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Artykuły w czasopismach na temat "EGFR"
Chemmalar, S., A. R. Intan Shameha, Che Azurahanim Che Abdullah, Nor Asma Ab Razak, Loqman Mohamad Yusof, Mokrish Ajat, Kim Wei Chan i Md Zuki Abu Bakar Zakaria. "Busting the Breast Cancer with AstraZeneca’s Gefitinib". Advances in Pharmacological and Pharmaceutical Sciences 2023 (4.12.2023): 1–26. http://dx.doi.org/10.1155/2023/8127695.
Pełny tekst źródłaRengifo, Charles E., Rancés Blanco, Damián Blanco, Mercedes Cedeño, Milagros Frómeta i Enrique Rengifo Calzado. "Immunohistochemical Characterization of Three Monoclonal Antibodies Raised against the Epidermal Growth Factor and Its Receptor in Non-Small-Cell Lung Cancer: Their Potential Use in the Selection of Patients for Immunotherapy". Journal of Biomarkers 2013 (11.12.2013): 1–9. http://dx.doi.org/10.1155/2013/627845.
Pełny tekst źródłaJezierska, Michalina, Anna Owczarzak i Joanna Stefanowicz. "Dimethylarginines in Children after Anti-Neoplastic Treatment". Medicina 58, nr 1 (11.01.2022): 108. http://dx.doi.org/10.3390/medicina58010108.
Pełny tekst źródłaAl-Shaibani, Eshrak, Taylor Young, Eshetu Atenafu, Verna Cheung, Safwan Alsibai, Vikas Gupta, Dawn C. Maze, Marta Beata Davidson, Aniket Banker i Hassan Sibai. "Impact of Kidney Dysfunction on Overall Survival in Myeloproliferative Neoplasms: A Single-Center Retrospective Study". Blood 142, Supplement 1 (28.11.2023): 6439. http://dx.doi.org/10.1182/blood-2023-189318.
Pełny tekst źródłaMaennling, Amaia Eleonora, Mehmet Kemal Tur, Marcus Niebert, Torsten Klockenbring, Felix Zeppernick, Stefan Gattenlöhner, Ivo Meinhold-Heerlein i Ahmad Fawzi Hussain. "Molecular Targeting Therapy against EGFR Family in Breast Cancer: Progress and Future Potentials". Cancers 11, nr 12 (20.11.2019): 1826. http://dx.doi.org/10.3390/cancers11121826.
Pełny tekst źródłaHuang, Hsien-Neng, Pin-Feng Hung, Yai-Ping Chen i Chia-Huei Lee. "Leucine Zipper Downregulated in Cancer-1 Interacts with Clathrin Adaptors to Control Epidermal Growth Factor Receptor (EGFR) Internalization and Gefitinib Response in EGFR-Mutated Non-Small Cell Lung Cancer". International Journal of Molecular Sciences 25, nr 3 (23.01.2024): 1374. http://dx.doi.org/10.3390/ijms25031374.
Pełny tekst źródłaNicholson, Christopher J., Samuel J. Roth, Arudhir Singh, Caitlin Brown, Simon P. Fricker, Jon Hu i Samantha Dale Strasse. "Abstract C052: Circumventing EGFR inhibitor resistance in NSCLC using transomics". Molecular Cancer Therapeutics 22, nr 12_Supplement (1.12.2023): C052. http://dx.doi.org/10.1158/1535-7163.targ-23-c052.
Pełny tekst źródłaKumar, Sachin, Jeff Vassallo, Kalpana Nattamai, Jose A. Cancelas i Hartmut Geiger. "EGFR Signaling in Osteoblasts Regulates Circadian Rhythm of HSPC in Circulation". Blood 126, nr 23 (3.12.2015): 665. http://dx.doi.org/10.1182/blood.v126.23.665.665.
