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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
- 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 59: Appendix A lIew polymorphic probe 0
- Page 62 and 63: Nudeic 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
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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
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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.
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cDNA sequence analysis Sequence ana
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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
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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