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Journal articles on the topic 'BRAF35'

Author: Grafiati

Published: 1 April 2023

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1

Rugerio-Martínez, Claudia Ivette, Daniel Ramos, Abel Segura-Olvera, et al. "Dp71 Point Mutations Induce Protein Aggregation, Loss of Nuclear Lamina Integrity and Impaired Braf35 and Ibraf Function in Neuronal Cells." International Journal of Molecular Sciences 23, no. 19 (2022): 11876. http://dx.doi.org/10.3390/ijms231911876.

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Dystrophin Dp71 is the most abundant product of the Duchenne muscular dystrophy gene in the nervous system, and mutations impairing its function have been associated with the neurodevelopmental symptoms present in a third of DMD patients. Dp71 is required for the clustering of neurotransmitter receptors and the neuronal differentiation of cultured cells; nonetheless, its precise role in neuronal cells remains to be poorly understood. In this study, we analyzed the effect of two pathogenic DMD gene point mutations on the Dp71 function in neurons. We engineered C272Y and E299del mutations to exp

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Mi LEE, Young, and Wankee KIM. "Association of human kinesin superfamily protein member 4 with BRCA2-associated factor 35." Biochemical Journal 374, no. 2 (2003): 497–503. http://dx.doi.org/10.1042/bj20030452.

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A large portion of human kinesin superfamily protein member 4 (KIF4) is associated with the nuclear matrix during the interphase, while a small portion is found in the cytoplasm. During mitosis, it is associated with chromosomes throughout the entire process. In the present study, we identified a protein that interacts with KIF4 using a yeast two-hybrid system, co-immunoprecipitation and co-fractionation. This protein is BRCA2-associated factor 35 (BRAF35) containing a non-specific DNA binding high-mobility-group domain and a kinesin-like coiled-coil domain. It appeared that the interaction be

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Hakimi, M. A., D. A. Bochar, J. Chenoweth, W. S. Lane, G. Mandel, and R. Shiekhattar. "A core-BRAF35 complex containing histone deacetylase mediates repression of neuronal-specific genes." Proceedings of the National Academy of Sciences 99, no. 11 (2002): 7420–25. http://dx.doi.org/10.1073/pnas.112008599.

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Zanchetta, Melania E., Luisa M. R. Napolitano, Danilo Maddalo, and Germana Meroni. "The E3 ubiquitin ligase MID1/TRIM18 promotes atypical ubiquitination of the BRCA2-associated factor 35, BRAF35." Biochimica et Biophysica Acta (BBA) - Molecular Cell Research 1864, no. 10 (2017): 1844–54. http://dx.doi.org/10.1016/j.bbamcr.2017.07.014.

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Ceballos-Chavez, M., S. Rivero, P. Garcia-Gutierrez, et al. "Control of neuronal differentiation by sumoylation of BRAF35, a subunit of the LSD1-CoREST histone demethylase complex." Proceedings of the National Academy of Sciences 109, no. 21 (2012): 8085–90. http://dx.doi.org/10.1073/pnas.1121522109.

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Lee, Belinda, Angelyn Anton, Margaret Lee, et al. "Examining progression-free survival in first- and second-line treatment for BRAF-mutant metastatic colorectal cancer (CRC)." Journal of Clinical Oncology 35, no. 4_suppl (2017): 728. http://dx.doi.org/10.1200/jco.2017.35.4_suppl.728.

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728 Background: BRAF mutated (BRAFm) CRC represents ~10% of all CRC and is associated with significantly poorer prognosis. However, responses to chemotherapy do still occur. Some data suggest that the poor prognosis associated with BRAFm CRC is dominated by substantially poorer second line PFS (PFS2), whereas first line PFS (PFS1) was similar for both BRAFm and BRAF wildtype (BRAFwt) CRC. Using a large multicenter dataset, our study aimed to examine PFS1 and PFS2 in BRAFm versus BRAFwt CRC. Methods: Prospectively collected data from the Treatment of Recurrent and Advanced Colorectal Cancer (TR

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Osterlund, Pia J., Emerik Osterlund, Aki Uutela, et al. "Resectability, conversion and resections rates, and outcomes in RAS&BRAF wildtype (wt), RAS mutant (mt) and BRAFmt metastatic colorectal cancer (mCRC) subgroups in the prospective Finnish RAXO-study." Journal of Clinical Oncology 39, no. 15_suppl (2021): 3532. http://dx.doi.org/10.1200/jco.2021.39.15_suppl.3532.

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3532 Background: Outcomes of metastasectomy varies with RAS and BRAF-status, but the effect on resectability, conversion and resection rates has not been extensively studied. Methods: The prospective Finnish RAXO study (NCT01531621) included 1086 patients 2011-2018 (Osterlund et al TLRHE 2021, Isoniemi et al BJS 2021) of which 906 were included in this secondary endpoint analysis. Excluded had missing KRAS/ NRAS/ BRAF-V600E test, were untreatable or had an atypical BRAF mutation. We studied repeated centralized resectability assessment, conversion and resectability rates in mCRC, and overall s

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Braithwaite, Matthew, Christopher Duane Nevala-Plagemann, Kelsey Baron, Benjamin Haaland, Lisa M. Pappas, and Ignacio Garrido-Laguna. "Real-world outcomes of patients with BRAF-mutated mCRC treated in the United States." Journal of Clinical Oncology 38, no. 15_suppl (2020): 4030. http://dx.doi.org/10.1200/jco.2020.38.15_suppl.4030.

