This document discusses cancer formation (carcinogenesis) through the interaction of activator and repressor proteins with CpG islands and methylation. During normal DNA transcription and expression, activator proteins are needed, but after neoplastic transformation, promoter regions become hypermethylated due to mutations, energy levels, and chronic inflammation. This hypermethylation prevents transcription factor binding, while mutations allow expression through hypomethylated promoter regions and aberrant ligand signaling pathways.

1. “EFRUZHU
CANCER (CARCİNOGENESİS) THEORY”
ACTİVATOR-REPPRESSOR PROTEİNS AND CPG İSLANDS
METHYLATİONS.
DETAİLED COMMENTS 9. = VOİCED 9.
NORMAL DNA SEQUENCE GENES TRANSCRİPTİON EXPRESSİON NEED
ACTİVATOR PROTEİNS. BUT AFTER NEOPLASTİC TRASFORMATİON
THİS PRMOTER REGİONS GENERALLY DEPENDENCE OF ENERGY,
MUTATİONS GROUP AND CHRONİC İNFAMMATİON DEGREE/LEVEL
ARE HYPERMETHYLATED AND SUPPRESSOR/REPPRESSOR PROTEİN
SHOULD NOT PERMİT TO TRANSCRİPTİON EXPRESSİON.ON THE
CONTRARY MUTATİONS GROUP İDENTİTY SEQUENCE GENES
TRANSCRİPTİON EXPRESİON DOMİNANTLY POSSİBLE BY ACTİVATOR
PROTEİNS İN THE PROMOTER REGİON TO BE
HYPOMETHYLATED.LİGAND SİGNALİNG FROM OUTSİDE VİA
MUTATİONAL RECEPTOR,ABERRANT SİGNALİNG PATHWAYS(NİTRİC
OXİDE-GUANİLATE CYCLASE-CYCLİC MONO PHOSPHATE+CALCİUM