Selected Articles from This Issue

Abstract

Highlights| July 15 2022 Selected Articles from This Issue Author & Article Information Online Issn: 1557-3265 Print Issn: 1078-0432 ©2022 American Association for Cancer Research2022American Association for Cancer Research Clin Cancer Res (2022) 28 (14): 2975. https://doi.org/10.1158/1078-0432.CCR-28-14-HI Related Content A commentary has been published: RASGRF1 Fusions Activate Oncogenic RAS Signaling and Confer Sensitivity to MEK Inhibition A commentary has been published: Pembrolizumab in Combination with Neoadjuvant Chemoradiotherapy for Patients with Resectable Adenocarcinoma of the Gastroesophageal Junction A commentary has been published: Phase Ib/II Trial of Ribociclib in Combination with Binimetinib in Patients with NRAS-mutant Melanoma View more A commentary has been published: Safety and Efficacy of Irradiation Boost Based on 18F-FET-PET in Patients with Newly Diagnosed Glioblastoma View less Views Icon Views Article contents Figures & tables Video Audio Supplementary Data Peer Review Share Icon Share Facebook Twitter LinkedIn MailTo Tools Icon Tools Get Permissions Cite Icon Cite Search Site Article Versions Icon Versions Version of Record July 15 2022 Citation Selected Articles from This Issue. Clin Cancer Res 15 July 2022; 28 (14): 2975. https://doi.org/10.1158/1078-0432.CCR-28-14-HI Download citation file: Ris (Zotero) Reference Manager EasyBib Bookends Mendeley Papers EndNote RefWorks BibTex toolbar search Search Dropdown Menu toolbar search search input Search input auto suggest Search Advanced Search Neuroblastoma RAS viral oncogene homolog (NRAS)-mutant melanoma makes up 15%–25% of all melanomas, has a poor prognosis, and has no approved targeted therapies. Enhanced mitogen-activated protein kinase (MAPK) pathway signaling and cell cycle checkpoint dysregulation are characteristic of most NRAS-mutant melanomas. Simultaneous inhibition of MAPK kinase (MEK) and cyclin-dependent kinase 4/6 (CDK4/6) has shown synergistic antitumor activity in several preclinical models of NRAS-mutant melanoma. The regimen of the MEK inhibitor binimetinib and the selective CDK4/6 inhibitor ribociclib is a rational combination to assess in an NRAS-mutant melanoma population for toxicity and efficacy. In this phase Ib/II study, Schuler and colleagues demonstrate that the combination of ribociclib + binimetinib achieved target inhibition and tolerability consistent with the known profile of the two agents. Antitumor activity was observed particularly in NRAS-mutant melanomas with concurrent genetic alterations in cell cycle regulators. Dual timepoint FET-PET acquisition might improve the definition of glioblastoma location and... You do not currently have access to this content.