HYPOTHESIS FOR TARGET THERAPY IN AML

Leukemic cells do not like Mesenchymal transformation, therefore MEK amplification is an absolute must in treatment.
2.  The primary dysfunction in AML is Histone Deacetylation
but Histone deacetyl transferase inhibitors will work in some cases because of the variety of deacetylation or heterogeneity of molecules involved
3.  Amplification of the NF-kB signal transduction may help some patient
4. Growth factors and Androgen  may help some patients
5. Insulin may help some subset of patients
6. we predict that MTOR inhibition will have a very limited effect (except in those with specific gene discussed yesterday)
7. Velcade will not work in patients with NACA-1

so combination of the future
chemoth and MEK amplification agents
Histone Deacetylase inhibitors and MEK amplifiers
Histone Deacetylator Androgen and MEK amplifiers
MTOR-ANDROGEN-MEK amplifier
androgen will be added to pt with TIF2