ArticleJournal of neuropathology and experimental neurology2011
p16INK4A and p14ARF tumor suppressor pathways are deregulated in malignant rhabdoid tumors.
Article in Journal of neuropathology and experimental neurology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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Who cites it
28 citing papers in PubMed, 49 citations in OpenAlex.
- PIWIL4: from biological characteristics to disease pathogenesis and clinical applications.Frontiers in oncology · 2026Review
- SMARCB1-related schwannomatosis and other SMARCB1-associated phenotypes: clinical spectrum and molecular pathogenesis.Familial cancer · 2025Review
- Dysregulation of noncoding RNA in chordoma; implications in identifying potential targets for novel therapeutic approaches.Molecular biology reports · 2024Review
- Review
- Atypical Teratoid/Rhabdoid Tumor of the Central Nervous System in Children under the Age of 3 Years.Cancer research and treatment · 2021Article
- Factors Affecting the Outcomes of Patients with Malignant Rhabdoid Tumors: A Population-Based Study.International journal of medical sciences · 2021Article
- SWI/SNF complex heterogeneity is related to polyphenotypic differentiation, prognosis, and immune response in rhabdoid tumors.Neuro-oncology · 2020Article
- Efficacy of High-Dose Chemotherapy and Three-Dimensional Conformal Radiation for Atypical Teratoid/Rhabdoid Tumor: A Report From the Children's Oncology Group Trial ACNS0333.Journal of clinical oncology : official journal of the American Society of Clinical Oncology · 2020Article
- Article
- Dangerous liaisons: interplay between SWI/SNF, NuRD, and Polycomb in chromatin regulation and cancer.Genes & development · 2019Review
- MDM2 and MDM4 Are Therapeutic Vulnerabilities in Malignant Rhabdoid Tumors.Cancer research · 2019Article
- p53 Is a Master Regulator of Proteostasis in SMARCB1-Deficient Malignant Rhabdoid Tumors.Cancer cell · 2019Article
- Embryonal Tumors of the Central Nervous System in Children: The Era of Targeted Therapeutics.Bioengineering (Basel, Switzerland) · 2018Review
- Cancer epigenetics: Moving forward.PLoS genetics · 2018Review
- 2-O, 3-O desulfated heparin mitigates murine chemotherapy- and radiation-induced thrombocytopenia.Blood advances · 2018Article
- Phosphorylation of pRb: mechanism for RB pathway inactivation in MYCN-amplified retinoblastoma.Cancer medicine · 2017Article
- Inhibition of DNA damage repair by the CDK4/6 inhibitor palbociclib delays irradiated intracranial atypical teratoid rhabdoid tumor and glioblastoma xenograft regrowth.Neuro-oncology · 2016Article
- Dual function of MDM2 and MDMX toward the tumor suppressors p53 and RB.Genes & cancer · 2016Review
- Generation of a mouse model of atypical teratoid/rhabdoid tumor of the central nervous system through combined deletion of Snf5 and p53.Cancer research · 2015Article
- Intramedullary megakaryocytes internalize released platelet factor 4 and store it in alpha granules.Journal of thrombosis and haemostasis : JTH · 2015Article
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
Abstract
Malignant rhabdoid tumors (MRTs) are aggressive tumors associated with mutations in the SMARCB1 gene. In experimental systems, the loss of SMARCB1 is hypothesized to alter p16(INK4A) pathways resulting in the repression of tumor suppressors. To determine whether these pathways are deregulated in human MRT, we used immunohistochemistry on tissue microarrays to evaluate p16(INK4A)/E2F1/RB and p14(ARF)/MDM2/p53 pathways in 25 atypical teratoid/rhabdoid tumors (AT/RT) and 11 non-CNS MRT. p16(INK4A) was negative or showed focal weak expression. p16(INK4A) downstream targets CDK4/cyclin D1/ppRB were variably expressed at moderate to low levels; E2F1 was negative. Unexpectedly, p14(ARF) expression was seen in many cases, which correlated positively with p53 and inversely with MDM2 immunostaining in AT/RT. TP53 mutational analysis in 19 of 25 AT/RT and in 8 of 11 non-CNS MRT cases showed point mutations in only 3 AT/RT cases, suggesting that p53 expression was driven mainly by p14(ARF). Finally, nucleophosmin, a protein that stabilizes p53, was positive in most cases and colocalized with p53. Together, these data suggest that, in MRT, there is deregulation not only of p16(INK4A) but also of the p14(ARF) pathway. These results provide insights into cell cycle deregulation in the pathogenesis of human MRT and may aid in the design and evaluation of potential therapies for these tumors.
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