2007PA112203.

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Elghazi, Lynda. "Développement du pancréas : rôle de ligands spécifiques de récepteurs à activité tyrosine kinase." Paris 7, 2002. http://www.theses.fr/2002PA077074.

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Books on the topic "Tyrosine Kinase (RTK) Pathway"

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Fleischmann, Roy. Signalling pathway inhibitors. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199642489.003.0081.

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Oral, small-molecule signalling pathway inhibitors, including ones that inhibit the JAK and SyK pathways, are currently in development for the treatment of rheumatoid arthritis (RA). Tofacitinib is an orally administered small-molecule inhibitor that targets the intracellular Janus kinase 3 and 1 (JAK1/3) molecules to a greater extent than JAK2 while baricitinib (formerly INCB028050) predominantly inhibits JAK1/2. Many of the proinflammatory cytokines implicated in the pathogenesis of RA utilize cell signalling that involves the JAK-STAT pathways and therefore inhibition of JAK-STAT signalling
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Book chapters on the topic "Tyrosine Kinase (RTK) Pathway"

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McDermott, Martina, and Norma O’Donovan. "Analysis of Receptor Tyrosine Kinase (RTK) Phosphorylation by Immunoblotting." In Methods in Molecular Biology. Springer New York, 2014. http://dx.doi.org/10.1007/978-1-4939-1789-1_1.

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Helman, Aharon, and Ze’ev Paroush. "Detection of RTK Pathway Activation in Drosophila Using Anti-dpERK Immunofluorescence Staining." In MAP Kinase Signaling Protocols. Humana Press, 2010. http://dx.doi.org/10.1007/978-1-60761-795-2_24.

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Samelson, Lawrence E., Mark Egerton, Pamela M. Thomas, and Ronald L. Wange. "The T Cell Antigen Receptor Tyrosine Kinase Pathway." In Advances in Experimental Medicine and Biology. Springer US, 1992. http://dx.doi.org/10.1007/978-1-4615-3396-2_2.

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Chu, Yaya, Mitchell S. Cairo, and Auke Beishuizen. "Resistance to Bruton’s Tyrosine Kinase Signaling Pathway Targeted Therapies." In Resistance to Targeted Anti-Cancer Therapeutics. Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-030-24424-8_6.

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He, Lijuan, and Kalina Hristova. "Quantification of the Effects of Mutations on Receptor Tyrosine Kinase (RTK) Activation in Mammalian Cells." In Methods in Molecular Biology. Springer New York, 2014. http://dx.doi.org/10.1007/978-1-4939-1789-1_8.

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Nakai, Masamichi, Satoshi Tanimukai, Keiko Yagi, et al. "Amyloid β induces phosphorylation and translocation of MARCKS through tyrosine kinase-activated PKC-δ signaling pathway in microglia." In Neuroscientific Basis of Dementia. Birkhäuser Basel, 2001. http://dx.doi.org/10.1007/978-3-0348-8225-5_27.

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Di Palma, Michael, Manuel Narvaez, Mariana Pita-Rodríguez, et al. "Co-immunoprecipitation (Co-IP) of G Protein-Coupled Receptor (GPCR)-Receptor Tyrosine Kinase (RTK) Complexes from the Dorsal Hippocampus of the Rat Brain." In Co-Immunoprecipitation Methods for Brain Tissue. Springer New York, 2018. http://dx.doi.org/10.1007/978-1-4939-8985-0_13.

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Patranabis, Somi. "Recent Advances in the Therapeutic Development of Receptor Tyrosine Kinases (RTK) against Different Types of Cancer." In Protein Kinase - New Opportunities, Challenges and Future Perspectives [Working Title]. IntechOpen, 2021. http://dx.doi.org/10.5772/intechopen.98497.

