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Artykuły w czasopismach na temat "Mutation BRAFV600E"
Lee, Min Hee, Seong Eun Lee, Dong Wook Kim, Min Jeong Ryu, Sung Jin Kim, Sung Joong Kim, Yong Kyoung Kim i in. "Mitochondrial Localization and Regulation of BRAFV600E in Thyroid Cancer: A Clinically Used RAF Inhibitor Is Unable to Block the Mitochondrial Activities of BRAFV600E". Journal of Clinical Endocrinology & Metabolism 96, nr 1 (1.01.2011): E19—E30. http://dx.doi.org/10.1210/jc.2010-1071.
Pełny tekst źródłaSahm, Felix, David Capper, Matthias Preusser, Jochen Meyer, Albrecht Stenzinger, Felix Lasitschka, Anna-Sophie Berghoff i in. "BRAFV600E mutant protein is expressed in cells of variable maturation in Langerhans cell histiocytosis". Blood 120, nr 12 (20.09.2012): e28-e34. http://dx.doi.org/10.1182/blood-2012-06-429597.
Pełny tekst źródłaChakraborty, Dhritiman, Sunil Shakya, Sanjana Ballal, Shipra Agarwal i Chandrasekhar Bal. "BRAFV600E and TERT promoter mutations in paediatric and young adult papillary thyroid cancer and clinicopathological correlation". Journal of Pediatric Endocrinology and Metabolism 33, nr 11 (26.11.2020): 1465–74. http://dx.doi.org/10.1515/jpem-2020-0174.
Pełny tekst źródłaDiamond, Eli L., Benjamin Durham, Ahmet Dogan, Mariko Yabe, Kseniya Petrova-Drus, Raajit K. Rampal, Raajit K. Rampal i in. "Phase 2 Trial of Single-Agent Cobimetinib for Adults with Histiocytic Neoplasms". Blood 142, Supplement 1 (28.11.2023): 1812. http://dx.doi.org/10.1182/blood-2023-187508.
Pełny tekst źródłaSong, Eyun, Meihua Jin, Ahreum Jang, Min Ji Jeon, Dong Eun Song, Hye Jin Yoo, Won Bae Kim, Young Kee Shong i Won Gu Kim. "Mutation in Genes Encoding Key Functional Groups Additively Increase Mortality in Patients with BRAFV600E-Mutant Advanced Papillary Thyroid Carcinoma". Cancers 13, nr 22 (22.11.2021): 5846. http://dx.doi.org/10.3390/cancers13225846.
Pełny tekst źródłaKaneko, Masanao, Mitsuko Nakashima, Kiichi Sugiura, Natsuki Ishida, Satoshi Tamura, Shinya Tani, Mihoko Yamade i in. "Both MLH1 deficiency and BRAFV600E mutation are a unique characteristic of colorectal medullary carcinoma: An observational study". Medicine 102, nr 38 (22.09.2023): e35022. http://dx.doi.org/10.1097/md.0000000000035022.
Pełny tekst źródłaAscierto, Paolo A., David Minor, Antoni Ribas, Celeste Lebbe, Anne O'Hagan, Niki Arya, Mary Guckert i in. "Phase II Trial (BREAK-2) of the BRAF Inhibitor Dabrafenib (GSK2118436) in Patients With Metastatic Melanoma". Journal of Clinical Oncology 31, nr 26 (10.09.2013): 3205–11. http://dx.doi.org/10.1200/jco.2013.49.8691.
Pełny tekst źródłaMorris, Van K., Kanwal Pratap Singh Raghav, Arvind Dasari, Michael J. Overman, Bryan K. Kee, Benny Johnson, Christine Megerdichian Parseghian i in. "Utility of circulating tumor DNA in the clinical management of patients with BRAFV600E metastatic colorectal cancer." Journal of Clinical Oncology 39, nr 3_suppl (20.01.2021): 119. http://dx.doi.org/10.1200/jco.2021.39.3_suppl.119.
