Добірка наукової літератури з теми "BRAFV600E oncogene"
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Статті в журналах з теми "BRAFV600E oncogene":
Algazi, Alain Patrick, Megan Othus, Benjamin Newell Voorhies, Kari Lynn Kendra, Shaker R. Dakhil, Amy K. Harker-Murray, Christopher D. Lao, et al. "Clinical outcomes in patients with BRAFV600 mutant melanoma and undetectable circulating tumor DNA treated with dabrafenib and trametinib." Journal of Clinical Oncology 38, no. 15_suppl (May 20, 2020): 10059. http://dx.doi.org/10.1200/jco.2020.38.15_suppl.10059.
Rogounovitch, Tatiana I., Svetlana V. Mankovskaya, Mikhail V. Fridman, Tatiana A. Leonova, Victor A. Kondratovitch, Natalya E. Konoplya, Shunichi Yamashita, Norisato Mitsutake, and Vladimir A. Saenko. "Major Oncogenic Drivers and Their Clinicopathological Correlations in Sporadic Childhood Papillary Thyroid Carcinoma in Belarus." Cancers 13, no. 13 (July 5, 2021): 3374. http://dx.doi.org/10.3390/cancers13133374.
Perna, Daniele, Florian A. Karreth, Alistair G. Rust, Pedro A. Perez-Mancera, Mamunur Rashid, Francesco Iorio, Constantine Alifrangis, et al. "BRAF inhibitor resistance mediated by the AKT pathway in an oncogenic BRAF mouse melanoma model." Proceedings of the National Academy of Sciences 112, no. 6 (January 26, 2015): E536—E545. http://dx.doi.org/10.1073/pnas.1418163112.
Kaabouch, Meryem, Hafsa Chahdi, Naima Azouzi, Mohammed Oukabli, Issam Rharrassi, Adil Boudhas, Hassan Jaddi, et al. "BRAFV600E hot spot mutation in thyroid carcinomas: first Moroccan experience from a single-institution retrospective study." African Health Sciences 20, no. 4 (December 16, 2020): 1849–56. http://dx.doi.org/10.4314/ahs.v20i4.40.
Wang, Liye, Qianyi Lu, Kuikui Jiang, Ruoxi Hong, Shusen Wang, and Fei Xu. "BRAF V600E Mutation in Triple-Negative Breast Cancer: A Case Report and Literature Review." Oncology Research and Treatment 45, no. 1-2 (November 24, 2021): 54–61. http://dx.doi.org/10.1159/000520453.
Zurnadzhy, Liudmyla, Tetiana Bogdanova, Tatiana I. Rogounovitch, Masahiro Ito, Mykola Tronko, Shunichi Yamashita, Norisato Mitsutake, Serhii Chernyshov, Sergii Masiuk, and Vladimir A. Saenko. "The BRAFV600E Mutation Is Not a Risk Factor for More Aggressive Tumor Behavior in Radiogenic and Sporadic Papillary Thyroid Carcinoma at a Young Age." Cancers 13, no. 23 (November 30, 2021): 6038. http://dx.doi.org/10.3390/cancers13236038.
Hosier, Gregory W., and Matthew T. Roberts. "Initial response of renal cell carcinoma to vemurafenib in a patient treated for metastatic melanoma." Canadian Urological Association Journal 10, no. 9-10 (September 13, 2016): 306. http://dx.doi.org/10.5489/cuaj.3652.
Chabanet, Tamer Basel, Shannon Steinberg, Peisheng Zhang, and Mary Jo Turk. "Elucidating the oncogene-driven regulatory T cell responses during melanoma tumorigenesis." Journal of Immunology 196, no. 1_Supplement (May 1, 2016): 74.1. http://dx.doi.org/10.4049/jimmunol.196.supp.74.1.
Kidger, Andrew M., Linda K. Rushworth, Julia Stellzig, Jane Davidson, Christopher J. Bryant, Cassidy Bayley, Edward Caddye, Tim Rogers, Stephen M. Keyse, and Christopher J. Caunt. "Dual-specificity phosphatase 5 controls the localized inhibition, propagation, and transforming potential of ERK signaling." Proceedings of the National Academy of Sciences 114, no. 3 (January 4, 2017): E317—E326. http://dx.doi.org/10.1073/pnas.1614684114.
