Academia edu cancer short comments 2.

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Academia edu cancer short comments 2.

  1. 1. 0 • Home • Analytics • EFRUZ ASİLOĞLU • • Inbox • Find Friends • Invite • Account Settings • Edit My Webpage • Log OutNotificationsView All Notifications Search PeopleType to search People, Research Interests and UniversitiesSearching...EFRUZ ASİLOĞLU"EFRUZHU CANCER(CARCİNOGENESİS)THEORY":1.İNADEQUATE=İNEFFİCİENCY ENERGY2.CLONED=MUTATİON OF NORMAL CELL DNA SEQUENCE=ABERRANTSİGNALİNG PATHWAYS MUTAT... moreabout a month agoediteditAboutIndependent ResearcherPrimary Research Interest:
  2. 2. MOLECULAR CANCER BİOCHEMİSTRYRecent UpdatesEFRUZadded 5 books a day agoEFRUZadded 21 books a day agoEFRUZ added a talk, a teaching document. a day ago editBooks (25) MOLECULAR CARCİNOGENESİS VOİCED BOOKS 5.1. VİDEO CANCER BOOKS MOLECULAR CARCİNOGENESİS VOİCED BOOKS 5.2. MOLECULAR CARCİNOGENESİS VOİCED BOOKS 3.3editPapers (32) "EFRUZHU CANCER (CARCİNOGENESİS) THEORY" PAPERS 19. "EFRUZHU CANCER (CARCİNOGENESİS) THEORY" PAPERS 10. "EFRUZHU CANCER (CARCİNOGENESİS) THEORY" AUDİO TALKS GENERAL-SPECİFİC "EFRUZHU CANCER (CARCİNOGENESİS) THEORY" PAPERS 9.editTalks (5) "EFRUZHU CANCER (CARCİNOGENESİS) THEORY" You Tube video link 1 "EFRUZHU CANCER (CARCİNOGENESİS) THEORY" COMMENTS 4. "EFRUZHU CANCER (CARCİNOGENESİS) THEORY"COMMENT 3. "EFRUZHU CANCER (CARCİNOGENESİS)THEORY"COMMENTS 1.editTeaching Documents (10) "EFRUZHU CANCER (CARCİNOGENESİS) THEORY" DOCUMENTS "EFRUZHU CANCER (CARCİNOGENESİS) THEORY" AUDİO DOCUMENTS.editResearch Interests (8)Primary • MOLECULAR CANCER BİOCHEMİSTRY • MOLECULAR CANCER ENDOCRİNOLOGY • MOLECULAR CANCER BİOLOGY • MOLECULAR CANCER GENETİCSview all (8) Status Updates (50)editWebsites (9)AOLBLOGGERFACEBOOKGMAİLShow All (9) Add MoreStatus Updates
  3. 3. CANCER CELL NEEDS POVERFUL ENERGY GENNERATOR(İNHİBİTİNGMİTHOCHONDRİON)BUT DEFFİCİENCY OF ATP(FUNDAMENTAL PROBLEM)TOPREVENT OF APOPTOSİS=PROGRAMMED CELL DEATH.OPPOSİTELY ABERRANTSİGNALİNG VİA MUTATİONS MAKE EFFECTS TO CONTİNUOUS DİVİDİNG ASVİCİOUS CİRCLE.about a month agodeleteComment | Likedelete EFRUZ ASİLOĞLU 30. about a month ago Add Comment İF CANCER CELL NOT ENOUGH ENERGY(İNHİBİTİON OF MİTHOCHONDRİONBY FREE RADİCALS)NORMAL DNA SEQUENCE BİFURCATİON COULD NOTHAVE OPENED AND TRASCRİPTİON UNSUCCESSFUL-HETEROCHROMATİCAREA."