ArticleCancer discovery2016
Chromosomal Instability Affects the Tumorigenicity of Glioblastoma Tumor-Initiating Cells.
Article in Cancer discovery, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 papers.
What it found
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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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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.
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Who cites it
56 citing papers in PubMed, 62 citations in OpenAlex.
- A tumour-host feed-forward loop contributes to the growth of chromosomal instability-induced tumours.EMBO reports · 2026Article
- Chromosomal Instability Drives Glioblastoma Heterogeneity and Therapeutic Opportunities.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Review
- Molecular features unique to circulating tumor DNA enable the tumor-naïve liquid biopsy of glioblastoma.NPJ precision oncology · 2026Article
- Simultaneous CRISPR/Cas9-induced double-strand breaks are lethal in models of pancreatic cancer.The Journal of clinical investigation · 2026Article
- Loss of DIAPH3 accelerates glioma genesis in mice.Cell death & disease · 2026Article
- Key genes altered in glioblastoma based on bioinformatics (Review).Oncology letters · 2025Review
- Therapy enhancing chromosome instability may be advantageous forNAR cancer · 2025Article
- Review
- Chromosomal instability: a key driver in glioma pathogenesis and progression.European journal of medical research · 2024Review
- Chromosomal instability as an architect of the cancer stemness landscape.Frontiers in cell and developmental biology · 2024Review
- Chromosomal instability in aneuploid acute lymphoblastic leukemia associates with disease progression.EMBO molecular medicine · 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
- Diverse microtubule-targeted anticancer agents kill cells by inducing chromosome missegregation on multipolar spindles.PLoS biology · 2023Article
- Breast cancer stem cells tolerate chromosomal instability during tumor progression via c-Jun/AXL stress signaling.Heliyon · 2023Article
- CAMK2D serves as a molecular scaffold for RNF8-MAD2 complex to induce mitotic checkpoint in glioma.Cell death and differentiation · 2023Article
- Improving Localized Radiotherapy for Glioblastoma via Small Molecule Inhibition of KIF11.Cancers · 2023Article
- HPV16 E6 induces chromosomal instability due to polar chromosomes caused by E6AP-dependent degradation of the mitotic kinesin CENP-E.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- Systematic in vitro analysis of therapy resistance in glioblastoma cell lines by integration of clonogenic survival data with multi-level molecular data.Radiation oncology (London, England) · 2023Article
- A pluripotent developmental state confers a low fidelity of chromosome segregation.Stem cell reports · 2023Article
- Article
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
unlabelledTumors are dynamic organs that evolve during disease progression with genetic, epigenetic, and environmental differences among tumor cells serving as the foundation for selection and evolution in tumors. Tumor-initiating cells (TIC) that are responsible for tumorigenesis are a source of functional cellular heterogeneity, whereas chromosomal instability (CIN) is a source of karyotypic genetic diversity. However, the extent that CIN contributes to TIC genetic diversity and its relationship to TIC function remains unclear. Here, we demonstrate that glioblastoma TICs display CIN with lagging chromosomes at anaphase and extensive nonclonal chromosome copy-number variations. Elevating the basal chromosome missegregation rate in TICs decreases both proliferation and the stem-like phenotype of TICs in vitro Consequently, tumor formation is abolished in an orthotopic mouse model. These results demonstrate that TICs generate genetic heterogeneity within tumors, but that TIC function is impaired if the rate of genetic change is elevated above a tolerable threshold. SIGNIFICANCE: Genetic heterogeneity among TICs may produce advantageous karyotypes that lead to therapy resistance and relapse; however, we found that TICs have an upper tolerable limit for CIN. Thus, increasing the chromosome missegregation rate offers a new therapeutic strategy to eliminate TICs from tumors. Cancer Discov; 6(5); 532-45. ©2016 AACR.This article is highlighted in the In This Issue feature, p. 461.
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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.