Дисертації з теми "NSCLP"
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Bianco, Anna Monica Rosaria. "Characterization of novel genes insolved in non syndromic cleft lip with or with out cleft palate (NSCLP)." Doctoral thesis, Università degli studi di Trieste, 2010. http://hdl.handle.net/10077/3735.
Повний текст джерелаNon-syndromic cleft lip with or without cleft palate (NSCLP) is one of the most common birth defect. Genetic studies on human populations have identified numerous predisposing factors, as MYH9 and JARID2, whose role during palatogenesis remains obscure. In order to improve our knowledge on pathogenetic mechanisms, we carried out expression studies during mouse palate development using RNA in situ hybridization. As reference genes (Tgfb3, Irf6, Pvrl1, Foxe1 and Tp63) known to be required for correct palate formation, Jarid2 and Myh9 are expressed in the epithelial cells of the palatine processes before and at the time of contact. Then, this signal decreases and eventually disappears concomitantly with the degradation of the medial epithelial cells. Consistent with these observations, RT-PCR carried out on dissected palatal shelves detected products of Myh9 and Jarid2 from embryonic day E14.0 to E15.0 with a pick at E14.5, the stage when shelves appose in the midline. Taken together, these expression studies strongly support the association studies that designate these genes as predisposing factors for NSCLP. In multifactorial diseases as NSCLP once genetic studies demonstrate association, a major challenge is to identify mutations. In this regard, we started analyzing two in linkage disequilibrium SNPs (rs3752462 of MYH9 and rs2076056 of JARID2) that could be involved in defective splicing mechanisms, as hypothesized on the basis of their localization within splice sites. Using a hybrid minigene assay, however, we demonstrated that none of the allelic variants lead to any aberrant products at least in HeLa cells, the model used for this study. Moreover, we investigated whether alternative splicing events of the Myh9 gene detected in cochlea and brain (Li et al., 2008) could also be found in other tissues and palate. A small insertion of 12 bp between exon 4 and 5 (loop1) due to an alternative splicing was detected in all adult tissues analyzed. The same insertion was not detected in embryonic tissues, such as palatal samples at different stages of development, and brain. These results suggest that the genomic region of loop1 should be investigated in all risk haplotypes to search for pathogenetic variants. In conclusion, further investigations should be planned to explore the role of MYH9 and JARID2 in orofacial development in order to dissect signaling pathways during palate formation and identify the causative variants contributing to NSCLP.
XXII Ciclo
1973
Krüger, Marcus. "Molekulare und funktionale Charakterisierung der neuronalen bHLH Transkritptionsfaktoren NSCL-1 und NSCL-2." [S.l.] : [s.n.], 2002. http://deposit.ddb.de/cgi-bin/dokserv?idn=969337183.
Повний текст джерелаPegoraro, Ilan Emanuel Moreira. "NSCL in the ETSI M2M platform." Master's thesis, Universidade de Aveiro, 2014. http://hdl.handle.net/10773/14704.
Повний текст джерелаThe evolution of every day gadgets into smart-devices able to react to their surrounding environment is enabling the development of novel applications aiming revolutionize the industry related to this technology. Currently much attention has been given to standardizing IoT and M2M in order to build an interoperable foundation that will enable the growth of the future Internet, where devices will communicate without, or at least minimizing, human intervention. In this dissertation is presented in first place issues such as: heterogeneity, scalability, addressing and the first approach taken by the ETSI M2M standard. Subsequently, is presented the ETSI M2M vision and high-level architecture together with current work in this area. Finally an implementation of the network middleware is going to be presented along with further testing.
A evolução dos dispositivos do dia a dia em dispositivos inteligentes capazes de reagir ao ambiente que os rodeia está a permitir a criação de novas aplicações que visam revolucionar a industria. Atualmente tem-se dado muita atenção a estandardização da Internet das Coisas e comunicações máquinaa- máquina, com o objetivo de construir uma fundação interoperável que permitirá o crescimento futuro da Internet, onde os dispositivos irão comunicar sem, ou com mínima, intervenção humana. Nesta dissertação é apresentado em primeiro lugar requisitos como heterogeneidade, escalabilidade, endereçamento e a primeira abordagem feita pelo standard M2M do ETSI. Consequentemente, é a apresentada a visão e a arquitetura e o trabalho realizado nesta área. Por fim é apresentada a implementação da componente de rede realizada nesta dissertação juntamente com os respetivos testes.
Chater, Emily. "Novel therapeutic targets in NSCLC resistance to Erlotinib." Thesis, Imperial College London, 2017. http://hdl.handle.net/10044/1/50699.
