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Since assessment of the IgV<sub>H</sub> antibody DNA changes is difficult to perform, the presence of either [[cluster of differentiation]] [[CD38|38]] ([[CD38]]) or Z-chain–associated protein kinase-70 ([[ZAP-70]]) may be surrogate markers of high risk subtype of CLL.<ref name="pmid16983131"/> Their expression correlates with a more immature cellular state and a more rapid disease course.
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In addition to the immunoglobulin variable-region [[heavy chain]] (IgV<sub>H</sub>) gene mutation status, the prognosis of patients with CLL is dependent on the genetic changes within the neoplastic cell population. These genetic changes can be identified by fluorescent probes to chromosomal parts using a technique referred to as [[fluorescent in situ hybridization]] (FISH).<ref name="pmid16983131"/> Four main genetic aberrations are recognized in CLL cells that have a major impact on disease behavior.<ref name="pmid11136261">{{cite journal | author = Dohner H|year=2000|title=Genomic aberrations and survival in chronic lymphocytic leukemia |journal=NEJM|volume=343|issue=26|pages=1910–6|pmid=11136261|url=http://content.nejm.org/cgi/content/full/343/26/1910 | doi = 10.1056/NEJM200012283432602 | author-separator = , | author2 = Stilgenbauer S | author3 = Benner A | author4 = "" | display-authors = 4 | last5 = Kröber | first5 = Alexander | last6 = Bullinger | first6 = Lars | last7 = Döhner | first7 = Konstanze | last8 = Bentz | first8 = Martin | last9 = Lichter | first9 = Peter}}</ref>
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# Trisomy 12, an additional chromosome 12, is a relatively frequent finding occurring in 20–25% of patients and imparts an intermediate prognosis.
# Deletion of the long arm of chromosome 13 (del 13q) is the most common abnormality in CLL with roughly 50% of patients with cells containing this defect. These patients have the best prognosis and most will live many years, even decades, without the need for therapy. The gene targeted by this deletion is a segment coding for microRNAs miR-15a and miR-16-1.<ref>{{Cite pmid|19347736}}</ref><ref>{{Cite pmid|23216588}}</ref> Studies have found the miR-15a/16-1 microRNA cluster to function as a tumour suppressor, with the oncogene BCL2 as its target.<ref name="pmid18931683">{{cite journal| author=Bonci D, Coppola V, Musumeci M, Addario A, Giuffrida R, Memeo L et al.| title=The miR-15a-miR-16-1 cluster controls prostate cancer by targeting multiple oncogenic activities. | journal=Nat Med | year= 2008 | volume= 14 | issue= 11 | pages= 1271–7 | pmid=18931683 | doi=10.1038/nm.1880 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=18931683 }}</ref>
====Array-based karyotyping====
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