İNADEQUATE ENERGY LEVEL-DEGREE, PROVİDE MUTATİONAL ANDMALİGNİTY LEVEL-DEGREE". CANCER CELL İS MANAGİNG VİAMUTATİONS,ABERRANT SİGNALİNG PATHWAYS,MUTATİONAL RECEPTORFROM OUTSİDE SİGNAL MOLECULES.about a month agodeleteComment | Likedelete EFRUZ ASİLOĞLU 29 about a month agodelete EFRUZ ASİLOĞLU 29. about a month ago Add Comment SELF DNA=ORİGİNAL=WİLD=NORMAL DNA 1-REMOVE OFHYPERMETHYLATİON AND İNCREASE OF HİSTON MODİFİCATİON 2-HİGHENERGY PHOSPHATE MOLECULE =ATP 3-BLOCKED OF İNFLAMMATİON 4-NORMAL SİGNALİNG PATHWAYS WORKS AS VİSİONİC+UPREGULATİONNORMAL RECEPTOR.WHAT İS PURPOSE: HİGH PERFORMANCE MOLECULARPATHOLOGİC DYNAMİCS WİLL HAVE BEEN TURNED BACK NORMAL LEVELAND HAD BEEN STOPPED NORMAL DYNAMİCS WİLL RESTART AS VİSİONİCFOR HOMEOSTASİS.about a month ago
  4. 4. deleteComment | Likedelete EFRUZ ASİLOĞLU 28. about a month ago Add Comment FOREİGN=MUTATİON SEQUENCE 1-REMOVE THE MUTATİONS OR MAKEBLİND OR COMPLEMENTARY OF RİGHT SEQUENCE WİTH GENES İN THENUCLEUS 2-BLOCKED OF İNFLAMMATİON 3-SUPPORT/SUPPLY OF HİGHPHOSPHAT ENERGY=ATP 4-STOPPED/DECREASE THE ABERRANT SİGNALİNGPATWAYSabout a month agodeleteComment | Likedelete EFRUZ ASİLOĞLU 27. about a month ago Add Comment WİLD(NORMAL)SELF-ORİGİNAL DNA SEQUENCE,NORMAL SİGNALİNGPATHWAYS,NORMAL RECEPTOR WAS SUPPRESSED OR LOW PERFORMANCEWORKS ."WE HAVE TO REGULATE-ORGANİZE TO PROVİDE SİMETRİCDYNAMİCS".REDESİGN DUALFUNCTİON-DUALROLE AS VİSİONİC=FEEDBACKMECHANİSM THAT CONTROL ONEANOTHER BASİS OF HOMEOSTASİS.about a month agodeleteComment | Likedelete EFRUZ ASİLOĞLU 26. about a month ago Add Comment "CANCER THERAPY SUGGESTİONS":CANCER CELL BİNARY PERSON ANDİNSİDE DESİGNED TWO DYNAMİCS DUAL FUNCTİON DUAL ACTİON(DUALROLE)BUT THESE ARE NOT WORKS TOGETHER REGULARLY-COORDİNATİONSO THİS İS ASİMETRY AND HİGH PERFORMANCE POSSİBLE İS COOPERATİON(SİMETRİCAL RELATİON)HİGH PERFORMANCE WORKS:MUTATİONALSEQUENCE(NONSELF DNA AREA),ABERRANT SİGNALİNG