Повний текст джерелаHolgersson, Georg. "Prognostic Factors in Non-Small Cell Lung Cancer (NSCLC)." Doctoral thesis, Uppsala universitet, Experimentell och klinisk onkologi, 2017. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-327925.
Повний текст джерелаStamatkin, Christopher W. "PHOSPHATIDYLINOSITOL 3-KINASE (PI3K) AS A THERAPEUTIC TARGET IN NSCLC." UKnowledge, 2014. http://uknowledge.uky.edu/pharmacy_etds/58.
Повний текст джерелаChatterjee, Saradiya. "Role of TLR7 in non-small cell lung carcinona (NSCLC)." Paris 6, 2013. http://www.theses.fr/2013PA066063.
Повний текст джерелаLung cancer accounts for over 1 million deaths per year with a 5-year survival of 8-12%. Stimulation of TLRs by the natural ligands like the PAMPs and DAMPs results in a proinflammatory signaling cascade. We have shown that stimulation of lung cancer cell lines with TLR7 agonist lead to tumor cell survival and chemoresistance in vitro. We studied the effect of TLR7 agonists on A549 and LL/2 cells injected in NOD/SCID and C57BL/6 mice either treated or not with cisplatin. Loxoribine has a pro-tumoral effect on A549 cells and induces chemoresistance in NOD/SCID mice. Blockade of TLR7 with IRS661 reversed the pro-tumoral effect of TLR7 agonist on A549 cells. CL264 was also found to have a pro-tumoral effect on LL/2 cells and induced chemoresistance in NOD/SCID mice. On the other hand CL264 at lower concentration induces an anti-tumoral effect on LL/2 cells while at a higher concentration demonstrated a pro-tumoral effect in C57BL/6 mice. We also demonstrated an overall bad prognostic value for higher expression of TLR7 by tumoral cells among NSCLC patients treated and not treated with neoadjuvant chemotherapy. These results suggest a pro- tumoral role and induction of chemoresistance by TLR7 in NSCLC patients. Use of TLR7 agonist as therapeutic option is recommended based on the TLR7 expression level for individual NSCLC patients. TLR7 antagonist holds promise for treatment of NSCLC in future
Recondo, Gonzalo. "Resistance Mechanisms to ALK Tyrosine Kinase Inhibitors (TKIs) in NSCLC." Thesis, Université Paris-Saclay (ComUE), 2019. http://www.theses.fr/2019SACLS248/document.
Повний текст джерелаThe molecular study and classification of lung adenocarcinomas has led to the development of selective targeted therapies aiming to improve disease control and survival in patients. The anaplastic lymphoma kinase (ALK) is a tyrosine kinase receptor from the insulin tyrosine kinase receptor family, with a physiologic role in neural development. Gene rearrangements involving the ALK kinase domain occur in ~3-6% of patients with lung adenocarcinoma. The fusion protein dimerizes leading to transactivation of the ALK kinase domain in a ligand-independent and constitutive manner. Lorlatinib is a third generation ALK inhibitor with high potency and selectivity for this kinase in vitro and in vivo, and elevated penetrance in the central nervous system. Lorlatinib can overcome resistance mediated by over 16 secondary kinase domain mutations occurring in 13 residues upon progression to first - and second - generation ALK TKI. In addition, treatment with lorlatinib is effective for patients who have been previously treated with a first and a second generation or a second generation ALK TKI upfront and is currently approved for this indication. The full spectrum of biological mechanisms driving lorlatinib resistance in patients remains to be elucidated. It has been recently reported that the sequential acquisition of two or more mutations in the kinase domain, also referred as compound mutations, is responsible for disease progression in about 35% of patients treated with lorlatinib, mainly by impairing its binding to the ALK kinase domain. However, the effect of these compound mutations on the sensitivity to the repertoire of ALK inhibitors can vary, and other resistance mechanisms occurring in most patients are unknown. My PhD thesis aimed at exploring resistance to lorlatinib in patients with ALK-rearranged lung cancer through spatial and temporal tumor biopsies and development of patient-derived models. Within the institutional MATCH-R study (NCT02517892), we performed high-throughput whole exome, RNA and targeted next-generation sequencing, together with plasma sequencing to identify putative genomic and bypass mechanisms of resistance. We developed patient-derived cell lines and characterized novel mechanisms of resistance and personalized treatment strategies in vitro and in vivo. We characterized three mechanisms of resistance in four patients with paired biopsies. We studied the induction of epithelial-mesenchymal transition (EMT) by SRC activation in a patient-derived cell line exposed to lorlatinib. Mesenchymal cells were sensitive to combined SRC and ALK co-inhibition, showing that even in the presence of an aggressive and challenging phenotype, combination strategies can overcome ALK resistance. We identified two novel ALK kinase domain compound mutations, F1174L/G1202R, C1156Y/G1269A, occurring in two patients treated with lorlatinib. We developed Ba/F3 cell models harboring single and compound mutations to study the differential effect of these mutations on lorlatinib resistance. Finally, we characterized a novel mechanism of resistance caused by NF2 loss of function at the time of lorlatinib progression through the development of patients derived PDX and cell lines, and in vitro validation of NF2 knock-out with CRISPR/CAS9 gene editing. Downstream activation of mTOR was found to drive lorlatinib resistance by NF2 loss of function and was overcome by providing treatment with mTOR inhibitors.This study shows that mechanisms of resistance to lorlatinib are more diverse and complex than anticipated. Our findings also emphasize how longitudinal studies of tumor dynamics allow deciphering TKI resistance and identifying reversing strategies
Baghai, Tabassom. "ATF3 as a Key Regulator of Cisplatin Cytotoxicity: Combining ATF3 Inducing Agents Enhances Cisplatin Activity in NSCLC." Thesis, Université d'Ottawa / University of Ottawa, 2018. http://hdl.handle.net/10393/37963.