Pełny tekst źródłaSmyrk, Thomas C., David Tougeron, Stephen N. Thibodeau, Shalini Singh, Andrea Muranyi, Kandavel Shanmugam, Thomas M. Grogan, Steven R. Alberts, Qian Shi i Frank A. Sinicrope. "Detection of the BRAFV600E protein in human colon carcinomas by a mutation-specific antibody." Journal of Clinical Oncology 31, nr 15_suppl (20.05.2013): 3576. http://dx.doi.org/10.1200/jco.2013.31.15_suppl.3576.
Pełny tekst źródłaChoi, Yun-Suk, Seong-Woon Choi i Jin-Wook Yi. "Prospective Analysis of TERT Promoter Mutations in Papillary Thyroid Carcinoma at a Single Institution". Journal of Clinical Medicine 10, nr 10 (18.05.2021): 2179. http://dx.doi.org/10.3390/jcm10102179.
Pełny tekst źródłaRozprawy doktorskie na temat "Mutation BRAFV600E"
Radom, Mickaëlle. "Rôle de la NADPH oxydase 4 (NOX4) dans la dédifférenciation des cellules tumorales thyroïdiennes porteuses de la mutation BRAFV600E". Electronic Thesis or Diss., université Paris-Saclay, 2024. http://www.theses.fr/2024UPASL012.
Pełny tekst źródłaThe radioiodine therapy (RAI) constitutes the main treatment for differentiated thyroid cancer (DTC). This metabolic radiotherapy is based on the expression at thyroid cell basal membrane of the iodine transporter (NIS) encoded by SLC5A5 gene. BRAFV600E oncogene driver mutation is present in 40 to 60% of DTC. Locally advanced and metastatic papillary thyroid cancer (PTC) harboring BRAFV600E mutation have poor prognosis. BRAFV600E oncogene is a strong activator of MAPK signaling leading to a dedifferentiation process, which is associated with SLC5A5 gene repression and radioiodine therapy refractoriness. The RAI uptake constitutes a major challenge for treatment of patients and in this sense a new therapeutic approach consists of thyroid cell redifferentiation strategy. Our previous studies showed that BRAFV600E controls the NADPH oxidase (NOX4) expression and NOX4- derived ROS repress SLC5A5 gene. NOX4 inhibition reinduces NIS expression and the reversibility suggests a contribution to an epigenetic mechanism. The objective of the thesis was to determine the molecular and mechanistic events induced by NOX4-derived ROS that contribute to the repression of genes involved in differentiation process and in the efficiency of metabolic radiotherapy. Our results showed that NOX4 generates specific oxidative damage to DNA, which promotes the retention of epigenetic actors such as DNMTs through interaction with DNA repair proteins, thereby disrupting the DNA binding of thyroid differentiation transcription factors, PAX8 and NKX.2.1, and preventing gene transcription for prolonged periods. We also demonstrated an effect of BRAF/MEK inhibitors used clinically in NOX4- dependant epigenetic mechanism and a clinical interest of NOX4 inhibition in addition to BRAF/MEK inhibition in thyroid differentiation gene reinduction
Touat, Mahdi. "Mécanismes et implications thérapeutiques de l'hypermutation dans les gliomes Mechanisms and Therapeutic Implications of Hypermutation in Gliomas Mismatch Repair Deficiency in High-Grade Meningioma: A Rare but Recurrent Event Associated With Dramatic Immune Activation and Clinical Response to PD-1 Blockade Buparlisib in Patients With Recurrent Glioblastoma Harboring Phosphatidylinositol 3-Kinase Pathway Activation: An Open-Label, Multicenter, Multi-Arm, Phase II Trial Hyman DM. BRAF Inhibition in BRAFV600-Mutant Gliomas: Results From the VE-BASKET Study Glioblastoma Targeted Therapy: Updated Approaches From Recent Biology Successful Targeting of an ATG7-RAF1 Gene Fusion in Anaplastic Pleomorphic Xanthoastrocytoma With Leptomeningeal Dissemination Ivosidenib in IDH1-Mutated Advanced Glioma". Thesis, université Paris-Saclay, 2020. http://www.theses.fr/2020UPASL071.
