FLT3LG
Overview
FLT3LG (FLT3 Ligand) encodes the cytokine ligand for the FLT3 receptor tyrosine kinase, a key regulator of hematopoietic stem cell survival and differentiation. In cancer genomics, FLT3LG is notable in extra-cranial malignant rhabdoid tumors (MRT) where it falls within MRT-specific super-enhancers, suggesting epigenetic deregulation rather than direct mutation as the mechanism of altered expression. FLT3LG has established roles in stem-cell self-renewal and differentiation programs.
Alterations observed in the corpus
- FLT3LG is flagged within MRT-specific super-enhancers in extra-cranial malignant rhabdoid tumors (n=40); the super-enhancer landscape in MRT is characterized by gain at HOX clusters and other developmental loci downstream of SMARCB1 loss; FLT3LG and STAT3 co-occur within these MRT-specific super-enhancers, both having prior roles in stem-cell self-renewal and differentiation. PMID:26977886
Cancer types (linked)
- MRT / MRTL — FLT3LG falls within MRT-specific super-enhancers (present in >=50% of MRT, absent in fetal brain and hESC), suggesting epigenetic activation downstream of SMARCB1 loss in extra-cranial rhabdoid tumors. PMID:26977886
Co-occurrence and mutual exclusivity
- FLT3LG super-enhancer activation co-occurs with STAT3 super-enhancer coverage and with the broader HOX-cluster super-enhancer landscape driven by SMARCB1 loss in MRT. PMID:26977886
Therapeutic relevance
- FLT3LG super-enhancer activation in MRT nominates epigenetic dependencies as candidate therapeutic targets; no direct FLT3LG-targeting clinical data are reported in this corpus. PMID:26977886
Open questions
- Whether FLT3LG super-enhancer activation translates to increased FLT3LG protein secretion and paracrine FLT3 signaling in MRT, or represents a passenger epigenetic event, has not been tested. PMID:26977886
Sources
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