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4030 Background: BRAF mutations portend a poor prognosis in metastatic colorectal cancer (mCRC). Recent trials have hypothesized that using more aggressive triplet-based chemotherapy regimens such as FOLFOXIRI in the frontline setting may improve outcomes in this patient population. In this study, we utilized real-world data to assess whether FOLFOXIRI is being used in the United States (US) and compared survival outcomes in BRAF mutated (BRAFmt) mCRC stratified by first line (1L) therapy. Methods: The nationwide Flatiron Health EHR-derived de-identified database was reviewed for patients diag

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Hernandez-Aya, Leonel Fernando, Matthew Burke, Jenna M. Collins, et al. "Real-world treatment patterns and clinical outcomes of advanced melanoma patients following disease progression on anti-PD-1-based therapy." Journal of Clinical Oncology 38, no. 15_suppl (2020): e22036-e22036. http://dx.doi.org/10.1200/jco.2020.38.15_suppl.e22036.

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e22036 Background: Despite the success of anti-programmed cell death-1 (PD-1) based therapies that prolong survival in advanced melanoma, some patients experience disease progression. Real-world treatment patterns and outcomes after progression on anti-PD-1 based regimens are unknown. Methods: Adults with advanced melanoma and a record of disease progression on anti-PD-1 treatment (alone or in combination) between 1 Sept 2014–31 Jan 2019 were selected from the Flatiron Health Oncology electronic medical record (EMR) database for this retrospective study. Index progression date was defined as a

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Trunk, Andrew, Matthew Braithwaite, Christopher Nevala-Plagemann, Lisa Pappas, Benjamin Haaland, and Ignacio Garrido-Laguna. "Real-World Outcomes of Patients With BRAF-Mutated Metastatic Colorectal Cancer Treated in the United States." Journal of the National Comprehensive Cancer Network 20, no. 2 (2022): 144–50. http://dx.doi.org/10.6004/jnccn.2021.7059.

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Background: BRAF mutations portend a poor prognosis in metastatic colorectal cancer (mCRC). Whether these patients may benefit from more aggressive frontline chemotherapy with a triplet regimen such as FOLFOXIRI remains unclear. We used real-world data from a cohort of patients in the United States to assess the BRAF testing rate, determine the prevalence of FOLFOXIRI use, and compare survival outcomes in mCRC, stratified by BRAF mutation status and first-line therapy. Methods: A nationwide electronic health record–derived deidentified database was reviewed for patients diagnosed with mCRC bet

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Nordstrom, Beth L., Melissa Hamilton, Jenna M. Collins, et al. "Treatment patterns and outcomes following disease progression on anti-PD-1 therapies for advanced melanoma." Future Oncology 18, no. 11 (2022): 1343–55. http://dx.doi.org/10.2217/fon-2021-0340.

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Background: Anti-PD-1-based therapies prolong survival in advanced melanoma, but disease progression is common. This study evaluated treatment patterns and overall survival (OS) after anti-PD-1 progression. Methods: Retrospective data from patients with advanced melanoma and progression on anti-PD-1 treatment between 2014 and 2019 were taken from Flatiron Health, which reflects largely community practice. Treatment patterns and OS were analyzed for BRAF mutant (mt) and wild-type (wt) subgroups; OS was also examined across all patients. Results: Progression following anti-PD-1 was recorded for

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Vergidis, Joanna, Richard John Klasa, Youwen Zhou, Elena Moon, Debbie Jepson, and Kerry J. Savage. "Outcome and prognostic factors in BRAF mutation positive metastatic melanoma treated with a BRAF inhibitor: A population-based study in British Columbia." Journal of Clinical Oncology 31, no. 15_suppl (2013): e20045-e20045. http://dx.doi.org/10.1200/jco.2013.31.15_suppl.e20045.

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e20045 Background: BRAF mutations are present in approximately 40-60% of cutaneous melanomas. The BRAF inhibitor vemurafenib has demonstrated dramatic anti-tumour activity in phase III trials in BRAF mutation positive (BRAFm) metastatic/unresectable melanoma; however, there is limited data outside of clinical trials. Methods: All patients > 18 years of age, PS 0-2, with metastatic/unresectable melanoma considered for treatment with vemurafenib in British Columbia between March 2011 to December 2012 were identified. CNS disease, if present, had to be radiographically stable/asymptomatic and

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Ma, Michelle W., Joshua Andrew Farhadian, Erica Brooke Friedman, et al. "MicroRNA alterations associated with BRAF status in melanoma." Journal of Clinical Oncology 30, no. 15_suppl (2012): 8565. http://dx.doi.org/10.1200/jco.2012.30.15_suppl.8565.

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8565 Background: We hypothesize that BRAF mutations result in microRNA (miRNA) alterations which contribute to orchestrating the mutant BRAF’s oncogenic effects in melanoma. Our study is the first to examine the association between the BRAF mutation status in primary melanomas and the expression of miRNAs that target known tumor suppressors. Methods: 84 prospectively accrued melanoma patients at New York University Langone Medical Center were studied. DNA and total RNA were extracted from consecutive sections of formalin-fixed paraffin-embedded primary tissues. BRAF mutation status was determi

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Karreth, Florian, Markus Reschke, Bjoern Chapuy, Margaret A. Shipp, Roberto Chiarle, and Pier Paolo Pandolfi. "The BRAF Pseudogene Is a Proto-Oncogenic Competitive Endogenous RNA." Blood 124, no. 21 (2014): 263. http://dx.doi.org/10.1182/blood.v124.21.263.263.