Pełny tekst źródłaHigh tumor mutational burden (hypermutation) is observed in some gliomas; however, the mechanisms by which hypermutation develops and whether it predicts chemotherapy or immunotherapy response are poorly understood. Mechanistically, an association between hypermutation and mutations in the DNA mismatch-repair (MMR) genes has been reported in gliomas, but most MMR mutations observed in this context were not functionally characterized, and their role in causing hypermutation remains unclear. Furthermore, whether hypermutation enhances tumor immunogenicity and renders gliomas responsive to immune checkpoint blockade (e.g. PD-1 blockade) is not known. Here, we comprehensively analyze the clinical and molecular determinants of mutational burden and signatures in 10,294 gliomas, including 558 (5.4%) hypermutated tumors. We delineate two main pathways to hypermutation: a de novo pathway associated with constitutional defects in DNA polymerase and MMR genes, and a more common, post-treatment pathway, associated with acquired resistance driven by MMR defects in chemotherapy-sensitive gliomas recurring after temozolomide. Experimentally, the mutational signature of post-treatment hypermutated gliomas (COSMIC signature 11) was recapitulated by temozolomide-induced damage in MMR-deficient cells. While MMR deficiency was associated with acquired temozolomide resistance in glioma models, clinical and experimental evidence suggest that MMR-deficient cells retain sensitivity to the chloroethylating nitrosourea lomustine. MMR-deficient gliomas exhibited unique features including the lack of prominent T-cell infiltrates, extensive intratumoral heterogeneity, poor survival and low response rate to PD-1 blockade. Moreover, while microsatellite instability in MMR-deficient gliomas was not detected by bulk analyses, single-cell whole-genome sequencing of post-treatment hypermutated glioma cells demonstrated microsatellite mutations. Collectively, these results support a model where differences in the mutation landscape and antigen clonality of MMR-deficient gliomas relative to other MMR-deficient cancers may explain the lack of both immune recognition and response to PD-1 blockade in gliomas. Our data suggest a change in practice whereby tumor re-sequencing at relapse to identify progression and hypermutation could inform prognosis and guide therapeutic management
Tsai, Po-chin, i 蔡柏欽. "BRAFV600E mutation in anaplast thyroid carcinomas and multiple papillary thyroid carcinomas". Thesis, 2005. http://ndltd.ncl.edu.tw/handle/94263865585788514890.
Pełny tekst źródła國立中山大學
生物醫學科學研究所
93
Abstract: Activating point mutations of the BRAF gene have been recently reported to be restricted to papillary thyroid carcinomas (PTCs) and anaplastic thyroid carcinomas (ATCs) arising from PTCs among various benign and malignant thyroid tumors. A thymine-to-adenine transversion at nucleotide 1799 (T1799A), formerly designated as T1796A, in exon 15 resulting in a valine to glutamate substitution at residue 600 (V600E), formerly designated as V599E, was the only mutational site reported in thyroid cancer. We have previously shown that BRAFV600E mutations were detected in 49 of 105 (47%) PTCs but not in 5 follicular thyroid carcinomas (FTCs), 10 follicular adenomas, 3 Hürthle cell adenomas and 10 nodular goiters. In contrast to PTC, to date only few studies have been published concerning the frequency of BRAFV600E in ATCs and their coexisting differentiated thyroid carcinomas. In addition, there is no report concerning the BRAF status in multiple PTCs. In this study, paraffin-embedded tumor tissues of 25 patients with thyroid cancer (15 ATCs and 10 PTCs) were obtained from the Department of Pathology of Chang Gung Memorial Hospital-Kaohsiung. Nine ATCs were found to contain a coexisting differentiated carcinoma, including three follicular and six papillary carcinomas. Ten cases of PTC with multiple tumor foci were selected from a cohort of 105 PTCs as previously reported. Paraffin blocks containing tumor were sectioned followed by microdissection to obtain tissue for DNA extraction. Mutational hot spot in exon 15 (codon 600) of the BRAF gene were amplified by PCR and sequenced with an automatic sequencer. BRAFV600E mutations were detected in 3 of 15 (20%) ATCs. In the 9 coexisting differentiated carcinomas, 2 out of 6 PTCs harbored BRAF mutations but not in the three follicular carcinomas. In none of 3 ATCs with coexisting PTCs were mutations detectable in both tumor types. Among the ten cases of PTCs with multiple tumor foci, 5 cases demonstrated the same BRAF status in each tumor foci whereas 5 cases showed distinct BRAF status in different tumor foci. We conclude that the distinct BRAF status in anaplastic carcinoma and its coexisting differentiated carcinoma suggests that anaplastic carcinoma might not arise from differentiated carcinoma.The distinct BRAF status in different tumor foci of multiple papillary carcinomas suggests that multifocal tumors might not be formed through intrathyroidal lymphatic metastasis.
