Monday, June 23, 2014

Down the road of many cancers, our understanding is still increasing....

It is increasingly puzzling that Gene suppression could be one of the most powerful way to induce cancer and most likely to affect cellular migration in a process well identified as Metastasis.  This fact is true Whether you discuss RB1, or PTEN or in some cases BRCA2 or WT1. (or the Cadherins for that matter) In squamous cancer of the head and neck, suppression of the FAT1 has been clearly documented in the neoplastic transformation. The question is what can possibly  cause this decrease of gene expression affecting tumor suppressor.   Mutation is one mechanism we can't rule out or avoid or sometime even address.  The example of Colon cancer expressing KRAS Mutation comes to mind.  Wild type KRAS reassures the observer that the EGFR system is still intact and medication affecting this system could work.  But what is exactly the intact EGFR system.  There is increase evidences these gene mutations could be induced by Methylation.   This facts warrants further exploration as "demethylation" of specific genes could have a therapeutic effect.   This speculation also re-emphasized the fact that combining Anti-EGFR with de-methylating agent could open certain doors therapeutically in some diseases.  Along this line, one may assume that certain gene loss we observe actually remove certain list of genes from the "relative danger" of methylation.  The fact is the level of Methylation in certain cancer (MDS,Leukemic processes) needs further clarification.
Please do not forget that certain Cytokines may in fact promote methylation of genes that were not meant to that fate!

Package insert:"
Vectibix is an epidermal growth factor
receptor (EGFR) antagonist indicated
for the treatment of wild-type
KRAS
(exon 2) metastatic colorectal cancer
(mCRC) as determined by an FDA-approved test for this use"
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