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Receptor Tyrosine Kinases (RTKs) are an important class of receptors involved in regulating different cellular functions. The usual pathway of RTK activation involves specific ligand binding, dimerization and trans-autophosphorylation. Recently, RTK has been extensively studied as they have potential applications in targeted cancer therapy. RTK-based therapeutic strategies are promising because dysfunction of RTK is connected to a variety of diseases. More specifically, RTK has been widely associated with different types of cancer and related diseases. The chapter aims to cover recent advances and challenges in RTK related research, to get an overview of the problems and possibilities associated with targeted therapy. This will help in deciphering novel therapeutic applications in the future.
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Gaborit, Nadège, and Yosef Yarden. "Growth factors and associated signalling pathways in tumour progression and in cancer treatment." In Oxford Textbook of Cancer Biology, edited by Francesco Pezzella, Mahvash Tavassoli, and David J. Kerr. Oxford University Press, 2019. http://dx.doi.org/10.1093/med/9780198779452.003.0009.

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To gain increased proliferation, blood supply, invasiveness, and resistance to cytotoxic treatments, cancer cells continuously secrete polypeptide growth factors, or they utilize factors produced by the associated normal tissue and the immunological microenvironment. The growth factors relay biochemical messages by binding with receptor tyrosine kinases (RTKs) located at the cell surface. In response to activation and receptor auto-phosphorylation, RTKs mobilize diverse signalling pathways, which culminate in cytoplasmic and nuclear alterations, including activation of gene expression programmes. This chapter describes several well-characterized growth factors, highlights the cognate receptors and downstream signalling pathways, and exemplifies involvement of specific growth factors in maintenance of the hallmarks of cancer. An account of clinically approved drugs able to intercept growth factor signalling closes this chapter.
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Gaborit, Nadège, and Yosef Yarden. "Growth factors and associated signalling pathways in tumour progression and in cancer treatment." In Oxford Textbook of Cancer Biology, edited by Francesco Pezzella, Mahvash Tavassoli, and David J. Kerr. Oxford University Press, 2019. http://dx.doi.org/10.1093/med/9780198779452.003.0009_update_001.

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To gain increased proliferation, blood supply, invasiveness, and resistance to cytotoxic treatments, cancer cells continuously secrete polypeptide growth factors, or they utilize factors produced by the associated normal tissue and the immunological microenvironment. The growth factors relay biochemical messages by binding with receptor tyrosine kinases (RTKs) located at the cell surface. In response to activation and receptor auto-phosphorylation, RTKs mobilize diverse signalling pathways, which culminate in cytoplasmic and nuclear alterations, including activation of gene expression programmes. This chapter describes several well-characterized growth factors, highlights the cognate receptors and downstream signalling pathways, and exemplifies involvement of specific growth factors in maintenance of the hallmarks of cancer. An account of clinically approved drugs able to intercept growth factor signalling closes this chapter.
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Conference papers on the topic "Tyrosine Kinase (RTK) Pathway"

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Tohyama, Osamu, Junji Matsui, Kotaro Kodama, et al. "Abstract 1376: Receptor tyrosine kinase (RTK) signaling pathway in preclinical thyroid cancer models: Antitumor and antiangiogenic activity of lenvatinib to target VEGFR/FGFR/RET." In 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.am2015-1376.

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Daly, Roger J., Falko Hochgräfe, David R. Croucher, et al. "Abstract 3131: A novel tyrosine kinase signaling pathway in human basal breast cancer." 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.am2011-3131.

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Sanda, Takaomi, Jeffrey W. Tyner, Alejandro Gutierrez, et al. "Abstract 2809: Pathway dependence on the tyrosine kinase TYK2 in T-cell acute lymphoblastic leukemia." 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.am2011-2809.

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Suganuma, Masami, Keisuke Iida, Shota Yokoyama, Anchalee Rawangkan, Kozue Namiki, and Pattama Wongsirisin. "Abstract 2376: AXL receptor tyrosine kinase stimulates cell softening and cancer progression via Rac signaling pathway." In 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.am2018-2376.

