
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
Molecular Oncology, Markers, Clinical Correlates |
Departments of1 Medicine, Hematology, and Oncology, 2 Cardiology, and 3 Neurology and 4 Institute of Clinical Chemistry and Laboratory Medicine, University of Münster, Münster, Germany; 5 Department of Abdominal and Vascular Surgery, University of Cologne, Cologne, Germany; and 6 European Laboratory Association, Ibbenbüren, Germany
ABSTRACT
Novel high-throughput analyses in molecular biology allow sensitive and rapid identification of disease-related genes and drug targets. We have used quantitative real-time reverse transcription-PCR reactions (n = 23,000) to analyze expression of all human receptor tyrosine kinases (n = 56) in malignant tumors (n = 313) of different origins and normal control samples (n = 58). The different tumor types expressed very different numbers of receptor tyrosine kinases: whereas brain tumors and testicular cancer expressed 50 receptor tyrosine kinases, acute myeloid leukemia (AML) samples expressed only 20 different ones. Specimens of similar tumor origin exhibited characteristic receptor tyrosine kinase expression patterns and were grouped together in hierarchical cluster analyses. When we focused on specific tumor entities, receptor tyrosine kinases were identified that were disease and/or stage specific. Leukemic blasts from AML bone marrow samples differed significantly in receptor tyrosine kinase expression compared with normal bone marrow and purified CD34+ cells. Among the differentially expressed receptor tyrosine kinases, we found FLT3, c-kit, CSF1 receptor, EPHB6, leukocyte tyrosine kinase, and ptk7 to be highly overexpressed in AML samples. Whereas expression changes of some of these were associated with altered differentiation patterns (e.g., CSF1 receptor), others, such as FLT3, were genuinely overexpressed in leukemic blasts. These data and the associated database (http://medweb.uni-muenster.de/institute/meda/research/) provide a comprehensive view of receptor tyrosine kinase expression in human cancer. This information can assist in the definition of novel drug targets.
This article has been cited by other articles:
![]() |
B. Dolniak, E. Katsoulidis, N. Carayol, J. K. Altman, A. J. Redig, M. S. Tallman, T. Ueda, R. Watanabe-Fukunaga, R. Fukunaga, and L. C. Platanias Regulation of Arsenic Trioxide-induced Cellular Responses by Mnk1 and Mnk2 J. Biol. Chem., May 2, 2008; 283(18): 12034 - 12042. [Abstract] [Full Text] [PDF] |
||||
![]() |
M. Camos, J. Esteve, P. Jares, D. Colomer, M. Rozman, N. Villamor, D. Costa, A. Carrio, J. Nomdedeu, E. Montserrat, et al. Gene Expression Profiling of Acute Myeloid Leukemia with Translocation t(8;16)(p11;p13) and MYST3-CREBBP Rearrangement Reveals a Distinctive Signature with a Specific Pattern of HOX Gene Expression. Cancer Res., July 15, 2006; 66(14): 6947 - 6954. [Abstract] [Full Text] [PDF] |
||||
![]() |
C. Xue, J. Wyckoff, F. Liang, M. Sidani, S. Violini, K.-L. Tsai, Z.-Y. Zhang, E. Sahai, J. Condeelis, and J. E. Segall Epidermal Growth Factor Receptor Overexpression Results in Increased Tumor Cell Motility In vivo Coordinately with Enhanced Intravasation and Metastasis Cancer Res., January 1, 2006; 66(1): 192 - 197. [Abstract] [Full Text] [PDF] |
||||
![]() |
C. Muller-Tidow, S. Diederichs, E. Bulk, T. Pohle, B. Steffen, J. Schwable, S. Plewka, M. Thomas, R. Metzger, P. M. Schneider, et al. Identification of Metastasis-Associated Receptor Tyrosine Kinases in Non-Small Cell Lung Cancer Cancer Res., March 1, 2005; 65(5): 1778 - 1782. [Abstract] [Full Text] [PDF] |
||||
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
| Cancer Research | Clinical Cancer Research |
| Cancer Epidemiology Biomarkers & Prevention | Molecular Cancer Therapeutics |
| Molecular Cancer Research | Cancer Prevention Research |
| Cancer Prevention Journals Portal | Cancer Reviews Online |
| Annual Meeting Education Book | Meeting Abstracts Online |