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Journal articles on the topic 'Deletion bras long'

Author: Grafiati

Published: 4 June 2021

Last updated: 17 February 2022

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1

Mistry, Matthew, Nataliya Zhukova, Daniele Merico, et al. "BRAF Mutation and CDKN2A Deletion Define a Clinically Distinct Subgroup of Childhood Secondary High-Grade Glioma." Journal of Clinical Oncology 33, no. 9 (2015): 1015–22. http://dx.doi.org/10.1200/jco.2014.58.3922.

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Purpose To uncover the genetic events leading to transformation of pediatric low-grade glioma (PLGG) to secondary high-grade glioma (sHGG). Patients and Methods We retrospectively identified patients with sHGG from a population-based cohort of 886 patients with PLGG with long clinical follow-up. Exome sequencing and array CGH were performed on available samples followed by detailed genetic analysis of the entire sHGG cohort. Clinical and outcome data of genetically distinct subgroups were obtained. Results sHGG was observed in 2.9% of PLGGs (26 of 886 patients). Patients with sHGG had a high f

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Lhermitte, Benoit, Eric Guerin, Elisa Ruhland, et al. "TBIO-17. INTEGRATIVE ANALYSES OF BRAFv600e MUTATED GLIOMAS: FROM MOLECULAR BIOLOGY TO RADIOLOGY AND TREATMENTS." Neuro-Oncology 22, Supplement_3 (2020): iii469—iii470. http://dx.doi.org/10.1093/neuonc/noaa222.844.

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Abstract BRAFv600e mutation is encountered mostly in low-grade pediatric gliomas (LGG) and epileptogenic glioneuronal tumors, such as gangliogliomas (GG). Less frequently this mutation is present in high-grade glial (HGG) or glioneuronal tumors. Recent publications were highlighting BRAF mutation and CDKN2A deletion, as independent prognostic factors linked to a worst outcome in LGGs. We studied retrospectively a monocentric cohort of 12 LGGs (9 GG and 3 pilocytic astrocytomas) and 9 HGG (5 “de novo” tumors and 4 with a long past of LGG evolution) with BRAFv600e positivity. The patients were a

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Lassaletta, Alvaro, Michal Zapotocky, Matthew Mistry, et al. "Therapeutic and Prognostic Implications of BRAF V600E in Pediatric Low-Grade Gliomas." Journal of Clinical Oncology 35, no. 25 (2017): 2934–41. http://dx.doi.org/10.1200/jco.2016.71.8726.

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Purpose BRAF V600E is a potentially highly targetable mutation detected in a subset of pediatric low-grade gliomas (PLGGs). Its biologic and clinical effect within this diverse group of tumors remains unknown. Patients and Methods A combined clinical and genetic institutional study of patients with PLGGs with long-term follow-up was performed (N = 510). Clinical and treatment data of patients with BRAF V600E mutated PLGG (n = 99) were compared with a large international independent cohort of patients with BRAF V600E mutated-PLGG (n = 180). Results BRAF V600E mutation was detected in 69 of 405

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Nobre, Liana, Michal Zapotocky, Vijay Ramaswamy, et al. "Outcomes of BRAF V600E Pediatric Gliomas Treated With Targeted BRAF Inhibition." JCO Precision Oncology, no. 4 (September 2020): 561–71. http://dx.doi.org/10.1200/po.19.00298.

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PURPOSE Children with pediatric gliomas harboring a BRAF V600E mutation have poor outcomes with current chemoradiotherapy strategies. Our aim was to study the role of targeted BRAF inhibition in these tumors. PATIENTS AND METHODS We collected clinical, imaging, molecular, and outcome information from patients with BRAF V600E–mutated glioma treated with BRAF inhibition across 29 centers from multiple countries. RESULTS Sixty-seven patients were treated with BRAF inhibition (pediatric low-grade gliomas [PLGGs], n = 56; pediatric high-grade gliomas [PHGGs], n = 11) for up to 5.6 years. Objective

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Nobre, Liana, Michal Zapotocky, Vijay Ramaswamy, et al. "LGG-55. OUTCOME OF BRAF V600E PEDIATRIC GLIOMAS TREATED WITH TARGETED BRAF INHIBITION." Neuro-Oncology 22, Supplement_3 (2020): iii377. http://dx.doi.org/10.1093/neuonc/noaa222.433.

