Proteomics

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Translatome proteomics of human AML cells treated with FLT3 inhibitors quizartinib, crenolanib, gilteritinib

ABSTRACT: Internal tandem duplications (ITD) in the receptor tyrosine kinase FLT3 occur in 25% of acute myeloid leukemia (AML) patients and lead to constitutive activation of FLT3, driving leukemia cell survival and proliferation. Quizartinib, crenolanib and gilteritinib are second-generation FLT3 inhibitors (FLT3i) in phase III trials or clinical use for the targeted treatment of FLT3-ITD+ AML. However, they demonstrated only limited benefit and were not curative. A full understanding of cellular resistance factors contributing to this poor response is lacking. Here, we examined cell-autonomous pathways modulated by FLT3i using global translatome and phosphoproteome proteomics to identify non-genetic resistance mechanisms.

INSTRUMENT(S): Q Exactive HF

ORGANISM(S): Homo Sapiens (human)

TISSUE(S): Cell Suspension Culture, Leukocyte

DISEASE(S): Acute Leukemia

SUBMITTER: Sebastian Koschade  

LAB HEAD: Christian Münch

PROVIDER: PXD023125 | Pride | 2022-08-25

REPOSITORIES: Pride

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20200520_GT_SK_3-3_Plex1_F.msf Msf
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20200520_GT_SK_3-3_Plex1_F10.raw Raw
20200520_GT_SK_3-3_Plex1_F11.raw Raw
20200520_GT_SK_3-3_Plex1_F12.raw Raw
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Publications

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]

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