HINTS OF TARGET THERAPY!  JUST DO IT AND THANK ME LATER!

Proposed cytosine cycle.

" Five-hydromethylcytosine (hmC) is generated from 5-methylcytosine (mC) through oxidation catalyzed by the TET family of oxygenases. HmC may then be deaminated by members of the AID/APOBEC family and the resulting 5-hydroxymethyluracyl (hmU) is excised by thymine–DNA glycosylase (TDG), or another DNA glycosylase. This initiates the base excision repair process (BER), leading to replacement of hmU by an unmethylated cytosine. Further oxidation of hmC by TET enzymes may lead to 5-formylcytosine (fC) or 5-carboxylcytosine (caC). These modified cytosines may be specifically recognized and excised by TDG, leading to subsequent BER activity. CaC may also be converted to cytosine by a not yet identified decarboxylase. Oxidation of mC may also impair their recognition by maintenance methyltransferase DNMT1 and allow replication-dependent demethylation. A: abasic (apurinic/apyrimidinic) site."(Mercher et al)
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Disruptive antibody

PDZK1 is a scaffold protein that connects plasma membrane proteins and regulatory components, regulating their surface expression in epithelial cells apical domains. It may be involved in the coordination of a diverse range of regulatory processes for ion transport and second messenger cascades. In complex with SLC9A3R1, it may cluster proteins that are functionally dependent in a mutual fashion and modulate the trafficking and the activity of the associated membrane proteins. It may also play a role in the cellular mechanisms associated with multidrug resistance through its interaction with ABCC2 and PDZK1IP1. May potentiate the CFTR chloride channel activity. PDZK1 functions to connect SCARB1 with the cellular machineries for intracellular cholesterol transport and/or metabolism and may be involved in the regulation of proximal tubular Na(+)-dependent inorganic phosphate cotransport therefore playing an important role in tubule function (life science research)
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IDAX gene blocks the devil (Dvl) and therefore the Wnt, and through Caspase 3, regulate the TET2.
Block the PDZ locus on the Devil and you can get Leukemia under control!

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FOR ANGIOSARCOMA ,  GO TO YOUNG'S NOTE

II

Abstract

Background:

Angiogenesis is the process of new blood vessel formation

,

and is regulated by angiogenic growth factors

including vascular endothelial growth factor (VEGF)

.

Angiosarcomas are rare, aggressive vascular tumours

.

Studies were performed to investigate the expression of angiogenicgrowth factors in angiosarcoma

,

and to assess vascular targeted agents for the treatment of angiosarcoma

.

Methods:

In vitro studies compared

two human cutaneous angiosarcoma cell lines (ASM and ISO-HAS) with human dermal microvascular endothelial cells (HuD MECs).

The cell lines were compared in functional assays

,

including cell viability, cell differentiaiton and cell migration assays, and protein expression profiled using antibody arrays. Cell responses to vascular targeted agents were compared including response to bevacizumab an anti-VEGF antibody, axitinib a VEGFreceptor (VEGFR) tyrosine

kinase inhibitor

,

selumetinib a MEK inhibitor and DMXAA a vascular disrupting agent.'