title: AKT as locus of cancer phenotype.
abstract: Cancer robustness is generated by the positive feedback loops. The positive loops hyperactivate AKT locus forming a cancer phenotype in leukemia, lymphoma, myeloma, plasmocytoma, sarcoma and carcinoma. The positive loops inducing AKT hyperphosphorylation increase activity of the AKT locus and the nodal associated and interconnected signaling genes. Only genes expressed above the threshold in the AKT signaling interactome networks, participate in the formation of the complex cancer phenotype. AKT is the switching locus for the cancer phenotype. The phenotype formation and maintenance is regulated by the AKT locus through an entropy/enthalpy processes. Targeting the AKT by locus chemotherapy, changing redox balance (antioxidant/oxidant), affects phosphorylation and activity of the AKT, inducing conversion of the positive feedback loops and disappearance of the malignant phenotype.
authors.affiliation: Department of Surgery, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts, 02115.
authors.forename: Ziv
authors.initials: Z
authors.lastname: Radisavljevic
mesh_terms: D000818:Animals; D006801:Humans; D009369:Neoplasms / Q000378:metabolism* / Q000473:pathology; D010766:Phosphorylation / Q000235:genetics / Q000502:physiology; D051057:Proto-Oncogene Proteins c-akt / Q000235:genetics / Q000378:metabolism*; D015398:Signal Transduction / Q000235:genetics / Q000502:physiology
chemical_list: D051057:Proto-Oncogene Proteins c-akt
keywords: AKT LOCUS; CANCER PHENOTYPE; HEMATOLOGICAL MALIGNANCY; POSITIVE FEEDBACK LOOPS; SOLID CANCERS