Letteratura scientifica selezionata sul tema "Poumon – Cancer non à petites cellules – Génétique"
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Articoli di riviste sul tema "Poumon – Cancer non à petites cellules – Génétique":
Bonnette, Pierre. "Résections carcinologiques limitées des cancers non à petites cellules du poumon". Bulletin du Cancer 99, n. 11 (novembre 2012): 1069–75. http://dx.doi.org/10.1684/bdc.2012.1654.
Sève, P., e C. Dumontet. "β-tubuline de classe III et cancer du poumon non à petites cellules". Revue des Maladies Respiratoires 27, n. 4 (aprile 2010): 383–86. http://dx.doi.org/10.1016/j.rmr.2010.03.006.
Thomas, P., M. Dahan, M. Riquet, G. Massart, P. E. Falcoz, L. Brouchet, F. Le Pimpec Barthes, C. Doddoli, E. Martinod e E. Fadel. "Pratiques chirurgicales dans le traitement du cancer primitif non à petites cellules du poumon". Revue des Maladies Respiratoires 25, n. 8 (ottobre 2008): 1031–36. http://dx.doi.org/10.1016/s0761-8425(08)74419-x.
Cherif, H., S. Bacha, S. Habibech, I. Moussa, S. Agerbi, H. Racil, A. Chabbou e N. Chaouch. "Évènements osseux dans le cancer du poumon non à petites cellules avec métastases osseuses". Revue des Maladies Respiratoires 35 (gennaio 2018): A211. http://dx.doi.org/10.1016/j.rmr.2017.10.483.
Assié, J. B., L. Greiller, A. Cortot e M. Wislez. "Le traitement périopératoire dans le cancer du poumon non à petites cellules a priori résécables". Revue des Maladies Respiratoires Actualités 15, n. 1 (giugno 2023): 1S27–1S32. http://dx.doi.org/10.1016/s1877-1203(23)00016-2.
Eberst, G., D. Vernerey, C. Laheurte, V. Kaulek, A. Meurisse, L. Cuche, P. Jacoulet et al. "Valeur pronostique de la lymphopénie T CD4 + dans le cancer du poumon non à petites cellules". Revue des Maladies Respiratoires Actualités 13, n. 1 (gennaio 2021): 124. http://dx.doi.org/10.1016/j.rmra.2020.11.254.
Bernard, Galaad, Guillaume Klausner, Eivind Blais, Charles-Henry Canova, Jean Bourhis e Idriss Troussier. "Place de la radiothérapie stéréotaxique dans le cancer du poumon non à petites cellules en oligoprogression". Revue Médicale Suisse 18, n. 784 (2022): 1125–33. http://dx.doi.org/10.53738/revmed.2022.18.784.1125.
Mohamed Lemine, S. O., K. Rim, A. Sourour, H. Mohamed Moustapha, Y. Ilhem e K. Samy. "Facteurs pronostiques des patients atteints d’un cancer du poumon non à petites cellules de stade III". Revue des Maladies Respiratoires Actualités 14, n. 1 (gennaio 2022): 103. http://dx.doi.org/10.1016/j.rmra.2021.11.123.
Riquet, M., C. Rivera, C. Pricopi, A. Badia, A. Arame, A. Dujon, C. Foucault, F. Le Pimpec-Barthes e E. Fabre. "Facteurs pronostiques cliniques et paracliniques dans la chirurgie du cancer du poumon non à petites cellules". Revue de Pneumologie Clinique 71, n. 5 (ottobre 2015): 264–74. http://dx.doi.org/10.1016/j.pneumo.2015.06.001.
Capelle, H., C. Tummino, M. Gouitaa, J. Birnbaum, N. Ausias, D. Charpin, L. Grellier e M. Montana. "Intérêt des tests allergologiques par intradermoréaction chez les patients traités pour cancer du poumon non à petites cellules". Le Pharmacien Hospitalier et Clinicien 49, n. 2 (giugno 2014): e152-e153. http://dx.doi.org/10.1016/j.phclin.2014.04.308.
Tesi sul tema "Poumon – Cancer non à petites cellules – Génétique":
Planque, Chris. "Expression de kallicreines tissulaires humaines dans les cancers broncho-pulmonaires non à petites cellules". Tours, 2005. http://www.theses.fr/2005TOUR4042.
Evaluation of 8 human tissue kallikrein gene expression (15 genes) in lung cancer showed that, except for KLK8, all kallikrein gene transcription resulted in synthesis of a major mRNA encoding kallikrein protein. Altogether, we identified 24 KLK transcripts in lung tissue and 11 mRNA were never described yet. We also quantified using real-time RT-PCR those KLK gene expression in normal and tumoral lung tissues Our results revealed that KLK10 and KLK11 displayed similar expression in normal and tumor lung tissues, whereas KLK5 and KLK7 differential expression was correlated with tumor histotype. KLK13 and KLK14 expression was altered in patients with or without lymph nodes metastasis. The KLK6 and KLK8 genes were highly over-expressed in NSCLC compared to normal lung tissue. Moreover, increased expression of KLK6 and KLK8 genes correlated with negative patient prognosis suggesting that proteins encoded by those genes may be involved in neo-plastic progression
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.
