Editing Centrosome (section)

=== Numeric aberrations ===
The presence of an inadequate number of centrosomes is very often linked to the appearance of [[genome instability]] and the loss of tissue differentiation.<ref name=Lingle2002 /><ref>{{Cite journal
 | title = Centrosome amplification and instability occurs exclusively in aneuploid, but not in diploid colorectal cancer cell lines, and correlates with numerical chromosomal aberrations
 | year = 2000
 | journal = Genes Chromosomes Cancer
 | pages = 183–190
 | volume = 27
 | pmid = 10612807
 | pmc = 4721570
 | last1 = Ghadimi     | first1 =  B.M.
 | last2 =  Sackett     | first2 =  D.L.
 | last3 =  Difilippantonio     | first3 =  M.J.
 | last4 =  Schrock     | first4 =  E.
 | last5 =  Neumann     | first5 =  T.
 | last6 =  Jauho     | first6 =  A.
 | last7 =  Auer     | first7 =  G.
 | last8 =  Ried     | first8 =  T. | doi=10.1002/(SICI)1098-2264(200002)27:2<183::AID-GCC10>3.0.CO;2-P
 | issue = 2
 }}</ref> However, the method to count the centrosome number (with two centrioles to each centrosome) is often not very precise, because it is frequently assessed using [[fluorescence microscope|fluorescence microscopy]], which does not have high enough [[optical resolution]] to resolve centrioles that are very close to each other. Nevertheless, it is clear that the presence of an excess of centrosomes is a common event in human tumors. It has been observed that loss of the [[TP53|tumor-suppressor p53]] produces superfluous centrosomes,<ref>{{Cite journal
 |title        = Abnormal centrosome amplification in the absence of p53
 |year         = 1996
 |journal      = Science
 |pages        = 1744–1747
 |volume       = 271
 |doi          = 10.1126/science.271.5256.1744
 |last1        = Fukasawa
 |first1       = K.
 |last2        = Choi
 |first2       = T.
 |last3        = Kuriyama
 |first3       = R.
 |last4        = Rulong
 |first4       = S.
 |last5        = Woude
 |first5       = Vande G.F.
 |issue        = 5256
 |pmid         = 8596939
 |bibcode      = 1996Sci...271.1744F
 |s2cid        = 20139983
 |url          = https://zenodo.org/record/1231068
 |access-date  = 2019-09-09
 |archive-date = 2020-11-15
 |archive-url  = https://web.archive.org/web/20201115203136/https://zenodo.org/record/1231068
 |url-status   = live
}}</ref> as well as deregulating other proteins implicated in [[cancer]] formation in humans, such as [[BRCA1]] and [[BRCA2]]. (For references, see <ref name=Nigg2002 />.) An excess of centrosomes can be generated by very different mechanisms: specific reduplication of the centrosome, cytokinesis failure during [[cell division]] (generating an increase in chromosome number), cell fusion (such as in cases of infection by specific viruses) or ''de novo'' generation of centrosomes. At this point, there is insufficient information to know how prevalent these mechanisms are ''in vivo'', but it is possible that the increase in centrosome numbers due to a failure during cell division might be more frequent than appreciated, because many "primary" defects in one cell (deregulation of the [[cell cycle]], defective [[DNA]] or [[chromatin]] metabolism, failure in the [[spindle checkpoint]], etc.) would generate a failure in cell division, an increase in [[ploidy]] and an increase in centrosome numbers as a "secondary" effect.<ref>{{Cite journal
 | title = Aurora-A overexpression reveals tetraploidization as a major route to centrosome amplification in p53–/– cells
 | year = 2002
 | journal = EMBO J
 | pages = 483–492
 | volume = 21
 | doi = 10.1093/emboj/21.4.483
 | last1 = Meraldi     | first1 =  P.
 | last2 =  Honda     | first2 =  R.
 | last3 =  Nigg     | first3 =  E.A. | pmid=11847097 | pmc=125866
 | issue = 4
 }}</ref><ref>{{Cite journal
 | title = From polyploidy to aneuploidy, genome instability and cancer
 | year = 2004
 | journal = Nat Rev Mol Cell Biol
 | pages = 45–54
 | volume = 5
 | pmid = 14708009
 | last1 = Storchova     | first1 =  Z.
 | last2 =  Pellman     | first2 =  D.
 | doi = 10.1038/nrm1276
 | issue = 1
 | s2cid = 11985415
 }}</ref>