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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.
Pełny tekst źródłaApproved for entry into archive by Verônica Esteves (vevenesteves@gmail.com) on 2017-09-28T17:29:03Z (GMT) No. of bitstreams: 2 license_rdf: 0 bytes, checksum: d41d8cd98f00b204e9800998ecf8427e (MD5) Dissertação Carolina Barbara - AVALIAÇÃO DE POLIMORFISMOS NO.pdf: 2844302 bytes, checksum: d3ce9355ae4a9633c9b9e0c88ce683c5 (MD5)
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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 źródłaCONTE, ALEXIA. "INTEGRATION OF MODELING AND EXPERIMENTS TO DEFINE PRINCIPLES OF EGFR ACTIVATION AND UBIQUITINATION". Doctoral thesis, Università degli Studi di Milano, 2016. http://hdl.handle.net/2434/362616.
Pełny tekst źródłaMagalhães, Paula Lima. "Imunomarcação dos receptores de EGF (EGFR e c-ErbB2) no carcinoma de células escamosas em cães". Universidade Federal de Goiás, 2017. http://repositorio.bc.ufg.br/tede/handle/tede/7724.
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Squamous cell carcinoma (SCC) is one of the most common malignant cutaneous tumors in all species, as well as in the human species, ranging from young animals to the elderly. It has development associated with environmental factors such as prolonged exposure to solar rays and epidermal hypopigmentation. According to the literature, 80% of malignancies originate in environmental stimuli, due to exposure to carcinogens. Despite the multifactorial etiology, the search for clarification of the causes and mechanisms of cancer evolution must be incessant, since innumerable neoplasms can be prevented, especially when induced by exogenous factors. The aim of this study was to study canine cutaneous SCC in the light of different histomorphological patterns of the neoplasia, evaluating its immunophenotype response to EGFR and c-erbB2 epidermal growth factor receptors. For that, the cases of canine SCC were analyzed from the archive of the Animal Pathology Sector of the EVZ / UFG from 2006 to 2015. For the epidemiological study, registration information was considered, including breed, sex, age and anatomical location. Regarding the histomorphological evaluation and malignancy criteria, the lesions were classified according to the system recommended by the Müller e Kirk’s. Anti-EGFR (HER1) and anti-c-erbB-2 (HER2) antibodies were used for the immunohistochemical study to better understand the role of these proteins in the mechanisms involved in the genesis, proliferation and evolution of SCC in dogs. Considering the histomorphological and immunophenotypic analyzes, the correlation between its variables was tested, and a correlation was verified between the EGFR immunostaining and the degree of SCC differentiation (r = 0.26, p = 0.02). On the other hand, there was no correlation between c-erbB2 immunostaining and histomorphological differentiation (r = 0.02; p = 0.83). When the correlation between EGFR and c-erbB2 immunoblots was tested, a positive correlation was also observed, but not statistically significant (r = 0.21, p = 0.06). It is concluded that there is a propensity that the increase in EGFR immunoexpression is directly proportional to the degree of SCC differentiation, and that it does not occur with c-erbB2 immunostaining. Also, SCCs in dogs seems to exhibit simultaneous increase of EGF receptor immunostaining.
O carcinoma de células escamosas (CCE) é um dos tumores cutâneos malignos mais comuns em todas as espécies animais, assim como na espécie humana, podendo acometer desde animais jovens a idosos. Tem desenvolvimento associado a fatores ambientais como exposição prolongada aos raios solares e hipopigmentação epidermal. Os estudos revelam que, 80% das neoplasias malignas têm origem em estímulos ambientais, em decorrência a exposição a carcinógenos. Apesar da etiologia multifatorial, a busca pelo esclarecimento das causas e dos mecanismos de evolução do câncer deve ser incessante, pois inúmeras neoplasias podem ser prevenidas, especialmente quando induzidas por fatores exógenos. Assim, este trabalho teve por objetivo estudar o CCE cutâneo canino à luz dos diferentes padrões histomorfológicos da neoplasia, avaliando o seu imunofenótipo quanto aos receptores do fator de crescimento epidérmico EGFR e c-erbB2. Para tal, foram avaliadas os casos de CCE canino provenientes do arquivo do Setor de Patologia Animal da EVZ/UFG no período de 2006 a 2015. Para o estudo epidemiológico foram consideradas as informações de registro, incluindo raça, sexo, idade e localização anatômica. Quanto à avaliação histomorfológica e critérios de malignidade, as lesões foram classificadas de acordo com o sistema preconizado por Müller e Kirk’s. Para o estudo imunoistoquímico foram utilizados os anticorpos anti-EGFR (HER1) e anti-c-erbB-2 (HER2), com o intuito de melhor compreender a participação dessas proteínas nos mecanismos envolvidos na gênese, proliferação e evolução do CCE em cães. Considerando as análises histomorfológica e imunofenotípica foi testada a correlação entre suas variáveis, sendo constatada correlação entre a imunomarcação para EGFR e o grau de diferenciação do CCE (r=0,26; p=0,02). Por outro lado, não houve correlação entre a imunomarcação de c-erbB2 e a diferenciação histomorfológica (r=0,02; p=0,83). Quando testada a correlação entre as imunomarcações de EGFR e c-erbB2, também foi observada correlação positiva, porém sem significância estatística (r=0,21; p=0,06). Conclui-se que há propensão de que o aumento na imunoexpressão de EGFR seja diretamente proporcional ao grau de diferenciação do CCE, sendo que o mesmo não ocorre com a imunomarcação de c-erbB2. Também, os CCE em cães parecem apresentar aumento simultâneo da imunomarcação dos receptores de EGF.