Spourquet, Catherine, Ophélie Delcorte, Pascale Lemoine, Nicolas Dauguet, Axelle Loriot, Younes Achouri, Maija Hollmén, et al. "BRAFV600E Expression in Thyrocytes Causes Recruitment of Immunosuppressive STABILIN-1 Macrophages." Cancers 14, no. 19 (September 26, 2022): 4687. http://dx.doi.org/10.3390/cancers14194687.
Дисертації з теми "BRAFV600E oncogene":
COLLEONI, CRISTINA. "Dissecting the non-cell autonomous effects of oncogene activation on hematopoiesis." Doctoral thesis, Università Vita-Salute San Raffaele, 2023. https://hdl.handle.net/20.500.11768/137018.
In hematopoietic stem and progenitor cell (HSPC) gene therapy (GT), insertional mutagenesis may result in oncogene activation, increasing the risk of leukemia in patients. Moreover, hBRAFV600E-expressing human HSPCs transplanted into immune-deficient mice, even in small numbers, induce lethal bone marrow (BM) failure. This aggressive phenotype is due to the engagement of senescence, characterized by cell cycle blockade and a senescence-associated secretory phenotype, affecting also non-mutated bystander cells. Thus, it is fundamental to describe oncogene activation in HSPCs, since it poses risks before the malignant transformation. To investigate the fate of senescent cells in the presence or absence of an active immune system, we transplanted NSG or immune-competent (WT) mice with mouse (m) HSPCs transduced with lentiviral vectors expressing mBrafV600E, an N-truncated version (mBraf-trunc), or GFP as control. In NSG recipients, mBraf-trunc and mBrafV600E expression caused dose-dependent lethality and reduced cellularity, the latter resulting in a more aggressive phenotype. As opposed to the humanized model, only mBrafV600E-lymphoid cells were impaired, but not bystander cells. Transcriptional profiling showed upregulated cell cycle inhibitor genes Cdkn2d and Cdk2ap2, not Cdkn2a or Cdkn1a. Hallmarks upregulated were TNFα signaling, oxidative stress pathways, and apoptosis. Downregulated processes were ribosome biogenesis, interferon signaling, and innate (MHC class II) and adaptive immune response. Instead, in WT recipients, we observed reduced lethality (only 60%) and complete clearance of oncogene-expressing cells in the surviving mBrafV600E mice, suggesting that the immunological competence of recipients promotes a more efficient clearance of senescent cells. Transcriptional analysis showed similar immune suppression to NSG, but upregulated hallmarks were related to cell cycle, G2/M checkpoint, E2F targets, DNA replication, and repair processes in B cells. This suggests that B cells are potentially escaping senescence and returning to the cell cycle. This study aspires to identify species-specific or universal biomarkers for pre-clinical and clinical GT studies and to recognize factors determining the resilience/clearance of senescent cells, suggesting strategies for their elimination.
Tran, Sieu. "Oncogene-induced senescence and the role of p53 in BRAFV600E melanoma." Thesis, The University of Sydney, 2014. http://hdl.handle.net/2123/13286.
Azouzi, Naima. "Etude de l’implication de la NADPH oxydase NOX4 et du stress oxydatif dans la radiorésistance des cancers papillaires de la thyroïde exprimant l’oncogène BRAFV600E." Thesis, Université Paris-Saclay (ComUE), 2016. http://www.theses.fr/2016SACLS416.
