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Journal articles on the topic 'V600 type mutation'

Author: Grafiati

Published: 24 April 2022

Last updated: 30 July 2025

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1

Moon, J. J. "Novel Approach for Detection of BRAF and KRAS Mutations Using ARMS (amplification refractory mutation system) Primers for Colon Cancer Therapeutic Response Prediction." American Journal of Clinical Pathology 162, Supplement_1 (2024): S130—S131. http://dx.doi.org/10.1093/ajcp/aqae129.289.

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Abstract Introduction/Objective KRAS and BRAF V600E mutations are confirmed predictive biomarkers for anti-EGFR monoclonal antibody therapy response and prognosis for colorectal cancer and often considered mutually exclusive with few exceptions (0.05% of mCRC cases). We have developed a multiplex PCR assay utilizing ARMS (amplification refractory mutation system) Primers and Probes for screening and further testing of BRAF mutation status in a 2 step process. Methods/Case Report The Multiplex PCR Assay or BRAF/KRAS mutation was designed as a 5 color assay. Primers and Probes consisted of Wild

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Rojo, Federico, Trinidad Caldes, Sandra Zazo, et al. "Prevalence of low-penetrance KRAS (codons 12/13 and 61) and BRAF mutations in metastatic colorectal carcinoma." Journal of Clinical Oncology 30, no. 15_suppl (2012): e14147-e14147. http://dx.doi.org/10.1200/jco.2012.30.15_suppl.e14147.

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e14147 Background: In patients with metastatic colorectal cancer (mCRC), activating mutations within KRAS, which result in EGFR-independent intracellular signal transduction activation, are found in approximately 35-40% of patients with mCRC have been significantly associated with lack of response to cetuximab or panitumumab therapy. Although current guidelines recommend testing for frequent KRAS codons 12/13 mutations, emerging data indicate that additional KRAS and BRAF mutations are also predictive of non-responsiveness to anti-EGFR antibodies in mCRC. This study is aimed to analyze the pre

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Fülöp, László, Katalin Götzer, Erzsébet Csernák, Danyil Szergejevics Kuznyecov, and Erika Tóth. "Rapid BRAF mutation detection in melanoma patients by immunohistochemistry." Journal of Universal Science Online 4, no. 1 (2017): 1–5. http://dx.doi.org/10.17202/juso.2017.4.1.

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The V600E mutation is the most common (~90%) activating mutation of the BRAF gene. BRAF mutations have been frequently investigated in melanoma, colorectal cancer and papillary thyroid carcinoma. The importance of the detection of BRAF mutations has been rising by the routine use of Braf inhibitor therapy. We evaluated the usefulness of the BRAF V600E mutation-specific monoclonal antibody (VE1) in metastatic melanoma patients. To confirm the results of immunohistochemistry (IHC), we used COBAS 4800 BRAF V600 mutation test and PCR amplification followed by Sanger sequencing.36 of 105 patients h

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Erika, Pino, Benítez Claudia, Aristizábal Clara, et al. "Frequency of BRAF V600E/E2/D and V600K/R/M mutations in patients with malignant melanoma unresectable stage III-IIIC–IV from May to August-2021 at Unigem in Medellin." International Journal of Molecular Biology Open Access 6, no. 1 (2023): 8–12. http://dx.doi.org/10.15406/ijmboa.2023.06.00146.

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Background: Melanoma is the most aggressive skin cancer type and is responsible for 80% of deaths from this entity. It is considered one of the tumors with the highest mutational load, with approximately 50% of cases in codon 600 of the BRAF gene. Objective: To determine the frequency of BRAF V600E/E2/D and BRAF V600K/R/M mutations in patients with malignant melanoma unresectable stage III-IIIC – IV, during the period May-2018 and August-2021, at UNIGEM, in Medellín. Methodology: Observational, retrospective study, which included 154 paraffin-embedded biopsies from patients with stage III-IIIC

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Jones, Jeremy C., Lindsay A. Renfro, Humaid O. Al-Shamsi, et al. "Non-V600BRAF Mutations Define a Clinically Distinct Molecular Subtype of Metastatic Colorectal Cancer." Journal of Clinical Oncology 35, no. 23 (2017): 2624–30. http://dx.doi.org/10.1200/jco.2016.71.4394.

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Purpose Molecular diagnostic testing has become an integral part of the evaluation of patients with metastatic colorectal cancer (CRC). Expanded mutational testing, such as next-generation sequencing (NGS), often identifies mutations with unclear clinical or prognostic implications. One such example is BRAF mutations that occur outside of codon 600 (non-V600 BRAF mutations). Methods We conducted this multicenter, retrospective cohort study to characterize the clinical, pathologic, and survival implications of non-V600 BRAF mutations in metastatic CRC. We pooled patients in whom non-V600 BRAF m

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Huang, Helen J., Benoit Devogelaere, Gerald Steven Falchook, et al. "BRAF mutation testing with a novel, rapid, fully automated molecular diagnostics prototype platform." Journal of Clinical Oncology 31, no. 15_suppl (2013): 11086. http://dx.doi.org/10.1200/jco.2013.31.15_suppl.11086.

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11086 Background: Mutations in the BRAF gene provide actionable targets for cancer therapy in melanoma and other tumor types. Novel, fast, and accurate diagnostic systems are needed for further implementation of personalized therapy. Methods: The molecular diagnostics (MDx) prototype platform (Biocartis, Mechelen, Belgium) is a fully integrated real-time PCR-based system with high sensitivity (1% mutant in wild-type [wt] background) and fast turnaround time (< 90 minutes), which requires no sample preparation and <2 min hands-on time. Archival formalin-fixed paraffin-embedded tumor sampl

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Karbel, Hadeel Abdul Elah, Sura Salman Ejam, and Ali Zaki Naji. "Immunohistochemical Study Using Monoclonal VE1 Antibody Can Substitute the Molecular Tests for Apprehension of BRAF V600E Mutation in Patients with Non-small-Cell Lung Carcinoma." Analytical Cellular Pathology 2019 (November 5, 2019): 1–6. http://dx.doi.org/10.1155/2019/2315673.

