ArticleOncogene2014
Whole chromosome instability resulting from the synergistic effects of pRB and p53 inactivation.
Article in Oncogene, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.
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Who cites it
34 citing papers in PubMed, 57 citations in OpenAlex.
- Telomere Dysfunction in Human Astrocytes Drives Acrocentric Chromosome Instability and Nucleolar Reorganization.bioRxiv : the preprint server for biology · 2026Article
- Cell cycle dysregulation: a central hub in colitis-associated colorectal carcinogenesis.Frontiers in immunology · 2026Review
- Methylation sites of human papillomavirus 16 as potential biomarkers for cervical cancer progression.Frontiers in oncology · 2025Article
- Genomic and transcriptomic profiling of combined small-cell lung cancer through microdissection: unveiling the transformational pathway of mixed subtype.Journal of translational medicine · 2024Article
- Exosomes from Adipose-Tissue-Derived Stem Cells Induce Proapoptotic Gene Expression in Breast Tumor Cell Line.International journal of molecular sciences · 2024Article
- Comprehensive Analysis of the Mechanism of Anoikis in Hepatocellular Carcinoma.Genetics research · 2024Article
- Permission to pass: on the role of p53 as a gatekeeper for aneuploidy.Chromosome research : an international journal on the molecular, supramolecular and evolutionary aspects of chromosome biology · 2023Review
- Establishment and validation of an immune infiltration predictive model for ovarian cancer.BMC medical genomics · 2023Article
- Seeing is believing: the impact of RB on nuclear organization.Cell cycle (Georgetown, Tex.) · 2023Article
- Inactivation of RB1, CDKN2A, and TP53 have distinct effects on genomic stability at side-by-side comparison in karyotypically normal cells.Genes, chromosomes & cancer · 2023Article
- Suppression of Chromosome Instability Limits Acquired Drug Resistance.Molecular cancer therapeutics · 2022Article
- Hepatocellular Carcinoma: Current Therapeutic Algorithm for Localized and Advanced Disease.Journal of oncology · 2022Review
- Cold and heterogeneous T cell repertoire is associated with copy number aberrations and loss of immune genes in small-cell lung cancer.Nature communications · 2021Article
- Construction and Validation of a Reliable Six-Gene Prognostic Signature Based on the TP53 Alteration for Hepatocellular Carcinoma.Frontiers in oncology · 2021Article
- Are Molecular Alterations Linked to Genetic Instability Worth to Be Included as Biomarkers for Directing or Excluding Melanoma Patients to Immunotherapy?Frontiers in oncology · 2021Review
- Cep55 overexpression promotes genomic instability and tumorigenesis in mice.Communications biology · 2020Article
- Retinoblastoma: Etiology, Modeling, and Treatment.Cancers · 2020Review
- Protein expression profiling identifies differential modulation of homologous recombination by platinum-based antitumor agents.Cancer chemotherapy and pharmacology · 2020Article
- RBL1 (p107) functions as tumor suppressor in glioblastoma and small-cell pancreatic neuroendocrine carcinoma in Xenopus tropicalis.Oncogene · 2020Article
- Centromere mechanical maturation during mammalian cell mitosis.Nature communications · 2019Article
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
Whole chromosome instability (CIN) is a common feature of cancer cells and has been linked to increased tumor evolution and metastasis. Several studies have shown that the loss of the pRB tumor suppressor causes mitotic defects and chromosome mis-segregation. pRB is inactivated in many types of cancer and this raises the possibility that the loss of pRB may be a general cause of CIN in tumors. Paradoxically, retinoblastoma tumor cells have a relatively stable karyotype and currently the circumstances in which pRB inactivation causes CIN in human cancers are unclear. Here we utilize a fluorescence in situ hybridization-based approach to score numerical heterogeneity in chromosome copy number as a readout of CIN. Using this technique, we show that high levels of CIN correlate with the combined inactivation of pRB and p53 and that this association is evident in two independent panels of cancer cell lines. Retinoblastoma cell lines characteristically retain a wild-type TP53 gene, providing an opportunity to test the relevance of this functional relationship. We show that retinoblastoma cell lines display mitotic defects similar to those seen when pRB is depleted from non-transformed cells, but that the presence of wild-type p53 suppresses the accumulation of aneuploid cells. A similar synergy between pRB and p53 inactivation was observed in HCT116 cells. These results suggest that the loss of pRB promotes segregation errors, whereas loss of p53 allows tolerance and continued proliferation of the resulting, genomically unstable cancer cells. Hence, it is the cooperative effect of inactivation of both pRB and p53 tumor suppressor pathways that promotes CIN.
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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.