CDC45L gene
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an essential protein required to the initiation of DNA replication. Cdc45 is a member of the highly conserved multiprotein complex including Cdc6/Cdc18, the minichromosome maintenance proteins (MCMs) and DNA polymerase, which is important for early steps of DNA replication in eukaryotes.
this gene talks to ORC1,   a six subunits protein complex essential for the initiation of the DNA replication that serves as a template for this initiation.While other ORC subunits are stable throughout the cell cycle, the levels of this protein vary during the cell cycle, which has been shown to be controlled by ubiquitin-mediated proteolysis after initiation of DNA replication. (Mcm protein)This protein is found to be selectively phosphorylated during mitosis. It is also reported to interact with MYST histone acetyltransferase 2 (MYST2/HBO1), a protein involved in control of transcription silencing.^{[2]  wikipedia}

MYST2 has been shown to interact with Androgen receptor,^[2] ORC1L^[1] and Vimentin.<sup>[4][5]
=============================LINKING ANDROGEN HORMONE STIMULATION TO GENE SILENCING !

TOP2A</sup>

 WIKIPEDIA
This gene encodes a DNA topoisomerase, an enzyme that controls and alters the topologic states of DNA during transcription. This nuclear enzyme is involved in processes such as chromosome condensation, chromatid separation, and the relief of torsional stress that occurs during DNA transcription and replication. It catalyzes the transient breaking and rejoining of two strands of duplex DNA which allows the strands to pass through one another, thus altering the topology of DNA. Two forms of this enzyme exist as likely products of a gene duplication event. The gene encoding this form, alpha, is localized to chromosome 17 and the beta gene is localized to chromosome 3. The gene encoding this enzyme functions as the target for several anticancer agents and a variety of mutations in this gene have been associated with the development of drug resistance. Reduced activity of this enzyme may also play a role in ataxia-telangiectasia.^[1]

 TOP2A has been shown to interact with HDAC1,^[2][3] CDC5L,^[4] Small ubiquitin-related modifier 1^[5] and P53.<sup>[6]

INHIBITORY iNTERACTION WITH BCL-2, A LIMITING FACTOR
DHFR
NCBI RESOURCE</sup>

Dihydrofolate reductase converts dihydrofolate into tetrahydrofolate, a methyl group shuttle required for the de novo synthesis of purines, thymidylic acid, and certain amino acids. While the functional dihydrofolate reductase gene has been mapped to chromosome 5, multiple intronless processed pseudogenes or dihydrofolate reductase-like genes have been identified on separate chromosomes. Dihydrofolate reductase deficiency has been linked to megaloblastic anemia. [provided by RefSeq, Jul 2008]

 CIT GENE LIKENKED THROUGH SEVERAL INTERMEDIARY TO THE RHO GENE WHOSE FUNCTIONS INCLUDE:
"The Rho family of GTPases is a family of small (~21 kDa) signaling G protein (more specific, a GTPase), and is a subfamily of the Ras superfamily. The members of the Rho GTPase family have been shown to regulate many aspects of intracellular actin dynamics, and are found in all eukaryotic organisms including yeasts and some plants. Three members of the family have been studied a great deal: Cdc42, Rac1, and RhoA. Rho proteins have been described as "molecular switches" and play a role in cell proliferation, apoptosis, gene expression, and multiple other common cellular functions.^[1][2]

WIKIPEDIA

CIT (gene) has been shown to interact with RHOB^[3] and RHOA.^[4][3]
 h CIT,^[4] ARHGEF3,^[5] ARHGDIG^[6] and RHPN2.^[7]
AND 

Human CNK1 Acts as a Scaffold Protein, Linking Rho and Ras Signal Transduction Pathways

 

AND  z Gene summary for CNKSR1:

This gene is a necessary element in receptor tyrosine kinase pathways, possibly as a tyrosine phosphorylation target.

It is involved in regulation of RAF in the MAPK pathway and may also play a role in a MAPK-independent pathway.

(provided by RefSeq, Jul 2008) 

 

====================================THESE ARE TARGET TO BLOCK TO AVOID SPILL OVER INTO MAJOR PATHWAYS!  IF YOU WANT TO STOP tHYROID CANCER TO FURTHER GROW!  BLOCK THE CONNECTIONS!

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