We are analyzing https://link.springer.com/article/10.1007/s10577-015-9505-5.

Title:
Centrosome amplification, chromosomal instability and cancer: mechanistic, clinical and therapeutic issues | Chromosome Research
Description:
Centrosomes, the main microtubule-organizing centers in most animal cells, are of crucial importance for the assembly of a bipolar mitotic spindle and subsequent faithful segregation of chromosomes into two daughter cells. Centrosome abnormalities can be found in virtually all cancer types and have been linked to chromosomal instability (CIN) and tumorigenesis. Although our knowledge on centrosome structure, replication, and amplification has greatly increased within recent years, still only very little is known on nature, causes, and consequences of centrosome aberrations in primary tumor tissues. In this review, we summarize our current insights into the mechanistic link between centrosome aberrations, aneuploidy, CIN and tumorigenesis. Mechanisms of induction and cellular consequences of aneuploidy, tetraploidization and CIN, as well as origin and effects of supernumerary centrosomes will be discussed. In addition, animal models for both CIN and centrosome amplification will be outlined. Finally, we describe approaches to exploit centrosome amplification, aneuploidy and CIN for novel and specific anticancer treatment strategies based on the modulation of chromosome missegregation rates.
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Keywords {🔍}

pubmed, google, scholar, article, cas, central, cancer, cell, centrosome, cells, instability, biol, chromosome, aneuploidy, amplification, human, nat, chromosomal, mitotic, res, protein, kinase, genet, sci, spindle, krämer, nature, tumor, van, oncogene, duensing, cycle, mol, proc, natl, acad, centrosomes, leukemia, tumorigenesis, mitosis, wang, science, missegregation, checkpoint, rev, myeloid, amon, aberrations, multipolar, mammalian,

Topics {✒️}

cre-loxp-controlled periodic aurora month download article/chapter p53-dependent apoptosis pathway ubiquitin-conjugating enzyme e2 high-risk human papillomavirus cyclin-dependent kinase 2 p53-dependent postmitotic checkpoint s-phase-targeting anticancer drugs radiation-induced mitotic catastrophe 17-n-allylamino-17-demethoxygeldanamycin aicar main microtubule-organizing centers microtubule-stabilizing agents epothilones carrillo-de-santa-pau bueno-de-mesquita hb syndrome-related myeloid disorders nci-60 drug-screening panel somatic copy-number alteration quantitative multi-parametric evaluation aneuploidy-selective antiproliferation compounds cdc20 promotes tumorigenesis full article pdf mutated ha-ras-1 allele centrosome-declustering drugs mediate inhibits centrosomal clustering dna damage occurs article cosenza centrosome amplification induced kinesin-related protein potential anticancer agent stolzenberg-solomon rz diaz-martinez la human tetraploid cells p53-dependent mechanism über asymmetrische zelltheilung von lilienfeld-toal acentriolar mitosis activates additional chromosomal abnormality privacy choices/manage cookies dna damage response robust spindle checkpoint van der burg stil−/− mouse embryos fielding ab bakhoum sf hsf1 activation supports ubch10 ubiquitin conjugase peloponese jm jr abnormal centrosome amplification multiple molecular targets integrin-linked kinase

Questions {❓}

Nigg EA (2002) Centrosome aberrations: cause or consequence of cancer progression?
Weaver BAA, Cleveland DW (2006) Does aneuploidy cause cancer?

Schema {🗺️}

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      description:Centrosomes, the main microtubule-organizing centers in most animal cells, are of crucial importance for the assembly of a bipolar mitotic spindle and subsequent faithful segregation of chromosomes into two daughter cells. Centrosome abnormalities can be found in virtually all cancer types and have been linked to chromosomal instability (CIN) and tumorigenesis. Although our knowledge on centrosome structure, replication, and amplification has greatly increased within recent years, still only very little is known on nature, causes, and consequences of centrosome aberrations in primary tumor tissues. In this review, we summarize our current insights into the mechanistic link between centrosome aberrations, aneuploidy, CIN and tumorigenesis. Mechanisms of induction and cellular consequences of aneuploidy, tetraploidization and CIN, as well as origin and effects of supernumerary centrosomes will be discussed. In addition, animal models for both CIN and centrosome amplification will be outlined. Finally, we describe approaches to exploit centrosome amplification, aneuploidy and CIN for novel and specific anticancer treatment strategies based on the modulation of chromosome missegregation rates.
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