looking into cancer resistance and the autoimmune syndromes

-Does chronic exposure to autoimmune diseases or antigen stimulate
a new set of genes
-does these gene include genes from cellular growth
or cellular growth in autoimmune diseases is limited by consequence of energy consumption
does blocking energy consumption a valid intervention in cancer cure
-is vitamin D deficiency linked to consumption or repression of this gene or lack of absorption
-what are the cytokines liberated during an autoimmune disease
-how does decrease of proliferation rate linked to resistance to apoptosis
-how necrosis, senescence, autophagy (type II programmed cell death) and mitotic disruptions can be brought to bear in cancer resistance
-detections of inhibitors to main pathways,
-does inhibition represent a valid option to cancer cure
-does inhibitions of pump/ion receptor a potential way of wining resistance to cancer therapy
-can amplifying c-MYC be a major therapeutic intervention given its effect on Bcl-2
-According to the ASCPB:"DNA methylation is established by DNA methyltransferase (DMT) enzymes that transfer a methyl group from S-adenosyl Met to the fifth carbon of cytosine. Depending on whether the recognition site is already methylated or not, these enzymes can largely be subdivided into maintenance and de novo DMTs. Maintenance DMTs conserve the methylation status of symmetrical (palindromic) sites after DNA replication by recognizing the hemimethylated locus and methylating the newly synthesized strand. Candaele et al. (pp. 1350–1364)"
dosing this Methylation may be a significant intervention in cancer resistance particularly in cancer that use the subterfuge of migrating at distant levels to recur (glioblastoma) 
-does combining 

-does Pomalidomide or vectibix increase the effect of Temozolimide 
-or is it Panobinostat (hydroxamic acid) the next enhancer of Temolomide!
-or is it Erivedge the next big thing? 
-what is the the cytokines involved or is there any?