Pełny tekst źródłaZhou, Caicun, Fumio Imamura, Ying Cheng, Isamu Okamoto, Byoung Chul Cho, Meng Chih Lin, Margarita Majem i in. "Early clearance of plasma EGFR mutations as a predictor of response to osimertinib and comparator EGFR-TKIs in the FLAURA trial." Journal of Clinical Oncology 37, nr 15_suppl (20.05.2019): 9020. http://dx.doi.org/10.1200/jco.2019.37.15_suppl.9020.
Pełny tekst źródłaLee, Eugine, Padraich Flahardy, Cameron Vergato, Stephen Siecinski, Justin Chen, Charles O’Donnell, Graeme Hodgson, Defne Yarar i Thomas McCauley. "Abstract 1726: Targeted epigenomic control of MYC as a strategy to treat EGFR inhibitor-resistant NSCLC". Cancer Research 84, nr 6_Supplement (22.03.2024): 1726. http://dx.doi.org/10.1158/1538-7445.am2024-1726.
Pełny tekst źródłaRozprawy doktorskie na temat "EGFR"
Barbosa, Keila Cardoso. "Estudo de polimorfismos dos genes EGF e EGFR em astrocitomas difusamente infiltrativos". Universidade de São Paulo, 2008. http://www.teses.usp.br/teses/disponiveis/5/5138/tde-24062008-150231/.
Pełny tekst źródłaINTRODUCTION: Diffusely infiltrative astrocytomas are the most frequent tumors of the Central Nervous System (CNS) with a rate of 5-7 new cases in 100,000 individuals per year. They are highly invasive, and they are associated to alterations in some genes as EGF (epidermal growth factor) and EGFR (epidermal growth factor receptor), which may increase mitogenic activity, leading to increase of proliferation, cellular maturation, apoptosis, angiogenesis, and metastasis. Genetic alterations, as presence of polymorphisms of single nucleotide change (SNP) could influence their expression level, and thus could be associated to increased risk in developing astrocytomas. In the present study, two SNP of non-coding region (c.-191C>A and c.-216G>T) and one SNP in exon 16 (c.2073A>T) of EGFR, and another SNP of non-coding region of EGF (c.61A>G) were analyzed. The SNPs were associated to EGFR expression level and to survival time. METHOD: a case-control study of 193 of diffusely infiltrative astrocytomas and 200 controls was carried out, with PCR amplification and enzymatic digestion, which products were analyzed in agarose gel or polyacrylamide gel electrophoresis stained by ethidium bromide. EGFR expression level was studied by real time PCR after RNA extraction followed by reverse transcription of tumor tissues compared to epileptic non-neoplastic brain tissues. Stastistical analysis were performed by chi-square, odds ratio (OR), 95% confidence interval (95% CI), Student-t test and Kaplan Meier. RESULTS: The polymorphic genotype frequency was different between case and controls for the polymorphism c.2073A>T. Patients with TT genotype presented lower risk to develop astrocytoma when compared to genotype AA (OR=0.51, CI95%=0.29- 0.99). No other correlation was observed for the remaining studied polymorphisms. There was neither correlation between the polymorphic genotypes and the EGFR expression levels nor with survival time. CONCLUSION: The present study showed a possible protection factor in developing astrocytomas for the patients harboring the genotype TT of c.2073A>T polymorphism of EFGR, thus the patients presenting TT genotype have lower risk to develop diffusely infiltrative astrocytoma than patients presenting the genotype AA.
Bauer, Philip [Verfasser]. "Der Einfluss der EGFR Expressionsdichte auf die EGFR Antikörper gerichteten Abwehrmechanismen / Philip Bauer". Kiel : Universitätsbibliothek Kiel, 2017. http://d-nb.info/1127044206/34.
Pełny tekst źródłaHamilton, S. J. "An investigation of EGFR binding and modulation of EGFR signalling pathways using synthetic peptides". Thesis, Queen's University Belfast, 2004. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.403480.
Pełny tekst źródłaBalko, Justin M. "THE PHARMACOGENOMICS OF EGFR-DEPENDENT NSCLC: PREDICTING AND ENHANCING RESPONSE TO TARGETED EGFR THERAPY". Lexington, Ky. : [University of Kentucky Libraries], 2009. http://hdl.handle.net/10225/1062.