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In patients with non-small-cell lung carcinoma (NSCLC), the analysis of BRAF V600E mutation has become more and more applied since the introduction of many mutation-targeted medications. In this regard, the advantage of immunohistochemistry (IHC) as a reliable diagnostic test substitute to other molecular studies has not been approved yet. Objective. To examine the dependability of using immunohistochemical method utilizing monoclonal VE1 antibody in the detection of BRAF V600 E mutation in patients with non-small-cell lung carcinoma and compare the results there with that of polymerase chain

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Mukonoweshuro, Chantel L., Emmanuelle Rousselle, and April A. Rose. "Abstract 5063: Exploring the mutational landscape of KRAS and NRAS in tumors with non-V600 BRAF mutations." Cancer Research 84, no. 6_Supplement (2024): 5063. http://dx.doi.org/10.1158/1538-7445.am2024-5063.

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Abstract Background: BRAF, a key modulator of the Mitogen-Activated Protein Kinase (MAPK) pathway, is observed in 7% of all cancers. Therapeutic response to MAPK inhibition (MAPKi) often relies on molecular distinctions between members of varying classes: Class 1 (V600), Class 2 and 3 (non-V600) BRAF mutants. Preliminary data indicates that co-occurring RAS mutations in non-V600 BRAF mutant cancers are less responsive to MAPKi treatment. This emphasizes the need to investigate the characteristics of RAS co-mutations in non-V600 BRAF mutant tumors. Methods: Genomic data was obtained from a coho

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Anderson, Steven, Kenneth J. Bloom, Dino U. Vallera, et al. "Multisite Analytic Performance Studies of a Real-Time Polymerase Chain Reaction Assay for the Detection of BRAF V600E Mutations in Formalin-Fixed, Paraffin-Embedded Tissue Specimens of Malignant Melanoma." Archives of Pathology & Laboratory Medicine 136, no. 11 (2012): 1385–91. http://dx.doi.org/10.5858/arpa.2011-0505-oa.

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Context.—A polymerase chain reaction–based companion diagnostic (cobas 4800 BRAF V600 Mutation Test) was recently approved by the US Food and Drug Administration to select patients with BRAF-mutant metastatic melanoma for treatment with the BRAF inhibitor vemurafenib. Objectives.—(1) To compare the analytic performance of the cobas test to Sanger sequencing by using screening specimens from phase II and phase III trials of vemurafenib, and (2) to assess the reproducibility of the cobas test at different testing sites. Design.—Specimens from 477 patients were used to determine positive and nega

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Kazandjian, Suzanne, Emmanuelle Rousselle, Matthew Dankner, et al. "The Clinical, Genomic, and Transcriptomic Landscape of BRAF Mutant Cancers." Cancers 16, no. 2 (2024): 445. http://dx.doi.org/10.3390/cancers16020445.

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Background: BRAF mutations are classified into four molecularly distinct groups, and Class 1 (V600) mutant tumors are treated with targeted therapies. Effective treatment has not been established for Class 2/3 or BRAF Fusions. We investigated whether BRAF mutation class differed according to clinical, genomic, and transcriptomic variables in cancer patients. Methods: Using the AACR GENIE (v.12) cancer database, the distribution of BRAF mutation class in adult cancer patients was analyzed according to sex, age, primary race, and tumor type. Genomic alteration data and transcriptomic analysis wa

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Yao, Ian, Sarah Dawson, Julian Higgins, Luke McGuinness, Alexandra McAleenan, and Kathreena M. Kurian. "Effectiveness of BRAF inhibitors in patients with BRAF V600 mutation positive glioma: a systematic review." Neuro-Oncology 21, Supplement_4 (2019): iv14. http://dx.doi.org/10.1093/neuonc/noz167.059.

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Abstract Background BRAF inhibitor treatment with vemurafenib and dabrafenib have produced significant increases in median overall survival for BRAF V600 mutation-positive melanoma patients and are in wide clinical use. BRAF inhibitors have also been used in an ad hoc fashion in BRAF V600 mutation-positive glioma in a number of glioma subtypes with varying prognoses. Methods An electronic search was performed on MEDLINE and Embase on February 1, 2019 to identify studies of any design that reported the outcome of patients with BRAF V600 mutation-positive glioma treated with BRAF inhibitors. Dat

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Ejam, Sura Salman, Israa Al-Humairi Abd Ali, Hadeel Abdulelah Karbel, and Mohammed Ali Al-Jabory. "Evaluation of BRAF v600 mutation by single strand conformation polymorphism-PCR (SSCP-PCR) in patients with interstitial lung disease." Medical Journal of Babylon 20, no. 4 (2023): 828–32. http://dx.doi.org/10.4103/mjbl.mjbl_575_23.

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Abstract Background: Many studies demonstrating a high predominance of pulmonary disease among individuals with interstitial lung disease (ILD), genomic examinations have recognized and initiated mutations in proto-oncogene B-Raf (BRAF) among patients with lung malignant growth. To support our hypothesis of being ILD could show a more vital event for framing into bronchogenic threat BRAFV600E change was examined. Objectives: To inquire about the frequency of BRAF (V600E) mutation in ILD with the possible evaluation of the presence of BRAF V600 mutation and such parameters as patient’s age, gen

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Bracht, Jillian Wilhelmina Paulina, Niki Karachaliou, Trever Bivona, et al. "BRAF Mutations Classes I, II, and III in NSCLC Patients Included in the SLLIP Trial: The Need for a New Pre-Clinical Treatment Rationale." Cancers 11, no. 9 (2019): 1381. http://dx.doi.org/10.3390/cancers11091381.

