Tuesday, February 25, 2014

and questions keep ringing the deep senses!

Does random phosphorylation induced by Casein and related decrease of AP-1 critical to Breast cancer (TNBC) development
can we equate or parallel depression of PTEN under HIF influence to Casein phosphorylation induced  depression of AP-1 in inducing cancers?
The same phosphorylation affect the RELA causing cross talking of the NOTCH and Catenins
all this putting center epigenetic phenomena to Neoplastic transformation
does this justify the cancer preventive force of certain anti-inflamatory drugs
can the effect of neoplastic prevention be linked to expression of c-fos
how does BCL-2 expression linked to c-fos
As easy at it sound, only certain facts leads to c-Fos expression...suggestion is overexpression of c-fos indicates that certain condition in the cell have been satisfied!
Are we in the belly of the beast when it comes to Breast and Pancreatic cancers,   Are we  at the bottom of the GTX combination used in Pancreatic cancer ?(the founders was talking of enzyme limiting activities and saturation?

check it out!

Casein kinase II is a negative regulator of c-Jun DNA binding and AP-1 activity

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