All content on this site is intended for healthcare professionals only. By acknowledging this message and accessing the information on this website you are confirming that you are a Healthcare Professional. If you are a patient or carer, please visit Know AML.
The aml Hub website uses a third-party service provided by Google that dynamically translates web content. Translations are machine generated, so may not be an exact or complete translation, and the aml Hub cannot guarantee the accuracy of translated content. The aml and its employees will not be liable for any direct, indirect, or consequential damages (even if foreseeable) resulting from use of the Google Translate feature. For further support with Google Translate, visit Google Translate Help.
The AML Hub is an independent medical education platform, sponsored by Daiichi Sankyo, Johnson & Johnson, and Syndax, and has been supported through an educational grant from the Hippocrate Conference Institute, an association of the Servier Group. The funders are allowed no direct influence on our content. The levels of sponsorship listed are reflective of the amount of funding given. View funders.
Now you can support HCPs in making informed decisions for their patients
Your contribution helps us continuously deliver expertly curated content to HCPs worldwide. You will also have the opportunity to make a content suggestion for consideration and receive updates on the impact contributions are making to our content.
Find out moreCreate an account and access these new features:
Bookmark content to read later
Select your specific areas of interest
View aml content recommended for you
The fms-like tyrosine kinase 3 (FLT3) receptor is activated by binding to the fms-like tyrosine kinase 3 ligand (FLT3L), which is expressed by acute myeloid leukemia (AML) cells and is thought to enhance proliferation through an autocrine process.1 The soluble FLT3L concentration (sFLT3Lc) has been shown to correlate with the extent of bone marrow aplasia following treatment, and this could provide a potential prognostic impact in outcomes for AML patients.2
In a letter to the editor of Haematologica, the authors outlined the prospective, monocentric, non-interventional FLAM/FLAL trial (NCT02693899) which aimed to assess the impact of the sFLT3Lc kinetic profile on outcomes in intensively treated adult patients with AML following 18-month first-line therapy protocols.3 Endpoints assessed in this trial were progression-free survival (PFS) and overall survival (OS). Patients recruited to this trial (n = 63), between May 2016 and January 2018, were treated according to the standard-of-care first-line therapy, in line with multicenter trial protocols. Plasma samples were collected on days 1, 8, 15, and 22 of induction for analysis of sFLT3Lc by ELISA (n = 62; median age = 59 years, range 29–71). Prognostic value was assessed according to refractory status following induction, relapse according to morphologic, cytogenetic, molecular, or immunophenotypic characteristics.
The authors concluded that the sFLT3Lc kinetic profile during induction appeared to be an early prognostic marker which could help to classify patients with AML, although these results will need to be validated in a larger cohort study.
References
Your opinion matters
What barriers do you encounter when conducting multiple MRD tests during treatment?