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BRAF V600 mutations have been found in 1–2% of non-small-cell lung cancer (NSCLC) patients, with Food and Drug Administration (FDA) approved treatment of dabrafenib plus trametinib and progression free survival (PFS) of 10.9 months. However, 50–80% of BRAF mutations in lung cancer are non-V600, and can be class II, with intermediate to high kinase activity and RAS independence, or class III, with impaired kinase activity, upstream signaling dependence, and consequently, sensitivity to receptor tyrosine kinase (RTK) inhibitors. Plasma cell-free DNA (cfDNA) of 185 newly diagnosed advanced lung a

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Kotani, Daisuke, Sebastián Mondaca, Aparna Parikh, et al. "Clinicopathological features, efficacy of anti-EGFR therapy, and survival outcomes in patients with BRAF non-V600 mutated metastatic colorectal cancer." Journal of Clinical Oncology 37, no. 4_suppl (2019): 659. http://dx.doi.org/10.1200/jco.2019.37.4_suppl.659.

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659 Background: BRAF non-V600 mutations occur in 2-3% of colorectal cancer. These mutants can be classified as RAS independent (class 2) or RAS dependent (class 3). We reported BRAF non-V600 mutations could be a negative predictive factor for anti-EGFR therapy in patients (pts) with pretreated metastatic colorectal cancer (mCRC), while mCRC pts with class 3 BRAF mutations could respond to anti-EGFR therapy because of its dependency on receptors and RAS. Methods: This study evaluates the efficacy to anti-EGFR therapy in a large cohort of pts with BRAF non-V600 mutated mCRC. Pts with mCRC referr

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Sasaki, Makiko, Takaya Shimura, Hirotada Nishie, et al. "BRAF K601E-mutated metastatic colorectal cancer in response to combination therapy with encorafenib, binimetinib, and cetuximab: A case report." World Journal of Gastrointestinal Oncology 16, no. 7 (2024): 3357–63. http://dx.doi.org/10.4251/wjgo.v16.i7.3357.

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BACKGROUND BRAF mutation has been recognized as a negative prognostic marker for metastatic colorectal cancer (mCRC), but these data are from common BRAF V600E-mutated mCRC. Combination therapy of BRAF inhibitor and anti-epidermal growth factor receptor (EGFR) antibody has been approved for BRAF V600E-mutated mCRC. However, BRAF non-V600 mutations are rare mutations, and their clinical behavior is not understood. Moreover, the BRAF K601E mutation is extremely rare in mCRC, and there have been no reports on its specific treatment. CASE SUMMARY Herein, we report the case of a 59-year-old female

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Xi, Liqiang, Evgeny Arons, Winnifred Navarro, et al. "Both variant and IGHV4-34–expressing hairy cell leukemia lack the BRAF V600E mutation." Blood 119, no. 14 (2012): 3330–32. http://dx.doi.org/10.1182/blood-2011-09-379339.

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Abstract Recently, the BRAF V600E mutation was reported in all cases of hairy cell leukemia (HCL) but not in other peripheral B-cell neoplasms. We wished to confirm these results and assess BRAF status in well-characterized cases of HCL associated with poor prognosis, including the immunophenotypically defined HCL variant (HCLv) and HCL expressing the IGHV4-34 immunoglobulin rearrangement. Fifty-three classic HCL (HCLc) and 16 HCLv cases were analyzed for BRAF, including 5 HCLc and 8 HCLv expressing IGHV4-34. BRAF was mutated in 42 (79%) HCLc, but wild-type in 11 (21%) HCLc and 16 (100%) HCLv.

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Neagu, Monica, Dobre Elena-Georgiana, Carolina Constantin, Mihaela Surcel, Adriana Munteanu, and Sabina Zurac. "Insights in genetic and epigenetic traits in cutaneous melanoma - new therapy targets." South East European Journal of Immunology 8, CITIM (2025): 044. https://doi.org/10.3889/seejim.2025.6106.

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The purpose of our study was to evaluate the genetic alterations that could affect the EGFR-RAS-RAF pathway in search of new druggable genetic targets. Materials and methods. Paraffin embedded samples from patients diagnosed with skin melanoma (n=22) were evaluated using droplet digital PCR (ddPCR) in comparison to benign nevi (n=15) and normal skin samples (n=15). Samples were diagnosed using histology and immunohistochemistry (IHC) evaluation. The study was operated in accordance with the principles of the Declaration of Helsinki (according to Annex 4, National Law 104/2004 and application H

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Shoushtari, Alexander Noor, Francisco Sanchez-Vega, Havish Kantheti, et al. "Therapeutic implications of a novel driver classification system for cutaneous and unknown primary melanomas." Journal of Clinical Oncology 37, no. 15_suppl (2019): 9539. http://dx.doi.org/10.1200/jco.2019.37.15_suppl.9539.

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9539 Background: Cutaneous and “unknown primary” melanomas frequently harbor alterations that activate the Mitogen Activated Protein Kinase (MAPK) pathway, and are often classified as BRAF, NRAS, NF1 mutant, or “triple wild type.” Multigene sequencing may identify additional oncogenic drivers, but the clinical impact of this information is unknown. Methods: Patients with BRAF inhibitor naïve melanoma underwent prospective tumor molecular profiling using a targeted capture-based assay (MSK-IMPACT), and demographic and treatment data were collected. Time to treatment failure was assessed for pat

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Bernocchi, Ottavia, Marianna Sirico, Silvia Paola Corona, et al. "Tumor Type Agnostic Therapy Carrying BRAF Mutation: Case Reports and Review of Literature." Pharmaceuticals 14, no. 2 (2021): 159. http://dx.doi.org/10.3390/ph14020159.