Fu, Shuai-Shuai, i 傅帥帥. "The Clinical Manifestations and Specific Gene Expressions in Conventional Papillary Thyroid Carcinoma with BRAFV600E Mutation and BRAF Pseudogene". Thesis, 2012. http://ndltd.ncl.edu.tw/handle/36854887744386801786.
Pełny tekst źródła國立陽明大學
解剖學及細胞生物學研究所
100
BRAFV600E is the most common point mutation found in papillary thyroid carcinomas (PTC). It may play an important role in the thyroid tumorgenesis by activating MAPK signal pathway and proposed to be a poor prognostic marker. However, the results in different studies are controversial. BRAF Pseudogene is a gene with DNA sequence similar to BRAF but having many stop codons which may not translate to a functional protein. BRAF Pseudogene was shown to activate MAPK signal pathway, but its role in thyroid cancer is still unclear. In this study, we investigated the effects of BRAFV600E mutation in the clinical manifestations, gene and protein expressions in patients with conventional PTC. The results showed that the frequency of the BRAFV600E mutation in Taiwan is high (73.1%). There is no significant difference in age, gender, tumor size, extrathyroidal invasion, nodal metastasis, distant metastasis and staging between patients with or without BRAFV600E mutation. High expression of BRAF and ERK proteins were observed in PTCs compared with normal tissues in immunohistochemistry (IHC) studies. Neither the expression of BRAF, ERK, NIS and glucotransporter 1 (GLUT1) in IHC, nor the detection of BRAF, p-ERK, and t-ERK in Western blotting correlates with BRAFV600E mutation. In the Q-PCR studies of thyroid differentiated genes, tumor invasion genes and GLUT1 expressions in PTCs, paired-normal thyroid tissues and nodular goiter tissues we found that the expression of NIS, TPO and TSHR in PTC were less than normal tissues (p<0.001, p=0.001, p<0.001, respectively). Besides, PTC expressed more MMP9 and GLUT1 than normal tissues (p<0.001, p<0.001, respectively). There is no significant difference between BRAF wild type (BRAFWT) and BRAFV600E in TPO, TSHR, MMP2, MMP9, GLUT1 and DcR3 gene expressions. However, PTCs with BRAFV600E expressed lower NIS mRNA level than BRAFWT (p=0.012). BRAF Pseudogene expression is high in conventional PTC (91.7%) and the frequency is similar in both BRAFV600E and BRAFWT. Furthermore, we overexpressed the pBRAFWT, pBRAFV600E and pBRAFpseudogene in WRO (differentiated thyroid follicular carcinoma cell line) and no significant difference in NIS, TPO, MMP9 and GLUT1 mRNA expressions were found among these three insertions. Our results showed that no significant difference in clinical- pathological features, gene and protein expressions between patients with conventional PTC harboring BRAFV600E mutation and BRAFWT in Taiwan. The only finding is the lower NIS gene expression in PTC harboring the BRAFV600E mutation suggesting the dedifferentiation of the tumor which may affect the I131 uptake in the subsequent radiotherapy. However, our present finding is not strong enough to indicate that BRAFV600E mutation is a poor prognostic marker affecting recurrent and mortality rates. Further studies are necessary to investigate the role of BRAFV600E mutation in PTC tumorigenesis.
