ABCC8 p.Asn676Lys
| Predicted by SNAP2: | A: N (72%), C: D (53%), D: N (97%), E: N (87%), F: D (63%), G: N (82%), H: N (57%), I: N (53%), K: N (82%), L: D (53%), M: D (53%), P: D (66%), Q: N (87%), R: D (53%), S: N (87%), T: N (93%), V: D (59%), W: D (66%), Y: D (63%), |
| Predicted by PROVEAN: | A: D, C: D, D: N, E: N, F: D, G: N, H: N, I: D, K: D, L: D, M: D, P: D, Q: N, R: D, S: N, T: N, V: D, W: D, Y: D, |
[switch to compact view]
Comments [show]
None has been submitted yet.
[hide] Pharmacogenomics in acute myeloid leukemia. Pharmacogenomics. 2009 Nov;10(11):1839-51. Roumier C, Cheok MH
Pharmacogenomics in acute myeloid leukemia.
Pharmacogenomics. 2009 Nov;10(11):1839-51., [PMID:19891558]
Abstract [show]
Acute myeloid leukemia (AML) in adults is a heterogeneous malignant pathology with a globally unfavorable prognosis. The classification of AML allows identification of subgroups with favorable prognosis. However, besides these specific subgroups, most patients will have an intermediate or unfavorable prognosis often resulting in induction failure, probably due to drug resistance of the leukemic blasts, and more frequently resulting in early relapse after achieving complete remission. This unfavorable situation leads to a strong need to develop new diagnostic and therapeutic options. However, development of these therapies and their efficient use requires a better understanding of the biology and the molecular pathogenesis of AML. Pharmacogenomics focuses on the genetic variation of drug-metabolizing enzymes, targets and transporters, and how these genetic variations interact to produce specific drug-related phenotypes. Potential genetic markers may serve to functionally subclassify patients by their disease and therefore influence the nature and intensity of treatment. This review summarizes important aspects of and recent advances in the field of pharmacogenomics in AML.
Comments [show]
None has been submitted yet.
No. Sentence Comment
231 An underlying resistance mechanism in patients resistant to PKC412 is an N676K mutation in the N-lobe of the FLT-3 gene [83].
X
ABCC8 p.Asn676Lys 19891558:231:73
status: NEW