Pełny tekst źródłaTitle from document title page (viewed on September 17, 2009). Document formatted into pages; contains: viii, 175 p : ill. (some col.). Includes abstract and vita. Includes bibliographical references (p. 103-123).
Januário, Mara Elisama da Silva. "Estudo da função de AP1y2 e Alix no direcionamento de proteínas para degradação em lisossomos ou liberação em vesículas extracelulares". Universidade de São Paulo, 2017. http://www.teses.usp.br/teses/disponiveis/17/17136/tde-23042018-164806/.
Pełny tekst źródłaLysosomal degradation of endocytosed membrane proteins occurs through the targeting of these proteins to intraluminal vesicles (ILVs), formed in the multivesicular bodies (MVBs) lumen, and the subsequent fusion of MVBs with lysosomes. Despite its importance in the degradation of transmembrane proteins, MVBs have another important function, the production and release of extracellular vesicles (EVs). In this process, the MVBs do not fuse with lysosomes, but fuse with the plasma membrane resulting in the release of these vesicles that reside within MVBs to the extracellular environment. Several proteins regulate the targeting of cargo to MVBs. Studies that delineated the functions of AP1 in protein trafficking, focused on complexes containing the ?1 subunit, which mediates transport between trans-Golgi network (TGN) and endosomes. However, the human genome encodes a second isoform of this subunit, named ?2. Evidences from the literature, as well as results from our research group, indicate that AP1?2 regulates transport pathways that are distinct from the pathways classically attributed to AP1. By performing EGF-uptake assays under ?1 or ?2 knockdown (KD) conditions, it was observed that ?2 is required for degradation of internalized EGF, effect also observed for the EGF receptor (EGFR) using cell surface biotinylation assays. These results demonstrate that the lysosomal degradation of the EGFEGFR complexes via the canonical MVBs pathway requires the AP1?2 complex, but not AP1?1. In parallel with this study, we also analyzed the molecular mechanism of HIV-1 Nef targeting to MVBs associated with the EVs release. Nef is an important determinant in the modulation of the intracellular environment for efficient HIV replication and progression to AIDS. Nef is actively secreted via EVs and its release may lead to apoptosis of bystander acceptor cells. Moreover, Nef reduces the levels of CD4 and MHC-I molecules in EVs. Despite the importance of Nef release in EVs, the molecular mechanism used by Nef to be exported via EVs is unknown. Nef physically interacts with the ESCRT machinery accessory protein Alix, an important player in the process of ILVs formation and cargo selection. EVs released from HeLa cells and CD4+ T lymphocytes under Alix KD conditions demonstrated a significant IV reduction in Nef release via EVs. These results indicate that Nef requires Alix for its efficient release in EVs.
Liccardi, G. "Nuclear EGFR modulation of DNA repair". Thesis, University College London (University of London), 2011. http://discovery.ucl.ac.uk/1335897/.
Pełny tekst źródłaHousden, B. "Notch targets and EGFR pathway regulation". Thesis, University of Cambridge, 2011. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.604264.
Pełny tekst źródłaLee, Richard William. "MET-EGFR dimerisation in lung adenocarcinoma is dependent on EGFR mutations and altered by MET kinase inhibition". Thesis, King's College London (University of London), 2017. https://kclpure.kcl.ac.uk/portal/en/theses/metegfr-dimerisation-in-lung-adenocarcinoma-is-dependent-on-egfr-mutations-and-altered-by-met-kinase-inhibition(3a738a35-f82d-4eb6-83a3-150160d12045).html.
Pełny tekst źródłaOliveira, Carolina Barbara Nogueira de, Ivan Andrade de Araújo Penna i Antonio Marcos Saraiva. "Avaliação de polimorfismos nos genes EGF e EGFR e a susceptibilidade à pré-eclâmpsia severa". Universidade Federal Fluminense, 2012. https://app.uff.br/riuff/handle/1/4715.
