Table 2.

Results of aCGH analysis

TumorsGenomic positionBAC(s)EventNo. gene(s)Representative gene(s) symbol and description
4, 17, 22, and 23Chr6:113168055-113666837RP11-79I12Loss2LOC389424, cell cycle protein p38-2G4 homologue; LOC442250, similar to SOCS-5
4, 10, 21, and 22Chr7:27746109-28559975RP11-17H7Gain4CREB5, cyclic AMP–responsive element binding protein 5
2, 4, 8, 10, 15, 22,Chr7:53864617-55274089RP11-14K11Amplification8EGFR, epidermal growth factor receptor
RP11-81B20
RP11-97P11
4, 10, 17, and 21Chr7:127774792-127909559RP11-144D22Gain5LOC284701; LOC402483, novel protein similar to septin; LOC346653
1, 10, 17, and 21-23Chr7:129745678-132155850RP11-829C10Gain15MKLN1, muskelin 1; PLXNA4, plexin A4
3-5, 10, 17, and 21-23Chr7:150340429-152159943RP11-236I4Gain23PRKAG2, protein kinase, AMP activated, γ2; RHEB, Ras homologue enriched in brain
RP11-43L19
4, 5, 8, 17, 22, and 23Chr9:21588345-23900188RP11-344A7Loss10CDKN2A, cyclin-dependent kinase inhibitor 2A, p16; CDKN2B, cyclin-dependent kinase inhibitor 2B, p16
RP11-441I5
RP11-458D17
RP11-11J1
RP11-476H4
RP11-346N23
RP11-418N2
1, 4, 5, 7, 15, 22, and 23Chr10:106023284-106201712RP11-101J13Loss4GSTO2, glutathione S-transferase ω2; C10orf80; KIAA1754; LOC387710
1, 4, 5, 7, 15, 22, and 23Chr10:119134985-120589963RP11-79A18Loss7CASC2, cancer susceptibility candidate 2
1, 4, 5, 7, 15, 22, and 23Chr10:135111183-135150439RP11-108K14Loss3Sprn, shadow of prion protein; LOC399832
3-5, 17, and 21-23Chr13:29592937-30684939RP11-121O19Loss13HMGB1, high-mobility group box 1; KATNAL1, katanin p60 subunit A-like 1; LOC387917; FLJ14834
RP11-64C21
RP11-63C16
3-5, 17, and 21-23Chr13:39103232-40367433RP11-53F19Loss6COG6, component of oligomeric Golgi complex 6; FOXO1A, forkhead box O1A
RP11-89L15
3-5, 17, and 21-23Chr13:41593291-42577676RP11-21H9Loss8DGKH, diacylglycerol kinase; AKAP11, A kinase (PRKA) anchor protein 11; TNFSF11, tumor necrosis factor (ligand) superfamily member 11; EPSTI1, epithelial stromal interaction 1 (breast)
RP11-34K15
4, 5, 17, and 21-23Chr13:48242971-50898649RP11-54G17Loss22DLEU1-2, Losseted in lymphocytic leukemia, 1 and 2; MLNR, motilin receptor; FNDC3, fibronectin type III domain 3
RP11-34F20
RP11-58C16
4, 5, 7, 15, 17, and 21Chr14:57910104-58786387RP11-2L22Loss11DACT1, dapper homologue 1, antagonist of β-catenin; DAAM1, dishevelled associated activator of morphogenesis 1
5, 7, 15, 17, and 21Chr14:69440807-70531028RP11-18G18Loss14MAP3K9, MAPK kinase kinase 9
5, 7, 15, 17, and 21Chr14:77626345-79602555RP11-46L17Loss2NRXN3, neurexin 3; LOC388001
4, 5, 7, 8, 22, and 23Chr21:29921601-31102834RP11-96H21Loss33KRTAP, keratin-associated proteins; CLDN8, claudin 8
4, 5, 17, 22, and 23Chr22:31113067-31577786RP11-70F2Loss5SYN3, synapsin III; TIMP3, tissue inhibitor of metalloproteinase
  • NOTE: Defining regions frequently amplified or deleted in malignant brain tumors. A total of 36 BACs corresponding to 19 discrete loci were identified by aCGH as either gained or lost in at least 25% of the brain tumors analyzed. Contiguous BACs are shown with a vertical line, and the genomic position for each BAC(s) incorporates the genomic distance between BACs immediately proximal and distal to the known region of amplification or deletion. Each locus is identified as being a region of loss, gain (increase in one or two copies generally of an entire chromosome or chromosomal arm), or amplification (multiple copies of a particular locus). The total number of genes that map to each region is also shown with examples of either known or potential target genes.