Liffers, Katrin [Verfasser], i Katrin [Akademischer Betreuer] Lamszus. "Identifikation von Resistenzmechanismen gegenüber EGFR-Tyrosinkinase Inhibitoren in EGFR-amplifizierten und EGFRvIII-positiven Glioblastomen / Katrin Liffers. Betreuer: Katrin Lamszus". Hamburg : Staats- und Universitätsbibliothek Hamburg, 2015. http://d-nb.info/107464249X/34.
Pełny tekst źródłaKramer, Elizabeth L. "Role of the EGFR Pathway in Lung Remodeling and Disease". University of Cincinnati / OhioLINK, 2009. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1250206890.
Pełny tekst źródłaHennes, Nadine Regina. "Untersuchungen zur Expression und Lokalisation des epidermalen Wachstumsfaktors (EGF) und seines Rezeptors (EGFR) im Intestinaltrakt des Schweines". Diss., kostenfrei, 2008. http://edoc.ub.uni-muenchen.de/9013/.
Pełny tekst źródłaEscalante, Escalante Paula Isabel. "Polimorfismos genéticos de P53, COX-2 , EGF y EGFR como marcadores de riesgo de cáncer de laringe". Tesis, Universidad de Chile, 2017. http://repositorio.uchile.cl/handle/2250/147248.
Pełny tekst źródłaEl carcinoma escamoso de laringe es una enfermedad altamente invalidante ya que puede afectar la capacidad del habla, respiración y deglución del paciente que lo sufre. Los principales factores causales identificados son cigarro y alcohol. Las vías de respuesta inflamatoria, proliferativa y de reparación de ADN pueden contribuir al riesgo de cáncer de laringe. El objetivo de este estudio es determinar asociaciones entre variantes genéticas COX-2 rs20417, COX-2 rs689466, EGF rs4444903, EGFR rs2227983, P53 rs1042522 y el riesgo de cáncer de laringe en la población chilena. Se realizó un estudio casos y controles, con 100 pacientes con cáncer escamoso de laringe y 139 voluntarios adultos sin cáncer. La genotipificación se realizó mediante PCR-RLFP. Se observa que estos polimorfismos son capaces de incrementar el riesgo de cáncer de laringe asociado a la combinación de consumo de tabaco y alcohol en una razón de 0,34 veces para COX-2 rs20417, 0,5 veces para EGF rs4444903, 0,56 veces para P53 rs1042522, 1,72 veces para EGFR rs2227983 y 4,7 veces para COX-2 rs689466. Esto sugiere que las variantes COX-2 rs20417, COX-2 rs689466, EGF rs4444903, EGFR rs2227983 y P53 rs1042522 actúan como modificadores de riesgo de cáncer de laringe.
Laryngeal squamous cell carcinoma is a kind of cancer that can be highly disabling to the patient, affecting speech, swallowing and respiratory skills, and leading to impaired quality of life. Smoking and alcohol abuse are principal risk factors linked to this disease. Inflammation signaling pathways, mitogens and DNA repair genes are factors that can be involved in carcinogenesis. The aim of this research is to assess the effect of COX-2 rs20417, COX-2 rs689466, EGF rs4444903, EGFR rs2227983, P53 rs1042522 single nucleotide polymorphisms in the risk of laryngeal cancer development in Chilean population. For this case control study, we recruited 100 cancer patients and 139 healthy volunteers. SNP genotype was analyzed from genomic DNA by PCR-RFLP. We observed that these SNPs are capable of increase the smoking plus alcohol risk of laryngeal cancer in a ratio of 0,34 fold for COX-2 rs20417 SNP, 0,5 fold for EGF rs4444903 SNP, 0,56 fold for P53 rs1042522 SNP, 1,72 fold for EGFR rs2227983 SNP and 4,7 fold for COX-2 rs689466 SNP. These findings suggest that COX-2 rs20417, COX-2 rs689466, EGF rs4444903, EGFR rs2227983 and P53 rs1042522 single nucleotide polymorphisms acts as risk modifier factors for laryngeal cancer.
