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2012 | 12 | 2 | 74-103
Article title

Badania kliniczno-molekularne w oponiakach

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EN
Clinical and molecular studies in meningiomas
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PL
Abstracts
EN
Aim: The aim of our study was to evaluate the frequency of deletions on chromosomes 1, 9, 10, 14, 18 and 22 in 75 benign and 15 atypical meningiomas and correlate them with clinical findings. Methods: Paired normal and tumour DNA samples obtained from the patients operated on, were analyzed for loss of heterozygosity (LOH), using 24 microsatellite markers and PCR techniques. Results: Statistical analysis showed that deletions on chromosomes 14 and 18 were significantly associated with WHO grade of the meningiomas (p=0.048 and p=0.03, respectively). In addition, LOH on chromosome 14 was significantly associated with tumour size (p=0.048), as the risk of developing a tumour larger than 4 cm in diameter was 6-times greater than the risk of developing tumour with diameter below 4 cm. The most frequent genetic abnormality inmeningiomas is 22 LOH, which was confirmed in the present study in which high frequency of such abnormality was observed (66%). There was a clear associations between chromosome 22 status and histological subtype. LOH on chromosome 22 was more frequent in fibrous meningiomas than in the meningothelial variant (p=0.001). Besides that, there was a relationship between 22 LOH status and tumour location: the frequency of LOH in skull base meningiomas was significantly lower compared to parasagittal meningiomas (p=0.0004). Conclusions: These results indicated that allelic loss on chromosomes 9, 10, 14, 18 and 22 may be associated with meningioma pathogenesis and progression.
PL
Cel: Celem pracy była ocena częstości występowania delecji na chromosomach 1., 9., 10., 14., 18. i 22. w 75 łagodnych i 15 atypowych oponiakach oraz skorelowania ich z niektórymi danymi klinicznymi. Materiał i metoda: Sparowane próbki prawidłowego, pochodzącego z leukocytów krwi obwodowej DNA oraz DNA oponiaka zostały zbadane pod kątem utraty heterozygotyczności (LOH) za pomocą 24 markerów mikrosatelitarnych i techniki reakcji łańcuchowej polimerazy (PCR). Materiał pochodził od chorych operowanych. Wyniki: Analiza statystyczna wykazała, że delecje na chromosomach 14. i 18. były w istotny sposób związane ze stopniem WHO oponiaków (odpowiednio p=0,048 i p=0,03). Co więcej, LOH na chromosomie 14. był istotnie statystycznie związany z rozmiarem oponiaka (p=0,048), jako że ryzyko wzrostu nowotworu o średnicy powyżej 4 cm było 6-krotnie większe niż ryzyko rozwoju mniejszego guza. Najczęściej występującą nieprawidłowością genetyczną w oponiakach jest LOH na chromosomie 22., co zostało potwierdzone w przedstawionym materiale, w którym zmianę tę zaobserwowano w 66% przypadków. Występował silny związek pomiędzy zmianami na chromosomie 22. a podtypem histologicznym nowotworu. Utrata heterozygotyczności na chromosomie 22. była częstsza w oponiakach włóknistych niż w meningotelialnych (p=0,001). Ponadto obserwowano związek pomiędzy obecnością LOH na 22. chromosomie a umiejscowieniem oponiaka: częstość LOH w guzach podstawy czaszki była znacząco mniejsza w porównaniu z oponiakami przystrzałkowymi (p=0,0004). Wnioski: Powyższe wyniki wskazują, że utrata heterozygotyczności na chromosomach 9., 10., 14., 18. i 22. może mieć związek z patogenezą i progresją oponiaka.
Discipline
Publisher

Year
Volume
12
Issue
2
Pages
74-103
Physical description
Contributors
  • Klinika Neurochirurgii i Onkologii Centralnego Układu Nerwowego Uniwersytetu Medycznego w Łodzi., djask@o2.pl
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