CARISSIMI, Elvira. "BRAFV600E MUTATION, TISSUE INHIBITOR OF METALLOPROTEINASE-1 UPREGULATION AND NF-KB ACTIVATION: CLOSING THE LOOP ON THE PAPILLARY THYROID CANCER TRILOGY". Doctoral thesis, 2011. http://hdl.handle.net/10447/95098.
Pełny tekst źródłaCzęści książek na temat "Mutation BRAFV600E"
Po, Joseph W., Yafeng Ma, Alison W. S. Luk, David Lynch, Bavanthi Balakrishnar, Daniel Brungs, Farhad Azimi i in. "Single-Cell Analysis of BRAFV600E and NRASQ61R Mutation Status in Melanoma Cell Lines as Method Generation for Circulating Melanoma Cells". W Methods in Molecular Biology, 277–86. New York, NY: Springer US, 2021. http://dx.doi.org/10.1007/978-1-0716-1205-7_21.
Pełny tekst źródłaSterlich, Katharina, i Milen Minkov. "Childhood Langerhans Cell Histiocytosis: Epidemiology, Clinical Presentations, Prognostic Factors, and Therapeutic Approaches". W Rare Diseases [Working Title]. IntechOpen, 2021. http://dx.doi.org/10.5772/intechopen.96543.
Pełny tekst źródłaHoperia, Victoria, Alexander Larin, Joanna Gwiedzska, Kirk Jensen, Aneeta Patel, Andrew Bauer i Vasyl Vasko. "Detection of BRAFV600E Mutation in May-Grunwald Stained Thyroid FNA Samples Can Help in Identification of Cancers with a High Risk of Extra-Thyroidal Extension and Metastases". W CLINICAL - Thyroid Cancer, P3–665—P3–665. The Endocrine Society, 2011. http://dx.doi.org/10.1210/endo-meetings.2011.part4.p11.p3-665.
Pełny tekst źródłaSait, Sameer Farouk, Morgan Freret i Matthias Karajannis. "Pediatric High-Grade Glioma". W Neuro-Oncology Compendium for the Boards and Clinical Practice, redaktorzy Maciej M. Mrugala, Na Tosha N. Gatson, Sylvia C. Kurz, Kathryn S. Nevel i Jennifer L. Clarke, 267—C18.P333. Oxford University PressNew York, 2023. http://dx.doi.org/10.1093/med/9780197573778.003.0018.
Pełny tekst źródłaStreszczenia konferencji na temat "Mutation BRAFV600E"
Pace, Margaret, Vladislava O. Melnikova, Kerry Brandl, Larry Kahn, Jacky Woo i Darren W. Davis. "Abstract 3159: BRAFV600E mutation analysis in circulating tumor cells". W Proceedings: AACR 102nd Annual Meeting 2011‐‐ Apr 2‐6, 2011; Orlando, FL. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/1538-7445.am2011-3159.
Pełny tekst źródłaRan, Leili, Devan Murphy, Jessica Sher, Zhen Cao, Shangqian Wang, Edward Walczak, Youxin Guan i in. "Abstract A15: Modeling sporadic gastrointestinal stromal tumor with BRAFV600E mutation". W Abstracts: Advances in Sarcomas: From Basic Science to Clinical Translation; May 16-19, 2017; Philadelphia, PA. American Association for Cancer Research, 2018. http://dx.doi.org/10.1158/1557-3265.sarcomas17-a15.
Pełny tekst źródłaZhou, Biting, Kailun Xu, Yingkuan Shao, Xi Zheng i Shu Zheng. "IDDF2020-ABS-0070 Proteomic analysis of colorectal cancer with BRAFV600E mutation". W Abstracts of the International Digestive Disease Forum (IDDF), 22–23 November 2020, Hong Kong. BMJ Publishing Group Ltd and British Society of Gastroenterology, 2020. http://dx.doi.org/10.1136/gutjnl-2020-iddf.59.
