ReviewLeukemia2002
PML a target of translocations in APL is a regulator of cellular senescence.
Review in Leukemia, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 35 citations in OpenAlex.
- Unraveling senescence in cancer: mechanistic complexities and therapeutic opportunities.Molecular biology reports · 2025Review
- Role of senescence induction in cancer treatment.World journal of clinical oncology · 2018Review
- MG132-induced progerin clearance is mediated by autophagy activation and splicing regulation.EMBO molecular medicine · 2017Article
- The PML domain of PML-RARα blocks senescence to promote leukemia.Proceedings of the National Academy of Sciences of the United States of America · 2014Article
- The tumor suppressor PML specifically accumulates at RPA/Rad51-containing DNA damage repair foci but is nonessential for DNA damage-induced fibroblast senescence.Molecular and cellular biology · 2014Article
- New Strategies to Direct Therapeutic Targeting of PML to Treat Cancers.Frontiers in oncology · 2013Article
- Androgen receptor drives cellular senescence.PloS one · 2012Article
- A manually curated network of the PML nuclear body interactome reveals an important role for PML-NBs in SUMOylation dynamics.International journal of biological sciences · 2010Review
- DNA damage signaling and p53-dependent senescence after prolonged beta-interferon stimulation.Molecular biology of the cell · 2006Article
- Interferons alpha and gamma induce p53-dependent and p53-independent apoptosis, respectively.Oncogene · 2005Article
- Promyelocytic leukemia protein-induced growth suppression and cell death in liver cancer cells.Cancer gene therapy · 2005Article
- Retinoic acid syndrome in NOD/scid mice induced by injecting an acute promyelocytic leukemia cell line.Leukemia · 2004Article
- Treatment of acute promyelocytic leukemia: strategy toward further increase of cure rate.Leukemia · 2003Review
- Article
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Authors and funding
1 author at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
PML is the most frequent fusion partner of the RARalpha in the specific translocations associated with acute promyelocytic leukemia (APL). Models to explain the origin of this leukemia propose a block in cell differentiation due to aberrant repression of retinoic acid responsive genes and/or disruption of the function of the PML-containing nuclear bodies. Recently, PML has been identified as a regulator of replicative senescence and the premature senescence that occurs in response to oncogenic ras. This review discusses the idea that senescence is a general tumor suppressor mechanism related to terminal differentiation and disrupted during the establishment of APL and other cancers. According to this idea the PML-RARalpha fusion protein promotes leukemogenesis not only through repression of retinoic acid responsive genes, but also by way of interfering with several tumor suppressor proteins that cooperate to establish senescence. Retinoids and other drugs effective against APL do so by re-establishment of the senescence program, which also includes features of cell differentiation.
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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.