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Gene FLT3
Variant V592G
Impact List missense
Protein Effect gain of function
Gene Variant Descriptions FLT3 V592G lies within a region important for maintaining kinase activity in the Flt3 protein (UniProt.org). V592G results in constitutive phosphorylation of Flt3, activation of Stat3/5, Akt, and Erk signaling, and is transforming in culture (PMID: 18068628).
Associated Drug Resistance
Category Variants Paths

FLT3 mutant FLT3 act mut FLT3 V592G

FLT3 mutant FLT3 exon14 FLT3 V592G

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Transcript NM_004119.3
gDNA chr13:g.28034144A>C
cDNA c.1775T>G
Protein p.V592G
Source Database RefSeq
Genome Build GRCh38/hg38
Transcript gDNA cDNA Protein Source Database Genome Build
NM_004119.2 chr13:g.28034144A>C c.1775T>G p.V592G RefSeq GRCh38/hg38
NM_004119.3 chr13:g.28034144A>C c.1775T>G p.V592G RefSeq GRCh38/hg38
NM_004119 chr13:g.28034144A>C c.1775T>G p.V592G RefSeq GRCh38/hg38

Filtering

  • Case insensitive filtering will display rows if any text in any cell matches the filter term
  • Use simple literal full or partial string matches
  • Separate multiple filter terms with a space. Any order may be used (i. e. a b c and c b a are equivalent )
  • Filtering will only apply to rows that are already loaded on the page. Filtering has no impact on query parameters.
  • Use quotes to match on a longer phrase with spaces (i.e. "mtor c1483f")

Sorting

  • Generally, the default sort order for tables is set to be first column ascending; however, specific tables may set a different default sort order.
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Molecular Profile Indication/Tumor Type Response Type Therapy Name Approval Status Evidence Type Efficacy Evidence References
FLT3 V592G Advanced Solid Tumor sensitive Midostaurin Preclinical - Cell culture Actionable In a preclinical study, Rydapt (midostaurin) inhibited FLT3-induced phosphorylation of ERK1/2 and reduced growth of transformed cells expressing FLT3 V592G in culture (PMID: 18068628). 18068628
FLT3 V592G acute myeloid leukemia predicted - sensitive Sorafenib Case Reports/Case Series Actionable In a clinical case study, Nexavar (sorafenib) and Droxia (hydroxyurea) treatment resulted in complete remission with no minimal residual disease, and continued Nexavar (sorafenib) treatment plus Vidaza (azacytidine) treatment resulted in sustained response for at least 60 months in a patient with acute myeloid leukemia harboring FLT3 V592G, along with NPM1 W288fs and TET2 T556fs (PMID: 32984009). 32984009