The combined status of ATM and p53 link tumor development with therapeutic response

• Published in: Genes & development Vol. 23; no. 16; pp. 1895 - 1909
• Main Authors: Jiang, Hai, Reinhardt, H. Christian, Bartkova, Jirina, Tommiska, Johanna, Blomqvist, Carl, Nevanlinna, Heli, Bartek, Jiri, Yaffe, Michael B., Hemann, Michael T.
• Format: Journal Article
• Language: English
• Published: United States Cold Spring Harbor Laboratory Press 15.08.2009
• Subjects: Animals; Antineoplastic Agents - pharmacology; Antineoplastic Agents - therapeutic use; Apoptosis - drug effects; Ataxia Telangiectasia Mutated Proteins; ATM; Breast Neoplasms - drug therapy; Breast Neoplasms - physiopathology; Cancer; Cell Cycle Proteins - metabolism; Cell Line, Tumor; Checkpoint Kinase 2; chemotherapy; DNA-Binding Proteins - deficiency; DNA-Binding Proteins - metabolism; DNA-PK; Drug Resistance, Neoplasm; Female; Humans; MEDICIN; MEDICINE; Mice; Mice, Nude; mouse models; Neoplasms - drug therapy; Neoplasms - physiopathology; NIH 3T3 Cells; p53; Protein-Serine-Threonine Kinases - deficiency; Protein-Serine-Threonine Kinases - metabolism; Research Paper; Signal Transduction; Survival Analysis; Tumor Suppressor Protein p53 - metabolism; Tumor Suppressor Proteins - deficiency; Tumor Suppressor Proteins - metabolism

While the contribution of specific tumor suppressor networks to cancer development has been the subject of considerable recent study, it remains unclear how alterations in these networks are integrated to influence the response of tumors to anti-cancer treatments. Here, we show that mechanisms commo...