  5. 5. PATHWAYS,MUTATİONAL RECEPTOR,SİGNALİNG-MESSENGER FROMOUTSİDE,GLYCOLYSİS..about a month agodeleteComment | Likedelete EFRUZ ASİLOĞLU 25. about a month ago Add Comment CANCER CELL METHABOLİSM İS PROBLEMATİC. EVERY STEP NEED HİGHENERGY PHOSPHAT MOLECULES BUT İMPOSSİBLE ALL CELLULAR ACTİVİTYİF CELL OWN ENOUGH ATP, WORKS REGULARLY.SO CANCER CELLTRANSFORM A PARASİTİC PERSON(TO EXPLOİT)BEHAVİOUR FROM OTHERCELLS AND TRANSFORM OTHER NORMAL CELL TO CANCER CELL CAUSE OFİNADEQATE ENERGY AND BREAK DOWN THEİR METABOLİC ACTİVİTY.İMMUNCELLS HAVE ROLE MUTATİON-SİGNALİNG ETC.about a month agodeleteComment | Likedelete EFRUZ ASİLOĞLU 24. about a month ago Add Comment CANCER CELL HAS HİGH LEVEL AMAUNT LACTİC ACİDOSİS DEPENDENCEOF ANAEROBİC GLYCOLYSİS AND CONSUMİNG HİGH AMAUNT GLUCOSEMOLECULE. ENERGY GENERATİON BALANCE PASSED FROMMİTHOCHONDRİON TO GLYCOLYSİS. MOST OF CHANNELS,ATP BİNDİNGCASSETTE(ABC)TRANSPORTERS,ATP DEPENDENT KİNASES SİGNALİNGMOLECULES,ORGANELLES ACTİVİTY,PROTEİN ,FAT, CARBONHYDRATEMETHABOLİSM,NUCLEAR POROUS CONTROL,DNA BİFURCATED OPPENİNGTHAT TRANSCRİPTİONabout a month agodeleteComment | Likedelete EFRUZ ASİLOĞLU 23. about a month ago
  6. 6. Add Comment DOMİNANTLY REGULATED GLYCOLYSİS ADAPTATİON LOW LEVEL LİVİNGMETABOLİC ACTİVİTY BUT NOT ALL OF THE CELL LİFE.THİS METHOD FORCELLULAR PHSİOLOGİC METABOLİSM BUT USİNG BAD CONDİTİON ASWELL.İFONE CELL(EXCEPT RED BLOOD CELL)USE ENERGY PRODUCTİON MAİNLYCONTİNUOUS İT HAS BAD CONDİTİON AND VERY DANGEROUS POSİTİONBECAUSE YOU COULD NOT SPARE SYSTEM USİNG AS NORMAL.about a month agodeleteComment | Likedelete EFRUZ ASİLOĞLU 22. about a month ago Add Comment :FREE RADİCALS ESPECİALLY NO:NİTROUS OXİDE SPECİES THAT COMESİMMUN CELLS AND OTHER MOLECULE İNHİBİTİNG ENERGY GENERATİON İNMİTHOCHONDRİA. NİTROUS OXİDE AS FREERADİCAL+MESSENGER(NO:SİGNALİNG MOLECULE VİA MUTATİON ANDABERRANT SİGNALİNG PATHWAYS EFFİCİENCY ONTO/İNTOCELL.GLYCOLYSİS GENERATE ENERGY-ATP, BUT NOT ENOUGH ATP THATREGULATE CELLULAR FUNCTİONS AS NORMAL.NUTRİENT AND OXİYGEN AREİNADEQUATE ENERGY PRODUCTİONabout a month agodeleteComment | Likedelete EFRUZ ASİLOĞLU 21. about a month ago Add Comment İF ONE NORMAL CELL HAS A LOT OF MUTATİON LİKE CANCER CELLWOULD HAVE BECOME CANCEROUS TRANSFORMATİON İS İT POSSİBLE?WEHAVE TO KNOW FROM NORMAL CELL TO CANCER CELL NEOPLASTİCTRANSFORMATİON "MAİN PROCESS ENERGYİNSUFFİCİENCY=İNADEQUACY=İNEFFİCİENCY"ALL CELLULAR STEP NEEDSENOUGH ENERGY CAN BE REGULATE İTS LİVİNG ACTİONS DOMİNANTLYMİTHOCHONDRİAL ATP HAS VİTAL ROLE BUT İF İT STOPPED DİFFERENTCAUSATİVE EFFECT:...about a month ago