Bollée, Guillaume. "Rôle de l'Heparin-Binding Epidermal Growth Factor (HB-EGF) et du récepteur EGFR dans la glomérulonéphrite extracapillaire". Paris 7, 2011. http://www.theses.fr/2011PA077140.
Pełny tekst źródłaCrescentic glomerulonephritis or rapidly progressive glomerulonephritis (RPGN) is the most severe form of glomerular disease. Glomerular injury manifests as a proliferative histological pattern, accumulation of T cells and macrophages, proliferation of intrinsic glomerular cells, accumulation of cells in Bowman's space ("crescents"), and rapid deterioration of renal function. Here we show de novo induction of heparin-binding epidermal growth factor-like growth factor (HB-EGF) in intrinsic glomerular epithelial cells (podocytes) from mice with RPGN induced by nephrotoxic serum and also in human RPGN. HB-EGF induction increases phosphorylation of the EGFR/ErbB 1 receptor in mice with RPGN. In HB-EGF-deficient mice, EGFR activation in glomeruli is absent and the course of RPGN is markedly improved. Autocrine HB-EGF induces a phenotypic switch in podocytes in vitro. Conditional deletion of the Egfr gene from podocytes of mice alleviates crescentic glomerulonephritis and the clinical features that accompany RPGN. Pharmacological blockade of EGFR also prevents nephrotic syndrome, infiltration of T cells and macrophages, necrotizing crescentic glomerulonephritis, acute renal failure and death in mice. This approach is effective even when started 4 days after the induction of experimental RPGN. The deleterious effects of EGFR activation may be mediated by activation of STAT3 and the severity of RPGN in mice is reduced by the administration of a STAT3 inhibitor. Our results suggest that targeting the HB-EGF/EGFR pathway could be clinically beneficial for treatment of human RPGN
Roetzer, Silvia. "Fraktionierte lokoregionale Radioimmuntherapie mit 213Bi-anti-EGFR-MAk". Diss., Ludwig-Maximilians-Universität München, 2013. http://nbn-resolving.de/urn:nbn:de:bvb:19-160591.
Pełny tekst źródłaPfäffle, Heike. "Defective DNA repair in EGFR-mutant lung cancer". Diss., Ludwig-Maximilians-Universität München, 2013. http://nbn-resolving.de/urn:nbn:de:bvb:19-162407.
Pełny tekst źródłaWillems, Sofie Henriëtte. "ADAMs as EGFR ligand sheddases in prostate cancer". Thesis, University of Cambridge, 2011. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.609342.
Pełny tekst źródłaAlves, Alice Manuela Santos. ""EGFR, e Lesões Displásticas do Colo do Útero"". Master's thesis, Instituto de Ciências Biomédicas Abel Salazar, 2010. http://hdl.handle.net/10216/57198.
Pełny tekst źródłaWhite, Audrey Lucille, i Audrey Lucille White. "Signaling Crosstalks: EGFR and TAZ in Breast Cancer". Thesis, The University of Arizona, 2017. http://hdl.handle.net/10150/625241.
Pełny tekst źródłaLee, Tang-Cheng Threadgill David W. "Functional analysis of EGFR using a conditional allele". Chapel Hill, N.C. : University of North Carolina at Chapel Hill, 2008. http://dc.lib.unc.edu/u?/etd,1730.
Pełny tekst źródłaTitle from electronic title page (viewed Sep. 16, 2008). "... in partial fulfillment of the requirements for the degree of Doctor of Philosophy in the Curriculum of Genetics & Molecular Biology." Discipline: Genetics and Molecular Biology; Department/School: Medicine.
Alves, Alice Manuela Santos. ""EGFR, e Lesões Displásticas do Colo do Útero"". Dissertação, Instituto de Ciências Biomédicas Abel Salazar, 2010. http://hdl.handle.net/10216/57198.
Pełny tekst źródłaLue, Hui-wen. "LIV-1 Promotes Prostate Cancer Epithelial-to-Mesenchymal Transition and Metastasis Through HB-EGF Shedding and EGFR-mediated ERK Signaling". Digital Archive @ GSU, 2012. http://digitalarchive.gsu.edu/biology_diss/115.
Pełny tekst źródłaSu, Hsin-Yuan. "Therapeutic Potential of EGFR Derived Peptides in Breast Cancer". Diss., The University of Arizona, 2013. http://hdl.handle.net/10150/293486.
