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Appendix A lIew polymorphic probe 011 chromosome 22: NBl7 (D22S181) Nllc/. Acids Res. 19:686, 1991 AileII' polymOlphic probe 011 chromosome 22: NB35 (D22S182) Nllc/. Adds Res. 19:686, 1991 A lIew polymorphic probe 011 chromosome 22: NB84 (D22Sl83) Nllc/. Acids Res. 19:687, 1991 A lIew polymorphic probe 011 chromosome 22q: NB129 (D22S193) Nllc/. Acids Res. 19:687, 1991 A new polymO/phic probe 011 chromosome 22: NB5 (D22S20l) Nllc/. Acids Res. 19:1963, 1991 59
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GENES ON CHROMOSOME 22 INVOLVED IN
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PROMOTmCOMMIssm Promotor: Prof. Dr.
Page 6 and 7:
Contents List of abbreviations 9 Ch
Page 9: List of abbreviations APC bp DCC FA
Page 13 and 14: 1 Cancer is a genetic disease It is
Page 15 and 16: transformation came from somatic ce
Page 17 and 18: to tumorigenesis if a mutation inac
Page 19 and 20: is that this interaction inactivate
Page 21 and 22: endogenous wt p53 by forming mixed
Page 23 and 24: Recent studies in these families ha
Page 25 and 26: In about 15% of all colon tumors an
Page 27 and 28: e explained by assuming that the nu
Page 29 and 30: 3.6 The NFl gene Neurofibromatosis
Page 31 and 32: 4 MENINGIOMA 4.1 Cells of origin In
Page 33 and 34: fossa and foramen magnum), convexit
Page 35 and 36: early cell cultures the presence of
Page 37 and 38: gene (Dumanski et aI., NNFF consort
Page 39 and 40: et aI., 1991b; Larsson et aI., 1990
Page 41 and 42: 6 References Aaltonen LA, Peltomiik
Page 43 and 44: (1988) SV40 large tumor antigen for
Page 45 and 46: 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 61 and 62: Nuefeic Adds Research, Vol. 19, No.
Page 63: Nucleic Acids Research, Vol, 19, No
Page 67 and 68: Cytogenetic, Molecular Genetic and
Page 69 and 70: abnormalities, histopathological an
Page 71 and 72: D22S193, D22Sn, D22S56 and NF2 were
Page 73 and 74: (71 %) of the 93 meningiomas comple
Page 75 and 76: #22 status No. Sex/Age (y,) Site of
Page 77 and 78: #22 status No. SexlAge (yr) Site of
Page 79 and 80: #22 status No. Sex/Age (yr) Site of
Page 81 and 82: Table 3. Summary of chromosomal fin
Page 83 and 84: No. Days in Karyotypes and/or clona
Page 85 and 86: No. Days in Karyotypes and/or clona
Page 87 and 88: 112 12.1 122 123 1).1 132 133 .. '
Page 89 and 90: abnormalities were found, whereas i
Page 91 and 92: Discussion This series of meningiom
Page 93 and 94: finding that the majority of grade
Page 95 and 96: Dumanski JP, Roule~lU GA, Nordenskj
Page 97: Zucman J, Delattre 0, Desmaze C, Pl
Page 100 and 101: 100
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
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chromosome 22 in a major percentage
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110
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Lekanne Deprez et al. matosis 2 (NF
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Lekanne Deprez et a!. Figure I Basi
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Lekanne Deprez et al. A S ""'~"' n
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Lekanne Deprez et aL beling DNA res
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120
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Introduction Meningiomas are primar
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Hybrid cell lines, The somatic cell
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6A (data not shown), These data sug
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Isolation and characterization of t
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probably caused by the less efficie
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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
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involve loss of both the MNl and th
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D, van der Kwast TH, Zwarthoff BC (
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142
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144
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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
Page 166 and 167:
166
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wijzen, die rnogelijk voor rneninge
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170
Page 172 and 173:
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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