p16 methylation in pituitary adenomas - p16 in pituitary adenomas (Nov/06/2005 )
i have been gettin contradictory reviews on the role of p16 gene in pituitary tumors, i have also come close to establishing that p16 is one of the most common tumor suppressor genes which is silenced in the tumors but,not many articles voice the same. i wish to get an opinion from here as well if p16 really plays any kind of role, especially its methylation which thereby leads to tumors .....
-researcher_81-
It is very commonly deleted or methylated in some types of leukemias.
-tap14-
QUOTE (researcher_81 @ Nov 6 2005, 11:40 PM)
i have been gettin contradictory reviews on the role of p16 gene in pituitary tumors, i have also come close to establishing that p16 is one of the most common tumor suppressor genes which is silenced in the tumors but,not many articles voice the same. i wish to get an opinion from here as well if p16 really plays any kind of role, especially its methylation which thereby leads to tumors .....
1. The cancer has lots of faces and masks and shapes and forms and features. This depends on the scenary of carcinogenesis -and the last depends on lots of reasons....even nutrition (methyl defficiency or not...)...So. there is no great surprise about contradictions....Some class of cancers is "p16 involved..."
2. It's difficult to predict if "p16 hypermethylated type cancer" differs significantly from "p16 damaged type cancer"
Theoretically this is possible and practically - the answer is interesting and important...are there any carcinogenes who damage p16 directly??
3. For experimental investigation U need very precise device to modify exactly p16 and no more...
4. Theoretically, U can damage any chain in DNA methylation system - aproximately - 100 targets starting from Serine (or even glycolysis way), folate subsystems and finishing directly suprresing DNA methylases - when there appears undermethylathion on p16 maybe depends on chance too ..I've read recently - when methyl defficient diet was used, it was observed in the beginning- THE GLOBAL HYPOmethylation of total DNA, and later - hypermethylation of some genes - this depends on geometrical-physical features of chromatine...is possible to study this question using google more deep...i'm not the great specialist in the role of p16...but interested in the cancerogenesis model...veteran too...T A Edisson made great job being 80 years
I.m from Vilnius, Lithuania - theoretician trying to improve The global model of carcinogenesis - much more wide, that B.Vogelstein proposed...
GOOD LUCK
-urba-