Letteratura scientifica selezionata sul tema "Carcinome pulmonaire non à petites cellules – génétique"
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Articoli di riviste sul tema "Carcinome pulmonaire non à petites cellules – génétique":
Mahou, H., S. Joobeur, H. Mribah, S. Bel Haj Mohamed, N. Fahem, J. El Ghoul, S. Cheikh Mhamed, N. Skhiri, N. Rouetbi e A. El Kamel. "Le carcinome broncho-pulmonaire non à petites cellules : survie et facteurs pronostiques". Revue des Maladies Respiratoires 29 (gennaio 2012): A152. http://dx.doi.org/10.1016/j.rmr.2011.10.736.
Fournel, L., P. Boudou-Rouquette, M. Prieto, C. Guinet, J. Arrondeau, D. Damotte, M. Wislez et al. "Le nivolumab augmente la pression artérielle pulmonaire chez les patients traités pour carcinome pulmonaire non à petites cellules". Revue des Maladies Respiratoires Actualités 13, n. 1 (gennaio 2021): 117. http://dx.doi.org/10.1016/j.rmra.2020.11.243.
Pezzetta, Edgardo, Claude Haller, Sebastien Deglise, Jannick Rey, Zrad El-Lamaa, Hans-Beat Ris e Angelika Bischof-Delaloye. "Chirurgie: 1. Place du FDG PET-Scan dans la prise en charge chirurgicale du carcinome pulmonaire non à petites cellules". Revue Médicale Suisse 62, n. 2465 (2004): 81–92. http://dx.doi.org/10.53738/revmed.2004.62.2465.0081.
Francoz, S., R. B. Blasco, M. Cañamero, P. Dubus, M. Baccarini e M. Barbacid. "R19 – Oral C-Raf, acteur clé dans la signalisation de l’oncogène K-Ras dans le carcinome pulmonaire non à petites cellules". Bulletin du Cancer 97, n. 4 (ottobre 2010): S23. http://dx.doi.org/10.1016/s0007-4551(15)30936-x.
Francoz, S., R. B. Blasco, M. Canamero, P. Dubus, M. Baccarini e M. Barbacid. "R166 - Oral, Club Mex-H Ciblage in vivo de la voie de signalisation MAPK dans le carcinome pulmonaire non à petites cellules induit par l’oncogène K-Ras". Bulletin du Cancer 97, n. 4 (ottobre 2010): S81—S82. http://dx.doi.org/10.1016/s0007-4551(15)31087-0.
Sarrut, D., D. Perol, P. Pommier e C. Carrie. "Radiothérapie avec blocage respiratoire pour les grands insuffisants respiratoires atteints d'un carcinome pulmonaire non à petites cellules (Protocole RESPI 2000) : application à la modélisation des déformations d'organes par recalage déformable". Cancer/Radiothérapie 10, n. 6-7 (novembre 2006): 377–80. http://dx.doi.org/10.1016/j.canrad.2006.08.005.
Babey, H., P. Jamme, R. Gervais, J. B. Assié, R. Veillon, H. Doubre, M. Pérol et al. "Analyse FONctionnelle des mutations identifiées au voisinage de l’exon 14 du gène MET et efficacité du crizotinib chez des patients atteints d’un carcinome broncho-pulmonaire non à petites cellules de stade avancé (CBNPC) : étude GFPC-AFonMET". Revue des Maladies Respiratoires Actualités 13, n. 1 (gennaio 2021): 61. http://dx.doi.org/10.1016/j.rmra.2020.11.110.
Tesi sul tema "Carcinome pulmonaire non à petites cellules – génétique":
Renaud, Stéphane. "Impact de l’hypoxie sur la progression tumorale des cancers bronchiques non à petites cellules (CBNPC)". Thesis, Strasbourg, 2016. http://www.theses.fr/2016STRAJ117.
