ΔN-p73 is a transcriptional target of the PML/RARα oncogene in myeloid differentiation

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The p53 paralog TPp73 gene gives rise to a variety of functionally distinct polypeptides involved in the control of growth arrest, apoptosis and differentiation. Multiple TA (transactivation competent, pro-apoptotic and anti-proliferative) p73 carboxy-terminal splicing isoforms (α, β, γ, δ, ɛ, ζ, η and η₁) are expressed from the P1p73 promoter (reviewed by Giombini et al¹ and references therein). A second intragenic promoter, P2p73, controls the expression of dominant-negative (ΔN) variants that lack the amino-terminal transactivation domain and act as dominant-negative repressors of p53- and p73-dependent apoptosis (reviewed by Giombini et al¹ and references therein). Changes in TAp73 and ΔN-p73 expression rather than inactivating mutations within the TP73 gene, have been described in many human tumors.² Unlike acute lymphoid leukemias, which mainly display promoter CpG islands hypermethylation, acute myeloid leukemia is characterized by a relative enrichment of shorter TAp73 isoforms, and in the case of acute promyelocytic leukemia (APL), a peculiar lack of ΔN-p73 expression has been reported by our group.^{3, 4, 5}

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