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Abstract Children with pediatric gliomas harboring BRAF V600E mutation have a poor outcome with current chemoradiation strategies. Our aim was to study the role of targeted BRAF inhibition in these tumors. We collected clinical, imaging, molecular and outcome information from BRAF V600E glioma patients treated with BRAFi across 29 centers from multiple countries. Sixty-seven patients were treated with BRAFi (56 pediatric low grade gliomas, PLGG and 11 pediatric high grade gliomas, PHGG) for up to 5.6 years. Objective responses were observed in 80% of PLGGs compared to 28% with conventional che

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Nobre, Liana, Michal Zapotocky, Vijay Ramaswamy, et al. "PDCT-08. SUPERIOR OUTCOME FOR BRAF V600E PEDIATRIC GLIOMAS TREATED WITH TARGETED BRAF INHIBITION." Neuro-Oncology 21, Supplement_6 (2019): vi184—vi185. http://dx.doi.org/10.1093/neuonc/noz175.771.

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Abstract BACKGROUND Children with pediatric low grade glioma’s (PLGG) harboring BRAF V600E mutation have poor outcome due to relative resistance to chemo-radiation and higher risk of malignant transformation. However, the role of targeted BRAF inhibition in these tumors is poorly defined. METHODS We assembled an international cohort of children with BRAF V600E mutant gliomas treated with BRAF inhibition, from 29 centers participating in the PLGG taskforce, and collected response, survival and molecular parameters. RESULTS Sixty-seven patients were treated with BRAFi (56 PLGG and 11 high grade

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7

Lhermitte, Benoit, Eric Guerin, Agathe Chammas, et al. "BRAFv600e mutated gliomas: From biology to radiology and treatments." Journal of Clinical Oncology 37, no. 15_suppl (2019): e13552-e13552. http://dx.doi.org/10.1200/jco.2019.37.15_suppl.e13552.

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e13552 Background: BRAF V600E mutation is encountered in brain tumor, mostly low grade pediatric diffuse glioma (LGG) and epileptogenic glioneuronal tumor such as gangliogliomas (GG) or pleomorphic xanthoastrocytomas (PXA). Less frequently this mutation is present in high grade glial or glioneuronal tumors such as pleomorphic xanthoastrocytomas with anaplasia, anaplastic ganglioglioma, anaplastic diffuse astrocytomas or glioblastomas. Recently, few publications were highlighting differently the impact of BRAF mutation and CDKN2A deletion, as independent prognostic factors linked to a worst out

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Munir, Anum, Sajid Khan, and Shumaila Azam. "Computational drug ZINPIP-Analog an ultimate solution to cure conserved domains of mutant EGFR, ALK and BRAF Proteins in NSCLC." International Current Pharmaceutical Journal 4, no. 7 (2015): 396–401. http://dx.doi.org/10.3329/icpj.v4i7.23589.

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Mutations in different genes such as EGFR, ALK and BRAF results in non-small cell Lung cancer (NSCLC). The most ordinarily discovered EGFR mutations in patients with NSCLC are deletion in exon 29 or in 21. Mutations initiate the tyrosine kinase activity of EGFR and are connected with the affectability to small molecules results in the formation of NSCLC. The missense mutations of BRAF have been detected in exon 11 and 15. Mutation of ALK occurs as a result of small inversion. The primary objective of study was to design novel chemical compound to block the targeted sites for receptor proteins,

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Kissoon, Trisha, Sridharan Gururangan, Jesse Kresak, and Lance Governale. "PATH-52. ANAPLASTIC PILOMYXOID ASTROCYTOMA HARBORING BRAF FUSION, PTEN AND TERT MUTATIONS." Neuro-Oncology 21, Supplement_6 (2019): vi155. http://dx.doi.org/10.1093/neuonc/noz175.647.

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Abstract Pilomyxoid astrocytomas (PMA) are focal neoplasms that are often cured with total resection. We present a case of a progressive PMA with histologic and molecular features suggestive of malignant transformation. A 13-year old boy presented with headaches, diplopia, and seizures. He had previously been followed for 7 years by serial imaging for a cystic/solid enhancing mass in the right temporal lobe without biopsy that had remained stable up to 6 months prior to his current illness. MRI of brain demonstrated significant progression of the solid component with extension into the subepen

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Ashby, Cody, Eileen Boyle, Ruslana G. Tytarenko, et al. "Long-Term Follow-up Identifies Double Hit and Key Mutations As Impacting Progression Free and Overall Survival in Multiple Myeloma." Blood 132, Supplement 1 (2018): 110. http://dx.doi.org/10.1182/blood-2018-99-113045.

