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Mechanisms associated with t(7;12) acute myeloid leukaemia: from genetics to potential treatment targets

Denise Ragusa1,2, Liza Dijkhuis1, Cristina Pina1,2

  • 1College of Health, Medicine and Life Sciences, Division of Biosciences, Brunel University London, Uxbridge, UB8 3PH, U.K.

Bioscience Reports
|January 9, 2023
PubMed

Insights

Infant acute myeloid leukaemia (AML) with t(7;12) translocation is poorly understood. This review explores its biology and recent advances, offering potential therapeutic insights for this high-risk subtype.

Area of Science:

  • Hematology
  • Pediatric Oncology
  • Molecular Biology

Background:

  • Acute myeloid leukaemia (AML) in infants is rare but aggressive.
  • The t(7;12) translocation is a high-risk AML subtype specific to infants, with unclear leukaemogenesis mechanisms.
  • Ectopic MNX1 expression is a hallmark of t(7;12) AML, but its role in transformation remains elusive.

Approach:

  • Reviewing current literature on t(7;12) AML.
  • Analyzing recent studies utilizing advanced genome editing and murine models.
  • Investigating the biological features and mechanistic understanding of t(7;12) leukaemogenesis.

Key Points:

  • The t(7;12) translocation involves the MNX1 gene, but fusion transcripts are inconsistent.
  • Advances in genome editing enable precise recreation of the t(7;12) rearrangement.
  • Murine models provide valuable platforms for studying t(7;12) AML biology.

Conclusions:

  • Understanding t(7;12) biology is crucial for developing targeted therapies.
  • Recent mechanistic insights may lead to improved treatment strategies for infant AML.
  • Further research into this rare but aggressive AML subtype holds promise for better patient outcomes.

Keywords:
acute myeloid leukaemiacancerchromosomal translocationpaediatric

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