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Conselho Nacional de Desenvolvimento Científico e Tecnológico
Fundação Carlos Chagas Filho de Amparo à Pesquisa do Estado do Rio de Janeiro
Coordenação de Aperfeiçoamento de Pessoal de Nível Superior
Fundação Oswaldo Cruz. Instituto Nacional de Controle de Qualidade em Saúde (INCQS-Fiocruz)
Cerca de 10-15% das causas de mortalidade e morbidade materna em países desenvolvidos e 37% das causas de morte obstétricas diretas no Brasil podem ser associadas à pré-eclâmpsia. A pré-eclâmpsia é uma patologia multissistêmica definida por uma hipertensão associada a uma proteinúria, após a 20ª semana de gestação. As manifestações clínicas desta doença podem se apresentar como uma síndrome materna ou fetal e de acordo com a gravidade podem ser classificadas em leve ou severa e de início precoce ou tardio. Apesar do conhecimento limitado sobre esta patologia, existem fortes evidências de envolvimento do componente genético na etiologia da pré-eclâmpsia. O fator de crescimento epidérmico (EGF) desempenha um papel importante na regulação do crescimento, proliferação e diferenciação celular, através da ligação ao seu receptor, o EGFR. Acredita-se que este fator esteja relacionado com a regulação do crescimento e da função placentária durante a gestação. Variações na sequência do DNA desses genes podem levar a uma alteração nos níveis de transcrição gênica e, como consequência, ser responsável por mudanças nos níveis de produção e/ou atividade desses fatores. O polimorfismo EGF +61 G>A está associado com a produção in vitro da proteína EGF e os polimorfismos EGFR -216 G>T e -191 C>A estão correlacionados a mudanças na atividade do promotor e na expressão de RNAm desse gene. O objetivo geral do nosso estudo foi avaliar uma possível associação entre polimorfismos funcionais nos genes EGF (+61 G>A) e EGFR (-216 G>T e -191 C>A) e a susceptibilidade à pré-eclâmpsia severa na população de gestantes do Estado do Rio de Janeiro, através de um estudo caso-controle. Como objetivos específicos, além de analisarmos uma possível interação entre os polimorfismos no desenvolvimento da pré-eclâmpsia severa, buscamos associar os polimorfismos ao histórico familiar da doença. O estudo foi composto por dois grupos, pareados por etnia: um grupo caso composto por 98 mulheres com pré-eclâmpsia severa e um grupo controle com 98 mulheres saudáveis. Os polimorfismos EGF (+61 G>A) e EGFR (-216 G>T e -191 C>A) foram avaliados pela reação em cadeia da polimerase seguida por análise de polimorfismos por tamanho de fragmentos de restrição (PCR-RFLP). As variáveis categóricas, frequências alélicas e genotípicas foram comparadas através do teste do exato de Fisher, e o teste t de Student foi utilizado para comparação das variáveis contínuas em cada grupo. Os resultados demonstram que o alelo A do polimorfismo -191 do gene EGFR está associado com a susceptibilidade à pré-eclâmpsia severa (p<0,05). Não houve associação significativa entre os outros polimorfismos (EGF +61 G>A e EGFR -216 G>T) e a susceptibilidade à pré-eclâmpsia severa (p>0,05), assim como também não foi encontrada relação entre a interação dos polimorfismos, histórico familiar e o desenvolvimento da pré-eclâmpsia severa. Além desses resultados, também foram encontradas diferenças significativas ao avaliarmos as características demográficas e clínicas entre os grupos. Este é o primeiro estudo a avaliar associações entre pré-eclâmpsia severa e os polimorfismos -216 G>T e -191C>A do gene EGFR e o primeiro estudo na população brasileira a investigar a associação do polimorfismo EGF +61 G>A e a doença. Com esse achado, podemos sugerir que o polimorfismo, o -191C>A do gene EGFR, possa ser o responsável por alguma regulação na produção do EGFR, e que através dessa regulação possa desempenhar algum papel importante na susceptibilidade à pré-eclâmpsia severa em mulheres do Estado do Rio de Janeiro.