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Background: Precision medicine is based on molecular and genotypic patient characterization to define specific target treatment. BRAF mutation is an oncogenic driver, and the Cancer Genome Atlas has identified BRAF mutations in different cancer types. Tumor type agnostic therapy is based on targeting genomic alterations, regardless of tumor origin. In this context, novel therapeutic agents including BRAF and MEK inhibitors based on the molecular landscape in solid tumors have been investigated. Case presentation, Case 1: The first case is chemotherapy-refractory, BRAF V600E mutated intrahepati

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Negrao, Marcelo Vailati, Victoria M. Raymond, Richard B. Lanman, et al. "Molecular biology and treatment strategies for non-V600 BRAF-mutant NSCLC." Journal of Clinical Oncology 37, no. 15_suppl (2019): 3102. http://dx.doi.org/10.1200/jco.2019.37.15_suppl.3102.

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3102 Background: BRAF alterations (alts) account for ~4% of non-small cell lung cancers (NSCLC) with 50% being non-V600 alts. Because these alts are functionally heterogeneous and have a poorly characterized genomic landscape, determining appropriate treatment strategies is a challenge. Methods: The Guardant360 clinical database was queried for NSCLC patients (pts) with BRAF alts. Alts were categorized by clonality, type and class (1 and 2: BRAF monomer and dimer signaling; 3: requires co-occurring upstream RAS-mediated signaling). Functionality and drug screen assays were performed in Ba/F3 c

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Lee, Paul J., Katie Dennis, Rashna Madan, and Fang Fan. "BRAF V600 Mutational Status in Melanoma Correlates with Cytologic Features in Fine-Needle Aspirate Specimens." Acta Cytologica 63, no. 1 (2018): 10–16. http://dx.doi.org/10.1159/000491814.

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Melanomas are known as the great mimicker and must be considered in the differential diagnosis of any fine-needle aspirations (FNA). Despite recent advancements in understanding of the mutational landscape of melanomas, there still exists a divide between the genetic and morphologic correlates. A consecutive cohort of 39 FNA of clinically verified metastatic melanomas with concurrent BRAF V600 assessment were selected [positive (n = 18) and wild-type (n = 21)]. The melanoma cytology specimens were evaluated blinded to the BRAF mutation status in a dichotomized fashion for the presence of 8 sel

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Kosmidis, Christoforos S., Konstantina Papadopoulou, Chrysi Maria Mystakidou, et al. "Melanoma: BRAFi Rechallenge." Medicina 59, no. 5 (2023): 975. http://dx.doi.org/10.3390/medicina59050975.

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Melanoma is the most aggressive type of skin cancer. Half of melanoma cases are characterized by the mutation BRAF V600. The case presented concerns a 41-year-old patient with locally advanced melanoma, being positive in mutation BRAF V600. The patient underwent surgery and received additional targeted therapy as part of a clinical study. In subsequent disease progression, immunotherapy was used. When the disease progressed again while the patient was in a good performance status, targeted therapy was administered again, and a good response was noted, making the patient reach a statistically s

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Mangana, Joanna, Simone M. Goldinger, Katja Schindler, et al. "Analysis of BRAF and NRAS mutation status in advanced melanoma patients treated with anti-CTLA-4 antibodies: Association with overall survival?" Journal of Clinical Oncology 31, no. 15_suppl (2013): 9025. http://dx.doi.org/10.1200/jco.2013.31.15_suppl.9025.

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9025 Background: Ipilimumab and tremelimumab are human monoclonal antibodies against cytotoxic T-lymphocyte antigen-4 (CTLA-4). Ipilimumab was the first agent to show a statistically significant benefit in overall survival with durable-long-term responses for advanced melanoma patients both in first-and second-line setting. Up to date, there is no proven association between the BRAF-V600E mutation and the disease control rate (DCR) in response to Ipilimumab. Moreover, significantly shorter survival rates have been reported in patients harboring an NRAS mutation than in those without. This retr

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Stockman, David, Michael T. Tetzlaff, Tariq Al-Zaid, et al. "Differential clinical associations of BRAF and NRAS mutations among histologic types of cutaneous melanomas." Journal of Clinical Oncology 31, no. 15_suppl (2013): e20034-e20034. http://dx.doi.org/10.1200/jco.2013.31.15_suppl.e20034.

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e20034 Background: Previous studies have investigated whether BRAF and NRAS mutation status in melanoma correlate with histologic parameters and overall survival (OS), but evaluation of mutation groups irrespective of specific mutation among histologic types of melanoma has led to variability in the reproducibility of results. We tested the hypothesis that different histologic types of melanoma (nodular [NM] and superficial spreading [SSM]) have distinct clinical associations with specific BRAF and NRAS mutations. Methods: Primary tumor histology, BRAF/NRAS mutation status, and clinical outcom

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Kreitman, Robert J., Liqiang Xi, Winnifred Navarro, Maryalice Stetler-Stevenson, Evgeny Arons, and Mark Raffeld. "Presence and Absence of the BRAF V600E Mutation in Hairy Cell Leukemia and Its Variants." Blood 118, no. 21 (2011): 931. http://dx.doi.org/10.1182/blood.v118.21.931.931.

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Abstract Abstract 931 Background: Hairy cell leukemia (HCL) is a B-cell malignancy with distinctive immunophenotype. Purine analog therapy achieves durable complete remissions in 65–90% of patients. HCL variant (HCLv), recognized by the World Health Organization (WHO) as a different disease, lacks CD25, annexin A1 and/or TRAP, and responds poorly to purine analogs with only partial responses (PR) in <50% and lower overall survival (OS) from diagnosis. The recently described HCL variant expressing the immunoglobulin rearrangement IGHV4-34 also has poor response to purine analogs and OS, but

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Inic, Momcilo, Zorka Momcilo Inic, Milan Zegarac, Gordana Pupic, and Ivana Inic. "V600E mutations in metastatic melanoma: Case report." Journal of Clinical Oncology 31, no. 15_suppl (2013): e20002-e20002. http://dx.doi.org/10.1200/jco.2013.31.15_suppl.e20002.

