Table 1.
Year | Transgene | Strategy | Promoter | Inducer | Cellular Target | Phenotype | Ref. |
---|---|---|---|---|---|---|---|
1996 | PML-RARA | Conventional | CD11b | Myeloid lineage (BM, periphery) | Abnormal myelopoiesis. No APL | [52] | |
1997 | PML-RARA | Conventional | hCG | Myeloid lineage (BM, periphery) | Myeloid cells expansion in BM and spleen. AML-like with 30% penetrance after long (> 100 days) latency | [51] | |
1997 | PML-RARA | Conventional | hMRP8 | Myeloid lineage (BM, periphery) | APL-like disease (median 174 days) | [53] | |
2000 | RUNX1-ETO | Conditional | Tet | tTA | BM | Abnormal haematopoiesis. No AML | [60] |
2001 | RUNX1-ETO | Conventional | hMRP8 | Myeloid (neutrophils & monocytes) | AML-Only upon new-born treatment with ENU | [61] | |
2006 | Cbfb-MYH11 | Conditional | Cbfβ | Mx-iCre | BM (LSK) | AML-Aberrant myeloid progenitors, blocked megakaryotic differentiation. | [62] |
2008 | Mll-AF9 | Knock-in (Mll1; Mllex8-AF9 cDNA) | Mll | AML-Higher MLL-AF9 expression in HSCs than GMPs. | [63] | ||
2014 | MLL-ENL | Conditional | TRE (Col1a) | rtTA | LT-HS, pMeg/E, HSC, MPP, GMLP, CLP | AML- no leukaemia from HSC | [64] |
2016 | MLL-AF9 | Conditional | TRE (Hprt) | rtTA | LT-HSC, ST-HSC, CMP, GMP | AML-dependent on DOX dose and cellular origin | [65] |
2018 | MLL-ENL | Conditional | TRE (Hprt) | rtTA | LT-HSC, LMPP, CMP | AML-MLL-dependent on DOX dose and cellular target | [66] |
Conventional (DNA injection into Oocytes), Knock-in (homologous DNA recombination in ES cells), Conditional (regulated expression), LSK (lineage marker negative, Sca1+, cKit+), MPP (multipotent progenitors), GMLP (granulocyte-macrophage-lymphoid progenitors), CLP (common lymphoid progenitor), ST-HSC (short term hematopoietic stem cells), DOX (doxycycline).