On the road to cancer: aneuploidy and the mitotic checkpoint

By G. Kops, Beth A. Weaver, D. Cleveland. Nature Reviews. Cancer, 2005

1,237 citations recorded by the source corpus.

Subfields: Cell Biology, Molecular Biology, Oncology

View Paper: https://www.semanticscholar.org/paper/2e3037914fc22635583bdcbab75e354c90013117

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Citations in the corpus

Apoptosis and cancer: mutations within caspase genes (2009, background): “account for only a small fraction of all tumours, most cancers are caused by a mix of hereditary and environmental factors.(1) Identification of cancer”
How Taxol/paclitaxel kills cancer cells (2014, background): “Unattached kinetochores, which have not made stable attachments to microtubules, activate a signal transduction cascade that delays mitotic progression by inhibiting the anaphasepromoting complex/cyclosome (Kops et al., 2005; Lara-Gonzalez et al., 2012; Foley and Kapoor, 2013).”
Cell cycle kinases as therapeutic targets for cancer (2009, background): “Defects in the SAC can lead to premature separation of sister chromatids and could facilitate chromosomal instability (altered chromosome number), which is a frequent characteristic of cancer cell line”
An increased micronucleus frequency in peripheral blood lymphocytes predicts the risk of cancer in humans. (2006, background): “In contrast to chromosome breakage, whose role in early stages of carcinogenesis has extensively been studied, the significance of aneuploidy is still poorly understood, although it is well known that aneuploidy is a hallmark of the majority of human tumours, and is associated with high grade invasi”
The complexity of p53 stabilization and activation (2006, background): “Thus, it is not surprising that mutations that interfere with the function of key steps involved predispose to genome instability, cancer and other pathologies.(1) A central player in protecting the integrity of the genome is p53 (human p53 gene or protein), which is present at low levels under unpe”
The spindle assembly checkpoint. (2012, background): “uk point in the cell cycle can result in daughters with deviations from the normal karyotype, which in turn can result in a loss of fitness or, in the case of multicellular organisms, various diseases [2].”
Mitochondrial membrane permeabilization in cell death. (2007, background): “When cell death resulting from mitotic catastrophe is inhibited (for instance by overexpression of Bcl-2), the abortion of irregular mitoses is avoided and cells divide asymmetrically resulting in the generation of aneuploid daughter cells (397).”
Mad2 overexpression promotes aneuploidy and tumorigenesis in mice. (2007, neutral): “…assembly checkpoint is a signal transduction pathway that ensures that sister chromatids aligned at the metaphase plate do not separate prior to the bipolar attachment of all duplicated chromosomes to the mitotic spindle (Bharadwaj and Yu, 2004; Kops et al., 2005; Wassmann and Benezra, 2001).”
The impact of a negligent G2/M checkpoint on genomic instability and cancer induction (2007, background): “Chromosomal aberrations, including chromosome breaks or rearrangements, are reflective of genomic instability and are a hallmark of cancer cell”
Myc and cell cycle control. (2015, background): “struction key mitotic regulators such as cyclin B1 and securin, the separase inhibitor required for the correct anaphase [210,211].”
Cell cycle, CDKs and cancer: a changing paradigm (2009, background): “In addition, most tumours acquire genomic instability (GIN) that leads to additional mutations as well as chromosomal instability (CIN), a defect responsible for numerical changes in chromosome”
Boveri revisited: Chromosomal instability, aneuploidy and tumorigenesis (2009, background): “A surveillance mechanism called the mitotic checkpoint (also known as the spindle assembly checkpoint) is the primary guard against chromosome missegregatio”