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Abstract Introduction: The study of multiple myeloma (MM) genomics has identified many abnormalities that are associated with poor progression free survival (PFS) and overall survival (OS). Copy number abnormalities have been extensively studied in many datasets with long follow-up, however, the prognostic impact of mutations have not been extensively studied and available datasets have generally had a relatively short follow-up of 22-25 months, with one dataset being up to 5.4 years. These analyses have identified a range of mutations that are associated with prognosis, making it important to

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Basse, Clémence, Claire Morel, Céline Callens, et al. "Exploitation of Precision Medicine Trials Data: Examples of Long Responders From the SHIVA01 Trial." JCO Precision Oncology, no. 2 (November 2018): 1–11. http://dx.doi.org/10.1200/po.18.00048.

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Purpose Precision medicine trials constitute a precious source of molecular data with prospective clinical annotations allowing the exploration of patients’ subpopulations according to specific clinical or biological questions. Using the SHIVA01—the first randomized trial comparing molecularly targeted therapy on the basis of tumor molecular profiling versus conventional chemotherapy in metastatic cancer patients who failed standard of care therapy—annotated database, we report cases of patients treated in the trial with targeted therapy who experienced an objective response or prolonged disea

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Kilburn, Lindsay Baker, Nada Jabado, Andrea Franson, et al. "FIREFLY-1: A phase 2 study of the pan-RAF inhibitor DAY101 in pediatric patients with low-grade glioma." Journal of Clinical Oncology 39, no. 15_suppl (2021): TPS10056. http://dx.doi.org/10.1200/jco.2021.39.15_suppl.tps10056.

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TPS10056 Background: The mitogen-activated protein kinase (MAPK) signaling pathway is an essential pathway that regulates key cell functions such as growth, survival, and differentiation. Genomic alterations and dysregulation of the MAPK pathway including BRAF fusions, point mutations (e.g. BRAF V600) and in-frame deletions have been described in many different types of malignancies, including pediatric low-grade glioma (pLGG) and other pediatric cancers. The identification of the KIAA1549:BRAF fusion in 2008 led to deeper understanding of the genomic events driving growth of pLGG (Jones, Canc

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Durham, Benjamin, Jing Ma, Eunhee Kim, et al. "Unraveling the Molecular Basis of Langerhans and Non-Langerhans Cell Histiocytic Neoplasms through Whole Exome Sequencing." Blood 124, no. 21 (2014): 1887. http://dx.doi.org/10.1182/blood.v124.21.1887.1887.

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Abstract Systemic histiocytic disorders, including Langerhans cell histiocytosis (LCH) and the non-Langerhans cell histiocytic disorder Erdheim-Chester Disease (ECD) are clinically heterogeneous diseases whose underlying etiology has long been obscure. Recent identification of BRAF V600E mutations in ~50% of LCH and ECD patients, as well as mutations in MAP2K1 in ~25% of BRAF-wild type LCH patients has refined our understanding of these disorders as clonal malignancies driven by constitutive MAP kinase signaling. However, the compendium of mutations co-occurring with BRAF V600E and MAP2K1 muta

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Else, Monica, Stuart J. Blakemore, Jonathan C. Strefford, and Daniel Catovsky. "The association between deaths from infection and mutations of the BRAF, FBXW7, NRAS and XPO1 genes: a report from the LRF CLL4 trial." Leukemia 35, no. 9 (2021): 2563–69. http://dx.doi.org/10.1038/s41375-021-01165-w.

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AbstractCauses of death, in particular deaths due to infection, have not been widely studied in randomised trials in chronic lymphocytic leukaemia. With long-term follow-up (median 13 years) we examined the cause of death in 600/777 patients in the LRF CLL4 trial. Blood samples, taken at randomisation from 499 patients, were available for identifying gene mutations. Infection was a cause of death in 258 patients (43%). Patients dying of infection were more likely than those who died of other causes to have received ≥2 lines of treatment (194/258 [75%] versus 231/342 [68%], P = 0.04) and to hav

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15

Pramio, Dimitrius T., Paula C. Pennacchi, Silvya S. Maria-Engler, et al. "LINE-1 hypomethylation and mutational status in cutaneous melanomas." Journal of Investigative Medicine 64, no. 4 (2016): 899–904. http://dx.doi.org/10.1136/jim-2016-000066.