Повний текст джерелаDaskalos, Alexandros. "Deregulation of DNA methylation aand retrotransposon reactivation in NSCL." Thesis, University of Liverpool, 2011. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.539561.
Повний текст джерелаSouza, Cristiano de Pádua. "Perfil de expressão de microRNAs e seus alvos moleculares em carcinoma pulmonar." Botucatu, 2016. http://hdl.handle.net/11449/140150.
Повний текст джерелаResumo: Introdução: O câncer de pulmão é a principal causa de morte por câncer no mundo. Apesar dos avanços nas estratégias de diagnóstico e o desenvolvimento de novas terapias com alvos moleculares, pouco progresso tem sido observado quanto ao aumento de sobrevida dos pacientes. Portanto, a identificação de novos biomarcadores ainda é necessária para o desenvolvimento de novas terapêuticas para carcinomas pulmonares. Nesse contexto, os microRNAs (miRNAs) são moléculas promissoras, pois constituem uma classe de RNAs não-codantes reguladores da expressão gênica os quais têm sido evidenciados como biomarcadores diagnósticos, prognósticos e preditivos no câncer. Materiais e Métodos: Amostras de tecido pulmonar tumoral e normal de 38 pacientes com carcinoma de pulmão de células não pequenas (da sigla em inglês NSCLC), dos subtipos histológicos adenocarcinoma e carcinoma de células escamosas, foram avaliadas para a expressão global de miRNAs utilizando a plataforma TaqMan® Array Human MicroRNA card A v3.0 (Life Technologies). Os miRNAs com alterações na expressão (FC≥2,0) e p<0,05 foram considerados estatisticamente significativos. Os dados de expressão foram associados com a sobrevida global. Análises de bioinformática permitiram identificar genes-alvo regulados pelos miRNAs desregulados. A relação entre sobrevida global e a identificação de uma assinatura de expressão de miRNAs foi avaliada com objetivo de integrar nossos achados utilizando bancos de dados públicos. Resultados: Os resul... (Resumo completo, clicar acesso eletrônico abaixo)
Doutor
Campbell, Thomas. "The role of voltage-gated sodium channels in non-small cell lung cancer." Thesis, University of Manchester, 2013. https://www.research.manchester.ac.uk/portal/en/theses/the-role-of-voltagegated-sodium-channels-in-nonsmall-cell-lung-cancer(a65f4c5e-b217-483b-91d3-bb669965eb03).html.
Повний текст джерелаSchaal, Courtney. "Regulation of nAChRs and Stemness by Nicotine and E-cigarettes in NSCLC." Scholar Commons, 2016. http://scholarcommons.usf.edu/etd/6582.
Повний текст джерелаSarin, Navin [Verfasser]. "Cisplatin resistance is associated with altered signalling in NSCLC cells / Navin Sarin." Bonn : Universitäts- und Landesbibliothek Bonn, 2018. http://d-nb.info/1153467119/34.
Повний текст джерелаGIORDANO, 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.
Повний текст джерелаLung 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.
Petroff, Alev [Verfasser], and Christian [Akademischer Betreuer] Rübe. "Langzeitergebnisse radikal behandelter synchron vs. metachron oligometastasierter NSCLC / Alev Petroff ; Betreuer: Christian Rübe." Saarbrücken : Saarländische Universitäts- und Landesbibliothek, 2019. http://d-nb.info/1175950270/34.
