Abstract:
:Cohesin is a multi-protein complex composed of four core subunits (SMC1A, SMC3, RAD21, and either STAG1 or STAG2) that is responsible for the cohesion of sister chromatids following DNA replication until its cleavage during mitosis thereby enabling faithful segregation of sister chromatids into two daughter cells. Recent cancer genomics analyses have discovered a high frequency of somatic mutations in the genes encoding the core cohesin subunits as well as cohesin regulatory factors (e.g. NIPBL, PDS5B, ESPL1) in a select subset of human tumors including glioblastoma, Ewing sarcoma, urothelial carcinoma, acute myeloid leukemia, and acute megakaryoblastic leukemia. Herein we review these studies including discussion of the functional significance of cohesin inactivation in tumorigenesis and potential therapeutic mechanisms to selectively target cancers harboring cohesin mutations.
journal_name
BMB Repjournal_title
BMB reportsauthors
Solomon DA,Kim JS,Waldman Tdoi
10.5483/bmbrep.2014.47.6.092subject
Has Abstractpub_date
2014-06-01 00:00:00pages
299-310issue
6eissn
1976-6696issn
1976-670Xpii
2812journal_volume
47pub_type
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