Triple A therapy: the molecular underpinnings of the unique sensitivity of leukemic promyelocytes to anthracyclines, all-trans-retinoic acid and arsenic trioxide.

Jessica N Nichol, Nicolas Garnier, Wilson H Miller

Journal: Best practice & research. Clinical haematology 2015;27(1):19-31

PMID: 24907014

Full Text on Elsevier Science View on PubMed

Abstract

If looking for a mnemonic to remember the relevant facts about acute promyelocytic leukemia (APL), one just has to remember that APL is a disease of A's. It is acute and it is highly sensitive to treatment with anthracyclines, all-trans-retinoic acid (RA) and arsenic trioxide (ATO). The presence of fusions involving the retinoic acid receptor alpha (RARA) is without question the central player driving APL and dictating the response of this disease to these therapeutic agents. However, beyond this knowledge, the molecular mechanisms that contribute to the complicated pathogenesis and the response to treatment of APL are not completely defined. As more is understood about this hematological malignancy, there are more opportunities to refine and improve treatment based on this knowledge. In this review article, we discuss the response of APL to these "A" therapies.

Address: Division of Experimental Medicine, Department of Oncology, Segal Cancer Comprehensive Centre, Lady Davis Institute for Medical Research, Sir Mortimer B Davis Jewish General Hospital, McGill University, Montréal, Quebec H3T 1E2, Canada.; Division of Experimental Medicine, Department of Oncology, Segal Cancer Comprehensive Centre, Lady Davis Institute for Medical Research, Sir Mortimer B Davis Jewish General Hospital, McGill University, Montréal, Quebec H3T 1E2, Canada. Electronic address: [email protected].

DOI: 10.1016/j.beha.2014.04.009

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MeSH Terms: Anthracyclines, Antibiotics, Antineoplastic, Arsenic Trioxide, Arsenicals, Cell Differentiation, Cell Line, Tumor, Drug Resistance, Neoplasm, Gene Expression Regulation, Leukemic, Granulocyte Precursor Cells, Humans, Leukemia, Promyelocytic, Acute, Molecular Targeted Therapy, Neoplasm Proteins, Oncogene Proteins, Fusion, Oxides, Topoisomerase II Inhibitors, Transcription, Genetic, Tretinoin