Повний текст джерелаParikh, Ravi B. "DEFINITIVE PRIMARY THERAPY IN PATIENTS PRESENTING WITH OLIGOMETASTATIC NON-SMALL CELL LUNG CANCER (NSCLC)." Thesis, Harvard University, 2014. http://etds.lib.harvard.edu/hms/admin/view/47.
Повний текст джерелаBalko, 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.
Повний текст джерелаTitle 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).
Koch, Franziska [Verfasser]. "Humanes ex-vivo Lungentumormodell : Nutzung für Temperaturmessungen während der Thermoablation von NSCLC. / Franziska Koch." Greifswald : Universitätsbibliothek Greifswald, 2011. http://d-nb.info/1018242198/34.
Повний текст джерелаCarlson, Sarah Marie. "Student and Parent Perceptions of the Lunches Served Under the Revised Guidelines for the National School Lunch Program." Kent State University / OhioLINK, 2014. http://rave.ohiolink.edu/etdc/view?acc_num=kent1397165529.
Повний текст джерелаRamos, Alexis. "Cancer Genome Characterization with SNP Array and Whole-Exome Sequencing Analysis." Thesis, Harvard University, 2011. http://dissertations.umi.com/gsas.harvard:10036.
Повний текст джерелаUsó, Marco Marta. "ANALYSIS OF IMMUNOREGULATORY BIOMARKERS IN NON-SMALL CELL LUNG CANCER." Doctoral thesis, Universitat Politècnica de València, 2015. http://hdl.handle.net/10251/51283.
Повний текст джерела[ES] El cáncer de pulmón es una de las principales causas de muerte relacionada con cáncer en el mundo, siendo el tercer tipo de cáncer más común. El cáncer de pulmón no microcítico (CPNM) representa casi el 85% de todos los cánceres de pulmón y la supervivencia a los 5 años va desde el 50% en estadios IA hasta el 15% en estadios IIIA. Hasta el momento, no se han descubierto biomarcadores capaces de predecir la progresión de la enfermedad en pacientes tanto en estadios resecables como en estadios avanzados, por lo que existe una clara necesidad de realizar estudios centrados en la búsqueda de biomarcadores pronósticos y diagnósticos en los diferentes tipos de muestra disponibles, como por ejemplo sangre, tejido fresco y tejido parafinado. El campo de la inmunología tumoral ha cambiado en la última década y actualmente se sabe que el sistema inmune juega un papel clave en cáncer. Las células inmunes que infiltran el tumor son un componente más del microambiente tumoral. Pese a que son potencialmente capaces de eliminar los antígenos tumorales, estas células no pueden evitar la formación y progresión tumoral. Esto es debido a que el tumor adquiere diversos mecanismos de regulación del microambiente tumoral con el objetivo de escapar del ataque del sistema inmune, como por ejemplo liberación de factores que impiden el correcto funcionamiento de los mecanismos de reacción inmune, modulación de vías co-estimuladoras y reclutamiento y activación de células inmunoreguladoras como las células T reguladoras, las células mieloides supresoras y los macrófagos asociados a tumores. El estudio de marcadores relacionados con la respuesta inmune y concretamente con los procesos de inmunoregulación puede proporcionarnos información pronóstica y predictiva relevante sobre los pacientes con cáncer. Por todo ello, el principal objetivo de esta tesis doctoral es analizar la presencia de marcadores relacionados con la inmunoregulación y evaluar su posible correlación con las variables clínico-patológicas y pronósticas en pacientes con CPNM mediante el uso de técnicas fiables y aplicables en la práctica clínica como la PCR cuantitativa y la inmunohistoquímica. Así mismo, esto nos permitirá conocer en mayor profundidad las características inmunológicas del microambiente tumoral en pacientes con CPNM.
