Tobacco carcinogen-induced cellular transformation increases Akt activation in vitro and in vivo.
West
Kip A
KA
Cancer Therapeutics Branch, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD 20889-5105, USA.
Linnoila
Ilona R
IR
Brognard
John
J
Belinsky
Steven
S
Harris
Curtis
C
Dennis
Phillip A
PA
D000818:Animals; D017209:Apoptosis; D002273:Carcinogens; D002471:Cell Transformation, Neoplastic / Q000378:metabolism*; D002478:Cells, Cultured; D004789:Enzyme Activation; D066246:ErbB Receptors / Q000378:metabolism; D006801:Humans; D008175:Lung Neoplasms / Q000201:enzymology* / Q000517:prevention & control; D051379:Mice; D008805:Mice, Inbred A; D009602:Nitrosamines; D010766:Phosphorylation; D017346:Protein Serine-Threonine Kinases / Q000037:antagonists & inhibitors / Q000378:metabolism*; D011518:Proto-Oncogene Proteins / Q000037:antagonists & inhibitors / Q000378:metabolism*; D051057:Proto-Oncogene Proteins c-akt
D002273:Carcinogens; D009602:Nitrosamines; D011518:Proto-Oncogene Proteins; C016583:4-(N-methyl-N-nitrosamino)-1-(3-pyridyl)-1-butanone; D066246:ErbB Receptors; C494918:AKT1 protein, human; D017346:Protein Serine-Threonine Kinases; D051057:Proto-Oncogene Proteins c-akt