One of the major properties of the thyroid is iodine uptake from the bloodstream through an iodide transporter (NIS for Natrium Iodide Symporter). This capacity plays a key role in the thyroid hormones synthesis, but also in both diagnosis and treatment of thyroid cancer. However, due to a decrease or absence of the NIS expression in some tumors and metastases, patients become refractory to the metabolic radiotherapy and present a radioresistance, which cause a public health problem.The BRAFV600E oncogene, a potent activator of the MAP kinase pathway, is detected in 40-60% of papillary thyroid cancer (PTC), which represent 80% of total thyroid cancers. The BRAFV600E mutation is associated with the more aggressive thyroid tumors. However, the pharmacological inhibition of the MAP kinase pathway, constitutively induced by the BRAFV600E oncogene, is not able to restore alone the expression of NIS in patients with BRAFV600E mutated thyroid cancer. This suggests that other compensatory mechanisms may contribute to the radioresistance. A recent study in a mouse model demonstrated that downregulation of NIS by BRAFV600E oncogene is mediated through the TGF beta activation. An other showed that the expression of NIS is dependent on the redox status of the cell, suggesting a role for the reactive oxygen species (ROS). In cells, ROS can be produced by the NADPH oxidases (NOX/DUOX). The Thyroid gland expresses three of them: DUOX2, which is necessary for the thyroid hormones synthesis, but also DUOX1 and NOX4 whose the physiological role remains unknown. NOX4, which is overexpressed in the PTCs, has been shown to be a new key effector of the TGF beta pathway.In my thesis project, I was interested in studying the role of NOX4 in the negative regulation of NIS in BRAFV600E mutated CPT. The study of the mechanism, made from two human cell lines derived from BRAF-mutated papillary thyroid cancers (BCPAP and 8505C), has revealed that the oncogene BRAFV600E controls the expression of NOX4 at the transcriptional level via the TGF-beta/Smad3 pathway. These results were validated on both a rat thyroid cell line conditionnaly expressing BRAFV600E and on human thyrocytes in primary culture. Importantly, the use of antioxidants such as N-acetyl cysteine (NAC) or specific inhibition of NOX4 expression by RNA interference allow reinduction of NIS expression. These results, which show that ROS produced by NOX4 inhibit the expression of iodine transporter (NIS), establish a link between the oncogene BRAFV600E and NOX4. A comparative analysis of the NOX4 expression, made from 500 papillary thyroid cancers mutated or not for BRAF (TCGA data), confirms that NOX4 is significantly increased in BRAF-mutated cancers and that this is correlated with a decrease of NIS mRNA. Furthermore, the level of NOX4 is inversely related to thyroid differentiation score, suggesting that NOX4 might be involved in the dedifferentiation process. This study opens a new opportunity for optimizing the use of metabolic radiotherapy in the treatment of thyroid cancers refractory to radioiodine I131and makes NOX4 as a potential therapeutic target
Fenniche, Salma. "Rôle de la NADPH OXYDASE NOX4 dans la régulation de l'expression et de l'activité de CHD4 dans les tumeurs thyroïdiennes porteuses de la mutation BRAFV600E." Electronic Thesis or Diss., université Paris-Saclay, 2024. http://www.theses.fr/2024UPASL022.
Metabolic radiotherapy with radioiodine is the cornerstone of the treatment of distant metastases of differentiated thyroid cancers. This therapy depends on the expression at the basal membrane of thyrocytes of the Natrium Iodide Symporter 'NIS'. BRAFV600E mutation is present in 45 to 60% of papillary thyroid carcinomas, which represent 80% of thyroid cancers. The presence of this mutation is associated with the most aggressive thyroid tumors with low levels or absence of NIS expression. The loss of radioactive iodine uptake translates into resistance to metabolic radiotherapy, constituting a major issue for the treatment of patients with this cancer. One approach for treating patients refractory to metabolic radiotherapy is to increase iodine uptake.At the transcriptional level, our team has already shown, through a comparative analysis concerning approximately 500 PTCs from the TCGA database, that NOX4 was strongly expressed in PTCs-BRAFV600E compared to PTCs-BRAFwt. However, at the protein level, no link has been established between the BRAFV600E mutation and NOX4 in malignant and non-malignant tumors (BRAFV600E/BRAFwt). In my thesis project, we illustrate for the first time a positive correlation between the presence of BRAFV600E mutation and the overexpression of NOX4 protein in PTC tumor tissues. The overexpression of NOX4 was associated with an aggressive nature of tumors. Furthermore, we showed that 60% of infiltrating C-PTCs overexpress NOX4 independently of BRAF mutational status, suggesting that NOX4 could be considered as a potential co-marker of PTC aggressiveness. Interestingly, NOX4 protein was also overexpressed in non-malignant thyroid diseases (Basedow, goiters, and hyperplasias), with different subcellular localizations, suggesting a role for NOX4 in progression to thyroid malignancy.Furthermore, on a mechanistic level, our team has previously shown that BRAFV600E controls the expression of NOX4 under the effect of TGF-β/SMAD3 and that NOX4-derived ROS contribute to the repression of NIS. Inhibition of NOX4 promotes reactivation of the NIS. This reversibility suggests a contribution to an epigenetic mechanism. CHD4, a subunit of the NuRD remodeling complex, plays an essential role in gene repression. it was found to be strongly expressed in PTCs, in which it was associated with a poor prognosis. In this study, we showed that the TGF-β/SMAD3 pathway regulates the expression of CHD4 protein. The latter cooperates with DNMTs in repressing NIS in several thyroid tumor cells lines mutated for BRAFV600E. Furthermore, we showed that CHD4 responds to oxidative DNA damage induced by NOX4-derived ROS. Indeed, inhibition of NOX4 or its functional partner p22phox reduces the recruitment of CHD4 to chromatin. This recruitment depends on OGG1 and MSH6, two proteins involved in oxidative DNA damage repair. This study identifies CHD4 as a new therapeutic candidate in radioiodine-refractory thyroid cancers
GIGLIO, PAOLA. "Role of oncogenic BRAFV600E on cell death/survival decision in human skin melanoma." Doctoral thesis, Università degli Studi di Roma "Tor Vergata", 2016. http://hdl.handle.net/2108/201873.
