ReviewLeukemia2006
The role of p73 in hematological malignancies.
Review in Leukemia, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
18 citing papers in PubMed, 45 citations in OpenAlex.
- Isoform-specific disruption of theeLife · 2023Article
- A study of deregulated MMR pathways and anticancer potential of curcuma derivatives using computational approach.Scientific reports · 2021Article
- Targeting Post-Translational Modifications of the p73 Protein: A Promising Therapeutic Strategy for Tumors.Cancers · 2021Review
- 1-C Metabolism-Serine, Glycine, Folates-In Acute Myeloid Leukemia.Pharmaceuticals (Basel, Switzerland) · 2021Review
- DNA methylation and leukemia susceptibility in China: Evidence from an updated meta-analysis.Molecular and clinical oncology · 2016Article
- Article
- Mdm2 overexpression and p73 loss exacerbate genomic instability and dampen apoptosis, resulting in B-cell lymphoma.Oncogene · 2016Article
- Induction of TAp73 by platinum-based compounds to overcome drug resistance in p53 dysfunctional chronic lymphocytic leukemia.Leukemia & lymphoma · 2015Article
- Gene expression of WWOX, FHIT and p73 in acute lymphoblastic leukemia.Oncology letters · 2013Article
- Impact of aberrant DNA methylation patterns including CYP1B1 methylation in adolescents and young adults with acute lymphocytic leukemia.American journal of hematology · 2013Article
- A phase I study of immune gene therapy for patients with CLL using a membrane-stable, humanized CD154.Leukemia · 2010Article
- Loss of p73 promotes dissemination of Myc-induced B cell lymphomas in mice.The Journal of clinical investigation · 2010Article
- Targeting signal transduction pathways to eliminate chemotherapeutic drug resistance and cancer stem cells.Advances in enzyme regulation · 2010Review
- High-resolution analysis of aberrant regions in autosomal chromosomes in human leukemia THP-1 cell line.BMC research notes · 2009Article
- Article
- Review
- Article
- PU.1 binding to the p53 family of tumor suppressors impairs their transcriptional activity.Oncogene · 2008Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The P73 gene is a homologue of the P53 tumor suppressor. Owing to its structural similarity with p53, p73 was originally considered to have tumor suppressor function. However, the discovery of N-terminal truncated isoforms with oncogenic properties showed a 'two in one' structure of its product, p73 protein. The full-length variants are strong inducers of apoptosis, whereas the truncated isoforms inhibit proapoptotic activity of p53 and the full-length p73. Thus, p73 is involved in the regulation of cell cycle, cell death and development. Moreover, it plays a role in carcinogenesis and controls tumor sensitivity to treatment. p73 is commonly expressed in tumor cells in hematological malignancies. Overexpression of p73 protein and aberrant expression of its particular isoforms, with very low frequency of P73 hypermethylation or mutations, were found in malignant myeloproliferations, including acute myeloblastic leukemia. In contrast, hypermethylation and subsequent inactivation of the P73 gene are the most common findings in malignant lymphoproliferative disorders, especially acute lymphoblastic leukemia (ALL) and non-Hodgkin's lymphomas. Assessment of P73 methylation may provide important prognostic information, as was confirmed in patients with ALL. This review summarizes some aspects of p73 biology with particular reference to its possible pathogenetic role and prognostic significance in hematological malignancies.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.