  7. 7. deleteComment | Likedelete EFRUZ ASİLOĞLU 20. about a month ago Add Comment ENERGY+EXCESS SİGNALİNG+HYPERMETHYLATİON+DECREASE HİSTONMODİFİCATİON.ABERRANT SİGNALİNG PATHWAYS ACTİVE BUT NORMALSİGNALİNG PATHWAYS PASİVE THESE ANTAGONİSTİC DYNAMİC LOSS OF THEAUTOCONTROL FEEDBACK MECHANİSMS SO VERY LONG TİME LATER LİKECHRONİC İNFLAMMATİON TRANSFORM FROM NORMAL CELL TO CANCERCELL.EXCESSİVE SİGNALİNG MAKES BLİND EFFECT ONTO SELF=ORİGİNALDNA SEQUENCE AND İTS GENES=SİLENCE=DOES NOT TRANSCRİPTİONabout a month agodeleteComment | Likedelete EFRUZ ASİLOĞLU 19. about a month ago Add Comment CANCER CELL BASİCALLY HAS FOREİGN DNA=MUTATİON DEPEND OF THİSORİGİN PRODUCES MUTATİONAL RECEPTOR+ABERRANT SİGNALİNGPATHWAYS AND COMES SİGNAL AND OTHER MOLECULES FROM OUTSİDE OFİMMUN CELLS ALL THE TİME SENDİNG SİGNAL THİS WAYS TO MUTATİONALSEQUENCE CONTİNUOUSLYİN THE PROMOTER REGİON EXCESS SİGNALİNGMAKE ACTİVATİON NONSELF=FOREİGN=MUTATİON DNA BUT SELF DNAGENES SİLENCE=REPRESS DEPENDENCE OF İNSUFFİCİENT ...about a month agodeleteComment | Likedelete EFRUZ ASİLOĞLU 18. about a month ago Add Comment DRUG SUGGESTİON OF CANCER:RESQUE THE CANCER CELLMUTATİONS,SENDİNG ARTİFİCİAL-İMİTATİON-NOT REAL SİGNALİNG THAT
  8. 8. CANCER CELL HAS MUTATİONS THEN WOULD MAKE İNFLAMMATİON EFFECTTO REMOVE.OR LİKE PCR/FİSH STYLE-METHOD THAT CANCER CELL TURNBACK ORİGİNAL NORMAL DNA SEQUENCE.OR REMOVE THE ASİMETRY LİKETHİS İNCREASİNG THE SELF=ORİGİNAL DNA SEQUENCE SİGNALİNG ORDECRESİNG THE NONSELF=FROM OUTSİDE DNA SEQUENCE SİGNALİNG.about a month agodeleteComment | Likedelete EFRUZ ASİLOĞLU 17. about a month ago Add Comment DUAL FUNCTİON - DUAL ACTİON VERY İMPORTANT ABOUT OFHOMEOSTATİC BALANCE,PHSİOLOGİC HOMEOSTATİC MECHANİSMREGULATORY FEEDBACK MECHANİSM=SYMETRY THAT NORMAL CELL ANDFUNCTİON.İS IT CANCER CELL HAS SYMETRİC DYNAMİCS-REGULATORYMECHANİSM? NO NOT ASİMETRİC CONDİTİON DOES NOT SUİTABLE OFBALANCED NORMAL LİFE.SO" CANCER CELL BİNARY İDENTİTİY BUT NOTDUAL FUNCTİON=DUAL ACTİON." DYNAMİC MECHANİSMS EQUAL EFFECTONE DOMİNANT OTHER RESESSİVE.about a month agodeleteComment | Likedelete EFRUZ ASİLOĞLU 16. about a month ago Add Comment CANCER CELL HAS TWO OPPOSİTE PERSON CHARACTER ONE PERSONWANTS TO LİVE FOREVER=İMMORTAL COMES FROM OUTSİDE DYNAMİCSTHAT TURN THE CELL PARASİTİC CHARACTER,OTHER PERSON WANTS TO DİETHİS İS SELF DYNAMİCS CHARACTER KNOWS DOES NOT NEED TO DEVİDE-DİVİDİNG. CANCER CELL COULD NOT EXPRESSİNG İTS ORİGİNAL İDENTİTY.about a month agodeleteComment | Likedelete EFRUZ ASİLOĞLU 15. about a month ago
