Title |
Oncogenic protein tyrosine kinases
|
---|---|
Published in |
Cellular and Molecular Life Sciences, December 2004
|
DOI | 10.1007/s00018-004-4274-x |
Pubmed ID | |
Authors |
T. Naoe, H. Kiyoi |
Abstract |
FLT3, a member of the class III receptor tyrosine kinases (RTKs), is preferentially expressed on the cell surface of hematopoietic progenitors, and the ligand of FLT3 (FL) is expressed as a membrane-bound or soluble form by bone marrow stroma cells. It has been disclosed that FL-FLT3 interaction plays an important role in the maintenance, proliferation and differentiation of hematopoiesis. FLT3 is also expressed in a high proportion of acute myeloid leukemia (AML) and B-lineage acute lymphoblastic leukemia cells. Activating mutations of FLT3 are the most frequent genetic lesions in AML, and AML patients with FLT3 mutations have a worse prognosis than those with normal FLT3. Exploring the mechanism by which FLT3 mutations cause autoactivation and uncontrolled signaling might lead to a better understanding of how FLT3 becomes oncogenic and provide insights for the development of new drugs. |
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Geographical breakdown
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Russia | 1 | 2% |
Germany | 1 | 2% |
Belgium | 1 | 2% |
Switzerland | 1 | 2% |
Unknown | 53 | 93% |
Demographic breakdown
Readers by professional status | Count | As % |
---|---|---|
Researcher | 18 | 32% |
Professor | 7 | 12% |
Student > Master | 6 | 11% |
Student > Bachelor | 4 | 7% |
Student > Ph. D. Student | 3 | 5% |
Other | 8 | 14% |
Unknown | 11 | 19% |
Readers by discipline | Count | As % |
---|---|---|
Agricultural and Biological Sciences | 16 | 28% |
Medicine and Dentistry | 15 | 26% |
Biochemistry, Genetics and Molecular Biology | 10 | 18% |
Pharmacology, Toxicology and Pharmaceutical Science | 2 | 4% |
Chemistry | 2 | 4% |
Other | 3 | 5% |
Unknown | 9 | 16% |