Pełny tekst źródłaRaimbourg, Judith. "Effets du cisplatine sur la sensibilité des cancers bronchiques non à petites cellules EGFR sauvage aux inhibiteurs de tyrosine kinase anti EGFR". Thesis, Nantes, 2018. http://www.theses.fr/2018NANT1028/document.
Pełny tekst źródłaAnti-EGFR tyrosine kinase inhibitors (ITKs) have markedly improved the overall survival of patients with metastatic non-small cell lung cancer (NSCLC) with an EGFR activating mutation. In the absence of activating mutation, the benefit of these treatments is marginal and seems conditioned by the prior use of chemotherapy. In this study, prior exposure of wild-type EGFR NSCLC cells to sub-lethal doses of cisplatin induces an increase in EGFR phosphorylation increasing the sensitivity of these cells to erlotinib, anti-EGFR TKI, in vitro and in vivo, contrary to the effect observed on mutated EGFR cells. This activation of EGFR is related to the transactivation of the receptor by Src according to an independent mechanism of the EGFR ligands but involving IL6. This independent ligand activation of EGFR is correlated with the activation of the type 1 interferon pathway, in particular TBK1, IRF3, and the increase in the expression of two of their targeted genes IFIT1 and IFI27. Increasing expression of IFIT1 and IFI27 as well as IL6 are robust markers of cisplatin-induced ITK sensitization in vitro and in vivo. Finally the results of our study suggest an important role in this sensitization of the mitochondrial localization of EGFR, possibly induced by the phosphorylation of tyrosine 845, tyrosine target of Src. This sensitization could be related to the role played by the mitochondrial EGFR in the dynamics and the mitochondrial morphology as well as in the cellular metabolism
Bu, Yubai. "New synthetic routes to nitrogen heterocycles : natural products and novel drug scaffolds". Thesis, Loughborough University, 2017. https://dspace.lboro.ac.uk/2134/27482.
Pełny tekst źródłaMenezes, Sharleen Valerie. "Understanding the molecular mechanisms that underlie the anti-cancer activity of the metastasis suppressor, NDRG1 in the treatment of cancer". Thesis, The University of Sydney, 2018. http://hdl.handle.net/2123/20193.
Pełny tekst źródłaKvarnbrink, Samuel. "The importance og LRIG1 in lung cancer". Thesis, Umeå universitet, Onkologi, 2012. http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-57834.
Pełny tekst źródłaAlbuschat, Rica. "Neue EGFR-Tyrosinkinase-Inhibitoren mit Salicyloyl- oder Chinazolin-Teilstrukturen". [S.l.] : [s.n.], 2003. http://www.diss.fu-berlin.de/2003/189/index.html.
Pełny tekst źródłaSchäfer, Beatrix. "Transactivation of the EGFR Signal in Human Cancer Cells". Diss., lmu, 2004. http://nbn-resolving.de/urn:nbn:de:bvb:19-23041.
Pełny tekst źródłaBrown, K. E. "EGFR signalling and ommatidial orientation in the Drosophila eye". Thesis, University of Cambridge, 2004. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.596973.
Pełny tekst źródłaKlinghammer, Konrad [Verfasser]. "Primäre und sekundäre Resistenzmechanismen der EGFR Blockade / Konrad Klinghammer". Berlin : Medizinische Fakultät Charité - Universitätsmedizin Berlin, 2019. http://d-nb.info/1200409442/34.
Pełny tekst źródłaMao, Yanlan. "Adhesion molecules in Drosophila EGFR signalling and retinal development". Thesis, University of Cambridge, 2008. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.612274.
Pełny tekst źródłaAlbukhari, Ashwag. "Targeting EGFR signalling pathway in triple negative breast cancer". Thesis, University of Oxford, 2014. http://ora.ox.ac.uk/objects/uuid:85d4bb10-385e-4187-8576-cf04f15f2871.
Pełny tekst źródłaStrieder, Luciana Rocha [UNESP]. "Análise da proteína EGFR em carcinoma espinocelular de lábio". Universidade Estadual Paulista (UNESP), 2015. http://hdl.handle.net/11449/132902.
