PANCREATIC CANCER GENE (CONTINUED)

1' KRT20: keratin related gene, most likely of an early expression in neoplastic transformation
more predictive and diagnostic than of less therapeutic potential.

2-TEM 7: The blood vessels of Tumors seems to have an exclusive marker called Tumor Endothelial Marker or TEM.   Target therapy directed at this stuff may lead tumor to anoxic death by closing these vessels, at least that the wish of researchers, will follow their efforts!
Certainly this used as serologic marker or radiologically, can locate metastatic lesions.

3-MAP2K4" direct activator of the MAPK/c-JUNK through MAP8& 14. (Not the standard MAPK1)
but it also interact with an anchor called Filamin Though FLNC, filamin is actin binding protein, raising the issue of whether or not it is using this tract to quickly influence the Nucleus or whether it allows it to phosphorylate things right there!  we know its expression is, like the MTOR stimulated path, preserving survival!  Does this open the door to MTOR Inhibitor in Pancreatic cancer? Does expression of this pathway, an opportunity to introduce MTOR inhibitors?

4-BAT-26

please read this:
"BAT-26, an indicator of the replication error phenotype in colorectal cancers and cell lines" by

Hoang JM, Cottu PH, Thuille B, Salmon RJ, Thomas G, Hamelin R.

BAT 26 IS THEREFORE AN INDICATOR OF MICRO-SATELLITE INSTABILITY STATUS IN CANCER.

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5-ALOX12

6-TP53

7-BIRC5

8-NME1
9-ERBB2
10-GAS
11-TM4SF5

INTERESTING DEBATES

1.NF1 Mutation is upstream from
BRAF
and MTOR
But NF-1 is Mutated in Melanoma
can infusion of protein resulting from NF-1 be used to strengthen effect of MTOR inhibitor and BRAF inhibitor by maintaining these pathways open!

2.  Discriminating Redundancy in cellular language
same gene base corresponding to same Amino Acid
same receptors at membrane being sensitive by different stimuli
but when it comes to the RAS, nature and intensity need to matter and this also a function of tissue involved!
some time however the nature of the stimulus is more important particularly inside the cell where ie HP90 seems to stimulate more the CoN to achieve PTEN suppression. And you know that CoM stimulation raise Bcl2 level...we will say more in our upcoming article of langaue of the cell as it pertains to pathways!

3. PTEN is repressed by low expression of gene or mislocalization (reported PNUTS 'role) at Nuclear level or both?