ArticleLeukemia2004
Analysis of p73 expression pattern in acute myeloid leukemias: lack of DeltaN-p73 expression is a frequent feature of acute promyelocytic leukemia.
Article in Leukemia, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
12 citing papers in PubMed, 27 citations in OpenAlex.
- ΔNp73 isoform defines a TP53-mutant-like poor-risk subgroup of acute myeloid leukemia.Cell reports. Medicine · 2026Article
- Risk factors and remaining challenges in the treatment of acute promyelocytic leukemia.International journal of hematology · 2024Review
- A new signaling cascade linking BMP4, BMPR1A, ΔNp73 and NANOG impacts on stem-like human cell properties and patient outcome.Cell death & disease · 2018Article
- Clinical implications of the deregulated TP73 isoforms expression in cancer.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2018Review
- Emodin promotes the arrest of human lymphoma Raji cell proliferation through the UHRF1‑DNMT3A‑∆Np73 pathways.Molecular medicine reports · 2017Article
- Article
- Mechanisms, function and clinical applications of DNp73.Cell cycle (Georgetown, Tex.) · 2013Review
- Tumour suppressor genes in chemotherapeutic drug response.Bioscience reports · 2012Review
- p63 and p73 in human cancer: defining the network.Oncogene · 2007Review
- Differential expression of p73 isoforms in relation to drug resistance in childhood T-lineage acute lymphoblastic leukaemia.Leukemia · 2006Article
- Phosphoinositide 3-kinase/Akt signaling pathway and its therapeutical implications for human acute myeloid leukemia.Leukemia · 2006Review
- The role of p73 in hematological malignancies.Leukemia · 2006Review
Corrections and comments
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Authors and funding
8 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
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-p73alpha (TA-p73alpha), its spliced isoforms and N-terminal-deleted-p73 transcripts (DeltaN-p73). We detected p73 gene expression in AML irrespective of FAB (French-American-British) subtypes. Notably, the analysis of DeltaN-p73 expression, which has been reported to inactivate both p53 and p73 antitumor effects, revealed a rather peculiar pattern. In fact, DeltaN-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-RARalpha-positive M3 AML (P<0.01). Thus, the distinct gene expression profile of p73 further supports the notion that acute promyelocytic leukemia is a biologically different subset of AML.
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