From polyploidy to aneuploidy, genome instability and cancer
By Z. Storchová, D. Pellman. Nature reviews. Molecular cell biology, 2004
831 citations recorded by the source corpus.
Subfields: Cell Biology, Genetics, Plant Science
View Paper: https://www.semanticscholar.org/paper/c412777aefa95f2dfb38c22d2f1107f7897830c4
How researchers see this paper
The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.
In Cell Biology
- J. Raff
- D. Pellman
- Sarah P. Otto
- D. Cleveland
- Erich A. Nigg
- de Lange
- Beth A. Weaver
- Alec C. Kimmelman
In Genetics
In Plant Science
Citations in the corpus
- Forkhead Box M1 Regulates the Transcriptional Network of Genes Essential for Mitotic Progression and Genes Encoding the SCF (Skp2-Cks1) Ubiquitin Ligase (2005, background): “It is interesting that Foxm1 / MEFs generated by Medema and colleagues exhibit aneuploid genotypes (37), which are a hallmark of neoplastic transformation (58, 62).”
- How shelterin solves the telomere end-protection problem. (2010, background): “Tetraploid cells have been observed in the early stages of human tumorigenesis and are proposed to constitute a likely precursor for the genesis of aneuploidy (Storchova and Pellman 2004).”
- The evolutionary consequences of polyploidy. (2007, background): “stage in some cancers, facilitating a cascade of structural changes that disrupt normal controls to cell growth (Storchova and Pellman, 2004).”
- On the road to cancer: aneuploidy and the mitotic checkpoint (2005, background): “Such aberrant mitoses can be caused by polyploidization, which arises via previous cytokinesis defects, cell–cell fusion or from cells skipping mitosis altogether (endoreduplication”
- Centrioles, centrosomes, and cilia in health and disease. (2009, background): “two mechanisms is that only division failure will induce tetraploidization, which under in vivo conditions may favor the longterm survival of progeny from multipolar divisions (Nigg, 2002; Storchova and Pellman, 2004).”
- The “Polyploid Hop”: Shifting Challenges and Opportunities Over the Evolutionary Lifespan of Genome Duplications (2018, background): “Numerous studies have shown evidence of dysfunction in newly formed polyploids across kingdoms: in plants, fungi and animals, including notably cancer cells (Ramsey and Schemske, 2002; Storchova and Pellman, 2004; Comai, 2005; Yant and Bomblies, 2017).”
- Intratumor heterogeneity: the Rosetta stone of therapy resistance (2020, background): “Genomes of hybrid cells are often unstable (Duelli et al., 2007; Storchova and Pellman, 2004), which could lead to additional diversification associated with ploidy reduction, similar to a fusion-mediated ploidy conveyor in mature hepatocytes (Duncan et al.”
- Absolute quantification of somatic DNA alterations in human cancer (2012, methodology): “Subclonal mutations were identified using the model defined in equation (12).”
- Genetics and biology of pancreatic ductal adenocarcinoma. (2006, background): “The observation of polyploidy in association with aging and senescence and its observation in premalignant lesions have suggested that such an intermediate karyotype may play a role in the acquisition of aneuploidy (Storchova and Pellman 2004).”
- Cytokinesis failure generating tetraploids promotes tumorigenesis in p53-null cells (2005, background): “We focused on cells lacking p53 because (1) there is an epidemiological link between p53 loss and tetraploidy in Barrett’s oesophagus(11), (2) p53 loss facilitates the spontaneous formation of tetraploid cells in a variety of mouse and human cell types in culture(13), and (3) p53 loss is often requi”