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Abstract Non-coding RNAs have long been viewed as non-functional genomic relicts of evolution, but recetn findings have implicated their importance in physiology and disease. Recently, in vitro experiments demonstrated that the pseudogenes of PTEN and KRAS operate as natural miRNA decoys (competitive endogenous RNAs or ceRNAs) that regulate the expression of their parental genes. However, in vivo evidence for a causal role of pseudogenes in cancer development is lacking. To investigate whether the BRAF pseudogene (BRAFps) possesses oncogenic properties we generated transgenic mice carrying a T

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Qiang, Ya-Wei, Shiqiao Ye, Yu Chen, et al. "Mutant KRAS and Brafs Upregulate Stress Granules and Mediate Drug Resistance, Which Can be Modulated By Cox2 Inhibition in Multiple Myeloma." Blood 132, Supplement 1 (2018): 3166. http://dx.doi.org/10.1182/blood-2018-99-117459.

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Abstract Introduction: Mutant RAS leads to activation of the RAS/RAF/MEK/ERK pathway in approximately 50% of multiple myeloma (MM). Stress granules (SGs) are non-membranous structures composed of translational mRNAs, ribosomal proteins, and RNA-binding proteins, which form in response to different stress stimuli and chemotherapeutic treatment. TheKRAS effector pathway mediates the upregulation of SGs conferring resistance to chemotherapeutic agents in solid tumors. However, it is unclear if SGs are upregulated in KRAS mutant MM and if this is associated with chemotherapeutic resistance. The pu

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Duggan, Megan C., Andrew R. Stiff, Maryam Bainazar, et al. "Identification of NRAS isoform 2 overexpression as a mechanism facilitating BRAF inhibitor resistance in malignant melanoma." Proceedings of the National Academy of Sciences 114, no. 36 (2017): 9629–34. http://dx.doi.org/10.1073/pnas.1704371114.

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Activating mutations in BRAF are found in 50% of melanomas and although treatment with BRAF inhibitors (BRAFi) is effective, resistance often develops. We now show that recently discovered NRAS isoform 2 is up-regulated in the setting of BRAF inhibitor resistance in melanoma, in both cell lines and patient tumor tissues. When isoform 2 was overexpressed in BRAF mutant melanoma cell lines, melanoma cell proliferation and in vivo tumor growth were significantly increased in the presence of BRAFi treatment. shRNA-mediated knockdown of isoform 2 in BRAFi resistant cells restored sensitivity to BRA

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Xu, Zhiyuan, Cheng-Chia Lee, Arjun Ramesh, et al. "BRAF V600E mutation and BRAF kinase inhibitors in conjunction with stereotactic radiosurgery for intracranial melanoma metastases." Journal of Neurosurgery 126, no. 3 (2017): 726–34. http://dx.doi.org/10.3171/2016.2.jns1633.

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OBJECTIVE Recent advancements in molecular biology have identified the BRAF mutation as a common mutation in melanoma. The wide use of BRAF kinase inhibitor (BRAFi) in patients with metastatic melanoma has been established. The objective of this study was to examine the impact of BRAF mutation status and use of BRAFi in conjunction with stereotactic radiosurgery (SRS). METHODS This was a single-center retrospective study. Patient's charts and electronic records were reviewed for date of diagnosis of primary malignancy, BRAF mutation status, chemotherapies used, date of the diagnosis of CNS met

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Cybulska-Stopa, Bozena, Anna Malgorzata Czarnecka, Krzysztof Ostaszewski, et al. "Is the BRAF mutation still an unfavorable risk factor in patients with metastatic melanoma in the era of modern therapies?" Journal of Clinical Oncology 40, no. 16_suppl (2022): e21544-e21544. http://dx.doi.org/10.1200/jco.2022.40.16_suppl.e21544.

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e21544 Background: BRAF-mutated (MUT) melanoma is characterized by specific clinical features including more aggressive biological behavior than BRAF wild-type (WT) melanoma. BRAF mutations are historically known as negative prognostic factor for to shorter overall survival (OS) in patients with stage IV disease with melanoma. Methods: Consecutive patients with unresectable or metastatic melanoma started treatment with BRAF inhibitors (BRAFi), BRAFi and MEK inhibitors (MEKi) or IT (anti-PD-1 antibody) between 1/Jan/2013 and 31/Dec/2020. Clinical factors including age, gender, primary location

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Cybulska-Stopa, Bozena, Anna Malgorzata Czarnecka, Krzysztof Ostaszewski, et al. "Is the BRAF mutation still an unfavorable risk factor in patients with metastatic melanoma in the era of modern therapies?" Journal of Clinical Oncology 40, no. 16_suppl (2022): e21544-e21544. http://dx.doi.org/10.1200/jco.2022.40.16_suppl.e21544.

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e21544 Background: BRAF-mutated (MUT) melanoma is characterized by specific clinical features including more aggressive biological behavior than BRAF wild-type (WT) melanoma. BRAF mutations are historically known as negative prognostic factor for to shorter overall survival (OS) in patients with stage IV disease with melanoma. Methods: Consecutive patients with unresectable or metastatic melanoma started treatment with BRAF inhibitors (BRAFi), BRAFi and MEK inhibitors (MEKi) or IT (anti-PD-1 antibody) between 1/Jan/2013 and 31/Dec/2020. Clinical factors including age, gender, primary location

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Park, Jongwhi, Hope Lancero, Emon Nasajpour, et al. "STEM-15. THERAPY-INDUCED CHANGES BY BRAF AND MEK INHIBITORS IN BRAF V600E-MUTATED GLIOMA MODELS PROVIDE POTENTIAL NOVEL THERAPEUTIC OPPORTUNITIES." Neuro-Oncology 24, Supplement_7 (2022): vii34. http://dx.doi.org/10.1093/neuonc/noac209.132.

