No. Days in Karyotypes andlor clonal rearrangements {no. of cells] culture 35 6 45,XX,-22 [14]1 90,XXXX,-22,-22 [2] 37 9 39 49 14 50 14 53 28 54 35 46,XX"dd(2)(q22) [20] 45,XX,lq-,3q+,-10 [3]1 44.XX,2q·,·6,·7.lOp+.llp +, 13q+, 19q+ ,·22.22q +, + fragment [IO]I 45,XX,2qy 6,·7, lOp+, IIp+ ,·13, 19q+ ,·22,22q +, + fragment, + ring f3J1 46,XX [5] 45,XX,-22 [16] 45,XX,-22 [12]1 45,XX,,(17),-22 [3JI 44,XX,·22,tas(9; 17)(qter;pter)111 45,XX,-22 [1311 very aherrant tetraploid including tas 12} 43,XY,-14,-19,-22 [3]1 42,X,-Y,-14,-19,-22 [611 46,XY (61 55B~ 14 sse 10 55D 39 59 18 60' 35 64 49 69 32 45,XX,-22 [III 44,X,-X,-22 [811 40·43,idem,with random losses 151 45,XX,-22 12411 89,hypotetrapioid.-2212x],with additionHI tosses and rearrangements (lJ 45,XX,-22 [3JI 46,XX (2J 46,XX [16( 45,XX,-22 [4(1 46,XX [12J 46,XX [161 43,XX,der(1)t(l; J6)(p II ;qll),uic(6qter- > pI2:: 16q 11- >pter or 22q II-qter),-14, -16,-22 [16( 82
No. Days in Karyotypes and/or clonal rearrangements [no. of cellsJ culture 72 21 46,XX 116J 73 14 46,XX [16] 76 21 46,XX 123J 77 18 46,XY 120)J 78' 5 Very aberrant hypodiploid to hypotetraploid karyotype. Clonal aberrations: t(l;2)(q41?;q221),·19,19q+,22q+ [13J. Also many tas and HSR 81 25 56(54·59),X,·X, lp·, + Ip·, +3, +5,6q+, + 13, + 17, + 18,( + 19), +20,( +20),( +22), +various markers 19JI 46,XX [lJ 82 3 44,der(X), Y, 1 p.,t( 1 j6)(]l32;p2l),2q.,.4,·5q., +6q·,6p + ,der(7), 1 Oq +,12'1·, d,,(12)1(12; 17)(qlO;qlO),-15,-19,22q-,",,(22)1(2;22)(ql1 ;1;qll) 17JI idem,+additional aberrations:9q+ or ·9,1Ip+ or ·11.·21 (IOJ 85 14 46,XX [l6J 86 35 46,XX,I(7;14)(q35;qll-l2) 19JI 46,XX [3) 88 32 46,XX 118JI tetraploid 12] 89° 21 45,XX,-1l [JJI 47,XX,+X 14JI 46,XX 142J 90 38 46,XY 114JI tetraploid 14] 108 10 45,XX,-22116JI 44,XX,dic(l3;22)(pll;pll),-22 [4]1 44·45,XX,·22,and variable tas and whole arm translocations (61 III 28 45,XX,-22 112JI 44,XX,·22,dic or las involving chromosome 1914] 121 6 49 46,XX,22q- 17] 83
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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
- 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 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 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 115 and 116: Putative Tumor-suppressor Gene in M
- Page 117 and 118: 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
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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
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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
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Nawoord Dit boekje is 101 sland gek