Sunday, March 3, 2013

Smooth Muscle Myosin & Leukemia

1.SMMHC, a Smooth Muscle Myosin related marker of differentiation, but also implying the use of multiple regulatory genes that ultimately depress P53 as a way to decrease repair of DNA and allow leukemia to proceed with proliferation. this marker is  seen in Inv-16 Leukemia.  Through interaction with SMAD3, it affects TGF driven migration of leukemic cells.  It also interfere with ACTA 2, TGFBR-2 AND FBN-1,
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.


2.HOXD3
" 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).
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