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Abstract Combinations of the MEK inhibitor trametinib, and BRAF inhibitor dabrafenib (BRAFi+MEKi) show rapid and sustained responses in patients with BRAF V600E-mutated low-grade glioma, but tumor rebound after treatment discontinuation is frequent. Moreover, a lack of response is common in patient with high-grade glioma raising the need for further research into BRAFi+MEKi effects on tumors. We showed previously that BRAF V600E-mutated glioma cells positive for CD133 (Prominin-1), a marker of brain tumor stem cells, show decreased sensitivity to BRAFi, indicative of their role in promoting th

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Wichmann, Jürgen, Caroline Rynn, Thomas Friess, et al. "Preclinical Characterization of a Next-Generation Brain Permeable, Paradox Breaker BRAF Inhibitor." Clinical Cancer Research 28, no. 4 (2021): 770–80. http://dx.doi.org/10.1158/1078-0432.ccr-21-2761.

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Abstract Purpose: Disease progression in BRAF V600E/K positive melanomas to approved BRAF/MEK inhibitor therapies is associated with the development of resistance mediated by RAF dimer inducing mechanisms. Moreover, progressing disease after BRAFi/MEKi frequently involves brain metastasis. Here we present the development of a novel BRAF inhibitor (Compound Ia) designed to address the limitations of available BRAFi/MEKi. Experimental Design: The novel, brain penetrant, paradox breaker BRAFi is comprehensively characterized in vitro, ex vivo, and in several preclinical in vivo models of melanoma

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Gebhardt, Kathleen, Bayram Edemir, Elisabeth Groß, et al. "BRAF/EZH2 Signaling Represses miR-129-5p Inhibition of SOX4 Thereby Modulating BRAFi Resistance in Melanoma." Cancers 13, no. 10 (2021): 2393. http://dx.doi.org/10.3390/cancers13102393.

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Many melanomas are associated with activating BRAF mutation. Targeted therapies by inhibitors of BRAF and MEK (BRAFi, MEKi) show marked antitumor response, but become limited by drug resistance. The mechanisms for this are not fully revealed, but include miRNA. Wishing to improve efficacy of BRAFi and knowing that certain miRNAs are linked to resistance to BRAFi, we wanted to focus on miRNAs exclusively associated with response to BRAFi. We found increased expression of miR-129-5p during BRAFi treatment of BRAF- mutant melanoma cells. Parallel to emergence of resistance we observed mir-129-5p

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Tanaka, Yuka, Maho Murata, Che-Hung Shen, Masutaka Furue, and Takamichi Ito. "NECTIN4: A Novel Therapeutic Target for Melanoma." International Journal of Molecular Sciences 22, no. 2 (2021): 976. http://dx.doi.org/10.3390/ijms22020976.

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Malignant melanoma is the most common lethal skin cancer and causes death in a short time when metastasized. Although BRAF inhibitors (BRAFi) have greatly improved the prognosis of BRAF-mutated melanoma, drug resistance is a major concern even when they are combined with MEK inhibitors. Alternative treatments for BRAFi-resistant melanoma are highly anticipated. Nectin cell adhesion molecule 4 (NECTIN4) is highly expressed and associated with progression in tumors. We aimed to investigate the role of NECTIN4 in melanoma and its potency as a therapeutic target using 126 melanoma samples and BRAF

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Menzer, Christian, Alexander M. Menzies, Matteo S. Carlino, et al. "Targeted Therapy in Advanced Melanoma With Rare BRAF Mutations." Journal of Clinical Oncology 37, no. 33 (2019): 3142–51. http://dx.doi.org/10.1200/jco.19.00489.

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PURPOSE BRAF/MEK inhibition is a standard of care for patients with BRAF V600E/K–mutated metastatic melanoma. For patients with less frequent BRAF mutations, however, efficacy data are limited. METHODS In the current study, 103 patients with metastatic melanoma with rare, activating non-V600E/K BRAF mutations that were treated with either a BRAF inhibitor (BRAFi), MEK inhibitor (MEKi), or the combination were included. BRAF mutation, patient and disease characteristics, response, and survival data were analyzed. RESULTS Fifty-eight patient tumors (56%) harbored a non-E/K V600 mutation, 38 (37%

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Goldinger, Simone M., Carla Murer, Pascale Stieger, and Reinhard Dummer. "Upstream MAPK pathway inhibition: MEK inhibitor followed by a BRAF inhibitor in advanced melanoma patients." Journal of Clinical Oncology 31, no. 15_suppl (2013): 9071. http://dx.doi.org/10.1200/jco.2013.31.15_suppl.9071.

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9071 Background: The presence of activating BRAF mutations in about 60% of all metastatic melanomas (mM) has led to the development of inhibitors (i) targeting the RAF and MEK kinases. MEK is the downstream effector of BRAF. However, the blockage of the MAPK pathway is limited due to the development of resistance mechanisms. MEK resistance can confer cross-resistance to BRAF inhibition, whereas BRAF resistance is independent from the MAPK pathway. Hence, it seems reasonable to start a MAPK pathway inhibition by a BRAFi. An upstream inhibition beginning the treatment reversed with a MEKi follow

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Pelster, Meredith S., and Rodabe N. Amaria. "Combined targeted therapy and immunotherapy in melanoma: a review of the impact on the tumor microenvironment and outcomes of early clinical trials." Therapeutic Advances in Medical Oncology 11 (January 2019): 175883591983082. http://dx.doi.org/10.1177/1758835919830826.