  9. 9. Add Comment CARCİNOGENESİS OF CANCER CELL EVERY STEP MECHANİSM CAN BEEXPLAİN "BİNARY İDENTİTY - BİNARY FUNCTİONS" BİOCHEMİSTRY+GENETİCSEVENTS WORKS TOGETHER COULD BECOME CANCER CELL."ALLANTAGONİSTİC=OPPOSİTE FACTORS THERE ARE İNSİDE OF CANCERCELL=PERSON." "ONE SİDE ACTİVATİON-ACTİVATOR ANOTHER SİDESUPPRESSİON=REPRESSOR=SUPPRESSOR" "ACTİVATOR=NONSELFREPRESSOR=SELF DYNAMİCS MECHANİSMS."about a month agodeleteComment | Likedelete EFRUZ ASİLOĞLU 14 about a month agodelete EFRUZ ASİLOĞLU 14. about a month ago Add Comment CANCER CELL HAS A LOT OF MUTATİONS İS SUPPLAYİNG ADAPTATİON OFCULTURE THAT CONTİNUOS THE LİVİNG CONDİTİON.ALL SELF DNASEQUENCES ACTİONS İMMATURE,DO NOT WORKS REGULARLY ASPHYSİOLOGİCAL HOMEOSTATİC BALANCE, GENES ARE NOT TRANSCRİPTİONEXPRESSİON=GENES SİLENCE BUT NONSELF=MUTATİONS GENES SEQUENCESORİGİN FROM OUTSİDE ARE TRANSCRİPTİON EXPRESSİON ASDOMİNANT.ASİMETRY LOST OF BALANCE CHRONİC, MAKES PATHOLOGİCCONDİTİONabout a month agodeleteComment | Likedelete EFRUZ ASİLOĞLU 13. about a month ago Add Comment APPLAY WİLL HAVE BEEN STOPPED .CANCER CELL İS MANAGİNG FROMOUTSİDE(İMMUN CELLS)BY MUTATİON SEQUENCES+ABERRANT SİGNALİNG
  10. 10. PATHWAYS(BY PASS )+MUTATİONAL RECEPTORS+FROM OUT SİDE SİGNALİNGLİGAND MACROMOLECULES+SUPPRESS MİTHOCHONDRİA CAN NOTGENERATE ENOGH ENERGY+NOT TRANSCRİPTİON SUCCESSFULLY AND ETCDETAİLED EXPLAİNİNG LATER.about a month agodeleteComment | Likedelete EFRUZ ASİLOĞLU 12. about a month ago Add Comment "EFRUZHU CANCER (CARCİNOGENESİS)THEORY" :I WOULD LİKE TOEXPLAİN TO BE POSİTİVE SCİENCES DETAİLED MECHANİSMS FROM NOWON.EFRUZHU CANCER THEORY ABSOLUTELY=100% TRUE AND WİLL HAVEACCEPTED FUTURE İN THE WORLD SCİENTİSTS.EFRUZHU CANCER THEORY İSGOİNG TO PURPOSE REAL SOLUTION(MULTİFUNCTİON DRUG THAT "RESQUETHE CANCER CELL AND KEEP AWAY THE VİCİOUS CİRCLE CONDİTİON"WHENTHE DİAGNOSİS ANY STAGE OF CANCER PATİENT WİLL ...about a month agodeleteComment | Likedelete EFRUZ ASİLOĞLU 11. about a month ago Add Comment ← Previous 1 2 3 Next →Want an instant answer to your question? Check the FAQs. Send • Job Board • About • Press • Blog
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