Tumoral hypoxia, and his target HIF-1α, are linked to the epithelial to mesenchymal transition (EMT) in various solid tumors. EMT has been linked to chemotherapy resistance and metastases in many cancers. In this work, we have shown that tumoral hypoxia may help to define a worst prognosis in case of hypoxia after non-small cell lung cancer surgery (NSCLC). We have also shown that on NSCLC cell lines harboring activating EGFR mutations, hypoxia trough expression of HIF-1α, was able to induce EMT, with activation of different transcription factors according to cell mutational status: induction of SNAIL-1/SNAIL-2 in H1650 cell line harboring exon 19 deletion, induction of SNAIL-1/ZEB-1 in H1975 cell line harboring both exon 21 L858R and exon 20 T790M mutations. Considering all these data, it appears that HIF-1α may be considered a a new therapeutic target
Pallier, Karine. "Associations d'altérations génétiques et liens de coopérations oncogénique dans les cancers broncho-pulmonaires non à petites cellules". Paris 5, 2011. http://www.theses.fr/2011PA05T058.
Guérin, Célia. "Caractérisation de nouvelles mutations activatrices dépendantes de l'HGF dans le lobe N-terminal du domaine kinase du récepteur MET dans le cancer du rein héréditaire". Electronic Thesis or Diss., Université de Lille (2022-....), 2023. https://pepite-depot.univ-lille.fr/ToutIDP/EDBSL/2023/2023ULILS074.pdf.
Targeted therapies are currently revolutionizing the management of cancer patients, provided they present a targetable molecular alteration responsible for tumor progression. Receptor tyrosine kinases (RTKs) with activating mutations are major targets of targeted therapies, with EGFR as a representative example, whose mutations lead to its constitutive activation, making it independent of stimulation by its ligand.The MET receptor, another RTK in this family, has activating mutations in kidney and lung cancer. Indeed, type I papillary renal cell carcinoma (HPRC), an uncommon hereditary cancer, is unique in that over 80% of cases have MET activating mutations. In contrast, in non-small cell lung cancer (NSCLC), MET mutations lead to skipping of exon 14 encoding the juxtamembrane domain (MET ex14 mutations). This exon skipping leads to the loss of the juxtamembrane domain, a regulatory domain involved in the negative regulation of the receptor. In an original way from other RTK mutations, these mutations always require stimulation by HGF, the ligand of MET, making HGF production a parameter to be considered in the stratification of patients eligible for targeted therapies.Tyrosine kinase inhibitors (TKIs) directed against MET have very recently been approved for clinical use, offering real hope for patients with these mutations.Thanks to the development of high-throughput sequencing for diagnosis and the emergence of new resistance mutations following treatment with targeted therapies, the spectrum of mutations affecting TKIs is expanding considerably. The current challenge is no longer the detection of these mutations, but their functional interpretation, which can demonstrate their activating character or their targeting by TKIs.In this context, my thesis objective was to exploit sequencing data from patients suffering from HPRC or NSCLC to identify new MET activating mutations and characterize their activation mechanisms in order to determine their eligibility for potential treatment by TKIs.Thanks to a collaboration with the Institute Gustave Roussy, which centralizes sequencing data from HPRC patients, we have identified 8 previously undescribed mutations in a cohort of 158 patients, affecting the extracellular domain (V37A and R426P), the juxtamembrane domain (S1018P and G1086E) and the N-terminal lobe of MET kinase (H1086L, I1102T, C1125G and L1130S). In parallel, thanks to our collaboration with the Lille University Hospital, which centralizes data on 2808 NSCLC patients, we have identified 2 undescribed kinase domain mutations.First, we demonstrated in a fibroblast transformation model that the four N-terminal lobe mutations identified in HPRC are potential MET-activating mutations. Interestingly, although localized to the kinase, these mutations retain a dependence on HGF to induce cell transformation. Moreover, all four mutations are sensitive to TKIs directed against MET.In a second step, to better characterize these new activating mutations, we established T47D epithelial cell lines expressing two of the new activating mutations (H1086L and I1102T), which we compared with wild-type MET and MET ex14, known to retain its dependence on HGF. Our results confirm that both mutations require activation by HGF for activation of downstream signaling pathways and induction of responses such as cell motility. Transcriptomic analysis reveals significant similarities between the transcriptional programs of the MET I1102T, H1086L and MET exon14 mutations, highlighting their involvement in extracellular matrix remodeling and invasion. Xenografts of cells expressing these new mutations in mouse models demonstrate their ability to promote tumor growth [...]