Pełny tekst źródłaTazi, Abdellatif, Fanélie Jouenne, Emmanuelle Bugnet, Gwenaël Lorillon, Véronique Meignin, Aurélie Sadoux, Sylvie Chevret i Samia Mourah. "Clinical impact of BRAFV600E mutation in adult pulmonary Langerhans cell histiocytosis". W ERS International Congress 2019 abstracts. European Respiratory Society, 2019. http://dx.doi.org/10.1183/13993003.congress-2019.oa2141.
Pełny tekst źródłaBalint, Balazs, Karin van den Hurk, Sinead Toomey, Louise Unwin, Kieran Sheahan, Enda McDermott, Ian Murphy i in. "Abstract 23: Low incidence of BRAFV600E mutation among melanoma patients in Ireland." W Proceedings: AACR 104th Annual Meeting 2013; Apr 6-10, 2013; Washington, DC. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1538-7445.am2013-23.
Pełny tekst źródłaPhipps, Amanda I., Karen W. Makar, Anna E. Coghill, Andrea N. Burnett-Hartman, Michael N. Passarelli i Polly A. Newcomb. "Abstract 4510:BRAFV600E mutation status and survival after colorectal cancer diagnosis according to patient and tumor characteristics". W Proceedings: AACR 103rd Annual Meeting 2012‐‐ Mar 31‐Apr 4, 2012; Chicago, IL. American Association for Cancer Research, 2012. http://dx.doi.org/10.1158/1538-7445.am2012-4510.
Pełny tekst źródłaWu, Zihan, Xiaoyang Huang, Shaohui Huang, Xin Ding i Liansheng Wang. "Direct Prediction of BRAFV600E Mutation from Histopathological Images in Papillary Thyroid Carcinoma with a Deep Learning Workflow". W CSAI 2020: 2020 4th International Conference on Computer Science and Artificial Intelligence. New York, NY, USA: ACM, 2020. http://dx.doi.org/10.1145/3445815.3445840.
Pełny tekst źródłaKim, Eunhee, Stephen S. Chung, Jae H. Park, Young Rock Chung, Piro Lito, Julie Feldstein, Wenhuo Hu i in. "Abstract 3140: Context specific effects of the BRAFV600E mutation on hematopoiesis identifies novel models of BRAF mutant hematopoietic disorders". W Proceedings: AACR Annual Meeting 2014; April 5-9, 2014; San Diego, CA. American Association for Cancer Research, 2014. http://dx.doi.org/10.1158/1538-7445.am2014-3140.
Pełny tekst źródłaTanaka, Hiroki, Kie Horioka, Masahiro Yamamoto, Asari Masaru, Katsuhiro Okuda, Seiji Ohtani, Kosuke Yamazaki, Keiko Shimizu i Katsuhiro Ogawa. "Abstract 4081: Podoplanin expression in Kupffer cells and platelet deposition on the hepatic sinusoidal cells in the liver of transgenic mice with a hepatocyte-specific human BRAFV600E mutation". W Proceedings: AACR Annual Meeting 2018; April 14-18, 2018; Chicago, IL. American Association for Cancer Research, 2018. http://dx.doi.org/10.1158/1538-7445.am2018-4081.
Pełny tekst źródłaDeFazio, Anna, Tania Moujaber, Dariush Etemadmoghadam, Catherine Kennedy, Yoke-Eng Chiew, Rosemary L. Balleine, Catherine Saunders i in. "Abstract A25: BRAFV600E mutations in serous ovarian cancer and response to the BRAF inhibitor, dabrafenib." W Abstracts: AACR Special Conference: Advances in Ovarian Cancer Research: Exploiting Vulnerabilities; October 17-20, 2015; Orlando, FL. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/1557-3265.ovca15-a25.
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