{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"omics_type":["Unknown"],"volume":["10"],"submitter":["Simnica D"],"funding":["Deutsche Forschungsgemeinschaft"],"pubmed_abstract":["Drug-promoted cancers are increasingly recognized as a serious clinical problem in patients receiving BRAF inhibitory treatment. Here we report on a patient with <i>BRAF</i> mutant hairy cell leukemia and monoclonal B-cell lymphocytosis (MBL), who responded durably to BRAF/MEK inhibitors (BRAFi/MEKi) but experienced transformation of a <i>RAS</i> mutant MBL to chronic lymphocytic leukemia (CLL) with accelerated nodal progression. Hypothesizing that BRAFi triggered excessive MEK-ERK signaling in the MBL/CLL clone via the CRAF/RAS complex as previously described for BRAFi-induced cancers, BRAFi was discontinued inducing a rapid remission of the CLL on MEKi alone. Liquid biopsy monitoring showed a continuous increase of the MBL/CLL clone from the start of BRAFi/MEKi treatment followed by a ra"],"journal":["Frontiers in oncology"],"pagination":["540030"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC7517330"],"repository":["biostudies-literature"],"pubmed_title":["Targeting the Mutational Landscape of Bystander Cells: Drug-Promoted Blood Cancer From High-Prevalence Pre-neoplasias in Patients on BRAF Inhibitors."],"pmcid":["PMC7517330"],"pubmed_authors":["Ittrich H","Stein A","Bockemeyer C","Binder M","Simnica D"],"additional_accession":[]},"is_claimable":false,"name":"Targeting the Mutational Landscape of Bystander Cells: Drug-Promoted Blood Cancer From High-Prevalence Pre-neoplasias in Patients on BRAF Inhibitors.","description":"Drug-promoted cancers are increasingly recognized as a serious clinical problem in patients receiving BRAF inhibitory treatment. Here we report on a patient with <i>BRAF</i> mutant hairy cell leukemia and monoclonal B-cell lymphocytosis (MBL), who responded durably to BRAF/MEK inhibitors (BRAFi/MEKi) but experienced transformation of a <i>RAS</i> mutant MBL to chronic lymphocytic leukemia (CLL) with accelerated nodal progression. Hypothesizing that BRAFi triggered excessive MEK-ERK signaling in the MBL/CLL clone via the CRAF/RAS complex as previously described for BRAFi-induced cancers, BRAFi was discontinued inducing a rapid remission of the CLL on MEKi alone. Liquid biopsy monitoring showed a continuous increase of the MBL/CLL clone from the start of BRAFi/MEKi treatment followed by a ra","dates":{"release":"2020-01-01T00:00:00Z","publication":"2020","modification":"2025-04-25T23:45:33.265Z","creation":"2021-02-19T23:56:37Z"},"accession":"S-EPMC7517330","cross_references":{"pubmed":["33042833"],"doi":["10.3389/fonc.2020.540030"]}}