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Morozova, Olena, Sam Ng, Arjun Rao, Josh Stuart, David Haussler, and Sofie Salama. "Abstract A2-52: Pan-cancer analysis reveals distinct effects of receptor tyrosine kinase mutations on downstream pathway activities." In Abstracts: AACR Special Conference: Translation of the Cancer Genome; February 7-9, 2015; San Francisco, CA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1538-7445.transcagen-a2-52.

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Gao, Xuyuan, Hang Xu, James CM Ho, et al. "Abstract LB-196: EGFR-mutant lung adenocarcinomas mutation profiles reveal ARID1A might be a novel tyrosine kinase resistance pathway." In 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-lb-196.

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Cheng, Cliff. "Abstract 2093: HEC73543 is a novel potent, selective Flt3 receptor tyrosine kinase (RTK) Inhibitor for the treatment of refractory acute myeloid leukemia (AML)." In 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.am2017-2093.

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Milenković, Dejan A., Marko N. Živanović, Milan S. Dekić, Marijana Stanojević Pirković, and Jelena R. Đorović Jovanović. "CYTOTOXIC ACTIVITY AND MOLECULAR DOCKING STUDY OF 4- SUBSTITUTED FLAVYLIUM SALT." In 1st INTERNATIONAL Conference on Chemo and BioInformatics. Institute for Information Technologies, University of Kragujevac,, 2021. http://dx.doi.org/10.46793/iccbi21.466m.

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In the present manuscript, the cytotoxic activity of flavylium cation substituted at 4- position with phenyl (FC-4Ph) was tested to two cells lines (human colorectal carcinoma, HCT-116, and human fibroblast lung, MRC-5). In vitro cytotoxicity experiments were performed to elucidate the possible anticancer activity of tested substance. Investigated compound did not show cytotoxic effect on HCT-116 after 24 h, while after 72 h exerted significant effect. A significant selectivity towards colorectal carcinoma cells was observed. On the other hand, this compound did not show any effect on MRC-5 ce
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Ohashi, Kadoaki, Juliann Chmielecki, Ya-Lun Lin, et al. "Abstract 1897:RAS signaling pathway gene mutations and acquired resistance to EGFR tyrosine-kinase inhibitors in EGFR mutant lung cancer." In Proceedings: AACR 103rd Annual Meeting 2012‐‐ Mar 31‐Apr 4, 2012; Chicago, IL. American Association for Cancer Research, 2012. http://dx.doi.org/10.1158/1538-7445.am2012-1897.

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Yeh, Chih-Hsien, Jason Chia-Hsien Cheng, Yu-Chieh Tsai, et al. "Abstract 3872: Targeting EGFR/HER2 signaling pathway by a dual receptor tyrosine kinase inhibitor BIBW2992 for radiosensitization in murine urothelial carcinoma." In Proceedings: AACR 103rd Annual Meeting 2012‐‐ Mar 31‐Apr 4, 2012; Chicago, IL. American Association for Cancer Research, 2012. http://dx.doi.org/10.1158/1538-7445.am2012-3872.

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Reports on the topic "Tyrosine Kinase (RTK) Pathway"

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Rimm, David L. Outcome Based Screening for Prognostic Phospho-RTK (Receptor Tyrosine Kinase) Antibodies Using Tissue Microarrays. Defense Technical Information Center, 2002. http://dx.doi.org/10.21236/ada410085.

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Rimm, David. Outcome Based Screening for Prognostic Phospho-RTK (Receptor Tyrosine Kinase) Antibodies Using Tissue Microarrays). Defense Technical Information Center, 2004. http://dx.doi.org/10.21236/ada430123.

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Rimm, David L. Outcome Based Screening for Prognostic Phospho-RTK (Receptor Tyrosine Kinase) Antibodies Using Tissue Microarrays. Defense Technical Information Center, 2003. http://dx.doi.org/10.21236/ada420064.

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