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Fundação de Amparo à Pesquisa do Estado do Amazonas (FAPEAM)
O carcinoma espinocelular de lábio (CEC) é uma das neoplasias malignas mais comuns, acometendo principalmente lábio inferior devido à exposição solar. Este trabalho teve como objetivo avaliar 3 métodos de gradação histológica (OMS, BD e MRH), analisar a expressão da proteína EGFR no CEC de lábio, comparar com queilite actínica (QA) e correlaciona-las com o prognóstico. Dados de 53 pacientes com CEC de lábio foram coletados para a avaliação clinicopatológica e histológica. 22 casos de CEC e 19 de QA foram submetidos à reação imuno-histoquímica com a proteína EGFR e analisados por um analisador automatizado para avaliação da expressão proteica. A média de idade foi de 65 anos, 69,8% foram homens, o lábio inferior foi o local de predileção com 94,4% e 66,03% dos pacientes estavam em estadios precoces (T1+T2). 28 (52,83%) e 34 (64,15%) casos respectivamente foram graduados em baixo risco prognóstico ou grau 1 pelas escalas BD e OMS, o modelo MRH graduou a 29 (54,72%) casos como médio risco prognóstico ou grau 2. O modelo de gradação mais simples e fácil de ser aplicado em CEC de lábio foi a Escala BD e o mais eficaz, pois quando em alto grau histológico foi associado à menor sobrevida global (P=0,045). A sobrevida global foi de 87,8% em 5 anos. Estadiamento clínico avançado (T3+T4) e envolvimento linfonodal (N1) foram associados à menor sobrevida global e sobrevida livre de recorrência (P=0,002; 0,005; 0,007 e 0,01). O tratamento cirúrgico combinado ao radioterápico foi associado à menor sobrevida livre de recorrência (P=0,03). Na expressão da proteína EGFR não houve diferença estatisticamente significante entre QA e CEC de lábio. O CEC de lábio quando em estadios e graus histológicos avançados, é associado a um pior prognóstico, o diagnóstico precoce é essencial para a escolha do melhor tratamento e sobrevida dos pacientes, evitando mutilações e consequentemente, perda na qualidade de vida.
Lip squamous cell carcinoma (SCC) is one of the most common malignancies affecting especially lower lip due to sun exposure. This study aimed to evaluate three methods of histological grading (WHO, BD and MRH), analyze the expression of EGFR protein on the lip of SCC, compared with actinic cheilitis (AC) and correlates them with the prognosis. Data from 53 patients with lip SCC were collected for the clinicopathological and histological evaluation. 22 cases of SCC and 19 AC underwent immunohistochemical reaction with EGFR protein and analyzed by an automated analyzer for evaluation of protein expression. The average age was 65 years, 69,8% were men, lower lip was the site of predilection with 94,4% and 66,03% of patients were in early stages (T1 + T2). 52.83% and 64.15% cases respectively were graduates in low risk prognosis or grade 1 by BD and WHO scales, the MRH model graduated 54.72% cases as medium risk prognosis or grade 2. The simplest grading model and easy to apply in lip SCC was the BD scale and more efficient because when in high histological grade was associated with lower overall survival (P = 0.045). Overall survival was 87,8% at 5 years. Advanced clinical stage (T3 + T4) and lymph node involvement (N1) were associated with lower overall survival and recurrence-free survival (P = 0.002; 0.005; 0.007 and 0.01). Surgical treatment combined with radiotherapy was associated with lower recurrence-free survival (P = 0.03). The expression of EGFR protein had no statistically significant difference between AC and lip SCC. The lip SCC when in advanced stages and high histological grades, is associated with a worse prognosis, early diagnosis is essential for choosing the best treatment and survival of patients, avoiding mutilation and consequently, loss in quality of life.
FAPEAM: 1271/2012
Pretto, Guilherme Gonçalves. "EGFR na sequência DRGE, BARRETT e adenocarcinoma de esôfago". reponame:Biblioteca Digital de Teses e Dissertações da UFRGS, 2011. http://hdl.handle.net/10183/39671.
Pełny tekst źródłaSharif, Ariane. "Contrôle du phénotype astrocytaire par le couple TGFα-EGFR". Paris 6, 2005. http://www.theses.fr/2005PA066636.
Pełny tekst źródłaStrieder, Luciana Rocha. "Análise da proteína EGFR em carcinoma espinocelular de lábio /". São José dos Campos, 2015. http://hdl.handle.net/11449/132902.