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e20002 Background: Vemurafenib, a selective BRAF kinase inhibitor, is a new medicine against carcinoma.This work will discuss new approaches to the treatment of patients with metastatic melanoma, who have been proved to have BRAF V600 mutation. Methods: The 62-year-old patient was initially diagnosed in 2002 when the excision of melanoma of the left calf was performed. HP was Melanoma invasivum nodular, Breslow III, Clark IV, p T3, without angioinvasion. The stadium of illness was M1a (AJCC). Afterwards, she was operated four times. Chemyotherapy was performed with DTIC and in the further trea

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Dribnokhodova, O. P., E. A. Dunaeva, G. V. Leshkina, et al. "DETECTION OF SOMATIC MUTATIONS IN THE BRAF GENE BY PYROSEQUENCING." Siberian journal of oncology 20, no. 5 (2021): 75–83. http://dx.doi.org/10.21294/1814-4861-2021-20-5-75-83.

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Introduction. Detection of somatic mutations in the BRAF gene can be used in clinical oncology to clarify the diagnosis, select therapy and assess the prognosis of the disease. Pyrosequencing technology makes it possible to identify both already known and new mutations, as well as to determine the mutant allele ratio in the sample.The aim of the study was to develop the pyrosequencing-based method for detecting mutations in 592–601 codons of the BRAF gene.Material and Methods. The nucleotide sequences were obtained using «PyroMark Q24» instrument. The sensitivity and specificity of the method

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van Not, Olivier Jules, Alfonsus Johannes Maria van den Eertwegh, John B. A. G. Haanen, et al. "BRAF and NRAS mutation status and response to checkpoint inhibition in advanced melanoma." Journal of Clinical Oncology 39, no. 15_suppl (2021): 9558. http://dx.doi.org/10.1200/jco.2021.39.15_suppl.9558.

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9558 Background: The ability to analyze tumor mutation profiles has altered the oncology treatment landscape over the past decades. However, little is known about the effect of specific gene mutations on the response to immune checkpoint inhibitors (ICIs) in patients with advanced melanoma. Methods: All unresectable stage IIIc and IV patients with BRAF V600, NRAS mutations and BRAF and NRAS wild-type patients treated with anti-PD-1 or ipilimumab-nivolumab between 2012 and 2020 were included from the Dutch Melanoma Treatment Registry, a nationwide population-based registry. Outcomes were object

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Hersh, Evan, Michele Del Vecchio, Michael Paul Brown, et al. "A phase III trial of nab-paclitaxel versus dacarbazine in chemotherapy-naive patients with metastatic melanoma: A subanalysis based on BRAF status." Journal of Clinical Oncology 31, no. 15_suppl (2013): 9030. http://dx.doi.org/10.1200/jco.2013.31.15_suppl.9030.

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9030 Background: Activating mutations of BRAF V600 can be found in 40%-50% of melanomas and are related to poor prognosis. In a phase 3 trial for the treatment of metastatic melanoma (MM) in chemotherapy-naive patients, nab-paclitaxel (nab-P) vs dacarbazine (DTIC) demonstrated a significant improvement in the primary endpoint of progression-free survival (PFS), assessed by independent radiological review (IRR), and a trend toward prolonged overall survival (OS) at the interim survival analysis. The study also explored the effect of BRAF status on the efficacy parameters. Methods: Chemotherapy-

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Morelli, M. Pia, Michael J. Overman, Arvind Dasari, et al. "Heterogeneity of acquired KRAS and EGFR mutations in colorectal cancer patients treated with anti-EGFR monoclonal antibodies." Journal of Clinical Oncology 31, no. 15_suppl (2013): 3512. http://dx.doi.org/10.1200/jco.2013.31.15_suppl.3512.

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3512 Background: Although KRAS and EGFR extracellular domain acquired mutations were detected in two small cohorts and correlated with acquired resistance to anti-EGFR monoclonal antibodies (MAb), the frequency, co-occurrence, and distribution of these acquired mutations is unknown. In this study we evaluated the presence of acquired KRAS and EGFR mutations in cfDNA from CRC patients (pts) treated with anti-EGFR monoclonal antibody. Methods: Plasma was collected from EGFR-MAb refractory mCRC pts as part of the ATTACC (Assessment of Targeted Therapies Against Colorectal Cancer) program. Eligibl

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Lee, Jenny HJ, Matteo S. Carlino, Alexander M. Menzies, et al. "Circulating tumor DNA (ctDNA) using Guardant360 to predict response in BRAF V600 WT metastatic melanoma (MM) patients (pts) receiving immune checkpoint inhibitors (ICI)." Journal of Clinical Oncology 38, no. 15_suppl (2020): 10050. http://dx.doi.org/10.1200/jco.2020.38.15_suppl.10050.

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10050 Background: ctDNA detected by ddPCR predicts ICI response in MM, although its utility is limited to pts with known recurring mutations eg. BRAF, NRAS, KIT. We sought to overcome this limitation by using a next generation sequencing approach in BRAF V600 wild type (WT) MM pts. Methods: Plasma was collected at baseline and Week (wk) 6 in 35 BRAF V600 WT MM pts treated with ICI. Cell free (cf)DNA was analyzed using Guardant360 and only somatic non-synonymous and promoter variants were considered. Pts who failed cfDNA extraction at baseline were excluded (n = 3). Favorable ctDNA was defined

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Harle, Alexandre, Celine Gavoille, Olivier Bouche, et al. "cfDNA for accurate determination of RAS and BRAF mutations using OncoBEAM liquid biopsy in metastatic colorectal cancer patients: Results of the real-world multicentric ColoBEAM study." Journal of Clinical Oncology 37, no. 15_suppl (2019): 3542. http://dx.doi.org/10.1200/jco.2019.37.15_suppl.3542.

