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Chapter IV Familial anaplastic ependymoma: evidence of loss of chromosome 22 in tumor cells accepled for pllblication ill rhe 1. Neurol. NellroslI1g. P~)'chi(/tr)' 99
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GENES ON CHROMOSOME 22 INVOLVED IN
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PROMOTmCOMMIssm Promotor: Prof. Dr.
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Contents List of abbreviations 9 Ch
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List of abbreviations APC bp DCC FA
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1 Cancer is a genetic disease It is
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transformation came from somatic ce
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to tumorigenesis if a mutation inac
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is that this interaction inactivate
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endogenous wt p53 by forming mixed
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Recent studies in these families ha
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In about 15% of all colon tumors an
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e explained by assuming that the nu
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3.6 The NFl gene Neurofibromatosis
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4 MENINGIOMA 4.1 Cells of origin In
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fossa and foramen magnum), convexit
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early cell cultures the presence of
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gene (Dumanski et aI., NNFF consort
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et aI., 1991b; Larsson et aI., 1990
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6 References Aaltonen LA, Peltomiik
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(1988) SV40 large tumor antigen for
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Haber DA, Buckler AJ, Glaser T, Cal
Page 47 and 48: carcinomas. Genes Chrom Cancer 2:19
Page 49 and 50: Pelletier J, Breunin~ W, Kashtan CE
Page 51 and 52: Stratton MR, Darling J, Lantos PL,
Page 53: Chapter II Isolatioll alld characte
Page 56 and 57: SHORT COMMUNICATION TABLE 1 Charact
Page 59: Appendix A lIew polymorphic probe 0
Page 62 and 63: Nudeic Acids Research, Vol. 19, No.
Page 65: Chapter III Cytogenetic, molecular
Page 68 and 69: Introduction Meningiomas are consid
Page 70 and 71: defined by evaluating 6 histologica
Page 72 and 73: number of clonal chromosomal abnorm
Page 74 and 75: #22 status No. Sex/Age (yr) Site of
Page 76 and 77: #22 slattls No. SexiAge (yr) Site o
Page 78 and 79: #22 status No. Sex/Age (yr) Site of
Page 80 and 81: Table 2. Comparison of FISH, cytoge
Page 82 and 83: No. Days in Karyotypes andlor clona
Page 84 and 85: No. Days in Karyotypes and/or clona
Page 86 and 87: to map both breakpoints (data not s
Page 88 and 89: Statistical analyses concerning age
Page 90 and 91: Tuble 4. Frequency tables between d
Page 92 and 93: from adult patients, indicating tha
Page 94 and 95: Acknowledgements This study was sup
Page 96 and 97: McDermid HE, Duncan AMV, Higgins MJ
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Page 102 and 103: observed in 12 out of 30 analysed e
Page 104 and 105: A B c Figure 2. Cerebral scans. A.
Page 106 and 107: Genetic analysis Fresh tumor tissue
Page 108 and 109: chromosome 22 in a major percentage
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Page 112 and 113: Lekanne Deprez et al. matosis 2 (NF
Page 114 and 115: Lekanne Deprez et a!. Figure I Basi
Page 116 and 117: Lekanne Deprez et al. A S ""'~"' n
Page 118 and 119: Lekanne Deprez et aL beling DNA res
Page 120 and 121: 120
Page 122 and 123: Introduction Meningiomas are primar
Page 124 and 125: Hybrid cell lines, The somatic cell
Page 126 and 127: 6A (data not shown), These data sug
Page 128 and 129: Isolation and characterization of t
Page 130 and 131: probably caused by the less efficie
Page 132 and 133: A 1 2 3 4 5 6 7 8 kb 9.5 7.5 4.4 2.
Page 134 and 135: cDNA sequence analysis Sequence ana
Page 136 and 137: Discussion Characterization of the
Page 138 and 139: involve loss of both the MNl and th
Page 140 and 141: D, van der Kwast TH, Zwarthoff BC (
Page 142 and 143: 142
Page 144 and 145: 144
Page 146 and 147: CHROMOSOME 11 ABERRATIONS ebellopon
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E BP E HP E XO D B Control: I I II
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150
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152
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NF2 Mut.nions and Meningiomas vatin
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NF2 Mutations and Meningiomas A D B
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NF2 Mutations and Meningiomas Table
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NF2 Mutations and Meningiomas Natio
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chromosomal abnormalities and tumor
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expression of the MNI gene in one o
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166
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wijzen, die rnogelijk voor rneninge
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170
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172
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1) Lekanne Deprez RH, Groen NA, Lou
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het onderzoek onontbeerlijk was. Be
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