Regulating p73 isoforms in human tumours.

摘要: Although mutations in the TP73 gene are extremely rare human tumours, altered expression is common. In some most notably leukaemias and lymphomas, of reduced, suggesting a tumour suppressor role. contrast, over-expressed many other types, implying that it has oncogenic functions tumourigenesis. These conflicting scenarios can be reconciled by observations produces p53-like isoforms (TAp73) anti-p53 (DeltaTAp73). Thus, loss TAp73 or over-expression DeltaTAp73 should each promote transformation, balance opposing crucial factor. The mechanisms regulate therefore great interest. Recent data provide evidence for interacting roles ZEB1, p300, polymorphic 73 bp deletion intron 1 this process. Importantly, alterations to proposed regulatory pathway controlling isoform colorectal cancer associated with adverse clinico-pathological characteristics. Because p73 also chemosensitivity, these new findings prognostic information have potential guide future therapeutic decisions.