Fig. 5

Oncogenic collaboration of mutations with TET2^MT in animal models. Tet2^MT mice develop MPNs, AITL-like, AML-like, or T-ALL-like diseases when combined with Dnmt3A^R882H mutation or Dnmt3A deletion, and accelerated MPN or AML when combined with N-ras^G12D mutation. However, Tet2^MT mice develop AITL, AML, MPN, MDS/MPN, or mastocytosis when combined with RhoA^G17V, Flt3^ITD/AML1-ETO/Ncstn^MT, Jak2^V617F, Ezh2^MT/Asxl1^MT/Bcor^MT or Kit^D816V, respectively. All these mutant phenotypes resemble the disease phenotypes of patients having the same combinations of mutations. (Created with BioRender.com)