Malleter, Marine. "HEF1 et B2, deux cibles moléculaires potentielles dans le cancer broncho-pulmonaire non à petites cellules et leur mécanisme de régulation impliquant les miRNA". Nantes, 2010. https://archive.bu.univ-nantes.fr/pollux/show/show?id=925cf436-e879-412d-89dd-3327b04167e2.
The lung cancer is at the first place of the death at the world level and in France to. Today, the used molecular targets act on cells which has a speed proliferation, so the fact could explain their ineffectiveness on the non small cells lung cancer (NSCLC) which presents the particularities to have cells which have a slowly proliferation. So, it is very important to discover new molecular targets induced by new anti-cancer molecules which can act on these cells with the slowly proliferation. Previously the laboratory has identified two molecular targets HEF1 and B2 expressed in NSCLC. HEF1 is involved in numerous cellular functions such as apoptosis, cell proliferation, motility. B2 discovered and identified by the laboratory overlapped a part of the HEF1 genomic DNA. This 54 Kb non coding RNA is expressed in different tissues and specifically expressed in lung tissue as the HEF1 gene. Having regard the B2 RNA characteristics and the homology of sequence with HEF1, we put in evidence the existence of a regulation of the HEF1 gene by the B2 RNA. This regulation induced by B2 would be made by the miRNA mechanism. In fact, this large non-coding RNA would be a precursor of miRNA which could for some of them being directed against the HEF1 gene such as hsa-mir-146B. This miRNA overexpressed in NSCLC-N6 cells, has a high homology with the B2 gene and could regulate HEF1 gene on the exon 4. So these genes could be an approach of a new gene therapy whose the expression is modulated by cytostatic molecules such as the molecule A190 patented by the lab
Merle, Patrick. "Etude de ligands de l'ADN G-quadruplexe télomérique dans le traitement du glioblastome et cancer bronchique : approches combinatoires". Thesis, Clermont-Ferrand 1, 2011. http://www.theses.fr/2011CLF1MM14.
Lamy, Aude. "Contribution à l'étude des altérations du cycle cellulaire au cours du cancer bronchique primitif et des lésions précancéreuses". Rouen, 2002. http://www.theses.fr/2002ROUES010.
It is important to characterize the molecular changes occurring in precancerous lesions and invasive lung cancer the leading cause of cancer's mortality in industrial nations. In the first part of this work we studied the timing of aberrant methylation of CDKN2A and hRARb2 in primary cultures of precancerous lesions. Aberrant methylation of the CDKN2A gene promoter was found in 19 % of preinvasive lesions: (1) its frequency increased with the histological grade of the lesions, (2) methylation was significantly more frequent in patients with a previous history of lung or ENT cancer but was not influenced by tobacco or asbestos exposure, (3) there was no relationship between CDKN2A hypermethylation and the evolutivity of the lesions. In contrast, aberrant methylation of hRARb2 was not an early event of lung carcinogenesis in our study. In a second part of this work we found an altered expression of Cyclins B1 and B2 in 15 % of non-small cell lung cancer
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
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 [...]
Sève, Pascal. "Pharmacorésistance et cancer du poumon Non à petites cellules". Lyon 1, 2006. http://www.theses.fr/2006LYO10008.
MAGNIN, JEAN-LUC. "Etude de la survie a deux ans des cancers du poumon non anaplasiques a petites cellules non resecables non metastases". Aix-Marseille 2, 1989. http://www.theses.fr/1989AIX20079.
Piton, Nicolas. "Optimisation de la prise en charge diagnostique, pronostique et théranostique des carcinomes broncho-pulmonaires humains : des techniques d’imagerie in vivo à la biologie moléculaire. Ligation -dependent RT-PCR : a new specific and low-cost technique to detect ALK, ROS and RET rearrangements in lung adenocarcinoma A new assay for detection of theranostic gene translocations and MET exon 14 skipping in thoracic oncology. One-year perspective routine LD-RT-PCR in 413 newly diagnosed lung tumors STK11 mutations are associated with lower PDL1 expression in lung adenocarcinoma BRAF V600E mutation is not always present as expected ! A case report of lung and thyroid carcinomas A novel method for in vivo imaging of solitary lung nodules using navigational bronchoscopy and confocal laser microendoscopy". Thesis, Normandie, 2019. http://www.theses.fr/2019NORMR119.
Lung cancer is a serious and frequent condition for which the management strategies have been dramatically modified in recent years, from a diagnostic, prognostic and “theranostic” perspective, most notably with the introduction of “targeted therapies”. The latter have demonstrated dramatic improvement in both quality of life and survival rates of eligible patients, yet consequently highlight new complications in diagnosis, treatment options or technical considerations which can be attributed to the growing number of molecular alterations to be detected from limited tissue samples frequently encountered in thoracic oncology. This work combines 5 different research papers from 2 different angles: prognostic and “theranostic” molecular markers of lung cancer, as well as in vivo diagnostic procedures of lung cancer. The first angle encompasses 4 articles. The first two evaluate a new molecular technique, LD-RT-PCR, to detect gene translocation in lung cancer. The third article explores the association between STK11 mutations in lung cancer and the expression of PDL1. Finally, the fourth article is a case report illustrating the importance of a morphological approach to lung cancer. The second angle compares in vivo imaging techniques by endoscopy using confocal laser microendoscopy alongside a conventional microscopic approach