| Autor: |
Omura-Minamisawa M; Department of Pediatrics/Hematology-Oncology, University of California, San Diego 92103-8447, USA., Diccianni MB, Batova A, Chang RC, Bridgeman LJ, Yu J, de Wit E, Kung FH, Pullen JD, Yu AL |
| Jazyk: |
angličtina |
| Zdroj: |
Cancer research [Cancer Res] 2000 Dec 01; Vol. 60 (23), pp. 6573-6. |
| Abstrakt: |
p16 regulates the cell cycle pathway by inhibiting the cyclin Ds-cyclin-dependent kinase (CDK) 4/6-mediated phosphorylation of retinoblastoma protein (pRb). Previously, we reported that most primary T-cell acute lymphoblastic leukemia (T-ALL) harbored p16 inactivation and hyperphosphorylated pRb without cyclin Ds or CDK4/6 alterations. Therefore, inhibiting CDK4/6 may be an ideal therapeutic approach for p16 (-) T-ALL. UCN-01 (7-hydroxystaurosporine) is a potent antitumor agent that exerts its effects through the inhibition of CDKs. We now report that p16 protein expression status of T-ALL cells influences their sensitivity to UCN-01. In 36 primary T-ALL cells, the IC50s of UCN-01 in the 27 p16 (-) cells (43+/-52 nM) was significantly lower than that in the 9 p16 (+) cells (258+/-260 nM). Our results suggest that agents like UCN-01 may be useful as a p16-selective therapy for T-ALL. |
| Databáze: |
MEDLINE |
| Externí odkaz: |
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