About 10-15% of maternal deaths in development countries and approximately 37% of direct obstetrics deaths in Brazil can be assigned to preeclampsia. Preeclampsia is a multisystem disorder that usually occurs after 20 week of pregnancy and it is determined by the presence of hypertension associated with proteinuria. The clinical findings of preeclampsia can manifest as either a maternal syndrome or fetal syndrome. In addition, the preeclampsia can be classified as mild to severe, and in early or late-onset preeclampsia. Despite the limited knowledge of this pathology, there is a strong evidence of involvement of the genetic component in the etiology of preeclampsia. The epidermal growth factor (EGF) plays an important role in regulating cell growth, proliferation and differentiation, through binding its receptor, EGFR. Evidences suggest that this growth factor and its receptor are involved in growth regulation of placental function during the pregnancy. Variations in the DNA sequence in the EGF and EGFR genes can lead to an altered gene transcription and consequently can be responsible for changes in production and/or activity of these factors. The EGF +61 G>A polymorphism is significantly associated with in-vitro EGF protein production and the EGFR -216 G>T and -191 C>A polymorphisms are correlated with changes in promoter activity and expression of EGFR mRNA. The aim of this study was to verify the association between EGF +61 G>A, EGFR -216 G>T and -191 C>A polymorphisms and susceptibility to severe preeclampsia in the population of Rio de Janeiro through a case-control design. The specific objectives were to assess the association between these polymorphisms and the history family of preeclampsia, and also to analyze a possible interaction among these polymorphisms on the development of severe preeclampsia. The study was composed by two groups matched by ethnicity: the case group with 98 women with severe preeclampsia and the control group with 98 healthy women. Polymerase chain reaction restriction fragment length polymorphism analyses (PCR-RFLP) were performed to genotype EGF +61 G>A, EGFR -216 G>T and -191 C>A polymorphisms. Categorical variables, allelic and genotype frequencies were compared in each group applying Fisher´s exact test and a Student t test was used for continuous variables. The results showed that the A allele of the -191 C>A polymorphism of the EGFR gene is associated with susceptibility to severe preeclampsia (P<0,05). There were no significant association between severe preeclampsia and +61 G>A EGF and -216 G>T EGFR polymorphisms (P>0,05), as well as no correlation was found between the interaction of these polymorphisms, history family and the development of severe preeclampsia. We also found differences when we evaluated demographic and clinical characteristics between the two groups. This is the first study to assess the associations between -191 C>A and -216 G>T EGFR genetics polymorphisms and severe preeclampsia and the first study in Brazilian population to investigate the association between +61 G>A EGF polymorphism and severe preeclampsia. These findings suggest that the polymorphism-191C>A of the EGFR gene may be responsible for some regulation in the production of the EGFR, and that through this regulation this polymorphism might play an important role in the susceptibility to severe preeclampsia in women from Rio de Janeiro.
Vanlandingham, Phillip Allen. "Rab7 regulation of EGFR trafficking and signaling". Oklahoma City : [s.n.], 2009.
Znajdź pełny tekst źródłaKsiążki na temat "EGFR"
Haley, John D., i William John Gullick, red. EGFR Signaling Networks in Cancer Therapy. Totowa, NJ: Humana Press, 2008. http://dx.doi.org/10.1007/978-1-59745-356-1.
Pełny tekst źródłaCappuzzo, Federico. Guide to Targeted Therapies: EGFR mutations in NSCLC. Cham: Springer International Publishing, 2014. http://dx.doi.org/10.1007/978-3-319-03059-3.
Pełny tekst źródłaD, Haley John, i Gullick William John, red. EGFR Signaling Networks in Cancer Therapy / edited by John D. Haley, William John Gullick. New York, NY: Humana Press, 2008.