Planchard, David. "MAP Kinases et protéines de réparation dans les cancers pulmonaires non à petites cellules". Paris 11, 2009. http://www.theses.fr/2009PA11T113.
Maurin, Pauline. "Caractérisation fonctionnelle du complexe LKB1/STRADß au cil primaire et les conséquences au cours de la tumorigenèse". Thesis, Aix-Marseille, 2016. http://www.theses.fr/2016AIXM5065.
STK11 gene mutations were originally identified as responsible for the Peutz-Jeghers syndrome of which severity is mainly related to an increase incidence of tumor development. The product of this gene the serine/threonine kinase LKB1 gets its activity or its expression reduced, sometimes even lost, following somatic mutations in several types of cancer such as pancreas, liver but mainly from lung. Indeed, almost 30% of non-small cell lung carcinoma (NSCLC) does not express anymore or only an inactive form, has led to consider this kinase as tumor suppressor of importance. While there is no doubt of the involvement of its catalytic activity molecular mechanisms responsible for its tumor suppressor properties remain to be identified. Indeed, whereas its function as regulator of cellular metabolism through AMPK has been favor for a while, it is currently re-assess to benefit to its regulator function on canonical Wnt signaling. My thesis work, reinforce this eventuality in NSCLC. Indeed, among the two functional complexes formed by LKB1 through its association with STRADα or β pseudokinases, my results show that only the complex related to STRADβ is involved in the canonical Wnt pathway regulation. For that, LKB1/STRADβ complex localizes at primary cilia and participates to MARK3 kinase activation. These results strengthened by a STRADβ knockout mouse model and an a posteriori transcriptomic analysis of lung adenocarcinoma patient datasets related to their clinical records, suggest that LKB1 tumour suppressor activity is associated with its localization and its function at primary cilia participating in the activation of MARK3 and thus regulation of canonical Wnt signaling
Alzahouri, Kazem. "Pratiques diagnostiques pour les nodules pulmonaires isolés et le cancer du poumon non à petites cellules : caractérisation, déterminants et évaluations médico-économiques de l'introduction de la tomographie par émission de positon". Nancy 1, 2006. http://www.theses.fr/2006NAN11301.
Alifano, Marco. "Rôle du système neurotensine / récepteur de la neurotensine dans le carcinome pulmonaire non à petites cellules et le mésotheliome malin pleural". Paris 6, 2009. http://www.theses.fr/2009PA066003.
Rollin, Jérôme. "Expression comparée de deux anti-protéases, TFPI-2 et RECK, et des métalloprotéases MMP-2 et MMP-9 dans le cancer broncho-pulmonaire non à petites cellules". Tours, 2006. http://www.theses.fr/2006TOUR3303.
TFPI-2 and RECK are anti-proteases which regulate in vitro the activation of several MMP involve in cancer progression. We have demonstrated that gene expressions of these two inhibitors are decreased in 37% and 51% of non-small cell lung cancer tumours, respectively. In addition, hypermethylation of TFPI-2 gene promoter is associated with decreased expression of TFPI-2 gene in 50% of cases. On the other hand, the percentage of active forms of MMP-2 and MMP-9 was higher in tumours but did not significantly vary according to RECK or TFPI-2 gene expression. This study has also demonstrated that the survival time of patients with the MMP-2-735CC genotype was significantly shorter, despite tumour MMP-2 mRNA levels measured were significantly lower. In conclusion, these data support that TFPI-2 and RECK are likely contributing to inhibit tumour progression in NSCLC, but the exact mechanisms involved to regulate in vivo MMP remain to be identified
Galluzzi, Lorenzo. ""TripleC" : une étude de biologie des systèmes sur l'apoptose". Paris 11, 2008. http://www.theses.fr/2008PA11T093.
Picon, Agnès. "Etude des mécanismes transcriptionnels du gène codant pour la proopiomélanocortine dans la lignée humaine de carcinome bronchique à petites cellules DMS-79 : Endocrinologie et intéractions cellulaires". Paris 11, 1998. http://www.theses.fr/1998PA11T050.