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Epigenetic dysregulation is an important emerging hallmark of cutaneous melanoma development. The global loss of DNA methylation in gene-poor regions and transposable DNA elements of cancer cells contributes to increased genomic instability. Long interspersed element-1 (LINE-1) sequences are the most abundant repetitive sequence of the genome and can be evaluated as a surrogate marker of the global level of DNA methylation. In this work, LINE-1 methylation levels were evaluated in cutaneous melanomas and normal melanocyte primary cell cultures to investigate their possible association with bot

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16

Gerber, David E., Leena Gandhi, and Daniel B. Costa. "Management and Future Directions in Non-Small Cell Lung Cancer with Known Activating Mutations." American Society of Clinical Oncology Educational Book, no. 34 (May 2014): e353-e365. http://dx.doi.org/10.14694/edbook_am.2014.34.e353.

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Lung cancer accounts for a quarter of all cancer deaths. Non-small cell lung cancer (NSCLC) is currently segregated by the presence of actionable driver oncogenes. This review will provide an overview of molecular subsets of lung cancer, including descriptions of the defining oncogenes ( EGFR, ALK, KRAS, ROS1, RET, BRAF, ERBB2, NTRK1, FGFR, among others) and how these predict for response to small molecule tyrosine kinase inhibitors (TKIs) that are either clinically available or in clinical trial development for advanced NSCLC. Particular focus will be placed on subsets with EGFR mutated and A

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Zhang, Kang, Guanghui Wang, Chao Guo, et al. "Mutational landscapes and PD-L1 expression in non-small cell lung cancer." Journal of Clinical Oncology 37, no. 15_suppl (2019): 8541. http://dx.doi.org/10.1200/jco.2019.37.15_suppl.8541.

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8541 Background: Programmed death-ligand 1 (PD-L1) serves as a major predictive biomarker for immune checkpoint inhibitors in non-small cell lung cancer (NSCLC). However, the relationship between PD-L1 expression and genetic features of NSCLC remains unclear. The aim of this study was to explore the correlation between genetic profiles and PD-L1 expression in NSCLC. Methods: FFPE tumor and matched blood samples from 568 NSCLC (487 adenocarcinomas (ACAs) and 81 squamous carcinomas (SCAs)) patients were collected for NGS-based targeted panel sequencing. Genomic alterations including single nucle

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Lonial, Sagar, Venkata D. Yellapantula, Winnie Liang, et al. "Interim Analysis of the Mmrf Commpass Trial: Identification of Novel Rearrangements Potentially Associated with Disease Initiation and Progression." Blood 124, no. 21 (2014): 722. http://dx.doi.org/10.1182/blood.v124.21.722.722.

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Abstract The Multiple Myeloma Research Foundation (MMRF) CoMMpass trial (NCT0145429) is a longitudinal study of 1000 patients with newly-diagnosed multiple myeloma. The study opened July 2011 and now includes over 650 patients from 91 sites in the United States, Canada and European Union. Each patient is required to receive an approved proteasome inhibitor, immunumodulatory agent, or both. Enriched tumor and matched constitutional samples are comprehensively analyzed using Long-Insert Whole Genome Sequencing (WGS), Whole Exome Sequencing (WES) and RNA sequencing (RNAseq). Clinical parameters,

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Jaskula, Emilia, Janusz Lange, Mariola Sedzimirska, and Andrzej Lange. "Sorafenib Is Contributing to Salvage Chemotherapy and Is Effective Given Alone for Maintenance in AML FLT3 ITD Patients Relapsing Post Allo Hematopoietic Stem Cell Transplantation." Blood 124, no. 21 (2014): 5265. http://dx.doi.org/10.1182/blood.v124.21.5265.5265.

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Abstract Normal karyotype AML patients with FLT3 ITD have a higher risk of relapse than those lacking this mutation (Estey EH, Am J Hematol. 2013). Our comparative genomic hybridization study (77 patients) showed that AML cases with as compared to those without FLT3 ITD had significantly lower number of amplifications or deletions (number of total CNV aberrations: 18±4 vs 51±8, p=0.003). The latter observation in concert with that of others (Thiede, Blood 2002) suggest that FLT3 ITD mutation if present in normal karyotype patients is a key player in the pathogenesis of leukaemia and targeting

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Sharma, Kamal, August Stuart, Elliot M. Epner, and Thomas P. Loughran. "Overcoming Ibrutinib Resitance In Relapsed Chronic Lymphocytic Leukemia." Blood 122, no. 21 (2013): 4891. http://dx.doi.org/10.1182/blood.v122.21.4891.4891.

