ArticleOncogene1999
p73 at chromosome 1p36.3 is lost in advanced stage neuroblastoma but its mutation is infrequent.
Article in Oncogene, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.
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Who cites it
47 citing papers in PubMed, 119 citations in OpenAlex.
- Deciphering the Role of p53 and TAp73 in Neuroblastoma: From Pathogenesis to Treatment.Cancers · 2022Review
- p73 as a Tissue Architect.Frontiers in cell and developmental biology · 2021Review
- Silencing E3 Ubiqutin ligase ITCH as a potential therapy to enhance chemotherapy efficacy in p53 mutant neuroblastoma cells.Scientific reports · 2020Article
- Evasion of anti-growth signaling: A key step in tumorigenesis and potential target for treatment and prophylaxis by natural compounds.Seminars in cancer biology · 2015Review
- Preclinical activity of combined HDAC and KDM1A inhibition in glioblastoma.Neuro-oncology · 2015Article
- Tumor Suppressor Inactivation in the Pathogenesis of Adult T-Cell Leukemia.Journal of oncology · 2015Review
- WWP2-WWP1 ubiquitin ligase complex coordinated by PPM1G maintains the balance between cellular p73 and ΔNp73 levels.Molecular and cellular biology · 2014Article
- Identification of novel candidate compounds targeting TrkB to induce apoptosis in neuroblastoma.Cancer medicine · 2014Article
- Alterations of p63 and p73 in human cancers.Sub-cellular biochemistry · 2014Review
- N-(phosphonacetyl)-L-aspartate induces TAp73-dependent apoptosis by modulating multiple Bcl-2 proteins: potential for cancer therapy.Oncogene · 2013Article
- p73 expression is regulated by RNPC1, a target of the p53 family, via mRNA stability.Molecular and cellular biology · 2012Article
- Mutant p53 protein is targeted by arsenic for degradation and plays a role in arsenic-mediated growth suppression.The Journal of biological chemistry · 2011Article
- p73 in Cancer.Genes & cancer · 2011Article
- The connections between neural crest development and neuroblastoma.Current topics in developmental biology · 2011Review
- Association of a p73 exon 2 GC/AT polymorphism with colorectal cancer risk and survival in Tunisian patients.Virchows Archiv : an international journal of pathology · 2010Article
- Tracing the protectors path from the germ line to the genome.Proceedings of the National Academy of Sciences of the United States of America · 2010Article
- ATM regulates a RASSF1A-dependent DNA damage response.Current biology : CB · 2009Article
- N-myc augments death and attenuates protective effects of Bcl-2 in trophically stressed neuroblastoma cells.Oncogene · 2008Article
- The kinesin KIF1Bbeta acts downstream from EglN3 to induce apoptosis and is a potential 1p36 tumor suppressor.Genes & development · 2008Article
- Promoter hypermethylation profile of cell cycle regulator genes in pituitary adenomas.Journal of neuro-oncology · 2007Article
Corrections and comments
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Authors and funding
14 authors at 5 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
p73, a novel p53 family member, is a recently identified candidate neuroblastoma (NBL) suppressor gene mapped at chromosome 1p36.33 and was found to inhibit growth and induce apoptosis in cell lines. To test the hypothesis that p73 is a NBL suppressor gene, we analysed the p73 gene in primary human NBLs. Loss of heterozygosity (LOH) for p73 was observed in 19% (28/151) of informative cases which included 92 mass-screening (MS) tumors. The high frequency of p73 LOH was significantly associated with sporadic NBLs (9% vs 34%, P<0.001), N-myc amplification (10% vs 71%, P<0.001), and advanced stage (14% vs 28%, P<0.05). Both p73alpha and p73beta transcripts were detectable in only 46 of 134 (34%) NBLs at low levels by RT-PCR methods, while they were easily detectable in most breast cancers and colorectal cancers under the same conditions. They found no correlation between p73 LOH and its expression levels (P>0.1). We found two mutations out of 140 NBLs, one somatic and one germline, which result in amino acid substitutions in the C-terminal region of p73 which may affect transactivation functions, though, in the same tumor samples, no mutation of the p53 gene was observed as reported previously. These results suggest that allelic loss of the p73 gene may be a later event in NBL tumorigenesis. However, p73 is infrequently mutated in primary NBLs and may hardly function as a tumor suppressor in a classic Knudson's manner.
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