ArticleOncogene2006
Targeting cyclin D1, a downstream effector of INI1/hSNF5, in rhabdoid tumors.
Article in Oncogene, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 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
23 citing papers in PubMed, 67 citations in OpenAlex.
- What Have We Learnt from the Recent Multimodal Managements of Young Patients with ATRT?Cancers · 2025Article
- Attenuated expression of SNF5 facilitates progression of bladder cancer via STAT3 activation.Cancer cell international · 2021Article
- Malignant Rhabdoid Tumor of the Mediastinum: A Case Report and Literature Review.Journal of clinical imaging science · 2019Article
- Combined BRD4 and CDK9 inhibition as a new therapeutic approach in malignant rhabdoid tumors.Oncotarget · 2017Article
- Atypical teratoid/rhabdoid tumors-current concepts, advances in biology, and potential future therapies.Neuro-oncology · 2016Review
- Coordinating cell proliferation and differentiation: Antagonism between cell cycle regulators and cell type-specific gene expression.Cell cycle (Georgetown, Tex.) · 2016Review
- SMARCB1 (INI-1)-deficient carcinomas of the sinonasal tract.The American journal of surgical pathology · 2014Article
- Mechanisms by which SMARCB1 loss drives rhabdoid tumor growth.Cancer genetics · 2014Review
- Molecular pathways: SWI/SNF (BAF) complexes are frequently mutated in cancer--mechanisms and potential therapeutic insights.Clinical cancer research : an official journal of the American Association for Cancer Research · 2014Article
- The histone deacetylase inhibitor SAHA acts in synergism with fenretinide and doxorubicin to control growth of rhabdoid tumor cells.BMC cancer · 2013Article
- Update from the 2011 International Schwannomatosis Workshop: From genetics to diagnostic criteria.American journal of medical genetics. Part A · 2013Article
- Inhibition of EZH2 suppresses self-renewal and induces radiation sensitivity in atypical rhabdoid teratoid tumor cells.Neuro-oncology · 2013Article
- Novel cell lines established from pediatric brain tumors.Journal of neuro-oncology · 2012Article
- In vitro activities of novel 4-HPR derivatives on a panel of rhabdoid and other tumor cell lines.Cancer cell international · 2011Article
- p16INK4A and p14ARF tumor suppressor pathways are deregulated in malignant rhabdoid tumors.Journal of neuropathology and experimental neurology · 2011Article
- SWI/SNF nucleosome remodellers and cancer.Nature reviews. Cancer · 2011Review
- Therapeutically targeting cyclin D1 in primary tumors arising from loss of Ini1.Proceedings of the National Academy of Sciences of the United States of America · 2011Article
- Potent inhibition of rhabdoid tumor cells by combination of flavopiridol and 4OH-tamoxifen.BMC cancer · 2010Article
- Rhabdoid tumor: gene expression clues to pathogenesis and potential therapeutic targets.Laboratory investigation; a journal of technical methods and pathology · 2010Article
- The role of SMARCB1/INI1 in development of rhabdoid tumor.Cancer biology & therapy · 2009Review
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Rhabdoid tumors (RTs) are aggressive and currently incurable pediatric malignancies. INI1/hSNF5 is a tumor suppressor biallelically inactivated in RTs. Our previous studies have indicated that cyclin D1 is a key downstream target of INI1/hSNF5 and genesis and/or survival of RTs in vivo is critically dependent on the presence of cyclin D1. In this report, we have tested the hypothesis that therapeutic targeting of cyclin D1 is an effective means of treating RTs. We found that RNA interference of cyclin D1 in rhabdoid cells was sufficient to induce G1 arrest and apoptosis. Furthermore, we found that pharmacological intervention with low micromolar concentrations of N-(4-hydroxyphenyl)retinamide (4-HPR), which downmodulates cyclin D1, induced G1 arrest and apoptosis in rhabdoid cell lines. 4-HPR in combination with 4-hydroxy-tamoxifen (4OH-Tam), synergistically inhibited survival as well as anchorage-dependent and -independent growth of rhabdoid cells and caused synergistic induction of cell cycle arrest and apoptosis. 4-HPR and tamoxifen exhibited synergistic growth inhibition of RTs in xenograft models in vivo. The effects of combination of drugs were correlated to the depletion of cyclin D1 levels both in in vitro and in vivo tumor models. These results demonstrate that 4-HPR and tamoxifen are effective chemotherapeutic agents for RTs. We propose that downmodulation of cyclin D1 is a novel and effective therapeutic strategy for RTs.
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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.