IFI35 and Acute Myeloid Leukemia

Recent studies have identified an association between IFI35 (HGNC:5399) and acute myeloid leukemia (MONDO_0018874) by highlighting altered interferon signaling in a subset of AML patients. In a comprehensive analysis of 113 AML patients (PMID:38253683), patients with poor outcomes exhibited increased expression of interferon‐stimulated genes, including IFI35, suggesting its potential role as a prognostic biomarker.

This evidence comes from case report cohorts and multi‐patient studies where altered immune and metabolic pathways were linked to clinical outcomes. Although IFI35 has not been described as harboring specific pathogenic coding variants in AML, its upregulation appears to correlate with a more aggressive disease course in the context of a dysregulated interferon response.

The genetic data do not include direct reports of deleterious coding mutations in IFI35. Instead, the association is derived from transcriptomic profiling that detected elevated IFI35 levels among other interferon‐response genes, providing indirect genetic evidence rather than canonical variant discovery.

Functional studies specific to IFI35 in AML are currently lacking. However, its inclusion in a broader interferon‐mediated gene signature underscores a potential role in the disease’s molecular pathology. Confirmatory assays and more detailed mechanistic studies will be necessary to clarify the specific contribution of IFI35 to leukemogenesis.

There is no evidence of familial segregation or recurrent germline/somatic variants in IFI35 in AML patients, which limits the genetic evidence to expression correlation. This limitation is reflected in the overall strength of the association, where the available data indicate that IFI35 is a marker within a complex dysregulated immune network rather than a stand‐alone driver mutation.

In conclusion, while direct genetic alterations in IFI35 have not been reported, its differential expression in AML patients with poor clinical outcomes provides diagnostic insight that may inform risk stratification and future therapeutic research. Key take‑home message: Elevated IFI35 expression, as part of an interferon‐stimulated gene module, holds potential clinical utility in stratifying AML patients for prognosis and treatment decisions.

References

• Blood cancer journal • 2024 • Dysregulated immune and metabolic pathways are associated with poor survival in adult acute myeloid leukemia with CEBPA bZIP in‑frame mutations PMID:38253683

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