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      circMYBL2, a circRNA from MYBL2, regulates FLT3 translation by recruiting PTBP1 to promote FLT3-ITD AML progression

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          Abstract

          Sun et al identify a circular RNA, circMYBL2, that upregulates FLT3 translation to promote FLT3-ITD acute myeloid leukemia (AML) progression, suggesting a novel therapeutic target for FLT3-ITD AML.

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          Oncogenic Role of Fusion-circRNAs Derived from Cancer-Associated Chromosomal Translocations.

          Jlenia Guarnerio, Marco Bezzi, Jong Jeong … (2016)
          Chromosomal translocations encode oncogenic fusion proteins that have been proven to be causally involved in tumorigenesis. Our understanding of whether such genomic alterations also affect non-coding RNAs is limited, and their impact on circular RNAs (circRNAs) has not been explored. Here, we show that well-established cancer-associated chromosomal translocations give rise to fusion circRNAs (f-circRNA) that are produced from transcribed exons of distinct genes affected by the translocations. F-circRNAs contribute to cellular transformation, promote cell viability and resistance upon therapy, and have tumor-promoting properties in in vivo models. Our work expands the current knowledge regarding molecular mechanisms involved in cancer onset and progression, with potential diagnostic and therapeutic implications.
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            Acute myeloid leukaemia.

            Elihu Estey, Hartmut Döhner (2006)
            Acute myeloid leukaemia (AML) is a heterogeneous clonal disorder of haemopoietic progenitor cells and the most common malignant myeloid disorder in adults. The median age at presentation for patients with AML is 70 years. In the past few years, research in molecular biology has been instrumental in deciphering the pathogenesis of the disease. Genetic defects are thought to be the most important factors in determining the response to chemotherapy and outcome. Whereas significant progress has been made in the treatment of younger adults, the prospects for elderly patients have remained dismal, with median survival times of only a few months. This difference is related to comorbidities associated with ageing and to disease biology. Current efforts in clinical research focus on the assessment of targeted therapies. Such new approaches will probably lead to an increase in the cure rate.
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              Validation of ITD mutations in FLT3 as a therapeutic target in human acute myeloid leukaemia.

              Catherine Smith, Qi Wang, Chen-Shan Chin … (2012)
              Effective targeted cancer therapeutic development depends upon distinguishing disease-associated 'driver' mutations, which have causative roles in malignancy pathogenesis, from 'passenger' mutations, which are dispensable for cancer initiation and maintenance. Translational studies of clinically active targeted therapeutics can definitively discriminate driver from passenger lesions and provide valuable insights into human cancer biology. Activating internal tandem duplication (ITD) mutations in FLT3 (FLT3-ITD) are detected in approximately 20% of acute myeloid leukaemia (AML) patients and are associated with a poor prognosis. Abundant scientific and clinical evidence, including the lack of convincing clinical activity of early FLT3 inhibitors, suggests that FLT3-ITD probably represents a passenger lesion. Here we report point mutations at three residues within the kinase domain of FLT3-ITD that confer substantial in vitro resistance to AC220 (quizartinib), an active investigational inhibitor of FLT3, KIT, PDGFRA, PDGFRB and RET; evolution of AC220-resistant substitutions at two of these amino acid positions was observed in eight of eight FLT3-ITD-positive AML patients with acquired resistance to AC220. Our findings demonstrate that FLT3-ITD can represent a driver lesion and valid therapeutic target in human AML. AC220-resistant FLT3 kinase domain mutants represent high-value targets for future FLT3 inhibitor development efforts.
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                Author and article information

                Journal
                Title: Blood
                Publisher: American Society of Hematology
                ISSN (Print): 0006-4971
                ISSN (Electronic): 1528-0020
                Publication date Created: October 31 2019
                Publication date Created: August 06 2019
                Publication date (Print): October 31 2019
                Publication date (Electronic): August 06 2019
                Volume: 134
                Issue: 18
                Pages: 1533-1546
                Affiliations
                [1 ]MOE Key Laboratory of Gene Function and Regulation, State Key Laboratory for Biocontrol, Sun Yat-sen University, Guangzhou, China;
                [2 ]The First Affiliated Hospital of Sun Yat-sen University, Guangzhou, China; and
                [3 ]Department of Hematology, Guangdong Provincial People’s Hospital, Guangzhou, China
                Article
                DOI: 10.1182/blood.2019000802
                PMC ID: 6839953
                PubMed ID: 31387917
                SO-VID: bf13ab77-be84-4c61-844a-e132032a146c
                Copyright © © 2019
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