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The development of BRAF and MEK inhibitors (BRAFis and MEKis) and immune checkpoint inhibitors have changed the management of advanced stage melanoma and improved the outcomes of patients with this malignancy. However, both therapeutic approaches have limitations, including a limited duration of benefit in subsets of BRAF-mutant melanoma patients treated with targeted therapy and a lower overall response rate without a clear predictive biomarker in patients treated with checkpoint inhibitors. Preclinical and translational data have shown that BRAFis and MEKis alter the tumor microenvironment t

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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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Hicks, Hannah M., Veronica L. Espinoza, Sharon B. Sams, Nikita Pozdeyev, and Rebecca E. Schweppe. "Abstract 2434: The role of a more invasive phenotype in response to MAPK-directed therapies in thyroid cancer." Cancer Research 82, no. 12_Supplement (2022): 2434. http://dx.doi.org/10.1158/1538-7445.am2022-2434.

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Abstract Advanced papillary thyroid cancer (PTC) and anaplastic thyroid cancer (ATC) are the leading causes of endocrine cancer death. Mutations in the MAP kinase (MAPK) pathway are common in PTC and ATC, especially in BRAF, with a prevalence of 40-60%. Despite the importance of the MAPK pathway in thyroid cancer, therapies targeting this pathway are not approved for BRAF-mutant PTC patients. While the combination of BRAF and MEK inhibition is approved for patients with BRAF-mutant ATC, these patients often progress. An emerging mechanism of resistance to targeted therapies is an invasive phen

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Kefford, Richard, Wilson H. Miller, Daniel Shao-Weng Tan, et al. "Preliminary results from a phase Ib/II, open-label, dose-escalation study of the oral BRAF inhibitor LGX818 in combination with the oral MEK1/2 inhibitor MEK162 in BRAF V600-dependent advanced solid tumors." Journal of Clinical Oncology 31, no. 15_suppl (2013): 9029. http://dx.doi.org/10.1200/jco.2013.31.15_suppl.9029.

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9029 Background: Clinical data indicate that combining a BRAF and a MEK inhibitor (BRAFi, MEKi) may be more effective than BRAFi monotherapy in BRAF-mutant metastatic melanoma and that a MEKi may overcome or delay resistance to a BRAFi. Methods: This ongoing phase 1b/2 study is evaluating the combination of LGX818, a potent, selective BRAF inhibitor, and MEK162, a selective MEK1/2 inhibitor, in BRAFi-naive and -pretreated patients with BRAF-mutant tumors. The objective of the phase 1b part is to determine the maximum tolerated dose and/or recommended phase 2 dose (RP2D) for oral, daily LGX818

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Rossi, Ernesto, Giovanni Schinzari, Francesco Cellini, et al. "Dabrafenib-Trametinib and Radiotherapy for Oligoprogressive BRAF Mutant Advanced Melanoma." Biomedicines 11, no. 2 (2023): 394. http://dx.doi.org/10.3390/biomedicines11020394.

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The clinical management of metastatic melanoma has been changed by BRAF (BRAFi) and MEK inhibitors (MEKi), which represent a standard treatment for BRAF-mutant melanoma. In oligoprogressive melanoma patients with BRAF mutations, target therapy can be combined with loco-regional radiotherapy (RT). However, the association of BRAF/MEK inhibitors and RT needs to be carefully monitored for potential increased toxicity. Despite the availability of some reports regarding the tolerability of RT + target therapy, data on simultaneous RT and BRAFi/MEKi are limited and mostly focused on the BRAFi vemura

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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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Muldoon, Daniel, Guisheng Zhao, Carly Batt, Mallika Singh, and Theodore Nicolaides. "MODL-17. SHP2 INHIBITORS SHOW ACTIVITY AGAINST NF1-DEFICIENT GLIOMAS AND ENHANCE MAPK PATHWAY INHIBITION IN BRAF-V600E MUTANT GLIOMAS." Neuro-Oncology 22, Supplement_3 (2020): iii414. http://dx.doi.org/10.1093/neuonc/noaa222.591.

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Abstract INTRODUCTION Activation of the RAS-MAPK signaling cascade is common in pediatric gliomas. Based on the role of SHP2 in RAS pathway signaling, we hypothesized that NF1-deficient pediatric glioma models would respond to SHP2 inhibitor monotherapy whereas BRAF-V600E gliomas would not. However, we postulated that the latter would exhibit increased sensitivity to a BRAF inhibitor (BRAFi) in combination with SHP2i. Here we demonstrate that the SHP2 inhibitors SHP099 and RMC-4550 (SHP2i) show significant single-agent activity in vitro against NF1-deficient glioma cells and that the combinati

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Madej, Ewelina, Anna A. Brożyna, Agnieszka Adamczyk, et al. "Vemurafenib and Dabrafenib Downregulates RIPK4 Level." Cancers 15, no. 3 (2023): 918. http://dx.doi.org/10.3390/cancers15030918.