Znajdź pełny tekst źródłaRudzik, Nicholas James. A genetic analysis of the role of neuralized in the notch and EGFR pathways of Drosophila melanogaster. Ottawa: National Library of Canada, 1999.
Znajdź pełny tekst źródłaSaki, Mohammad. Radiolabeling of anti-EGFR antibody, Cetuximab, overcomes the radiotherapy resistance of Cetuximab resistant head and neck cancer cells. [S.l: s.n.], 2014.
Znajdź pełny tekst źródłaFaber, Anthony. Overcoming Resistance to EGFR Inhibitors in EGFR Mutant NSCLC. Elsevier Science & Technology, 2022.
Znajdź pełny tekst źródłaFaber, Anthony. Overcoming Resistance to EGFR Inhibitors in EGFR Mutant NSCLC. Elsevier Science & Technology Books, 2021.
Znajdź pełny tekst źródłaPatel, Harun M., Rahul Pawara i S. J. Surana. Third-Generation EGFR Inhibitors: Overcoming EGFR Resistance and Toxicity Problems. Elsevier, 2018.
Znajdź pełny tekst źródłaPatel, Harun M., Rahul Pawara i Sanjay J. Surana. Third Generation EGFR Inhibitors: Overcoming EGFR Resistance and Toxicity Problems. Elsevier, 2018.
Znajdź pełny tekst źródłaSchaeybroeck, Sandra Van. Egfr Activity As a Determinant of Response to Egfr-targeted Therapy. Leuven Univ Pr, 2006.
Znajdź pełny tekst źródłaCzęści książek na temat "EGFR"
Weiner, Louis M., i Christina Wu. "EGFR, Immunology". W Cancer Therapeutic Targets, 199–208. New York, NY: Springer New York, 2017. http://dx.doi.org/10.1007/978-1-4419-0717-2_27.
Pełny tekst źródłaWeiner, Louis M., i Christina Wu. "EGFR, Immunology". W Cancer Therapeutic Targets, 1–10. New York, NY: Springer New York, 2013. http://dx.doi.org/10.1007/978-1-4614-6613-0_27-2.
Pełny tekst źródłaBourdeanu, Laura, Ellen Liu, Suzanne Brint i David Langdon. "EGFR Resistance". W Resistance to Targeted Anti-Cancer Therapeutics, 103–16. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-70142-4_4.
Pełny tekst źródłaKobayashi, Kunihiko, i Hiroshi Kagamu. "EGFR Mutant". W Molecular Targeted Therapy of Lung Cancer, 167–89. Singapore: Springer Singapore, 2017. http://dx.doi.org/10.1007/978-981-10-2002-5_10.
Pełny tekst źródłaCooley, Laura A., Daniel G. Bausch, Marija Stojkovic, Waldemar Hosch, Thomas Junghanss, Marija Stojkovic, Waldemar Hosch i in. "eGFR, Concept of". W Encyclopedia of Intensive Care Medicine, 811–19. Berlin, Heidelberg: Springer Berlin Heidelberg, 2012. http://dx.doi.org/10.1007/978-3-642-00418-6_280.
Pełny tekst źródłaNoor, Zorawar S., i Jonathan W. Goldman. "EGFR Targeted Therapy". W Targeted Therapies for Lung Cancer, 1–30. Cham: Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-030-17832-1_1.
Pełny tekst źródłaBhutani, Manisha, i Helen Gharwan. "EGFR, Growth Factors". W Cancer Therapeutic Targets, 707–17. New York, NY: Springer New York, 2017. http://dx.doi.org/10.1007/978-1-4419-0717-2_72.
Pełny tekst źródłaSenellart, H., i J. Bennouna. "Anticorps anti-EGFR". W Les thérapies ciblées, 35–44. Paris: Springer Paris, 2008. http://dx.doi.org/10.1007/978-2-287-36008-4_2.
Pełny tekst źródłaBhutani, Manisha, i Helen Gharwan. "EGFR, Growth Factors". W Cancer Therapeutic Targets, 1–11. New York, NY: Springer New York, 2013. http://dx.doi.org/10.1007/978-1-4614-6613-0_72-3.
