Dataset Information
Translatome proteomics of primary human FLT3-ITD+ AML cells treated with FLT3 inhibitors quizartinib, crenolanib, gilteritinib
Ontology highlight
ABSTRACT:
INSTRUMENT(S): Q Exactive HF
ORGANISM(S): Homo Sapiens (human)
TISSUE(S): Blood Cell, Leukocyte, Blood
DISEASE(S): Acute Leukemia
SUBMITTER: 
Sebastian Koschade
LAB HEAD: Christian Münch
PROVIDER: PXD034081 | Pride | 2022-08-25
REPOSITORIES: Pride
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| 20220123_KKL_SK_T6_F.msf | Msf | |||
| 20220123_KKL_SK_T6_F1.raw | Raw | |||
| 20220123_KKL_SK_T6_F10.raw | Raw | |||
| 20220123_KKL_SK_T6_F11.raw | Raw | |||
| 20220123_KKL_SK_T6_F12.raw | Raw |
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Publications
Translatome proteomics identifies autophagy as a resistance mechanism to on-target FLT3 inhibitors in acute myeloid leukemia.
Leukemia 20220823 10
Internal tandem duplications (ITD) in the receptor tyrosine kinase FLT3 occur in 25 % of acute myeloid leukemia (AML) patients, drive leukemia progression and confer a poor prognosis. Primary resistance to FLT3 kinase inhibitors (FLT3i) quizartinib, crenolanib and gilteritinib is a frequent clinical challenge and occurs in the absence of identifiable genetic causes. This suggests that adaptive cellular mechanisms mediate primary resistance to on-target FLT3i therapy. Here, we systematically inve ...[more]