[CAT] El càncer de pulmó és una de les principals causes de mort relacionades amb càncer al món, sent a més a més el tercer tipus de càncer més comú. El càncer de pulmó no microcític (CPNM) representa el 85% de tots els casos de càncer de pulmó aproximadament i la supervivència als 5 anys continua sent molt baixa. Fins el moment, no s'han descobert biomarcadors capaços de predir la progressió de la malaltia tant en pacients en estadis inicials com en estadis avançats. Per aquest motiu, existeix una clara necessitat de realitzar estudis centrats en la recerca de biomarcadors pronòstics i predictius en els diferents tipus de mostres disponibles, com per exemple sang, teixit fresc i teixit parafinat. El camp de la immunologia tumoural ha canviat en l'última dècada i actualment se sap que el sistema immune exerceix un paper clau en el càncer. Les cèl¿lules immunològiques que infiltren el tumour són un component més del microambient tumoural. Malgrat que aquestes cèl¿lules són potencialment capaces d'eliminar el antígens tumourals, s'ha evidenciat que no poden previndre la formació i progressió tumoural. Una de les raons per les quals s'observa aquest fenomen és que el tumour adquireix diversos mecanismes de regulació del microambient tumoural. Aquests mecanismes es basen en l'alliberació de factors que impedeixen el correcte funcionament del sistema immune, la modulació de vies coestimuladores i el reclutament i activació de cèl¿lules immunoreguladores com poden ser les cèl¿lules T reguladores, les cèl¿lules mieloides supressores i els macròfags associats a tumour. L'estudi de marcadors relacionats amb la resposta immune i més concretament amb els processos d' immunoregulació pot proporcionar informació pronòstica i predictiva rellevant sobre els pacients amb càncer. Per tot això, el principal objectiu d'aquesta tesi doctoral és analitzar la presència de marcadors relacionats amb la immunoregulació i avaluar la seva possible correlació amb les variables clinicopatològiques i pronòstiques de pacients amb CPNM mitjançant l'ús de tècniques fiables i aplicables a la pràctica clínica com són la PCR quantitativa i la immunohistoquímica. Així mateix, aquestes anàlisis ens permetran conèixer amb major profunditat les característiques immunològiques del microambient tumoural de pacients amb CPNM.
Usó Marco, M. (2015). ANALYSIS OF IMMUNOREGULATORY BIOMARKERS IN NON-SMALL CELL LUNG CANCER [Tesis doctoral no publicada]. Universitat Politècnica de València. https://doi.org/10.4995/Thesis/10251/51283
TESIS
Zhang, Kai. "Developing Novel Carriers to Deliver Targeted Immunotoxins for the Treatment of Primary and Metastatic Non-Small Cell Lung Cancer." Thesis, Griffith University, 2017. http://hdl.handle.net/10072/365662.
Повний текст джерелаThesis (PhD Doctorate)
Doctor of Philosophy (PhD)
School of Medical Science
Griffith Health
Full Text
Schneeberger, Valentina. "Novel Roles of the Protein Tyrosine Phosphatase SHP2 in Non-small Cell Lung Cancer." Scholar Commons, 2014. https://scholarcommons.usf.edu/etd/5306.
Повний текст джерелаReuter, Cécile [Verfasser]. "Mutationsabhängige Aktivität von niedermolekularen reversiblen und irreversiblen Inhibitoren der EGFR Signalkaskade in NSCLC / Cécile Reuter." Köln : Deutsche Zentralbibliothek für Medizin, 2012. http://d-nb.info/1026215080/34.
Повний текст джерелаReinert, Christian Philipp [Verfasser]. "Einfluss von Lipoteichonsäuren von Staphylococcus aureus auf die Proliferation von NSCLC-Zelllinien / Christian Philipp Reinert." Gießen : Universitätsbibliothek, 2017. http://d-nb.info/1130119807/34.
Повний текст джерелаTam, Yee-san Issan, and 譚薏珊. "Epidermal growth factor receptor (EGFR) mutations and phosphorylation pattern in non-small cell lung cancer (NSCLC)." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2008. http://hub.hku.hk/bib/B40687673.
Повний текст джерелаBertram, Veit [Verfasser], and Rainer M. [Akademischer Betreuer] Bohle. "Quantitative Expressionsanalyse von TTF-1 in NSCLC und pulmonalen Metastasen / Veit Bertram ; Betreuer: Rainer M. Bohle." Saarbrücken : Saarländische Universitäts- und Landesbibliothek, 2019. http://d-nb.info/1197612076/34.
Повний текст джерелаLane, Keara M. "Negative feedback regulation as a means to constrain the oncogenic potential of mutant Egfr in NSCLC." Thesis, Massachusetts Institute of Technology, 2011. http://hdl.handle.net/1721.1/68427.
Повний текст джерелаCataloged from PDF version of thesis. Vita.
Includes bibliographical references.