Pełny tekst źródłaDistefano, Veronica, Maria Mannone, Irene Poli i Gert Mayer. "Clustering Trajectories to Study Diabetic Kidney Disease". W Communications in Computer and Information Science, 271–83. Cham: Springer Nature Switzerland, 2024. http://dx.doi.org/10.1007/978-3-031-57430-6_21.
Pełny tekst źródłaStreszczenia konferencji na temat "EGFR"
Lee, An-Chun, Chia-Cherng Yu, Yuan-Hung Wang i Yu-Ting Chou. "Abstract 5906: EGFR and SOX2 crosstalk determines EGFR-TKI". W 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.am2018-5906.
Pełny tekst źródłaAllen, Fred D., Clara F. Asnes, Alan Wells, Elliot L. Elson i Douglas A. Lauffenburger. "Alternative Pathways of Epidermal Growth Factor Receptor Mediated Contractile Force in NR6 Fibroblasts". W ASME 1999 International Mechanical Engineering Congress and Exposition. American Society of Mechanical Engineers, 1999. http://dx.doi.org/10.1115/imece1999-0403.
Pełny tekst źródłaWeng, Ting-Wei, Sheng-Yao Huang, Chun-Liang Lu, Chiun-Li Chin, Hao-Hung Tsai i I.-Fang Chung. "Distinguish EGFR+ and EGFR- patients in LA using CT images". W 2016 International Conference on Fuzzy Theory and Its Applications (iFuzzy). IEEE, 2016. http://dx.doi.org/10.1109/ifuzzy.2016.8004960.
Pełny tekst źródłaMilewska, Marta, Justin Micah Balko i Esther Penni Black. "Abstract 2896: MEK inhibition controls EGFR level in EGFR-dependent NSCLC cells via deregulated expression of EGF-like ligands". W 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.am2011-2896.
Pełny tekst źródłaMakinoshima, Hideki, Masahiro Takita, Shingo Matsumoto, Atsushi Yagishita, Satoshi Owada, Hiroyasu Esumi i Katsuya Tsuchihara. "Abstract 3361: EGFR signaling regulates aerobic glycolysis in EGFR-mutated lung adenocarcinoma". W 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.am2014-3361.
Pełny tekst źródłaRaimbourg, Judith, Mathilde Cabart, Marie-Pierre Joalland, Didier Decaudin, Ludmilla Deplater, Didier Lanoe, Jean-Yves Douillard, Jaafar Bennouna, François Vallette i Lisenn Lalier. "Abstract 2559: Optimisation of EGFR TKI efficiency wild-type EGFR lung cancer". W 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.am2015-2559.
Pełny tekst źródłaLee, Richard, Elena Ortiz-Zapater, Gregory Weitsman, Gilbert Fruhwirth, Will Owen, Tony Ng i George Santis. "EGFR mutations determine EGFR-MET crosstalk and MET inhibition in lung cancer". W Annual Congress 2015. European Respiratory Society, 2015. http://dx.doi.org/10.1183/13993003.congress-2015.pa539.
Pełny tekst źródłaHong, Shiao-Ya, Yi-Ping Shih, Tianhong Li, Kermit Carraway i Su Hao Lo. "Abstract A40: CTEN prolongs EGFR signaling by reducing ligand-induced EGFR degradation". W Abstracts: Third AACR International Conference on Frontiers in Basic Cancer Research - September 18-22, 2013; National Harbor, MD. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1538-7445.fbcr13-a40.
Pełny tekst źródłaMakhov, Peter, Alexander Kudinov, Alexander Deneka, Brian L. Egleston, Emmanuelle Nicolas, Kathy Q. Cai, Rohan Brebion i in. "Abstract 4452: Musashi-2 regulates EGFR/HER3 expression in NSCLC, cell proliferation and response to EGFR inhibitors in EGFR-mutant NSCLC". W 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.am2018-4452.
