Users' questions

What does FLT3 positive mean?

What does FLT3 positive mean?

The FLT3 gene codes for a protein called FLT3 that helps white blood cells grow. A mutation in this gene encourages the growth of too many abnormal leukemia cells. People with the FLT3 mutation have a very aggressive form of leukemia that’s more likely to come back after it’s treated.

What is FLT3 kinase?

The FLT3 gene provides instructions for making a protein called fms-like tyrosine kinase 3 (FLT3), which is part of a family of proteins called receptor tyrosine kinases (RTKs). Receptor tyrosine kinases transmit signals from the cell surface into the cell through a process called signal transduction.

What are FLT3 inhibitors?

FLT3 inhibitors are tyrosine kinase inhibitors (TKI) classified into first and next generation inhibitors based on their potency and specificity for FLT3 and their associated downstream targets.

Which is a negative regulator of FLT3 ITD?

We recently identified the PTP DEP-1/CD148/PTPRJ as a novel negative regulator of FLT3. This study addressed the role of DEP-1 for regulation of the acute myeloid leukemia (AML)–related mutant FLT3 internal tandem duplication (ITD) protein. Our experiments revealed that DEP-1 was expressed but dysfunctional in cells transformed by FLT3 ITD.

How does interference with FLT3 ITD inhibit cell transformation?

Interference with ROS production in 32D cells inhibited cell transformation by FLT3 ITD in a DEP-1–dependent manner, because RNAi-mediated depletion of DEP-1 partially abrogated the inhibitory effect of ROS quenching.

How does the FLT3 mutation prevent apoptosis?

The FLT3 Internal Tandem Duplication Mutation Prevents Apoptosis in Interleukin-3-Deprived BaF3 Cells Due to Protein Kinase A and Ribosomal S6 Kinase 1–Mediated BAD Phosphorylation at Serine 112 | Cancer Research Skip to main content AACR Publications Blood Cancer Discovery

Which is activator of STAT5 does FLT3 activate?

Previous studies have shown that FLT3/ITD activates the signal transducers and activators of transcription 5 (STAT5), p42/p44 mitogen-activated protein kinase [MAPK; extracellular signal-regulated kinase (ERK) 1/2], and phosphatidylinositol 3-kinase/Akt pathways.