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      MYBL2 (B-Myb): a central regulator of cell proliferation, cell survival and differentiation involved in tumorigenesis

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          Limitless cell proliferation, evasion from apoptosis, dedifferentiation, metastatic spread and therapy resistance: all these properties of a cancer cell contribute to its malignant phenotype and affect patient outcome. MYBL2 (alias B-Myb) is a transcription factor of the MYB transcription factor family and a physiological regulator of cell cycle progression, cell survival and cell differentiation. When deregulated in cancer cells, MYBL2 mediates the deregulation of these properties. In fact, MYBL2 is overexpressed and associated with poor patient outcome in numerous cancer entities. MYBL2 and players of its downstream transcriptional network can be used as prognostic and/or predictive biomarkers as well as potential therapeutic targets to offer less toxic and more specific anti-cancer therapies in future. In this review, we summarize current knowledge on the physiological roles of MYBL2 and highlight the impact of its deregulation on cancer initiation and progression.

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          Most cited references 135

          • Record: found
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          The hallmarks of cancer.

            • Record: found
            • Abstract: found
            • Article: not found

            Cellular senescence: when bad things happen to good cells.

            Cells continually experience stress and damage from exogenous and endogenous sources, and their responses range from complete recovery to cell death. Proliferating cells can initiate an additional response by adopting a state of permanent cell-cycle arrest that is termed cellular senescence. Understanding the causes and consequences of cellular senescence has provided novel insights into how cells react to stress, especially genotoxic stress, and how this cellular response can affect complex organismal processes such as the development of cancer and ageing.
              • Record: found
              • Abstract: found
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              The history and future of targeting cyclin-dependent kinases in cancer therapy.

              Cancer represents a pathological manifestation of uncontrolled cell division; therefore, it has long been anticipated that our understanding of the basic principles of cell cycle control would result in effective cancer therapies. In particular, cyclin-dependent kinases (CDKs) that promote transition through the cell cycle were expected to be key therapeutic targets because many tumorigenic events ultimately drive proliferation by impinging on CDK4 or CDK6 complexes in the G1 phase of the cell cycle. Moreover, perturbations in chromosomal stability and aspects of S phase and G2/M control mediated by CDK2 and CDK1 are pivotal tumorigenic events. Translating this knowledge into successful clinical development of CDK inhibitors has historically been challenging, and numerous CDK inhibitors have demonstrated disappointing results in clinical trials. Here, we review the biology of CDKs, the rationale for therapeutically targeting discrete kinase complexes and historical clinical results of CDK inhibitors. We also discuss how CDK inhibitors with high selectivity (particularly for both CDK4 and CDK6), in combination with patient stratification, have resulted in more substantial clinical activity.

                Author and article information

                [1 ]Max-Eder Research Group for Pediatric Sarcoma Biology, Institute for Pathology of the LMU Munich , Munich, Germany
                [2 ]INSERM Unit 830 ‘Genetics and Biology of Cancers’, Institut Curie Research Center , Paris, France
                [3 ]German Cancer Consortium (DKTK) , Munich, Germany
                [4 ]German Cancer Research Center (DKFZ) , Heidelberg, Germany
                Author notes
                [* ]Max-Eder Research Group for Pediatric Sarcoma Biology, Institute of Pathology of the LMU Munich , Thalkirchner Str. 36, Munich 80337, Germany. Tel: +49 89 218073716; Fax: +49 89 218073604; E-mail: thomas.gruenewald@
                Cell Death Dis
                Cell Death Dis
                Cell Death & Disease
                Nature Publishing Group
                June 2017
                22 June 2017
                1 June 2017
                : 8
                : 6
                : e2895
                Copyright © 2017 The Author(s)

                Cell Death and Disease is an open-access journal published by Nature Publishing Group. This work is licensed under a Creative Commons Attribution 4.0 International License. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in the credit line; if the material is not included under the Creative Commons license, users will need to obtain permission from the license holder to reproduce the material. To view a copy of this license, visit


                Cell biology


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