The discovery of EGFR kinase domain mutations in NSCLC patients who responded to tyrosine kinase inhibitors (TKIs) represented the first example of a targeted therapy for lung cancer. The dependence of these human tumors on sustained mutant receptor expression for survival, together with the discovery that ectopic expression of the receptor resulted in transformation, suggested that these mutations are causal events, and as such would be sufficient to induce tumor formation in the lung. To investigate this, and to further our understanding of how deregulated signaling through the mutant receptor could initiate tumor formation, we generated both a conditional and constitutive knock-in allele of one such mutation, L858R, at the endogenous murine Egfr locus. Expression of mutant Egfr failed to induce lung tumors in these mice; further analysis of the germline mutant mice revealed significant downregulation of the mutant receptor, and this was predominantly at the post-transcriptional level. These data suggest that normal cells can respond to an oncogenic lesion by upregulating negative feedback pathways to counteract the induction of aberrant signaling, and disabling these feedback mechanisms may be an essential component of the progression of EGFR mutant tumors. A multitude of positive and negative feedback loops converge on signaling pathways to ensure the appropriate output in response to a given stimulus. The role of oncogenes is typically thought of in terms of increasing the output of a signaling pathway, and while the contribution of the associated negative feedback loops is no doubt important, they have been afforded little attention. Recent studies have highlighted the existence of negative feedback mechanisms in established tumors and the integral role they play in shaping the signaling network, with a corresponding appreciation for how such feedback loops can profoundly influence therapeutic response. The capacity of negative regulators to modulate the oncogenic potential of a mutant protein in the context of tumor initiation has rarely been examined. Using a doxycyclineinducible system we recapitulate the aforementioned downregulation of mutant Egfr, initially observed in both tissues and MEFs derived from EgfrL858R mutant mice, in an ectopic cell culture expression system. We establish a role for ERK pathway signaling, and specifically DUSP6, in receptor degradation, and solidify the role of the E3 ligase, CULLIN5, in the downregulation of the mutant receptor. The existence of these negative feedback loops may explain the observation that mutation of EGFR is often coincident with gene amplification in NSCLC, and suggest that such amplification may primarily serve as a means to counteract the downregulation. The amplification of oncogenes is a recurring feature of many human tumors, but the contribution of gene amplification to particular stages of tumor development, or the molecular requirements for amplification to occur are unknown. EGFR is mutated and coincidentally amplified in NSCLC, but the relative contribution of mutation and amplification, both to tumor phenotype and therapeutic sensitivity, is not clear. The inability to model amplification in the mouse has contributed significantly to our limited mechanistic understanding of how gene amplification occurs in tumors. Using a yeast endonuclease, -Scel, and an allele that contains target sites for this enzyme engineered telomeric to mutant Egfr on chromosome 11, we attempted to initiate breakage-fusion-bridge (BFB) cycles in the lung, as these are thought to be a precursor to gene amplification. Our inability to elicit tumor formation using this strategy highlights the limitations in our understanding of how amplicons form in human tumors or the particular context required. While it would provide tremendous insight into mutant EGFR tumor development, a model of targeted gene amplification has thus far eluded us, and remains one of the significant challenges facing the mouse modeling community.
by Keara M. Lane.
Ph.D.
Abdo, Mustafa [Verfasser]. "Prediction of patients’ response to immune checkpoint inhibitors in the treatment of advanced NSCLC / Mustafa Abdo." Göttingen : Niedersächsische Staats- und Universitätsbibliothek Göttingen, 2021. http://d-nb.info/1228623848/34.
Повний текст джерелаStorti, Camila Baldin. "Perfil de expressão de genes associados aos telômeros em carcinoma pulmonar de células não pequenas (NSCLC)." Botucatu, 2018. http://hdl.handle.net/11449/153294.