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Vemurafenib and dabrafenib are BRAF kinase inhibitors (BRAFi) used for the treatment of patients with melanoma carrying the V600E BRAF mutation. However, melanoma cells develop resistance to both drugs when used as monotherapy. Therefore, mechanisms of drug resistance are investigated, and new molecular targets are sought that could completely inhibit melanoma progression. Since receptor-interacting protein kinase (RIPK4) probably functions as an oncogene in melanoma and its structure is similar to the BRAF protein, we analyzed the impact of vemurafenib and dabrafenib on RIPK4 in melanomas. Th

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Uebel, Anne, Stefanie Kewitz-Hempel, Edith Willscher, Kathleen Gebhardt, Cord Sunderkötter, and Dennis Gerloff. "Resistance to BRAF Inhibitors: EZH2 and Its Downstream Targets as Potential Therapeutic Options in Melanoma." International Journal of Molecular Sciences 24, no. 3 (2023): 1963. http://dx.doi.org/10.3390/ijms24031963.

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Activating BRAF mutations occurs in 50–60% of malignant melanomas. Although initially treatable, the development of resistance to BRAF-targeted therapies (BRAFi) is a major challenge and limits their efficacy. We have previously shown that the BRAFV600E signaling pathway mediates the expression of EZH2, an epigenetic regulator related to melanoma progression and worse overall survival. Therefore, we wondered whether inhibition of EZH2 would be a way to overcome resistance to vemurafenib. We found that the addition of an EZH2 inhibitor to vemurafenib improved the response of melanoma cells resi

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Schreck, Karisa, Andrew Morin, Guisheng Zhao, et al. "DDRE-13. DECONVOLUTING MECHANISMS OF RESISTANCE TO BRAF INHIBITORS IN BRAF V600E HUMAN GLIOMA." Neuro-Oncology 22, Supplement_2 (2020): ii64. http://dx.doi.org/10.1093/neuonc/noaa215.258.

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Abstract BACKGROUND While BRAF-targeted therapy can be effective in a subset of patients with glioma, resistance to treatment can emerge over time. The description and validation of mechanisms of resistance in BRAF-mutant glioma are not previously described. METHODS Pre- and post- BRAF inhibitor (BRAFi) or BRAFi/MEK inhibitor (MEKi) treated patient samples were obtained under IRB-approved protocols at University of Colorado Denver, UCSF, and Johns Hopkins. Targeted DNA sequencing or whole exome sequencing (WES), and RNA-seq were conducted on paired samples. Functional validation of putative re

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Romano, David, Lucía García-Gutiérrez, Nourhan Aboud, et al. "Proteasomal down-regulation of the proapoptotic MST2 pathway contributes to BRAF inhibitor resistance in melanoma." Life Science Alliance 5, no. 10 (2022): e202201445. http://dx.doi.org/10.26508/lsa.202201445.

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The RAS-RAF-MEK-ERK pathway is hyperactivated in most malignant melanomas, and mutations in BRAF or NRAS account for most of these cases. BRAF inhibitors (BRAFi) are highly efficient for treating patients with BRAFV600E mutations, but tumours frequently acquire resistance within a few months. Multiple resistance mechanisms have been identified, due to mutations or network adaptations that revive ERK signalling. We have previously shown that RAF proteins inhibit the MST2 proapoptotic pathway in a kinase-independent fashion. Here, we have investigated the role of the MST2 pathway in mediating re

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Thompson, Elizabeth L., Jiayi J. Hu, and Laura J. Niedernhofer. "The Role of Senescent Cells in Acquired Drug Resistance and Secondary Cancer in BRAFi-Treated Melanoma." Cancers 13, no. 9 (2021): 2241. http://dx.doi.org/10.3390/cancers13092241.

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BRAF is the most common gene mutated in malignant melanoma, and predominately it is a missense mutation of codon 600 in the kinase domain. This oncogenic BRAF missense mutation results in constitutive activation of the mitogen-activate protein kinase (MAPK) pro-survival pathway. Several BRAF inhibitors (BRAFi) have been developed to specifically inhibit BRAFV600 mutations that improve melanoma survival, but resistance and secondary cancer often occur. Causal mechanisms of BRAFi-induced secondary cancer and resistance have been identified through upregulation of MAPK and alternate pro-survival

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Wattson, Daniel A., Helen Alice Shih, Andrzej Niemierko, et al. "Survival patterns following brain metastases for patients with melanoma in the targeted therapy era." Journal of Clinical Oncology 31, no. 15_suppl (2013): 9064. http://dx.doi.org/10.1200/jco.2013.31.15_suppl.9064.

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9064 Background: Survival from metastatic melanoma (MM) has been significantly prolonged with the introduction of molecularly targeted therapy, including BRAF inhibitors (BRAFi) for patients (pts) with the V600E mutation. Here, we present the first data describing patterns of survival after diagnosis of brain metastases (BM) in a large cohort of these pts with long follow-up. Methods: A retrospective review of 191 MM pts accrued on multiple prospective trials between 2008–2012 was conducted. These trials assessed novel immunologic and targeted therapies in pts with both BRAF mutant (n=70) and

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Čepulytė, Rūta, Andrius Žučenka, and Valdas Pečeliūnas. "Combination of Dabrafenib and Trametinib for the Treatment of Relapsed and Refractory Multiple Myeloma Harboring BRAF V600E Mutation." Case Reports in Hematology 2020 (October 15, 2020): 1–5. http://dx.doi.org/10.1155/2020/8894031.