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3542 Background: Determination of KRAS, NRAS ( RAS) and BRAF mutations is a standard of care for the management of patients with metastatic colorectal cancer (mCRC). RAS mutations are well characterized resistance biomarkers to anti-EGFR antibodies and BRAF V600 mutations indicate poor prognosis. Tissue biopsy has traditionally been used to determine RAS and BRAF status, but liquid biopsy analysis of circulating tumor DNA (ctDNA) has demonstrated utility as a less invasive tool to expedite molecular testing results to the clinic. The ColoBEAM study reports the performance of plasma mutation te

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Beck, J. Thaddeus Thaddeus, Meredith McKean, Shirish M. Gadgeel, et al. "A phase 1, open-label, dose escalation and dose expansion study to evaluate the safety, tolerability, pharmacokinetics, and antitumor activity of PF-07799933 (ARRY-440) as a single agent and in combination therapy in participants 16 years and older with advanced solid tumors with BRAF alterations." Journal of Clinical Oncology 41, no. 16_suppl (2023): TPS3164. http://dx.doi.org/10.1200/jco.2023.41.16_suppl.tps3164.

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TPS3164 Background: Approved BRAF inhibitors (BRAFi) are inactive against RAF dimers. Accordingly, the acquisition of BRAF dimers ( e.g., through drug-acquired splice variants or BRAF amplification) may lead to therapy resistance. Non-V600 (class II and III) BRAF alterations that occur de novo in diverse tumor types also signal as dimers and therefore have no approved targeted therapeutic options. Additional liabilities of approved BRAFi include toxicity from paradoxical activation of wild-type (WT) RAF and limited brain penetration, a common primary and metastatic site for BRAF-altered cancer

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Jain, Sidharth S., A. Patrick IV McDeed, Megan E. McNamara, et al. "Abstract B047: Monitoring treatment response and toxicity in BRAF V600-mutant metastatic melanoma with circulating cell-free DNA." Clinical Cancer Research 30, no. 21_Supplement (2024): B047. http://dx.doi.org/10.1158/1557-3265.liqbiop24-b047.

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Abstract Background: The DREAMseq trial (EA6134, NCT02224781) was a national multi-center randomized phase III trial coordinated by ECOG-ACRIN that found that immune checkpoint inhibitor (IO) treatment achieves improved survival outcomes compared to targeted therapy (TT) in patients with BRAF V600-mutant metastatic melanoma. Still, approximately 40% of patients do not respond to IO, and existing biomarkers fail to distinguish this subset of patients who do not benefit from IO therapy. Additionally, as many as 80% of patients may experience immune- related adverse events (irAEs), which range fr

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Ma, Vincent The-Luc, Stephanie Daignault, Jessica Waninger, et al. "The impact of BRAF mutation status on clinical outcomes with single-agent PD-1 inhibitor versus combination ipilimumab/nivolumab." Journal of Clinical Oncology 38, no. 15_suppl (2020): 10024. http://dx.doi.org/10.1200/jco.2020.38.15_suppl.10024.

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10024 Background: Nearly half of all metastatic melanoma patients possess the BRAF V600 mutation. Several therapies are approved for BRAF mutant metastatic melanoma, but it is unclear if there is a differential outcome to various immunotherapy regimens. Our aim was to better assess if BRAF mutation status has any impact on survival to combination ipilimumab/nivolumab (I/N) versus single-agent PD-1 inhibitor (PD-1i). Methods: We performed a single center, retrospective analysis on a cohort of patients diagnosed with metastatic or unresectable melanoma from 2012 to 2019 at the University of Mich

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Nagel, Philipp D., Fenja M. Feld, Stephanie E. Weissinger, Albrecht Stenzinger, Peter Moeller, and Jochen K. Lennerz. "Absence Of BRAF and KRAS Hotspot Mutations In Primary Mediastinal and Other Diffuse Large B-Cell Lymphoma." Blood 122, no. 21 (2013): 4325. http://dx.doi.org/10.1182/blood.v122.21.4325.4325.

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Abstract Recently whole-exome-sequencing has identified oncogenic BRAF and KRAS mutations as likely drivers in diffuse-large B-cell lymphoma (DLBCL). It is currently unclear whether primary mediastinal B-cell lymphoma (PMBL), a clinicopathologically distinct variant of diffuse-large B-cell lymphoma, harbors such mutations. Here, we screened 100 samples (84 primary tumors and 16 cell lines), composed of 52 PMBL and 48 DLBCL samples for BRAF (V600/601) and KRAS (G12-K16) hotspot mutations using a sensitive pyrosequencing approach. All 100 samples were BRAF and KRAS wild-type. When combining our

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Pradelli, Lorenzo, and Paolo Ascierto. "[Clinical and economic evaluation of the introduction of the combinazion trametinib + dabrafenib in the management of advanced melanoma in the Italian market]." Farmeconomia. Health economics and therapeutic pathways 17, no. 3S (2016): 1–32. http://dx.doi.org/10.7175/fe.v17i3s.1279.

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Melanoma is the most aggressive type of all skin cancers. In Italy the incidence is increasing both in men and in women with 13,800 new cases expected in 2016. The advanced melanoma therapy has changed in recent years with the use of immunotherapy and targeted therapies. In particular, treatment with BRAF inhibitors in patients with advanced BRAF V600 mutated melanoma has shown high rates of rapid response and survival. Due to development of acquired resistance with disease progression the rapid response observed with BRAF inhibitor therapy is not long lasting. Combining a BRAF inhibitor with

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Abubaker, Khalid, Danyi Wang, Zheng Feng, et al. "Abstract 5245: Characterization of sub-clonal RAS/BRAF alterations in an anti-EGFR treated advanced CRC cohort using a liquid biopsy-based real world clinical genomics database." Cancer Research 82, no. 12_Supplement (2022): 5245. http://dx.doi.org/10.1158/1538-7445.am2022-5245.