Pełny tekst źródłaKoba, Hayato, Hideharu Kimura, Shingo Nishikawa, Taro Yoneda, Takashi Sone i Kazuo Kasahara. "Abstract 2268: Detection of T790M mutation in EGFR gene, an EGFR-TKI resistant mutation, in tumor samples unexposed to EGFR TKIs". W Proceedings: AACR 107th Annual Meeting 2016; April 16-20, 2016; New Orleans, LA. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/1538-7445.am2016-2268.
Pełny tekst źródłaRaporty organizacyjne na temat "EGFR"
Song, Yaowen, Shuiyu Lin, Jun Chen, Silu Ding i Jun Dang. First-line treatment with TKI plus brain radiotherapy vs TKI alone in EGFR-mutated non-small-cell lung cancer with brain metastases: a systematic review and meta-analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, styczeń 2023. http://dx.doi.org/10.37766/inplasy2023.1.0013.
Pełny tekst źródłaGoodrich, Jennifer S. EGFR Activation by Spatially Restricted Ligands. Fort Belvoir, VA: Defense Technical Information Center, czerwiec 2004. http://dx.doi.org/10.21236/ada426969.
Pełny tekst źródłaBacker, Joseph M. Development of Cu-64 labeled EGF for In Vivo PET Imaging of EGFR Expression. Office of Scientific and Technical Information (OSTI), lipiec 2009. http://dx.doi.org/10.2172/958568.
Pełny tekst źródłaHong, Xiaohua, Guangyao Wang, Chunmei Mo i Zhen Rong. Prognostic value of EGFR/p-EGFR in nasopharyngeal carcinoma: a protocol for systematic review and meta-analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, maj 2021. http://dx.doi.org/10.37766/inplasy2021.5.0010.
Pełny tekst źródłaLin, Chutong, Fengling Hu, Hongling Chu, Peng Ren, Shanwu Ma, Jingdi Wang, Jie Bai, Xuan Han i Shaohua Ma. The Role of EGFR-TKIs as Adjuvant Therapy in EGFR Mutation-Positive Early-Stage NSCLC: a meta-analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, październik 2020. http://dx.doi.org/10.37766/inplasy2020.10.0098.
Pełny tekst źródłaWang, Zexian, Yaru Guo, Xiaojin Wu, Xiaohan Qin, Zhiling Wan i Chen Liu. Bevacizumab plus Epidermal Growth Factor Receptor (EGFR)-Tyrosine Kinase Inhibitor versus EGFR-TKI alone for advanced EGFR-mutant non-small cell lung cancer: a meta-analysis of randomized clinical trials. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, grudzień 2023. http://dx.doi.org/10.37766/inplasy2023.12.0059.
Pełny tekst źródłaQin, Xiaohan, Yaru Guo, Xiaojin Wu, Zexian Wang, Zhiling Wan i Chen Liu. Chemotherapy plus Epidermal Growth Factor Receptor (EGFR)-Tyrosine Kinase Inhibitor versus EGFR-TKI alone for advanced EGFR-mutant non-small cell lung cancer: a meta-analysis of randomized clinical trials. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, styczeń 2024. http://dx.doi.org/10.37766/inplasy2024.1.0128.
Pełny tekst źródłaMarks, James. Structural Basis of EGFR Dimerization for Drug Design. Fort Belvoir, VA: Defense Technical Information Center, wrzesień 2000. http://dx.doi.org/10.21236/ada396569.
Pełny tekst źródłaLi, Chia-Wei. Role of IKKalpha in the EGFR Signaling Regulation. Fort Belvoir, VA: Defense Technical Information Center, wrzesień 2011. http://dx.doi.org/10.21236/ada610026.
Pełny tekst źródłaLi, Chia-Wei. Role of IKKalpha in the EGFR Signaling Regulation. Fort Belvoir, VA: Defense Technical Information Center, wrzesień 2012. http://dx.doi.org/10.21236/ada610027.
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