The Tribble with APL: A New Road to Therapy

Ruaidhrí Carmody; Karen Keeshan

doi:10.1016/j.ccell.2017.04.011

The Tribble with APL: A New Road to Therapy

Cancer Cell. 2017 May 8;31(5):612-613. doi: 10.1016/j.ccell.2017.04.011.

Authors

Ruaidhrí Carmody¹, Karen Keeshan²

Affiliations

¹ Centre for Immunobiology, Institute of Infection, Immunity and Inflammation, College of Medicine, Veterinary and Life Sciences, University of Glasgow, Glasgow, G12 8TA, UK.
² Paul O'Gorman Leukaemia Research Centre, College of Medicine, Veterinary and Life Sciences, Institute of Cancer Sciences, University of Glasgow, Glasgow, G12 0XB, UK. Electronic address: karen.keeshan@glasgow.ac.uk.

PMID: 28486101
DOI: 10.1016/j.ccell.2017.04.011

Abstract

The t(15;17) translocation generates a PML-RARα fusion protein causative for acute promyelocytic leukemia (APL). Li et al. now identify the pseudokinase stress protein TRIB3 as an important factor in APL disease progression and therapy resistance. Targeting the interaction of TRIB3 and PML-RARα using peptide technology provides a novel therapeutic approach.

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MeSH terms

Humans
Leukemia, Promyelocytic, Acute
Neoplasm Proteins / genetics*
Oncogene Proteins, Fusion / genetics
Translocation, Genetic
Tretinoin*

Substances

Neoplasm Proteins
Oncogene Proteins, Fusion
Tretinoin