Analysis of p73 expression pattern in acute myeloid leukemias: Lack of ΔN-p73 expression is a frequent feature of acute promyelocytic leukemia

M. G. Rizzo, E. Giombini, D. Diverio, M. Vignetti, A. Sacchi, U. Testa, F. Lo-Coco, G. Blandino

Research output: Contribution to journalArticle

Abstract

p73, the homologue of p53, is a nuclear protein whose ectopic expression, in p53+/+ and p53-/- cells, recapitulates the most well-characterized p53 effects, such as growth arrest, apoptosis and differentiation. Unlike p53, which is mutated in half of human cancers, p73 is rarely mutated. However, altered expression of the p73 gene has been reported in neuroblastoma, lung cancer, prostate cancer and renal cell carcinoma. To investigate the potential involvement of p73 in acute myeloid leukemias (AMLs), we analyzed 71 samples from AML patients for the expression pattern of N-terminal transactivation-p73α (TA-p73α), its spliced isoforms and N-terminal-deleted-p73 transcripts (ΔN-p73). We detected p73 gene expression in AML irrespective of FAB (French-American-British) subtypes. Notably, the analysis of ΔN-p73 expression, which has been reported to inactivate both p53 and p73 antitumor effects, revealed a rather peculiar pattern. In fact, ΔN-p73 transcript and protein were detectable in 27/28 (96.4%) cases of M0, M1, M2, M4, M5 and M6 AML and in 13/41 (31.7%) cases of PML-RARα-positive M3 AML (P

Original languageEnglish
Pages (from-to)1804-1809
Number of pages6
JournalLeukemia
Volume18
Issue number11
DOIs
Publication statusPublished - Nov 2004

Keywords

  • Acute myeloid leukemia
  • Acute promyelocytic leukemia
  • Isoform
  • p73

ASJC Scopus subject areas

  • Hematology
  • Cancer Research

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