title: The multi-hit hypothesis in basal-like breast cancer.
abstract: It has been known for many years that for a "normal" un-transformed cell to become immortal and subsequently tumorigenic requires multiple pro-oncogenic changes in the levels of protein expression and function. Genes most commonly associated with the process of oncogenesis include: p53 inactivating mutation; hDM2 overexpression; p16 reduced expression; K-/H-RAS activating mutation; PTEN inactivating mutation/deletion; EGFR activating mutation and overexpression; retinoblastoma inactivating mutation and deletion; Cyclin proteins overexpression; CD95 reduced expression; protective BCL-2 proteins overexpression; to name but just a few of such molecules.(1-5) That the minimally required specific proteins for oncogenesis are not known for many specific tumor types remains a challenge for the rational design of molecular targeted therapies.
authors: Department of Neurosurgery; Massey Cancer Center; Virginia Commonwealth University; Richmond, VA USA.
authors: Paul
authors: P
authors: Dent
mesh_terms: D000818:Animals; D001943:Breast Neoplasms / Q000235:genetics*; D002471:Cell Transformation, Neoplastic / Q000235:genetics*; D066246:ErbB Receptors / Q000235:genetics*; D005260:Female; D006801:Humans; D018295:Neoplasms, Basal Cell / Q000235:genetics*; D051059:PTEN Phosphohydrolase / Q000235:genetics*; D016159:Tumor Suppressor Protein p53 / Q000235:genetics*
chemical_list: D016159:Tumor Suppressor Protein p53; D066246:ErbB Receptors; D051059:PTEN Phosphohydrolase
keywords: EGFR; MCF10A; PTEN; basal-like breast cancer; mammary cells; oncogene; p53; soft agar; transformation; tumor suppressor
references: Mol Cancer Ther. 2005 Feb;4(2):243-55
references: 15713896
references: Cancer Biol Ther. 2012 Apr;13(6):369-78
references: 22313637
references: Cancer Biol Ther. 2010 Nov 1;10(9):903-17
references: 20855960
references: Cancer Biol Ther. 2012 May;13(7):567-74
references: 22406992
references: Cancer Biol Ther. 2012 Nov;13(13):1235-43
references: 22909976
references: Cancer Res. 2002 Jan 1;62(1):89-98
references: 11782364
references: Mol Cancer Ther. 2005 Feb;4(2):257-70
references: 15713897
references: Cancer Biol Ther. 2013 Mar;14(3):246-53
references: 23291982
references: Cancer Biol Ther. 2013 Sep;14(9):853-9
references: 23792586