ArticleNeoplasia (New York, N.Y.)2010
Telomere-centromere-driven genomic instability contributes to karyotype evolution in a mouse model of melanoma.
Article in Neoplasia (New York, N.Y.), 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 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
21 citing papers in PubMed, 24 citations in OpenAlex.
- LncRNAEpigenetics · 2026Article
- Three-Dimensional Organization of Telomeres: An Emerging Prognostic Biomarker in Multiple Myeloma.Cells · 2025Review
- First comparative proteomic andFrontiers in veterinary science · 2025Article
- LncRNAs in melanoma phenotypic plasticity: emerging targets for promising therapies.RNA biology · 2024Review
- Growth performance, reproductive status, and chromosomal instability in triploid Nile tilapias.Animal reproduction · 2024Article
- Transcriptional signatures underlying dynamic phenotypic switching and novel disease biomarkers in a linear cellular model of melanoma progression.Neoplasia (New York, N.Y.) · 2021Article
- Emerging Roles of C-Myc in Cancer Stem Cell-Related Signaling and Resistance to Cancer Chemotherapy: A Potential Therapeutic Target Against Colorectal Cancer.International journal of molecular sciences · 2019Review
- Effects of TIN2 on telomeres and chromosomes in the human gastric epithelial cell line GES-1.Oncology letters · 2018Article
- Review
- PRAME as an Independent Biomarker for Metastasis in Uveal Melanoma.Clinical cancer research : an official journal of the American Association for Cancer Research · 2016Article
- The Roles of miR-26, miR-29, and miR-203 in the Silencing of the Epigenetic Machinery during Melanocyte Transformation.BioMed research international · 2015Article
- c-MYC-induced genomic instability.Cold Spring Harbor perspectives in medicine · 2014Review
- Potential role of meiosis proteins in melanoma chromosomal instability.Journal of skin cancer · 2013Article
- Overcoming intratumor heterogeneity of polygenic cancer drug resistance with improved biomarker integration.Neoplasia (New York, N.Y.) · 2012Article
- Leukocyte telomere length predicts overall survival in hepatocellular carcinoma treated with transarterial chemoembolization.Carcinogenesis · 2012Article
- Mining gene expression signature for the detection of pre-malignant melanocytes and early melanomas with risk for metastasis.PloS one · 2012Article
- Article
- The interconnectedness of cancer cell signaling.Neoplasia (New York, N.Y.) · 2011Article
- Activation of the long terminal repeat of human endogenous retrovirus K by melanoma-specific transcription factor MITF-M.Neoplasia (New York, N.Y.) · 2011Article
- Epigenetic reprogramming as a key contributor to melanocyte malignant transformation.Epigenetics · 2011Article
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 2 countries.
Funding
Abstract
Aneuploidy and chromosomal instability (CIN) are hallmarks of most solid tumors. These alterations may result from inaccurate chromosomal segregation during mitosis, which can occur through several mechanisms including defective telomere metabolism, centrosome amplification, dysfunctional centromeres, and/or defective spindle checkpoint control. In this work, we used an in vitro murine melanoma model that uses a cellular adhesion blockade as a transforming factor to characterize telomeric and centromeric alterations that accompany melanocyte transformation. To study the timing of the occurrence of telomere shortening in this transformation model, we analyzed the profile of telomere length by quantitative fluorescent in situ hybridization and found that telomere length significantly decreased as additional rounds of cell adhesion blockages were performed. Together with it, an increase in telomere-free ends and complex karyotypic aberrations were also found, which include Robertsonian fusions in 100% of metaphases of the metastatic melanoma cells. These findings are in agreement with the idea that telomere length abnormalities seem to be one of the earliest genetic alterations acquired in the multistep process of malignant transformation and that telomere abnormalities result in telomere aggregation, breakage-bridge-fusion cycles, and CIN. Another remarkable feature of this model is the abundance of centromeric instability manifested as centromere fragments and centromeric fusions. Taken together, our results illustrate for this melanoma model CIN with a structural signature of centromere breakage and telomeric loss.
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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.