Pełny tekst źródłaBanca: Yasmin Rodarte Carvalho
Banca: Cláudia Malheiros Coutinho Camillo
Resumo: O carcinoma espinocelular de lábio (CEC) é uma das neoplasias malignas mais comuns, acometendo principalmente lábio inferior devido à exposição solar. Este trabalho teve como objetivo avaliar 3 métodos de gradação histológica (OMS, BD e MRH), analisar a expressão da proteína EGFR no CEC de lábio, comparar com queilite actínica (QA) e correlaciona-las com o prognóstico. Dados de 53 pacientes com CEC de lábio foram coletados para a avaliação clinicopatológica e histológica. 22 casos de CEC e 19 de QA foram submetidos à reação imuno-histoquímica com a proteína EGFR e analisados por um analisador automatizado para avaliação da expressão proteica. A média de idade foi de 65 anos, 69,8% foram homens, o lábio inferior foi o local de predileção com 94,4% e 66,03% dos pacientes estavam em estadios precoces (T1+T2). 28 (52,83%) e 34 (64,15%) casos respectivamente foram graduados em baixo risco prognóstico ou grau 1 pelas escalas BD e OMS, o modelo MRH graduou a 29 (54,72%) casos como médio risco prognóstico ou grau 2. O modelo de gradação mais simples e fácil de ser aplicado em CEC de lábio foi a Escala BD e o mais eficaz, pois quando em alto grau histológico foi associado à menor sobrevida global (P=0,045). A sobrevida global foi de 87,8% em 5 anos. Estadiamento clínico avançado (T3+T4) e envolvimento linfonodal (N1) foram associados à menor sobrevida global e sobrevida livre de recorrência (P=0,002; 0,005; 0,007 e 0,01). O tratamento cirúrgico combinado ao radioterápico foi associado à menor sobrevida livre de recorrência (P=0,03). Na expressão da proteína EGFR não houve diferença estatisticamente significante entre QA e CEC de lábio. O CEC de lábio quando em estadios e graus histológicos avançados, é associado a um pior prognóstico, o diagnóstico precoce é essencial para a escolha do melhor tratamento e sobrevida dos pacientes, evitando mutilações e consequentemente, perda na qualidade de vida
Abstract: Lip squamous cell carcinoma (SCC) is one of the most common malignancies affecting especially lower lip due to sun exposure. This study aimed to evaluate three methods of histological grading (WHO, BD and MRH), analyze the expression of EGFR protein on the lip of SCC, compared with actinic cheilitis (AC) and correlates them with the prognosis. Data from 53 patients with lip SCC were collected for the clinicopathological and histological evaluation. 22 cases of SCC and 19 AC underwent immunohistochemical reaction with EGFR protein and analyzed by an automated analyzer for evaluation of protein expression. The average age was 65 years, 69,8% were men, lower lip was the site of predilection with 94,4% and 66,03% of patients were in early stages (T1 + T2). 52.83% and 64.15% cases respectively were graduates in low risk prognosis or grade 1 by BD and WHO scales, the MRH model graduated 54.72% cases as medium risk prognosis or grade 2. The simplest grading model and easy to apply in lip SCC was the BD scale and more efficient because when in high histological grade was associated with lower overall survival (P = 0.045). Overall survival was 87,8% at 5 years. Advanced clinical stage (T3 + T4) and lymph node involvement (N1) were associated with lower overall survival and recurrence-free survival (P = 0.002; 0.005; 0.007 and 0.01). Surgical treatment combined with radiotherapy was associated with lower recurrence-free survival (P = 0.03). The expression of EGFR protein had no statistically significant difference between AC and lip SCC. The lip SCC when in advanced stages and high histological grades, is associated with a worse prognosis, early diagnosis is essential for choosing the best treatment and survival of patients, avoiding mutilation and consequently, loss in quality of life
Mestre
Lohse, Stefan [Verfasser]. "Charakterisierung rekombinanter IgA-Antikörper gegen den EGFR / Stefan Lohse". Kiel : Universitätsbibliothek Kiel, 2010. http://d-nb.info/1020002476/34.
Pełny tekst źródłaYin, Dongsheng [Verfasser]. "Biophysical studies of EGFR conformation and interaction / Dongsheng Yin". Bonn : Universitäts- und Landesbibliothek Bonn, 2019. http://d-nb.info/1208937553/34.
Pełny tekst źródłaRibeiro, Daniela Cotta. "Avaliação imunoistoquímica do EGFR / Her -1 em leucoplasias bucais". Universidade Federal de Minas Gerais, 2009. http://hdl.handle.net/1843/ZMRO-7V9KHX.
Pełny tekst źródłaA leucoplasia é a principal lesão cancerizável da boca. Fatores como a localização das lesões, hábito de tabagismo e atipia histológica têm sido associados ao potencial de transformação maligna dessas lesões, até o momento, no entanto, sem resultados definitivos. O EGFR é uma proteína de transmembrana, receptora de fatores de crescimento e com atividade tirosina quinase, pertencente à família dos receptores c-erbB. A expressão aumentada da proteína está relacionada com a progressão de tumores epiteliais, entre outras formas, através da alteração na proliferação celular. A proteína Ki-67 é um antígeno nuclear expressado em células proliferativas, muito utilizado como marcador de proliferação celular. A p27 é uma proteína com ação CDKI (inibidor das quinases dependentes de ciclina), que atua na inibição do ciclo celular. O objetivo do trabalho foi avaliar a associação da imunoexpressão do EGFR com atipia epitelial, tabagismo, localização das leucplasias e com a expressão de Ki-67 e p27. Avaliou-se ainda a associação entre a proliferação celular avaliada pelo Ki-67 e p27 com a atipia epitelial. Quarenta e oito lesões diagnosticadas como leucoplasias foram recuperadas do arquivo do laboratório de Patologia Bucal da FO-UFMG. As lâminas foram revisadas e dados clínicos (gênero, localização e tabagismo) recuperados. A imunoexpressão do EGFR mostrou associação positiva com a localização e com o total de célula positivas para p27. Não foi encontrada associação entre o EGFR e os demais dados clínico patológicos. Conclui-se que o EGFR está expresso em grande parte das leucoplasias bucais avaliadas independentemente do grau histológico de atipia. Os casos positivos para o EGFR foram localizados, em sua maioria, nas regiões de alto risco. As associações encontradas entre EGFR, localização das lesões e p27 devem ser melhor investigadas.