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Abstract Resistance to ibrutinib (PCI-32765) is uncommon and not well described. Here we describe a 78 year old Caucasian man with a long standing history of CLL originally diagnosed in 2004. He was treated at the James Cancer Hospital and Fellow Research Institute at the Ohio State University since that time and received multiple regimens including fludarabine and Rituxan based regimens under the care of John Byrd, MD. He progressed and more recently was on the clinical trial of ibrutinib for relapsed CLL, which he tolerated well and to which he had an excellent response for nearly 2 years. T

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Xie, Zhiyi, Lisa Chamberlain, Andrew Carson, et al. "Monitoring Minimal Residual Disease in Acute Myeloid Leukemia Using Genomic or cfDNA with MyMRD®, a Targeted NGS Panel." Blood 132, Supplement 1 (2018): 5268. http://dx.doi.org/10.1182/blood-2018-99-118971.

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Abstract Acute myeloid leukemia (AML) is a genetically and phenotypically heterogeneous disorder. Precision therapies for AML have been developed that target specific driver mutations. The efficacies of these therapies are variable, making it critical to determine successful therapies prior to patient relapse. For patients achieving a first complete remission, minimum residual disease (MRD) is an important prognostic factor, as MRD may provide a powerful and timely tool to evaluate therapeutic efficacy. There is a growing demand that new and promising drugs are approved as quickly as possible

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Misund, Kristine, Niamh Keane, Yan W. Asmann, et al. "Complementary Activation of Ccnd, MYC, RAS and NFkB By Mutations in Multiple Myeloma." Blood 128, no. 22 (2016): 355. http://dx.doi.org/10.1182/blood.v128.22.355.355.

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Abstract MYC expression is frequently dysregulated in multiple myeloma (MM). In one comprehensive study, MYC structural variations (SV) were found in nearly half of MM cases (Affer et al. Leukemia 2014). The prevalence was higher in hyperdiploid (HRD) tumors (65%) compared to non-hyperdiploid (NHRD) tumors (36%). The large amount of tumor DNA required for all of the genomic studies performed may have biased the samples analyzed (e.g., to those with higher tumor burdens). To validate the findings of recurrent MYC SV in another dataset, we analyzed the CoMMpass data. We analyzed long-insert whol

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Aktas-Samur, Anil, Mariateresa Fulciniti, Sanika Derebail, et al. "High Throughput Genomic Analysis Identifies Low-Risk Smoldering Multiple Myeloma." Blood 136, Supplement 1 (2020): 2. http://dx.doi.org/10.1182/blood-2020-139066.

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Multiple Myeloma is preceded by precursor states of monoclonal gammopathy of undermined significance (MGUS) and smoldering multiple myeloma (SMM). Studies have shown that progression to symptomatic MM five years after diagnosis is 1% for MGUS and 10% for SMM. However, based on the genomic background, this rate is highly variable, especially for SMM patients. Recent studies have evaluated the high-risk genomic features for SMM, but the genomic background of SMM patients who do not progress to MM after long-term follow-up (&gt;= 5 years) has not been described. Here, we evaluated genomic cha

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Kikuchi, Zensho, Ichiyo Shibahara, Tetsu Yamaki, et al. "TERT promoter mutation associated with multifocal phenotype and poor prognosis in patients with IDH wild-type glioblastoma." Neuro-Oncology Advances 2, no. 1 (2020). http://dx.doi.org/10.1093/noajnl/vdaa114.

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Abstract Background Although mutations in the promoter region of the telomerase reverse transcriptase (TERTp) gene are the most common alterations in glioblastoma (GBM), their clinical significance remains unclear. Therefore, we investigated the impact of TERTp status on patient outcome and clinicopathological features in patients with GBM over a long period of follow-up. Methods We retrospectively analyzed 153 cases of GBM. Six patients with isocitrate dehydrogenase 1 (IDH1) or H3F3A gene mutations were excluded from this study. Among the 147 cases of IDH wild-type GBM, 92 (62.6%) had the TER

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