Darp, Revati A. "Insights into the Role of Oncogenic BRAF in Tetraploidy and Melanoma Initiation." eScholarship@UMMS, 2021. https://escholarship.umassmed.edu/gsbs_diss/1129.
Héritier, Sébastien. "Bases moléculaires de l’histiocytose langerhansienne." Thesis, Université Paris-Saclay (ComUE), 2017. http://www.theses.fr/2017SACLS002.
Langerhans cell histiocytosis (LCH) is the most common type of histiocytosis owing to accumulation of pathologic CD1a+ CD207+ histiocytes. The identification of BRAFV600E in more than half of patients with LCH has launched a new field of investigation to study potential patient’s management benefits and implications from this molecular status.First, in BRAFV600E mutated LCH, we reported the effectiveness of BRAF inhibitors. Efficacy with no resistance to vemurafenib was reported in all cases with active LCH disease, especially for multi-system LCH with risk organ (MS RO+) involvement, confirming the driver status of this mutation in LCH. However, after discontinuation of this treatment administered during 2-6 months, many recurrences were observed.Then, we showed that children with BRAFV600E mutated LCH manifested more severe disease, comprised 87.8% of patients with MS RO+ involvement. Compared to patients with wild-type BRAF, patients with BRAFV600E more commonly displayed resistance to combined vinblastine and corticosteroid therapy (21.9% vs. 3.3%), showed a higher 5-year reactivation rate (42.8% vs. 28.1%) and had more long-term permanent consequences (27.9% vs. 12.6%).Moreover, we showed that BRAFV600E quantification in circulating cell-free DNA by droplet digital PCR is a relevant biomarker to monitor response to therapy for MS RO+ LCH and RO- LCH children who failed to respond to first line chemotherapy.Finally, after the screening of LCH biopsy (n=86) for the BRAF, KRAS, NRAS and PI3KCA most common mutations, leading to highlight one case with the PIK3CAE542K somatic mutation, 9 paired tumor-normal samples from children with LCH were analyzed by whole exome sequencing. Data showed a new BRAF recurrent mutation (n=2) in the 5′ splice sites of the intron 12. According to RNA analysis, this mutation would lead to the insertion of 3 amino acids (LLR) in the smaller N-terminal lobe of the BRAF kinase domain. Functional analysis is ongoing
Gagliardi, Sinforosa. "ERK5 is required for melanoma growth and is activated by oncogenic BRAF." Doctoral thesis, 2018. http://hdl.handle.net/2158/1125602.
Тези доповідей конференцій з теми "BRAFV600E oncogene":
Pringle, Daphne R., and Martin McMahon. "Abstract 308: Interrogating Goldilocks: Searching for mediators of oncogene overdose in engineered BRAFV600E inhibitor resistant melanoma cells." In Proceedings: AACR 107th Annual Meeting 2016; April 16-20, 2016; New Orleans, LA. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/1538-7445.am2016-308.
Kang, Byunghak, Julie In, Nicholas Zachos, David Huso, Shinji Maegawa, Jean-Pierre Issa, Hariharan Easwaran, and Stephen B. Baylin. "Abstract 4273: Oncogenic BRAFV600E drives stem cell niche factors-independent growth and tumorigenic transformation in colon organoids." In Proceedings: AACR 107th Annual Meeting 2016; April 16-20, 2016; New Orleans, LA. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/1538-7445.am2016-4273.