Biagiotti, M. "PEPTIDE-POLYMER CONJUGATES AS TOOLS TO SELECTIVELY TARGET EGFR". Doctoral thesis, Università degli Studi di Milano, 2014. http://hdl.handle.net/2434/244888.
Pełny tekst źródłaWoessner, N. C. "CHARACTERIZATION OF THE ROLE OF USP25 IN EGFR ENDOCYTOSIS". Doctoral thesis, Università degli Studi di Milano, 2015. http://hdl.handle.net/2434/261932.
Pełny tekst źródłaGIORDANO, FEDERICA. "Investigating the role of p65BTK as an emerging therapeutic target in NSCLC". Doctoral thesis, Università degli Studi di Milano-Bicocca, 2019. http://hdl.handle.net/10281/241339.
Pełny tekst źródłaLung cancer is the leading cause of cancer-related death worldwide both in men and women. In particular, Non-Small Cell Lung Cancer (NSCLC) is the most common subtype and is relatively insensitive to chemotherapy and radiation therapy. Despite the development of personalized molecular targeted therapies against specific driver mutations and the combination of chemotherapy with targeted therapy, lung cancer mortality remains very high because of intrinsic and acquired resistance. Thus, new strategies to overcome these limitations are needed. Recently, we discovered a new isoform of the Bruton Tyrosine Kinase (BTK), referred as p65BTK. We characterized p65BTK as a novel oncogene and a pivotal downstream effector of RAS. Moreover, we showed that its inhibition affected growth and survival of colon cancer cells and reverted resistance to chemotherapy. The aims of this project were: study the role of p65BTK in NSCLC cell biology and verify whether p65BTK may be a novel theranostic target in NSCLC. Studying a cohort of 382 patients, we observed that p65BTK was expressed in 50% of NSCLC patients’ tumors and its expression correlated with histotype, smoke habit and EGFR mutational status. In particular, we found p65BTK significantly more expressed in adenocarcinoma than in squamous carcinoma histotype and in non-smoker as compared to smoker patients. Moreover, its expression was significantly higher in non-smoker patients bearing wild type EGFR. Notably, these patients are not eligible for treatments with EGFR inhibitors due to a lack of EGFR mutation. By western blot analysis we confirmed p65BTK overexpression both in vitro, in NSCLC human cell lines with mutations in RAS or in one of the components of the RAS/MAPK pathway, and ex vivo, in tumor-derived primary cells from Kras/Trp53 null mice, suggesting that p65BTK overexpression correlate with a hyper-activated RAS/MAPK pathway also in NSCLC. Then, we showed that p65BTK inhibition by different BTK inhibitors (Ibrutinib, AVL-292, RN486) strongly impaired proliferation and clonogenicity of NSCLC cell lines with different genetic backgrounds. To determine if p65BTK could be a new theranostic target in NSCLC, representative resistant cell lines were treated with chemotherapy (Cisplatin, Gemcitabine, Pemetrexed) or EGFR-targeted therapy (Gefitinib, Erlotinib) alone or in combination with non-toxic concentrations of BTK inhibitors and then their viability was assessed. We found that BTK inhibitors were effective in re-sensitizing NSCLC cells scarcely responsive to the current treatments when used in combination with EGFR-targeted therapy or chemotherapy. However, the different BTK inhibitors’ combinations showed a better or worse synergy depending on which EGFR inhibitor or chemotherapeutic drug they were combined with. Thus, we demonstrate that p65BTK is overexpressed in NSCLC patients’ tumors and in human and murine NSCLC cells. Moreover, our data indicate p65BTK as an emerging actionable target in NSCLC and suggest that the combination of BTK inhibitors with chemotherapy or targeted therapy may represent a novel therapeutic approach to overcome drug resistance in NSCLC. As future perspectives, we will validate the effects of p65BTK inhibition in ex-vivo (spheroids derived from NSCLC cells) models and in in vivo mouse model of NSCLC.
