Gene Location [1]
Receptor tyrosine kinase/growth factor signaling
Variant Type
Deletion - In frame
Affected Exon Number
Protein Domain [2]
Protein kinase
ClinVar Prediction [3]
Likely pathogenic

FLT3 I836del is present in 0.04% of AACR GENIE cases, with acute myeloid leukemia, acute monoblastic and monocytic leukemia, acute myeloid leukemia with myelodysplasia-related changes, and B-cell lymphoblastic leukemia/lymphoma having the greatest prevalence [4].

Top Disease Cases with FLT3 I836del

Biomarker-Directed Therapies

Significance of FLT3 I836del in Diseases

Acute Myeloid Leukemia +

Myelodysplastic Syndromes +

Acute Leukemia +

Acute Biphenotypic Leukemia +

B-Cell Non-Hodgkin Lymphoma +

Chronic Myeloid Leukemia +

Chronic Myelomonocytic Leukemia +

Diffuse Large B-Cell Lymphoma +

Mature B-Cell Lymphoma/Leukemia +

Mediastinal Large B-Cell Lymphoma +

Secondary Acute Myeloid Leukemia +


1. Hart R and Prlic A. Universal Transcript Archive Repository. Version uta_20180821. San Francisco CA: Github;2015. https://github.com/biocommons/uta

2. The UniProt Consortium. UniProt: a worldwide hub of protein knowledge. Nucleic Acids Research. 2019;47:D506-D515.

3. Liu X, Wu C, Li C, and Boerwinkle E. dbNSFP v3.0: A one-stop database of functional predictions and annotations for human nonsynonymous and splice site SNVs. Human Mutation. 2015;37:235-241.

Liu X, Jian X, and Boerwinkle E. dbNSFP: A lightweight database of human nonsynonymous SNPs and their functional predictions. Human Mutation. 2011;32:894-899.

4. The AACR Project GENIE Consortium. AACR Project GENIE: powering precision medicine through an international consortium. Cancer Discovery. 2017;7(8):818-831. Dataset Version 8. This dataset does not represent the totality of the genetic landscape; see paper for more information.

5. All assertions and clinical trial landscape data are curated from primary sources. You can read more about the curation process here.