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number of clonal chromosomal abnormalities (chr abn). To analyze the latter variable the number of clonal chromosomal abnormalities was divided in two groups: ::;; 2 ehr abn or > 2 chr abn as seen by chromosome banding analysis. Resulls The 126 meningiomas that were studied are listed in table 1. This table shows the sex and age at surgery of the patients, the site of tumor origin, the histological subtype, grade, and the chromosome 22 status of the tumors. This series contains 13 tumors derived from 9 patients with two or more meningiomas, which were located at different sites, and 2 meningiomas from 2 sisters with NF2 (table 1). Of the liD single meningioma patients without evidence of NF2, 82 were from females (average age 55.3) and 28 were from males (average age 57.5). In the complete group of meningiomas the site of tumor origin was subdivided in convexity 52.9% of the cases, base 37.2%, falx 7.4% and intraventricular 2.5%. Histopathologically 52.3% of the meningiomas were transitional, 16.7% fibroblastic, 11.9% meningotheliomatous and 19.1 % were mixed or had a different sUbtype. Grading of the meningiomas resulted in 73% grade I (benign), 19.8% grade II (atypical) and 7.2% grade III (anaplastic) tumors. The chromosome 22 status (last 3 columns in table I) is the result of karyotyping, FISH and LOH analysis. These analyses were carried out depending on the quantity of material available. FISH analysis of freshly obtained tumor cells was applied only in the second half of this series and proved to be a very sensitive tool for the detection of (partial) loss of chromosome 22 (table I and 2). In total 97 tumors could be examined with at least one of these techniques. For the interpretation of (partial) loss of chromosome 22 and number of clonal chromosomal abnormalities in the tumors (below and table 4), the tumors 10, 133 and 177 were excluded because discrepancies between the methods were found. This was probably due to inhomogeneity in these tumors with regard to the percentage tumor vs normal cells. Tumor 16 was excluded because only one cell could be analyzed. This cell, however, showed a very abnormal karyotype, including loss of chromosome 22. Tumor 176 was excluded with regard to the interpretation of number of clonal chromosomal abnormalities because incomplete cytogenetic data were available. FfSH analysis in this tumor clearly showed loss of chromosome 22 (table I). Therefore, we established that in 66 72
(71 %) of the 93 meningiomas complete or partial loss of chromosome 22 was found. Table 1. Chal'actel'istics of patients with meningiomas #22 status No. Sex/Age Site of Histological Karyotype 2 FISH(% loss)} LOH' (yr) Tumor Subtype Origin1 (grade)l M/66 c T(D nc 3 F/60 C M (lQ -22* 4 FIS9 B T (Q -22 5 FISS B T(D 6 F/63 F T (lQ 7' F/62 C F(D -22,c -22 8 M/6S F(D 9 F/47 C T GQ der(22),C der(22) 10 F/67 F T(D -22,C 2n II Mf43 C Mill AlPs (1I) 12 F/43 C MGQ nc 13 F/41 B T(D 14 FI22 IV T GQ -22,C 15 FIS) B T(D 2n 16 M/68 IV M/H (Ill) -22,C? 17 M/49 B T (1) 18 MI73 c T(D -22 19 F/64 B T(D 73
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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
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 65: Chapter III Cytogenetic, molecular
Page 68 and 69: Introduction Meningiomas are consid
Page 70 and 71: defined by evaluating 6 histologica
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
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
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to playa role in the development of
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total sheared human genomic DNA bef
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Genomic cosmid contig spanning the
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probe A is conserved in hamster DNA
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Southerll, 1l0l1hern blots and evol
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The evolutionary conservation of th
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A " l ... aGAP~RAGC EPOV~SR~AGQGE ;
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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
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Curriculum vitae 30 juni 1965 gebor
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List of publications I) van 't Veer
Page 175 and 176:
Nawoord Dit boekje is 101 sland gek
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