Повний текст джерелаResumo: O câncer de pulmão é o câncer que apresenta maior mortalidade no mundo: >1,6 milhões de óbitos por ano segundo a Organização Mundial de Saúde (OMS), sendo o câncer de pulmão de células não pequenas (NSCLC) o tipo mais frequente (~ 85%) de carcinoma pulmonar. O NSCLC apresenta dois subtipos histológicos principais: adenocarcinoma (LUAD) e carcinoma de células escamosas (LUSC). Pesquisas têm sido realizadas objetivando identificar biomarcadores moleculares úteis como alvo terapêuticos em NSCLC e os telômeros têm sido considerado alvos promissores para terapias antitumoral, devido ao seu papel crucial na integridade, estabilidade e manutenção genômica. Telômeros humanos consistem em DNA repetitivo rico em G associado a proteínas do complexo shelterin e mantido pela ação da telomerase. Estudos recentes mostraram que a expressão de TERT (subunidade catalítica da telomerase) e de alguns componentes do complexo shelterin estão alterados em câncer de pulmão. No entanto, a correlação entre alterações na função telomérica e o desenvolvimento e progressão de NSCLC não foi elucidada. Portanto, o objetivo do presente estudo foi verificar alterações na expressão de genes associados aos telômeros, incluindo os ncRNAs associados à regulação e manutenção dos telômeros em NSCLC, no intuito de identificar novos biomarcadores associados ao desenvolvimento e progressão do NSCLC. Para tanto, foram realizadas análises de expressão de 50 genes associados aos telômeros em amostras de tecido tumoral e... (Resumo completo, clicar acesso eletrônico abaixo)
Abstract: According to the World Health Organization, lung cancer has a high mortality rate associated with >1.6 million deaths per year, being Non-small cell lung cancer (NSCLC) the most frequent type (~ 85%) of lung carcinoma. Lung adenocarcinoma (LUAD) and lung squamous cell carcinoma (LUSC) are the two major histological subtypes of NSCLC. Research efforts have been made to identify molecular biomarkers useful as therapeutic targets in NSCLC and telomere have been considered very promising targets for anticancer therapies due to their crucial role in genome integrity maintenance and stability. Human telomeres consist of repetitive G-rich DNA associated with proteins of the shelterin complex, maintained by the action of telomerase. Recent studies showed that expression of TERT (telomerase reverse transcriptase component) and of some of the shelterin components are altered in lung cancer. However, the mechanisms of telomere deregulation associated with NSCLC development and progression have not been elucidated. Therefore, our aim was to study expression changes affecting telomere-associated genes and ncRNAs associated with telomere regulation and maintenance in NSCLC. Such alterations may represent novel biomarkers associated with NSCLC development and progression. For this purpose, expression analyzes of 50 telomere-associated genes were performed in samples of tumor tissue and normal lung tissue, adjacent to the tumor, from patients with NSCLC. The following techniques were used: 1... (Complete abstract click electronic access below)
Mestre
Wang, Yu-Chieh. "Exploitation and Mechanistic Validation of Drug-combination Strategies to Overcome EGFR-inhibitor resistance in NSCLC cells." The Ohio State University, 2008. http://rave.ohiolink.edu/etdc/view?acc_num=osu1226515990.
Повний текст джерелаTam, Yee-san Issan. "Epidermal growth factor receptor (EGFR) mutations and phosphorylation pattern in non-small cell lung cancer (NSCLC)." Click to view the E-thesis via HKUTO, 2008. http://sunzi.lib.hku.hk/hkuto/record/B40687673.
Повний текст джерелаArthur, Muller [Verfasser], and Ursula [Akademischer Betreuer] Nestle. "Prospektive Evaluation des Verhaltens der Tumorgewebe bei NSCLC in der FDG-PET unter Strahlentherapie (Response PET/CT)." Freiburg : Universität, 2018. http://d-nb.info/1220225428/34.
Повний текст джерелаLinsel, Sören [Verfasser]. "Experimentelle Untersuchungen zum Proliferationsverhalten von NSCLC-Zelllinien unter Endotoxin-Stimulation : die Rolle des Cyclooxygenase-Metabolismus / Sören Linsel." Gießen : Universitätsbibliothek, 2016. http://d-nb.info/1102154792/34.
Повний текст джерелаMakowiecki, Christina Michaela [Verfasser]. "Potential der siRNA-Transfektion auf chemotherapieresistente NSCLC- und Pleuramesotheliomzellen - Auswirkungen auf Viabilität und Wachstumsverhalten / Christina Michaela Makowiecki." Tübingen : Universitätsbibliothek Tübingen, 2021. http://nbn-resolving.de/urn:nbn:de:bsz:21-dspace-1191334.
Повний текст джерелаKhaddam, Sinan M. D. "Difference in outcomes between central airway lesions requiring stents and lesions that donot in patients with NSCLC." University of Cincinnati / OhioLINK, 2019. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1553513958608363.
Повний текст джерелаSchulze, Arik Bernard [Verfasser], and Rainer Gerhard [Akademischer Betreuer] Wiewrodt. "Das RhCE-Protein beeinflusst die Prognose von Patienten mit NSCLC / Arik Bernard Schulze ; Betreuer: Rainer Gerhard Wiewrodt." Münster : Universitäts- und Landesbibliothek Münster, 2016. http://d-nb.info/1140588087/34.
Повний текст джерелаRoesner, Anuschka Josphine [Verfasser], and Gian [Akademischer Betreuer] Kayser. "Einfluss der PD-L1-Expression sowie von tumorinfiltrierenden Lymphozyten auf das Ansprechen von Immuncheckpoint-Inhibitoren im NSCLC." Freiburg : Universität, 2019. http://d-nb.info/1212795601/34.
Повний текст джерелаGRISTINA, Valerio. "Circulating cell-free DNA (cfDNA) and extracellular vesicles (EVs) as prognostic and predictive biomarkers in patients with advanced Non-Small Cell Lung Cancer (NSCLC): the LEXOVE prospective study." Doctoral thesis, Università degli Studi di Palermo, 2022. https://hdl.handle.net/10447/571952.