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Abstract Background: Anti-EGFR monoclonal antibodies are treatment options for RAS and BRAF V600 mutation-negative CRC patients. However, the literature suggests that CRC patients with sub-clonal RAS and BRAF mutations may still benefit from anti-EGFR therapies. The Guardant INFORM™ real-world clinical-genomic database was utilized to assess the impact of sub-clonal RAS and BRAF alterations detected in circulating tumor DNA (ctDNA) by the Guardant360® test on the clinical outcome of CRC patients treated with anti-EGFR therapy. Methods: Patients were selected from the Guardant INFORM™ database

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Johnson, Benny, Jonathan M. Loree, Alexandre A. Jacome, et al. "Atypical, Non-V600 BRAF Mutations as a Potential Mechanism of Resistance to EGFR Inhibition in Metastatic Colorectal Cancer." JCO Precision Oncology, no. 3 (December 2019): 1–10. http://dx.doi.org/10.1200/po.19.00102.

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PURPOSE Atypical, non-V600 BRAF ( aBRAF) mutations represent a rare molecular subtype of metastatic colorectal cancer (mCRC). Preclinical data are used to categorize aBRAF mutations into class II (intermediate to high levels of kinase activity, RAS independent) and III (low kinase activity level, RAS dependent). The clinical impact of these mutations on anti-EGFR treatment efficacy is unknown. PATIENTS AND METHODS Data from 2,084 patients with mCRC at a single institution and from an external cohort of 5,257 circulating tumor DNA (ctDNA) samples were retrospectively analyzed. Overall survival

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Liang, Yanke, Mathew E. Sowa, Katrina L. Jackson, et al. "Abstract 3425: The discovery and characterization of CFT1946: A potent, selective, and orally bioavailable degrader of mutant BRAF for the treatment of BRAF-driven cancers." Cancer Research 83, no. 7_Supplement (2023): 3425. http://dx.doi.org/10.1158/1538-7445.am2023-3425.

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Abstract The BRAF kinase plays a critical role in the MAPK signaling pathway and is mutated in ~8% of all human cancers including melanoma (~60%), thyroid (~60%), and lung adenocarcinoma (~10%). The most common mutation in BRAF is V600E (Class I), which is found in &gt;70% in these cancers. Despite the clinical success of approved small molecule inhibitors of BRAF V600E (vemurafenib, dabrafenib and encorafenib), this remains an area of unmet medical need because nearly all patients progress, due to either primary or acquired resistance. A bifunctional degradation activating compound (or Bi

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Tawbi, Hussein A., Caroline Robert, Jan C. Brase, et al. "Spartalizumab or placebo in combination with dabrafenib and trametinib in patients with BRAF V600-mutant melanoma: exploratory biomarker analyses from a randomized phase 3 trial (COMBI-i)." Journal for ImmunoTherapy of Cancer 10, no. 6 (2022): e004226. http://dx.doi.org/10.1136/jitc-2021-004226.

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BackgroundThe randomized phase 3 COMBI-i trial did not meet its primary endpoint of improved progression-free survival (PFS) with spartalizumab plus dabrafenib and trametinib (sparta-DabTram) vs placebo plus dabrafenib and trametinib (placebo-DabTram) in the overall population of patients with unresectable/metastatic BRAF V600-mutant melanoma. This prespecified exploratory biomarker analysis was performed to identify subgroups that may derive greater treatment benefit from sparta-DabTram.MethodsIn COMBI-i (ClinicalTrials.gov, NCT02967692), 532 patients received spartalizumab 400 mg intravenous

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Tsai, Katy K., Iwei Yeh, Adil Daud, and Ari Oglesby. "Phase II study of binimetinib with imatinib in patients with unresectable KIT-mutant melanoma." Journal of Clinical Oncology 39, no. 15_suppl (2021): TPS9594. http://dx.doi.org/10.1200/jco.2021.39.15_suppl.tps9594.

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TPS9594 Background: Immune checkpoint inhibitors (ICI) have transformed treatment for patients (pts) with advanced melanoma, as have BRAF/MEK inhibitors for pts with BRAF V600-mutant melanoma. However, pts with acral or mucosal melanomas are in particular need of more options given a lower objective response rate (ORR) to ICI, and lower incidence of BRAF V600 driver mutation. Such BRAF mutations are found in only 5-10% of acral/mucosal melanomas, while KIT mutations/amplifications are found in 10-20%. Even when present, a KIT alteration does not guarantee response to KIT inhibition, with only

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Chen, Jing, Ting Ye, Li Fan, Jieying Zhang, Rubo Cao, and Yanshen Liu. "Abstract 5764: Genomic profiling of cutaneous, acral and mucosal melanomas in Chinese populations." Cancer Research 82, no. 12_Supplement (2022): 5764. http://dx.doi.org/10.1158/1538-7445.am2022-5764.

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Abstract Background: Targeted therapies and immunotherapies have significantly improved the survival of patients with cutaneous melanoma. Nevertheless, patients with acral and mucosal melanomas show limited benefit. The proportion of acral and mucosal subtypes are much higher in Chinese populations than Caucasians. Therefore, it is of great interest to detail the genomic features of acral and mucosal melanomas and compare these with cutaneous melanoma. Methods: A total of 111 Chinese patients with melanoma treated in Union Hospital, Tongji Medical College, Huazhong University of Science and Te

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Subbiah, Vivek, Martin Gutierrez, Carey K. Anders, et al. "Trial in progress: Phase 1a/b study of PF-07284890 (brain-penetrant BRAF inhibitor) with/without binimetinib in patients with BRAF V600-mutant solid tumors." Journal of Clinical Oncology 39, no. 15_suppl (2021): TPS3152. http://dx.doi.org/10.1200/jco.2021.39.15_suppl.tps3152.

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TPS3152 Background: BRAF inhibitors have transformed treatment (Tx) for patients (pts) with BRAF V600-mutant cancers, but long-term efficacy is limited by disease progression in the brain, due to poor brain penetration. PF-07284890 is a potent, selective, highly brain-penetrant, small-molecule inhibitor of BRAF V600 mutations. This first in human study will assess the PK, safety, and preliminary clinical activity of PF-07284890, as monotherapy and in combination with binimetinib (MEK inhibitor), in pts with BRAF V600-mutated advanced solid tumors with/without brain metastases. Methods: Phase 1

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Mobark, Nahla Ali, Musa Alharbi, Yasser S. Bayoumi, et al. "DIPG-35. Personalized treatment for molecularly heterogeneous Diffuse midline glioma, H3 k27-altered Paediatric case." Neuro-Oncology 24, Supplement_1 (2022): i26. http://dx.doi.org/10.1093/neuonc/noac079.092.

