She, Qing-Bai <br/><br/>
Resistance to gefitinib in PTEN-null HER-overexpressing tumor cells can be overcome through restoration of PTEN function or pharmacologic modulation of constitutive phosphatidylinositol 3'-kinase/Akt pathway signaling.  [electronic resource] 

 -  Clinical cancer research : an official journal of the American Association for Cancer Research  Oct 2003 
 - 4340-6 p.  digital 
<br/><br/> Publication Type: Comparative Study; Journal Article 
<br/><br/><label>ISSN: </label>1078-0432 
<br/><br/><label>Subjects--Topical Terms: </label><br/>Breast Neoplasms--drug therapy<br/>Chromones--pharmacology<br/>Down-Regulation<br/>Drug Resistance, Neoplasm<br/>Enzyme Inhibitors--pharmacology<br/>Epidermal Growth Factor--antagonists & inhibitors<br/>Female<br/>Gefitinib<br/>Genes, Tumor Suppressor<br/>Humans<br/>Morpholines--pharmacology<br/>Phosphatidylinositol 3-Kinases--metabolism<br/>Phosphoinositide-3 Kinase Inhibitors<br/>Phosphoric Monoester Hydrolases--genetics<br/>Protein Serine-Threonine Kinases<br/>Proto-Oncogene Proteins--metabolism<br/>Proto-Oncogene Proteins c-akt<br/>Quinazolines--pharmacology<br/>Receptor, ErbB-2--antagonists & inhibitors<br/>Reverse Transcriptase Polymerase Chain Reaction<br/>Signal Transduction<br/>Transfection<br/>Tumor Cells, Cultured