Target Therapy for Extramedullary Relapse of FLT3 -ITD Acute Myeloid Leukemia: Emerging Data from the Field.
Andrea DuminucoCinzia MaugeriMarina ParisiElisa MauroPaolo Fabio FiumaraValentina RandazzoDomenico SalemiCecilia AgueliGiuseppe Alberto Maria PalumboAlessandra SantoroFrancesco Di RaimondoCalogero VetroPublished in: Cancers (2022)
FMS-like tyrosine kinase 3 (FLT3) is a receptor tyrosine kinase family member. Mutations in FLT3 , as well known, represent the most common genomic alteration in acute myeloid leukemia (AML), identified in approximately one-third of newly diagnosed adult patients. In recent years, this has represented an important therapeutic target. Drugs such as midostaurin, gilteritinib, and sorafenib, either alone in association with conventional chemotherapy, play a pivotal role in AML therapy with the mutated FLT3 gene. A current challenge lies in treating forms of AML with extramedullary localization. Here, we describe the general features of myeloid sarcoma and the ability of a targeted drug, i.e., gilteritinib, approved for relapsed or refractory disease, to induce remission of these extramedullary leukemic localizations in AML patients with FLT3 mutation, analyzing how in the literature, there is an important development of cases describing this promising potential for care.
Keyphrases
- acute myeloid leukemia
- tyrosine kinase
- epidermal growth factor receptor
- allogeneic hematopoietic stem cell transplantation
- newly diagnosed
- healthcare
- copy number
- systematic review
- palliative care
- genome wide
- stem cells
- big data
- dna methylation
- squamous cell carcinoma
- risk assessment
- machine learning
- gene expression
- mesenchymal stem cells
- immune response
- cancer therapy
- drug delivery
- quality improvement
- systemic lupus erythematosus
- transcription factor
- radiation therapy
- drug induced
- replacement therapy
- multiple myeloma
- genome wide identification