Al-Akhrass, Hussein. "Un rôle inédit de la sortiline dans le contrôle du transport rétrograde de l'EGFR pour limiter la croissance tumorale". Thesis, Limoges, 2017. http://www.theses.fr/2017LIMO0035/document.
Pełny tekst źródłaLung cancer is the third most common cancer in women and the second in men, it is the leading cause of cancer-related death worldwide, with an annual mortality of more than 1 million. Despite remarkable advances in targeted therapy, the majority of patients with lung cancer are diagnosed at an advanced stage where they do not experience a significant improvement in overall survival. Tyrosine kinase receptors such as the epidermal growth factor receptor (EGFR) transduce information from the microenvironment into the cell and activate homeostatic signalling pathways. Internalisation and degradation of EGFR after ligand binding limits the intensity of its proliferative signalling, thereby helping to maintain cell integrity. In cancer cells, deregulation of EGFR trafficking has a variety of effects on tumour progression. Here, we report that sortilin is a key regulator of EGFR internalisation. Loss of sortilin in tumour cells promotes cell proliferation by sustaining EGFR signalling at the cell surface, ultimately accelerating tumour growth. In lung cancer patients, sortilin expression decreases with increased pathologic grade, and the expression of SORT1 (the gene encoding sortilin) is strongly correlated with a better survival, notably in patients with high EGFR expression. Thus, sortilin is a novel regulator of EGFR intracellular trafficking acting by controlling receptor internalisation and limiting tumour growth
Das, Gupta Paromita Clinical School Prince of Wales Hospital Faculty of Medicine UNSW. "Gene profiling in soft tissue sarcoma: predictive value of EGFR in sarcoma tumour progression and survival". Publisher:University of New South Wales. Clinical School - Prince of Wales Hospital, 2007. http://handle.unsw.edu.au/1959.4/43259.
Pełny tekst źródłaRyan, Sean P. "Autosomal Recessive Polycystic Kidney Disease Epithelial Cell Model Reveals Multiple Basolateral EGF Receptor Sorting Pathways". Case Western Reserve University School of Graduate Studies / OhioLINK, 2010. http://rave.ohiolink.edu/etdc/view?acc_num=case1274887553.
Pełny tekst źródłaFraguas, Garcia Susanna. "Regulació de la regeneració anterior a través de la via egfr-3/egr-4 en la planària Schmidtea mediterranea". Doctoral thesis, Universitat de Barcelona, 2014. http://hdl.handle.net/10803/277417.
Pełny tekst źródłaDuring freshwater planarians regeneration, polarity and patterning programs play essential roles in determining whether a head or a tail regenerates at anterior or posterior-facing wounds. This decision is made very soon after amputation. The pivotal role of the Wnt/beta-•catenin and Hh signaling pathways in re-establishing anterior4 posterior polarity has been well documented. However, the mechanisms that control the growth and differentiation of the blastema in accordance with its anteriorposterior identity are less well understood. Conserved signa ling pathways play important roles in morphogenesis in all animals. One such pathway is the epidermal growth factor receptor (EGFR) pathway, which regulates multiple biological processes including cell proliferation, differentiation, apoptosis and cell survival. In this thesis, we show that silencing of Smed-egfr4 3, a planarian homologue of epidermal growth factor receptors, impairs regeneration and blastema growth in these organisms, probably by disrupting cellular differentiation. In order to better characterize the function of the EGFR signaling pathway during planarian regeneration, we conducted "Digital Gene Expression" analyses to identify putative target genes of Smed-egfr-3. One of the isolated candidate genes that is downregulated after silencing Smed-egfr-3 is egr-4, a member of the early growth response gene family. egr-4 is mainly expressed in the central nervous system and rapidly induced after different types of injury. While early egr-4 expression after injury is independent of EGFR signa ling, it becomes Smed-egfr4 34 dependent from the second day of regeneration. Functional analyses based on RNA interference (RNAi) reveals that egr-4 is required for head regeneration but not for posterior regeneration; egr-4 silencing impairs the formation of anterior blastemas; these animals exhibit either small cephalic ganglia or a total absence of new brain tissue. Single and combinatorial RNAi to target different elements of the Wnt/beta-•catenin pathway, together with expression analysis of brain4 and anterior4 specific markers, reveal that egr-4 is necessary for the brain primordia differentiation in the early stages of regeneration and it appears to antagonize the activity of the Wnt/~-catenin pathway to allow head regeneration. Our results suggest that a conserved EGFRjegr pathway plays an important role in cell differentiation during planarian regeneration and indicate an association between early brain differentiation and the progression of head regeneration.