{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,5,28]],"date-time":"2025-05-28T22:05:11Z","timestamp":1748469911739},"reference-count":43,"publisher":"Wiley","issue":"2","license":[{"start":{"date-parts":[[2007,1,22]],"date-time":"2007-01-22T00:00:00Z","timestamp":1169424000000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Neuropathology Appl Neurobio"],"published-print":{"date-parts":[[2007,4]]},"abstract":"<jats:p>Gangliogliomas and focal cortical dysplasias (FCDs) constitute glioneuronal lesions, which are frequently encountered in biopsy specimens of patients with pharmacoresistant focal epilepsy and relate to impaired differentiation and migration of neural precursors. However, their molecular pathogenesis and relationship are still largely enigmatic. Recent data suggest several components of the insulin\u2010pathway, including <jats:italic>TSC1<\/jats:italic> and <jats:italic>TSC2<\/jats:italic> mutated in tuberous sclerosis complex (TSC), to be altered in gangliogliomas and FCD with Taylor type balloon cells (FCD<jats:sub>IIb<\/jats:sub>). The proteins tuberin (TSC2) and hamartin (TSC1) constitute a tumour suppressor mechanism involved in cell\u2010cycle control. Hamartin and\/or tuberin were reported to colocalize and\/or interact with CDK1, cyclinB1 and cyclinA2 that are critically involved in cell\u2010size and cell\u2010growth control. Here, we have carried out mutational and expression analyses of <jats:italic>CDK1<\/jats:italic>, <jats:italic>cyclinB1<\/jats:italic> and <jats:italic>cyclinA2<\/jats:italic> in gangliogliomas and FCD<jats:sub>IIb<\/jats:sub>. Mutational screening was performed by single\u2010strand conformation polymorphism analysis in gangliogliomas (<jats:italic>n<\/jats:italic>\u2003=\u200320), FCD<jats:sub>IIb<\/jats:sub> (<jats:italic>n<\/jats:italic>\u2003=\u200335) and controls. <jats:italic>CyclinB1<\/jats:italic> revealed a polymorphism (G to A, cDNA Position 966, GenBank: NM_031966) in exon 7 with similar frequencies in FCD<jats:sub>IIb<\/jats:sub>, gangliogliomas and control specimens (FCD <jats:italic>n<\/jats:italic>\u2003=\u20039\/35; gangliogliomas <jats:italic>n<\/jats:italic>\u2003=\u20035\/20; control <jats:italic>n<\/jats:italic>\u2003=\u200320\/100). We used real\u2010time reverse transcription polymerase chain reaction to determine expression levels of <jats:italic>CDK1<\/jats:italic>, <jats:italic>cyclinB1<\/jats:italic> and <jats:italic>cyclinA2<\/jats:italic> in 10 FCD<jats:sub>IIb<\/jats:sub> and nine gangliogliomas compared with unaffected adjacent control tissue of the same patients. We observed significantly lower expression of <jats:italic>CDK1<\/jats:italic> and <jats:italic>cyclinA2<\/jats:italic> in FCD<jats:sub>IIb<\/jats:sub><jats:italic> vs.<\/jats:italic> controls whereas no significant expression differences were present for <jats:italic>CDK1<\/jats:italic>, <jats:italic>cyclinB1<\/jats:italic> and <jats:italic>cyclinA2<\/jats:italic> in gangliogliomas. Our data strongly argue against mutational events of <jats:italic>CDK1<\/jats:italic>, <jats:italic>cyclinB1<\/jats:italic> and <jats:italic>cyclinA2<\/jats:italic> to play a role in gangliogliomas or FCD<jats:sub>IIb<\/jats:sub>. However, a potential functional significance of lower expression for the cell\u2010size and cell\u2010cycle regulators <jats:italic>CDK1<\/jats:italic> and <jats:italic>cyclinA2<\/jats:italic> in FCD<jats:sub>IIb<\/jats:sub> composed of large dysplastic neurones and balloon cells needs to be further resolved.<\/jats:p>","DOI":"10.1111\/j.1365-2990.2006.00788.x","type":"journal-article","created":{"date-parts":[[2007,1,22]],"date-time":"2007-01-22T11:07:55Z","timestamp":1169464075000},"page":"152-162","source":"Crossref","is-referenced-by-count":14,"title":["Mutational and expression analysis of CDK1, cyclinA2 and cyclinB1 in epilepsy\u2010associated glioneuronal lesions"],"prefix":"10.1111","volume":"33","author":[{"given":"V.","family":"Schick","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"M.","family":"Majores","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"J.","family":"Fassunke","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"G.","family":"Engels","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"M.","family":"Simon","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"C. 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