![]() Wiley Interdiscip Rev Dev Biol 2016 5 : 659– 688. Polycomb and trithorax opposition in development and disease. ATP-dependent chromatin remodeling: genetics, genomics and mechanisms. Chromatin structure oligomers of the histones. Chromatin structure: a repeating unit of histones and DNA. Advances in therapy for pediatric sarcomas. 15 Weiss A, Gill J, Goldberg J, et al.Epidemiology and therapies for metastatic sarcoma. Children' s Oncology Group's 2013 blueprint for research: soft tissue sarcomas. Children's Oncology Group's 2013 blueprint for research: bone tumors. 12 Gorlick R, Janeway K, Lessnick S, et al.11 Clark MA, Fisher C, Judson I, et al.Systemic treatment in advanced soft tissue sarcoma: what is standard, what is new. 10 Frezza AM, Stacchiotti S, Gronchi A.New systemic therapy options for advanced sarcomas. Managing sarcoma: where have we come from and where are we going? Ther Adv Med Oncol 2017 9 : 637– 659. 8 Bleloch JS, Ballim RD, Kimani S, et al.Soft tissue sarcomas of adults: state of the translational science. 7 Borden EC, Baker LH, Bell RS, et al.Cloning and characterization of the Ewing's sarcoma and peripheral neuroepithelioma t(11 22) translocation breakpoints. 5 Zucman J, Delattre O, Desmaze C, et al.An evaluation of 85 cases of remarkable consistency of t(11 22)(q24 q12). 4 Turc-Carel C, Aurias A, Mugneret F, et al.Gene fusion with an ETS DNA-binding domain caused by chromosome translocation in human tumours. 3 Delattre O, Zucman J, Plougastel B, et al.Fusion of SYT to two genes, SSX1 and SSX2, encoding proteins with homology to the Kruppel-associated box in human synovial sarcoma. Identification of novel genes, SYT and SSX, involved in the t(X 18)(p11.2 q11.2) translocation found in human synovial sarcoma. 1 Clark J, Rocques PJ, Crew AJ, et al.Copyright © 2018 Pathological Society of Great Britain and Ireland. Understanding the functions of chromatin regulatory complexes and the mechanisms underpinning their roles in oncogenesis will be required for the design and development of new therapeutic strategies in sarcomas. Specifically, alterations to mammalian SWI/SNF (mSWI/SNF or BAF) ATP-dependent chromatin remodeling complexes and polycomb repressive complexes cause disease-specific changes in chromatin architecture and gene expression across a number of sarcoma subtypes. These genetic abnormalities most often result in global transcriptional misregulation via disruption of protein regulatory complexes which govern chromatin architecture. Hallmark tumor suppressor gene mutations and pathognomonic gene fusions collectively account for approximately one-third of all sarcomas. Soft-tissue sarcomas are increasingly characterized and subclassified by genetic abnormalities that represent underlying drivers of their pathology.
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