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Related Experiment Video

Updated: Aug 20, 2025

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Does IFITM3 link inflammation to tumorigenesis?

Jaewoong Lee1

  • 1School of Biosystems and Biomedical Sciences, College of Health Science, Korea University, Seoul 02841; Interdisciplinary Program in Precision Public Health, Korea University, Seoul 02841, Korea.

BMB Reports
|November 21, 2022
PubMed
Summary
This summary is machine-generated.

Chronic inflammation drives cancer development, often via cytokine signaling. This review explores how interferon-induced transmembrane protein 3 (IFITM3) contributes to B-cell malignancy, linking inflammation to leukemogenesis.

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Area of Science:

  • Immunology
  • Oncology
  • Molecular Biology

Background:

  • Chronic inflammation, driven by excessive cytokine signaling, is a known factor in tumorigenesis.
  • The antiviral protein interferon-induced transmembrane protein 3 (IFITM3) is induced by inflammatory responses.
  • IFITM3 has been unexpectedly implicated in the development of B-cell malignancies.

Approach:

  • This review discusses the role of inflammatory cytokines in upregulating IFITM3 expression.
  • It examines the mechanism by which IFITM3 contributes to B-cell malignancy and leukemogenesis.
  • The review synthesizes current understanding of IFITM3's oncogenic signaling pathways.

Key Points:

  • IFITM3, typically antiviral, exhibits oncogenic signaling in malignant B cells.
  • Upregulation of IFITM3 by inflammatory cytokines promotes B-cell tumorigenesis.
  • Understanding IFITM3's role clarifies how inflammatory proteins drive leukemogenesis.

Conclusions:

  • The study highlights IFITM3 as a critical link between inflammation and B-cell cancer.
  • Targeting IFITM3 or its regulatory pathways may offer therapeutic strategies for leukemias.
  • Further research is needed to fully elucidate IFITM3's oncogenic functions in hematological malignancies.