By B. Michael Ghadimi, Thomas Ried
This factor of Recent ends up in melanoma Research provides a accomplished overview of present realizing of chromosomal instability in melanoma and of ideas to take advantage of this knowledge for greater therapy of sufferers with melanoma. melanoma is a ailment of the chromosomes, and chromosomal instability in melanoma disrupts gene functionality by means of both inactivating tumor suppressor genes or activating growth-promoting oncogenes. The chromosomal foundation for those aberrations is both translocations, which switch the integrity of genes, or irregular numbers of chromosomes, a often called aneuploidy, which ends up in irregular gene expression degrees. Such structural or numerical chromosomal aberrations are particular for special tumor entities. The measure of chromosomal instability and the measure of intratumor heterogeneity have profound outcomes for ailment consequence and for healing stratification.
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Extra resources for Chromosomal Instability in Cancer Cells
Yale J Biol Med 86:453–461 Dalla-Favera R, Bregni M, Erikson J et al (1982) Human c-myc onc gene is located on the region of chromosome 8 that is translocated in Burkitt lymphoma cells. Proc Natl Acad Sci USA 79:7824–7827 De Bont R, van Larebeke N (2004) Endogenous DNA damage in humans: a review of quantitative data. Mutagenesis 19:169–185 de Graaf CA, van Steensel B (2013) Chromatin organization: form to function. Curr Opin Genet Dev 23:185–190 de Klein A, van Kessel AG, Grosveld G et al (1982) A cellular oncogene is translocated to the Philadelphia chromosome in chronic myelocytic leukaemia.
Nature 421:952–956 Goodarzi AA, Noon AT, Deckbar D et al (2008) ATM signaling facilitates repair of DNA double-strand breaks associated with heterochromatin. Mol Cell 31:167–177 Gostissa M, Ranganath S, Bianco JM, Alt FW (2009) Chromosomal location targets different MYC family gene members for oncogenic translocations. Proc Natl Acad Sci USA 106:2265– 2270 Halazonetis TD, Gorgoulis VG, Bartek J (2008) An oncogene-induced DNA damage model for cancer development. K. M. Kakadia Hastings PJ, Ira G, Lupski JR (2009) A microhomology-mediated break-induced replication model for the origin of human copy number variation.
2013a). A fourth approach to induce CIN in vivo is by disrupting the cohesion complex, a ring like structure that holds the sister chromatids together during interphase. , SA1), but also by deregulating upstream players such as pRb (Coschi et al. 2010; Manning et al. 2010; Van Harn et al. 2010). Similarly, various other genes have been knocked out in the mouse which indirectly affect chromosome segregation. E. Simon et al. Chromosome Cohesin Stag1 Securin Pttg1 Separase Espl1 Otherwise involved in mitosis Ccnb2 Mcm4 Chaos3 Chfr Tpx2 Lzts1 Kinetochore CenpA CenpB CenpC Hec1 Centrosome Aurora A Plk1 Plk4 Usp44 Microtubule Chromosome passengers APC INCENP Survivin Spindle assembly checkpoint Ccnb1 Mad1 Aurora B Cdc20 Mad2 Bub1 Cdh1 Mps1 BubR1 CenpE Ubch10 Bub3 Fig.
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