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Abstract Diffuse midline glioma, H3 k27-altered (DMG) is a type of Paediatric- type diffuse high grade gliomas according to the 2021 WHO CNS tumors Classification. Diffuse intrinsic pontine glioma (DIPG) is another acceptable related term when it located in the pons with fatal prognosis. The combination of H3K27M with BRAF V600 mutations rarely reported in DMG although more commonly in Paediatric-type low grade gliomas (Diffuse low-grade glioma, MAPK pathway-altered). We present a twenty-month-old boy, previously healthy, presented with 2 weeks history of unsteady gait, drooling, cranial nerve

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Szatkowska, Lidia, Jan Sieczek, Katarzyna Tekiela, et al. "Outcomes of Patients with Metastatic Melanoma—A Single-Institution Retrospective Analysis." Cancers 14, no. 7 (2022): 1672. http://dx.doi.org/10.3390/cancers14071672.

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Background: This study assessed risk factors and the results of treatment with anti-PD-1 antibodies and BRAF/MEK inhibitors for advanced malignant melanoma. Methods: A retrospective analysis was performed on 52 patients treated with immunotherapy and BRAF/MEK inhibitors for disseminated malignant melanoma. Results: The median follow-up was 31 months (6–108 months). The median PFS1 was 6 months (1–44 months). Second-line systemic treatment was applied in 27 patients (52%). The median PFS2 was 2 months (0–27 months), and the median OS was 31 months (6–108 months). Among the analyzed risk factors

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Kotani, Daisuke, Yoshinori Kagawa, Yuki Matsubara, et al. "TRIDENTE trial: A phase II study of rechallenge with encorafenib, binimetinib, and cetuximab in patients with RAS wild-type/BRAF V600E–mutant metastatic colorectal cancer." Journal of Clinical Oncology 41, no. 4_suppl (2023): TPS264. http://dx.doi.org/10.1200/jco.2023.41.4_suppl.tps264.

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TPS264 Background: The BEACON CRC trial demonstrated survival benefit of combination therapy with encorafenib (ENCO) + cetuximab (CET) +/- binimetinib (BINI) in patients with RAS wild-type (WT)/ BRAF V600E mutant metastatic colorectal cancer (mCRC). However, prognosis of those patients still be poor after the refractoriness to the BEACON combination therapy. One of resistant mechanisms to BRAF inhibitor has been reported as MAPK alterations including RAS mutation, similar to those for anti-EGFR antibody in patients with RAS/ BRAF V600E WT mCRC. Promising results of rechallenge therapy with ant

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Gupta, Avinash, Sharon Love, Anna Schuh, et al. "DOC-MEK: A double-blind randomized phase II trial of docetaxel with or without selumetinib (AZD6244; ARRY-142886) in wt BRAF advanced melanoma." Journal of Clinical Oncology 31, no. 15_suppl (2013): 9068. http://dx.doi.org/10.1200/jco.2013.31.15_suppl.9068.

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9068 Background: Inhibitors of mutant BRAF have transformed the treatment of melanoma for the 40% of patients whose tumors harbor V600 mutations. ERK1/2 is constitutively active in melanoma cells regardless of mutation status, and plays key roles in cell cycle entry, invasion, angiogenesis and in resistance to apoptosis. Selumetinib is a highly selective allosteric inhibitor of MEK1/2, suppressing pERK levels in melanoma independent of BRAF and NRAS mutation status. In melanoma cells, docetaxel induces mitochondrial dependent apoptosis by activation of Bax. Activation of ERK1/2 results in degr

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Loree, Jonathan M., Anthony Dowers, Dongsheng Tu, et al. "Expanded RAS and BRAF V600 testing as predictive biomarkers for single agent cetuximab in the randomized phase III CO.17 trial." Journal of Clinical Oncology 37, no. 4_suppl (2019): 537. http://dx.doi.org/10.1200/jco.2019.37.4_suppl.537.

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537 Background: KRAS/NRAS ( RAS) testing of exons 2, 3 and 4 is standard prior to anti-EGFR treatment in metastatic colorectal cancer and many consider BRAFV600 ( BRAF) mutations predictive. CO.17 was a randomized phase III trial comparing cetuximab vs best supportive care (BSC) in unselected patients (pts). Re-analysis tested only KRAS exon 2, thus the benefit of cetuximab in RAS/BRAF wild type (WT) pts is unclear. Methods: We retrospectively performed expanded RAS/BRAF testing using a highly sensitive digital PCR method (BEAMing; 1% allele frequency detection limit) on micro-dissected archiv

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Calegari, Maria Alessandra, Lisa Salvatore, Brunella Di Stefano, et al. "Clinical, Pathological and Prognostic Features of Rare BRAF Mutations in Metastatic Colorectal Cancer (mCRC): A Bi-Institutional Retrospective Analysis (REBUS Study)." Cancers 13, no. 9 (2021): 2098. http://dx.doi.org/10.3390/cancers13092098.

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Recently, retrospective analysis began to shed light on metastatic colorectal cancers (mCRCs) harboring rare BRAF non-V600 mutations, documenting a distinct phenotype and a favorable prognosis. This study aimed to confirm features and prognosis of rare BRAF non-V600 mCRCs compared to BRAF V600E and BRAF wild-type mCRCs treated at two Italian Institutions. Overall, 537 cases were retrospectively evaluated: 221 RAS/BRAF wild-type, 261 RAS mutated, 46 BRAF V600E and 9 BRAF non-V600. Compared to BRAF V600E mCRC, BRAF non-V600 mCRC were more frequently left-sided, had a lower tumor burden and displ

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