Figure 2
From: DNA mismatch repair and TP53 defects are early events in uterine carcinosarcoma tumorigenesis
Proposed model for histiogenesis of uterine carcinosarcomas. A normal progenitor cell may acquire a number of genetic mutations including defects in TP53 and DNA mismatch repair. Additional defects are acquired as the tumor differentiates into the carcinoma and sarcoma components. Shared molecular defects (present in the progenitor cell) will be present in both components. Molecular defects acquired later in histiogenesis will be discordant between the two components.
