Targeted therapies in gynecologic cancers.
With the rapid development of high-throughput techniques for identifying novel specific molecular targets in human cancer over the past few years, attention to targeted cancer therapy has dramatically increased. The term "targeted cancer therapy" refers to a new generation of drugs designed to interfere with a specific molecular target that is believed to play a critical role in tumor growth or progression, is not expressed significantly in normal cells, and is correlated with clinical outcome. There has been a rapid increase in the identification of targets that have potential therapeutic application. The clinical success of the small-molecule kinase inhibitor imatinib mesylate in chronic myeloid leukemia and gastrointestinal stromal tumors has accelerated the development of a new era of molecular targeted cancer therapy. The number of agents under preclinical and clinical investigation has grown accordingly. This emphasis on molecular biology and genetics has also resulted in significant changes in the treatment of gynecologic cancers. Several promising drugs targeting tyrosine kinases (EGFR and Her-2/Neu), mTOR, Raf kinase, proteasome, and histone deacetylases, as well as drugs affecting apoptosis and mitosis, are under development for clinical application. However, some clinical trials of p53 gene therapies and farnesyl transferase inhibitors have had limited success. In this review, we will focus on potential novel targets in gynecologic cancer and the development of targeted therapy and its clinical applications in gynecologic cancer.
Chon
Hye Sook
HS
Department of Gynecologic Medical Oncology, The University of Texas M. D. Anderson Cancer Center, 1515 Holcombe, Houston, TX 77030, USA.
Hu
Wei
W
Kavanagh
John J
JJ
D020533:Angiogenesis Inhibitors / Q000008:administration & dosage* / Q000627:therapeutic use; D000818:Animals; D000911:Antibodies, Monoclonal / Q000008:administration & dosage* / Q000627:therapeutic use; D061067:Antibodies, Monoclonal, Humanized; D000970:Antineoplastic Agents / Q000008:administration & dosage* / Q000627:therapeutic use; D017209:Apoptosis / Q000235:genetics; D016503:Drug Delivery Systems / Q000639:trends*; D019008:Drug Resistance, Neoplasm; D066246:ErbB Receptors / Q000037:antagonists & inhibitors / Q000378:metabolism; D005260:Female; D000077156:Gefitinib; D018014:Gene Transfer Techniques / Q000639:trends*; D005833:Genital Neoplasms, Female / Q000098:blood supply / Q000188:drug therapy* / Q000235:genetics / Q000378:metabolism; D006801:Humans; D009389:Neovascularization, Pathologic / Q000517:prevention & control; D016376:Oligonucleotides, Antisense / Q000235:genetics / Q000378:metabolism; D047428:Protein Kinase Inhibitors / Q000008:administration & dosage* / Q000627:therapeutic use; D019253:Proto-Oncogene Proteins c-bcl-2 / Q000235:genetics / Q000378:metabolism; D011799:Quinazolines / Q000008:administration & dosage / Q000627:therapeutic use; D018719:Erb-b2 Receptor Tyrosine Kinases / Q000276:immunology / Q000378:metabolism; D015398:Signal Transduction / Q000187:drug effects; D013792:Thalidomide / Q000008:administration & dosage / Q000627:therapeutic use; D013873:Thionucleotides / Q000235:genetics / Q000378:metabolism; D000068878:Trastuzumab
D020533:Angiogenesis Inhibitors; D000911:Antibodies, Monoclonal; D061067:Antibodies, Monoclonal, Humanized; D000970:Antineoplastic Agents; D066246:ErbB Receptors; D000077156:Gefitinib; D016376:Oligonucleotides, Antisense; D047428:Protein Kinase Inhibitors; D019253:Proto-Oncogene Proteins c-bcl-2; D011799:Quinazolines; D018719:Erb-b2 Receptor Tyrosine Kinases; D013792:Thalidomide; D013873:Thionucleotides; D000068878:Trastuzumab; C408162:oblimersen