THIS SUGGEST THAT BLOCKING MIGRATION AND IMMUNE BETA-2 RECEPTOR OF TGF COULD ADD TO ACUTE EOSINOPHILIC LEUKEMIA. BLOCKING NUCLEAR INTERNALIZATION OF THE BETA SUBUNIT OF THE CBF WOULD HELP IN THE CBF DRIVEN LEUKEMIA IN GENERAL.
" Mutations in this particular gene cause synpolydactyly and Brachydactyly. The product of the mouse Hoxd13 gene plays a role in axial skeleton development ...
remember the role of Anti-VEGF /MEK in people with gene that impairs morphogenesis. leukemia with this mutation could a get a trial!
3 MEIS, a cofactor to the "soul of AML" E3
remember we discussed the AML is characterized by suppression of NF-kB
that suppression is achieved by this MEIS over-expression. it is the over expression to
HOS protein which is
'The homologue of Slimb (HOS) F-box protein is a receptor of the Skp1-Cullin1-F-box protein (SCF(HOS)) E3 ubiquitin ligase, which mediates ubiquitination and degradation of beta-catenin and the inhibitor of NFkappaB, IkappaB.''
Stability of homologue of Slimb F-box protein is regulated by availability of its substrate.
You block this stuff, you release NF-kB, you slow down leukemia or at least decrease co-existing infection rates (role in transplant patients).