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Statistical analyses concerning age and sex were performed only on the sporadic meningioma cases, omitting the multiple meningioma and NF2 patients, to avoid any kind of bias. All the other analyses were carried out on the complete group minus the tumors described above in the case of loss of chromosome 22 or number of chromosomal abnormalities. When we looked at the age distribution, after correcting for population distribution (Damhuis et a!., 1993), we observed a biphasic curve in both male and female patients with a decline in incidence between the age of 50 to 54 years. Two other studies revealed a similar decline in number of female patients (Dumanski et a!., 1990; Vagner Capodano et a!., 1993), but one other study by Casalone et a!. (1990) did not. A subdivision of our patients in two groups J over and under 50 years of age at surgery I did not result in any significant association with one of the in the methods section mentioned variables. Therefore, Jarger studies are necessary to further investigate the significance of this incidence profile, if any. Other patient and tumor characteristics however revealed some interesting associations (table 4). Three of them were marginally significant: 1) We found that only 18.5% of the male meningiomas were located at the base, whereas 43.8% of the female tumors were observed at that site (P=0.058). 2) Female patients predominated in the group of meningiomas with :5 2 chromosomal abnormalities (74.3% versus 33.3%, P=0.06). 3) Loss of (parts of) chromosome 22 was found in 88.5 % of the grade WIll tumors but in only 64.2% of the grade I tumors (P=0.079). Statistically significant associations were observed in all the following instances: I) Grades WIll meningiomas were more often found in male than in female patients (46.4% versus 22%). 2) Base meningiomas were mostly grade I (88.9%) and grade WIll meningiomas were more frequently derived from the convexity (70.6%). 3) In 87.8% of the convexity meningiomas partial or complete loss of chromosome 22 was found, but in only 40.6% of the base tumors this was the case. All intraventricular and falx meningiomas showed (partial) loss of chromosome 22. 4) Almost all (92 %) base meningiomas had::; 2 chromosomal abnormalities, whereas 52.4% of the convexity tumors and only 14.3% of the intraventricular and falx meningiomas had $ 2 chromosomal abnormalities. 5) All fibroblastic meningiomas were grade I, while 60% of the meningothelial meningiomas were graded IIIIII and grade IIIIlI comprised only 27.4 % of all tumors analyzed. 6) Most (94.7%) of the fibroblastic meningiomas showed (partial) loss of chromosome 22. Tumors without loss of chromosome 22 were predominantly of the transitional type (74.1 %).7) In 78.6% of the grade II/III meningiomas> 2 chromosomal 88
abnormalities were found, whereas in only 17.5% of the grade I tumors this was the case. 8) Loss of (parts 01) chromosome 22 was observed in 94.4% of the tumors with> 2 chromosomal abnormalities but in only 47.2% of the meningiomas with:::;; 2 chromosomal abnormalities. 89
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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
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 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 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
Page 99 and 100: Chapter IV Familial anaplastic epen
Page 101 and 102: Familial anaplastic ependymoma: evi
Page 103 and 104: PATIENT A, born 1977, presented at
Page 105 and 106: Microscopic examination (patients A
Page 107 and 108: (Lekanne Deprez et aI., 1994). Tabl
Page 109 and 110: Chapter V A t(4;22) ill a meningiom
Page 111 and 112: Am. J. HI/m. Genet. 48:783-790, 199
Page 113 and 114: Putative Tumor-suppressor Gene in M
Page 119 and 120: Chapter VI Molecular clolling of a
Page 121 and 122: Molecular Cloning of a Gene Disrupt
Page 123 and 124: to playa role in the development of
Page 125 and 126: total sheared human genomic DNA bef
Page 127 and 128: Genomic cosmid contig spanning the
Page 129 and 130: probe A is conserved in hamster DNA
Page 131 and 132: Southerll, 1l0l1hern blots and evol
Page 133 and 134: The evolutionary conservation of th
Page 135 and 136: A " l ... aGAP~RAGC EPOV~SR~AGQGE ;
Page 137 and 138: postulates that the first AUG codon
Page 139 and 140:
Bijlsma EK, Brouwer~Mladin R, Bosch
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Tanaka N, Nishisho I, Yamamoto 1'.1
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Chapter VII Constitutional DNA-leve
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GENES, CHROMOSOMES & CANCER 9;124-1
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LfKANNf DfPREZ fT AL TABLE I. Cytog
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LEKANNE DEPRF2 ET AL could be that
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Chapter VIII Frequent NF2 gene tran
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Am.'. HIIIII. Gellet. 54:1022-1029,
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Lekanne Deprez ct al. Table I Oligo
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Table 2 Nfl Gene-Transcript Mutatio
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Lebnne Deprez et lli. observed at a
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Summary and Discussion Meningioma i
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translocation (Chapter V). These hy
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were derived from patients with mor
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Samenvatting Meningeomen zUn goedaa
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het gebied rondom het MNI gen te be
Page 171 and 172:
Curriculum vitae 30 juni 1965 gebor
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List of publications I) van 't Veer
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Nawoord Dit boekje is 101 sland gek
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