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Multiple myeloma (MM) is an incurable plasma cell neoplasia characterized by relapsed and/or refractory (R/R) disease course, which poses a major therapeutic challenge. New therapies, including BRAF V600E mutation targeting, may become a new treatment option for R/R MM. In combination with mitogen-activated protein kinase inhibitors (MEKi), BRAF inhibitors (BRAFi) could provide better tailored clinical management, although experience in this field is lacking. To this date, there is only one case describing R/R MM treatment with BRAFi vemurafenib and MEKi cobimetinib. This is the first case pre

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Park, Robin, Laércio Lopes da Silva, Sunggon Lee, and Anwaar Saeed. "Impact of BRAF mutations on prognosis and immunotherapy response in microsatellite instability/mismatch repair deficient metastatic colorectal cancer: A systematic review and meta-analysis." Journal of Clinical Oncology 39, no. 15_suppl (2021): 3557. http://dx.doi.org/10.1200/jco.2021.39.15_suppl.3557.

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3557 Background: Mismatch repair deficient/microsatellite instability high (dMMR/MSI-H) colorectal cancer (CRC) defines a molecular subtype with distinct clinicopathologic characteristics including an excellent response to immunotherapy. Although BRAF mutations are established as a negative prognostic marker in CRC, whether they retain their negative prognostic impact in or alter the response to immunotherapy in dMMR/MSI-H CRC remains unknown. Herein, we present a systematic review and meta-analysis of the impact of BRAF mutations on the overall survival (OS) and immune checkpoint inhibitor (I

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Röck, Ruth, Johanna E. Mayrhofer, Omar Torres-Quesada, et al. "BRAF inhibitors promote intermediate BRAF(V600E) conformations and binary interactions with activated RAS." Science Advances 5, no. 8 (2019): eaav8463. http://dx.doi.org/10.1126/sciadv.aav8463.

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Oncogenic BRAF mutations initiate tumor formation by unleashing the autoinhibited kinase conformation and promoting RAS-decoupled proliferative RAF-MEK-ERK signaling. We have engineered luciferase-based biosensors to systematically track full-length BRAF conformations and interactions affected by tumorigenic kinase mutations and GTP loading of RAS. Binding of structurally diverse αC-helix-OUT BRAF inhibitors (BRAFi) showed differences in specificity and efficacy by shifting patient mutation–containing BRAF reporters from the definitive opened to more closed conformations. Unexpectedly, BRAFi e

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Kotecha, Rupesh, Jacob A. Miller, Vyshak A. Venur, et al. "Melanoma brain metastasis: the impact of stereotactic radiosurgery, BRAF mutational status, and targeted and/or immune-based therapies on treatment outcome." Journal of Neurosurgery 129, no. 1 (2018): 50–59. http://dx.doi.org/10.3171/2017.1.jns162797.

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OBJECTIVEThe goal of this study was to investigate the impact of stereotactic radiosurgery (SRS), BRAF status, and targeted and immune-based therapies on the recurrence patterns and factors associated with overall survival (OS) among patients with melanoma brain metastasis (MBM).METHODSA total of 366 patients were treated for 1336 MBMs; a lesion-based analysis was performed on 793 SRS lesions. The BRAF status was available for 78 patients: 35 had BRAFmut and 43 had BRAF wild-type (BRAF-WT) lesions. The Kaplan-Meier method evaluated unadjusted OS; cumulative incidence analysis determined the in

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Leclair, Héloïse M., Nina Tardif, Anaïs Paris, Marie-Dominique Galibert, and Sébastien Corre. "Role of Flavonoids in the Prevention of AhR-Dependent Resistance During Treatment with BRAF Inhibitors." International Journal of Molecular Sciences 21, no. 14 (2020): 5025. http://dx.doi.org/10.3390/ijms21145025.

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BRAF and MEK inhibitors (BRAFi and MEKi) are the standard of care for the treatment of metastatic melanoma in patients with BRAFV600E mutations, greatly improving progression-free survival. However, the acquisition of resistance to BRAFi and MEKi remains a difficult clinical challenge, with limited therapeutic options available for these patients. Here, we investigated the therapeutic potential of natural flavonoids as specific AhR (Aryl hydrocarbon Receptor) transcription factor antagonists in combination with BRAFi. Experimental Design: Experiments were performed in vitro and in vivo with va

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Dummer, Reinhard, Caroline Robert, Marta Nyakas, et al. "Initial results from a phase I, open-label, dose escalation study of the oral BRAF inhibitor LGX818 in patients with BRAF V600 mutant advanced or metastatic melanoma." Journal of Clinical Oncology 31, no. 15_suppl (2013): 9028. http://dx.doi.org/10.1200/jco.2013.31.15_suppl.9028.

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9028 Background: LGX818, a potent and selective BRAF inhibitor (BRAFi) being investigated in BRAF V600 mutant melanoma, has unique biochemical properties with a dissociation half-time > 10 times longer than other BRAF inhibitors. Methods: A phase I trial of LGX818 administered orally once (qd) or twice (bid) daily in BRAF V600 tumors was initiated to define the maximum tolerated dose (MTD)/recommended phase II dose (RP2D) and to assess pharmacokinetics and clinical activity in BRAFi–naive or pretreated patients with BRAF V600 mutant advanced melanoma. Baseline assessment of biomarkers from

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Haselmann, Verena, Christoffer Gebhardt, Ingrid Brechtel, et al. "Liquid Profiling of Circulating Tumor DNA in Plasma of Melanoma Patients for Companion Diagnostics and Monitoring of BRAF Inhibitor Therapy." Clinical Chemistry 64, no. 5 (2018): 830–42. http://dx.doi.org/10.1373/clinchem.2017.281543.