Повний текст джерелаMüller, Benedikt Felix [Verfasser], and Ursula [Akademischer Betreuer] Klingmüller. "Interactions of EGFR/IGF-1R Signaling in NSCLC - A Systems Biology Approach / Benedikt Felix Müller ; Betreuer: Ursula Klingmüller." Heidelberg : Universitätsbibliothek Heidelberg, 2015. http://d-nb.info/1180501160/34.
Повний текст джерелаSeiz, Julia Raphaela [Verfasser]. "Rac1b-spezifische Effekte und Auswirkungen der 3D-Kultivierung auf Differenzierung und Signaltransduktion in NSCLC-Zelllinien / Julia Raphaela Seiz." Gießen : Universitätsbibliothek, 2019. http://d-nb.info/1199264474/34.
Повний текст джерелаKurian, Stefanie [Verfasser]. "Effects of combination therapy of PDE5 inhibitor sildenafil and multikinase inhibitors sorafenib and sunitinib in NSCLC / Stefanie Kurian." Gießen : Universitätsbibliothek, 2015. http://d-nb.info/1076760546/34.
Повний текст джерелаPamarthi, Pavan Kumar [Verfasser]. "Role of prostanoid receptor EP1 in the progression of non-small cell lung cancer (NSCLC) / Pavan Kumar Pamarthi." Gießen : Universitätsbibliothek, 2013. http://d-nb.info/106518395X/34.
Повний текст джерелаMüller, Benedikt [Verfasser], and Ursula [Akademischer Betreuer] Klingmüller. "Interactions of EGFR/IGF-1R Signaling in NSCLC - A Systems Biology Approach / Benedikt Felix Müller ; Betreuer: Ursula Klingmüller." Heidelberg : Universitätsbibliothek Heidelberg, 2015. http://nbn-resolving.de/urn:nbn:de:bsz:16-heidok-191984.
Повний текст джерелаJaber, Almahdi. "Oncogene driver mutations and copy number variation as markers for predicting drug resistance and disease outcome in NSCLC." Thesis, University of Leicester, 2017. http://hdl.handle.net/2381/39168.
Повний текст джерелаBesson, Florent. "Integrating PET-MR data for a multiparametric approach of tumour heterogeneity in non-small-cell lung cancer (NSCLC)." Thesis, université Paris-Saclay, 2020. http://www.theses.fr/2020UPASS081.
Повний текст джерелаTumor heterogeneity is an important factor of progression and resistance to treatment. Multiparametric PET-MRI imaging offers unique opportunities to characterize biological cellular processes, but has never been evaluated at the regional level in Non-Small Cell Lung Cancer (NSCLC), the leading cause of oncological death. A simultaneous dynamic multiparametric 18F-FDG PET-MRI approach has been developed to this end. This approach required the “in-house” implementation of the reference absolute PET quantitative method of glucose metabolism (Sokoloff's tri-compartmental model); the development of a method for correcting geometric distortions in diffusion weighted imaging, validated on phantom and clinically tested; the phantom validation of quantitative MRI methods (T1/T2 relaxometry), also clinically tested; and the "in-house" implementation of the Tofts compartmental model (extended version) for the evaluation of tumor vascularization by dynamic perfusion MRI. The results of our work, performed at the regional intra-tumor level, illustrate the heterogeneity of the regional interlinks between glucose metabolism and vascularization in NSCLC, two fundamental biological hallmarks of tumor progression, and show that an unsupervised tumor partitioning by Gaussian mixture model, integrating all the PET-MRI biomarkers of this project, individualizes 3 types of supervoxels, whose biological signature can be predicted with 97% accuracy by 4 dominant PET-MRI biomarkers, revealed by metaheuristic machine learning methods
Seiz, Julia [Verfasser]. "Rac1b-spezifische Effekte und Auswirkungen der 3D-Kultivierung auf Differenzierung und Signaltransduktion in NSCLC-Zelllinien / Julia Raphaela Seiz." Gießen : Universitätsbibliothek, 2019. http://d-nb.info/1199264474/34.
Повний текст джерелаSamek, Melanie [Verfasser]. "Erlotinib beim fortgeschrittenen nichtkleinzelligen Lungenkarzinom (NSCLC) : klinische Evaluation im Rahmen einer Phase IV Studie (Tarceva EAP) / Melanie Samek." Lübeck : Zentrale Hochschulbibliothek Lübeck, 2010. http://d-nb.info/1004771843/34.
Повний текст джерелаYang, Zheng. "Anti-cancer synergy of targeting pyruvate dehydrogenase kinase 1 (PDK1) in combination with EGFR-TKi in NSCLC therapy." Thesis, University of Macau, 2018. http://umaclib3.umac.mo/record=b3953612.
Повний текст джерела