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Association details:
| Biomarker: | FLT3 D835 |
|---|---|
| Cancer: | Acute Myelogenous Leukemia |
| Drug: | sorafenib (Multi-tyrosine kinase inhibitor, pan-RAF inhibitor) |
| Direction: | Sensitive |
Evidence:
Source:
Title:
Outcomes with sequential FLT3-inhibitor-based therapies in patients with AML
Published date:
10/08/2020
Excerpt:
A total of 239 patients with FLT3-ITD- and/or FLT3-D835-mutated AML who received FLT3i-based treatments (including single-agent or combination FLT3i therapies) were identified...Of 10 patients harboring D835 TKD mutations, 7 achieved CRc (70%): 4 received sorafenib (3 achieved CRc), 3 quizartinib (2 achieved CRc), and 3 midostaurin (2 achieved CRc) as induction FLT3i.
DOI:
10.1186/s13045-020-00964-5
Source:
Title:
Sorafenib treatment of FLT3-ITD+ acute myeloid leukemia: favorable initial outcome and mechanisms of subsequent nonresponsiveness associated with the emergence of a D835 mutation
Excerpt:
LICs bearing the D835 mutant have expanded during sorafenib treatment and dominated during the subsequent clinical resistance. These results suggest that sorafenib have selected more aggressive sorafenib-resistant subclones carrying both FLT3-ITD and D835 mutations, and might provide important leads to further improvement of treatment outcome with FLT3 inhibitors.
DOI:
https://doi.org/10.1182/blood-2011-06-363960