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Abstract BACKGROUND The current standard for determining eligibility of patients with metastatic melanoma for BRAF-targeted therapy is tissue-based testing of BRAF mutations. As patients are rarely rebiopsied, detection in blood might be advantageous by enabling a comprehensive assessment of tumor mutational status in real time and thereby representing a noninvasive biomarker for monitoring BRAF therapy. METHODS In all, 634 stage I to IV melanoma patients were enrolled at 2 centers, and 1406 plasma samples were prospectively collected. Patients were assigned to 3 separate study cohorts: study

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Huynh, Sandra, Laurent Mortier, Caroline Dutriaux, et al. "Combined Therapy with Anti-PD1 and BRAF and/or MEK Inhibitor for Advanced Melanoma: A Multicenter Cohort Study." Cancers 12, no. 6 (2020): 1666. http://dx.doi.org/10.3390/cancers12061666.

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Despite significant progress in melanoma survival, therapeutic options are still needed in case of progression under immune checkpoint inhibitors (ICI), and resistance to targeted therapies (TT) in BRAF-mutated melanomas. This study aimed to assess the safety of combined ICI and TT as a rescue line in real-life clinical practice. We conducted a study within the prospective French multicentric MelBase cohort, including patients treated with a combination of anti-PD1 (pembrolizumab/nivolumab) and BRAF inhibitor (BRAFi: dabrafenib/vemurafenib) and/or MEK inhibitors (MEKi: trametinib/cobimetinib)

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Switzer, Benjamin, Sabah Alaklabi, Arya Mariam Roy, et al. "Toxicity and outcomes of BRAF and MEK inhibitor “ramp-up” dosing strategies for patients with melanoma: A real-world institutional experience." Journal of Clinical Oncology 40, no. 16_suppl (2022): e21600-e21600. http://dx.doi.org/10.1200/jco.2022.40.16_suppl.e21600.

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e21600 Background: Combination BRAF inhibitor (BRAFi) and MEK inhibitor (MEKi) therapy is a widely accepted treatment option for patients (pts) with BRAF-V600E mutant melanoma. Although effective, these combinations exhibit high rates of adverse events (AEs), with 44% - 66% requiring dose modification or interruption and up to 26% discontinuing due to AEs in the adjuvant setting. Enhanced tolerance to BRAFi/MEKi is expected to improve pts quality of life and potentially enhance clinical outcomes. Clinicians at Roswell Park Comprehensive Cancer Center (RPCCC) have implemented a dose escalation

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San Lucas, F. Anthony, Scott Kopetz, Paul A. Scheet, and Eduardo Vilar Sanchez. "Discovering new targeted therapies for BRAF mutant-like colorectal cancers." Journal of Clinical Oncology 31, no. 15_suppl (2013): 3623. http://dx.doi.org/10.1200/jco.2013.31.15_suppl.3623.

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3623 Background: Approximately 10% of colorectal cancers (CRCs) harbor a BRAF mutation (BRAFm). Patients with BRAFm tumors have poor prognosis and are a therapeutic challenge. A BRAFm gene expression signature has been communicated (Popovici et al, JCO 2012), which can identify BRAFm tumors as well as BRAF wild-type tumors that display a similar expression pattern. Collectively, these tumors are termed BRAFm-like. Our goal was to validate this signature using next-generation sequencing and to discover novel therapies for BRAFm-like CRCs using a systems biology approach. Methods: We developed a

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Póvoa, Antónia Afonso, Elisabete Teixeira, Maria Rosa Bella-Cueto, et al. "Genetic Determinants for Prediction of Outcome of Patients with Papillary Thyroid Carcinoma." Cancers 13, no. 9 (2021): 2048. http://dx.doi.org/10.3390/cancers13092048.

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Papillary thyroid carcinoma (PTC) usually presents an excellent prognosis, but some patients present with aggressive metastatic disease. BRAF, RAS, and TERT promoter (TERTp) genes are altered in PTC, and their impact on patient outcomes remains controversial. We aimed to determine the role of genetic alterations in PTC patient outcomes (recurrent/persistent disease, structural disease, and disease-specific mortality (DSM)). The series included 241 PTC patients submitted to surgery, between 2002–2015, in a single hospital. DNA was extracted from tissue samples of 287 lesions (primary tumors and

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Weber, Jeffrey S., Keith T. Flaherty, Jeffrey R. Infante, et al. "Updated safety and efficacy results from a phase I/II study of the oral BRAF inhibitor dabrafenib (GSK2118436) combined with the oral MEK 1/2 inhibitor trametinib (GSK1120212) in patients with BRAFi-naive metastatic melanoma." Journal of Clinical Oncology 30, no. 15_suppl (2012): 8510. http://dx.doi.org/10.1200/jco.2012.30.15_suppl.8510.

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8510 Background: In preclinical models, the BRAFi/MEKi combination has demonstrated enhanced activity against BRAF-mutant cancer cells compared with either drug alone, delayed emergence of BRAFi resistance, and prevented BRAFi-related proliferative skin lesions. A 3-part study investigating the dabrafenib/trametinib combination was conducted in patients (pts) with V600 BRAF mutant solid tumors. Interim data from the study were previously reported (Infante, ASCO 2011); updated safety and efficacy data are presented. Methods: In Part 2, 125 pts with V600 BRAF mutant solid tumors enrolled, includ

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