DOI: 10.1158/0008-5472.can-03-3159. Genome-Wide Array-Based Comparative Genomic Hybridization Reveals Multiple Amplification Targets and Novel Homozygous Deletions in Pancreatic Carcinoma Cell Lines

Genome-Wide Array-Based Comparative Genomic Hybridization Reveals Multiple Amplification Targets and Novel Homozygous Deletions in Pancreatic Carcinoma Cell Lines

10.1158/0008-5472.can-03-3159

Crossref journal-article

American Association for Cancer Research (AACR)

Cancer Research (1086)

Abstract

Abstract Pancreatic carcinomas display highly complex chromosomal abnormalities, including many structural and numerical aberrations. There is ample evidence indicating that some of these abnormalities, such as recurrent amplifications and homozygous deletions, contribute to tumorigenesis by altering expression levels of critical oncogenes and tumor suppressor genes. To increase the understanding of gene copy number changes in pancreatic carcinomas and to identify key amplification/deletion targets, we applied genome-wide array-based comparative genomic hybridization to 31 pancreatic carcinoma cell lines. Two different microarrays were used, one containing 3,565 fluorescence in situ hybridization-verified bacterial artificial chromosome clones and one containing 25,468 cDNA clones representing 17,494 UniGene clusters. Overall, the analyses revealed a high genomic complexity, with several copy number changes detected in each case. Specifically, 60 amplicons at 32 different locations were identified, most frequently located within 8q (8 cases), 12p (7 cases), 7q (5 cases), 18q (5 cases), 19q (5 cases), 6p (4 cases), and 8p (4 cases). Amplifications of 8q and 12p were mainly clustered at 8q23–24 and 12p11–12, respectively, whereas amplifications on other chromosome arms were more dispersed. Furthermore, our analyses identified several novel homozygously deleted segments located to 9p24, 9p21, 9q32, 10p12, 10q22, 12q24, and 18q23. The individual complexity and aberration patterns varied substantially among cases, i.e., some cell lines were characterized mainly by high-level amplifications, whereas others showed primarily whole-arm imbalances and homozygous deletions. The described amplification and deletion targets are likely to contain genes important in pancreatic tumorigenesis.

Bibliography

Heidenblad, M., Schoenmakers, E. F. P. M., Jonson, T., Gorunova, L., Veltman, J. A., van Kessel, A. G., & HoÌglund, M. (2004). Genome-Wide Array-Based Comparative Genomic Hybridization Reveals Multiple Amplification Targets and Novel Homozygous Deletions in Pancreatic Carcinoma Cell Lines. Cancer Research, 64(9), 3052â3059.

Authors 7

Markus Heidenblad (first)
Eric F. P. M. Schoenmakers (additional)
Tord Jonson (additional)
Ludmila Gorunova (additional)
Joris A. Veltman (additional)
Ad Geurts van Kessel (additional)
Mattias Höglund (additional)

References 41 Referenced 65

Bardeesy N, DePinho RA Pancreatic cancer biology and genetics. Nat Rev Cancer, 2: 897-909, 2002. (10.1038/nrc949)
Griffin CA, Hruban RH, Morsberger LA, et al Consistent chromosome abnormalities in adenocarcinoma of the pancreas. Cancer Res, 55: 2394-9, 1995.
Gorunova L, Höglund M, Andrén-Sandberg Å, et al Cytogenetic analysis of pancreatic carcinomas: intratumor heterogeneity and nonrandom pattern of chromosome aberrations. Genes Chromosomes Cancer, 23: 81-99, 1998. (10.1002/(SICI)1098-2264(199810)23:2<81::AID-GCC1>3.0.CO;2-0)
Solinas-Toldo S, Wallrapp C, Müller-Pillasch F, Bentz M, Gress T, Lichter P Mapping of chromosomal imbalances in pancreatic carcinoma by comparative genomic hybridization. Cancer Res, 56: 3803-7, 1996.
Fukushige S, Waldman FM, Kimura M, et al Frequent gain of copy number on the long arm of chromosome 20 in human pancreatic adenocarcinoma. Genes Chromosomes Cancer, 19: 161-9, 1997. (10.1002/(SICI)1098-2264(199707)19:3<161::AID-GCC5>3.0.CO;2-W)
Mahlamäki EH, Höglund M, Gorunova L, et al Comparative genomic hybridization reveals frequent gains of 20q, 8q, 11q, 12p, and 17q, and losses of 18q, 9p, and 15q in pancreatic cancer. Genes Chromosomes Cancer, 20: 383-91, 1997. (10.1002/(SICI)1098-2264(199712)20:4<383::AID-GCC10>3.0.CO;2-O)
Curtis LJ, Li Y, Gerbault-Seureau M, et al Amplification of DNA sequences from chromosome 19q13.1 in human pancreatic cell lines. Genomics, 53: 42-55, 1998. (10.1006/geno.1998.5405)
Ghadimi BM, Schröck E, Walker RL, et al Specific chromosomal aberrations and amplification of the AIBI nuclear receptor coactivator gene in pancreatic carcinomas. Am J Pathol, 154: 525-36, 1999. (10.1016/S0002-9440(10)65298-4)
Jonson T, Gorunova L, Dawiskiba S, et al Molecular analyses of the 15q and 18q SMAD genes in pancreatic cancer. Genes Chromosomes Cancer, 24: 62-71, 1999. (10.1002/(SICI)1098-2264(199901)24:1<62::AID-GCC9>3.0.CO;2-4)
Abe T, Makino N, Furukawa T, et al Identification of three commonly deleted regions on chromosome arm 6q in human pancreatic cancer. Genes Chromosomes Cancer, 25: 60-4, 1999. (10.1002/(SICI)1098-2264(199905)25:1<60::AID-GCC9>3.0.CO;2-Y)
Kimura M, Abe T, Sunamura M, Matsuno S, Horii A Detailed deletion mapping on chromosome arm 12q in human pancreatic adenocarcinoma: identification of a 1-cM region of common allelic loss. Genes Chromosomes Cancer, 17: 88-93, 1996. (10.1002/(SICI)1098-2264(199610)17:2<88::AID-GCC3>3.0.CO;2-X)
Hilgers W, Tang DJ, Sugar AY, Shekher MC, Hruban RH, Kern SE High-resolution deletion mapping of chromosome arm 1p in pancreatic cancer identifies a major consensus region at 1p35. Genes Chromosomes Cancer, 24: 351-5, 1999. (10.1002/(SICI)1098-2264(199904)24:4<351::AID-GCC9>3.0.CO;2-Y)
Heidenblad M, Jonson T, Mahlamäki EH, et al Detailed genomic mapping and expression analyses of 12p amplifications in pancreatic carcinomas reveal a 3.5-Mb target region for amplification. Genes Chromosomes Cancer, 34: 211-23, 2002. (10.1002/gcc.10063)
Solinas-Toldo S, Lampel S, Stilgenbauer S, et al Matrix-based comparative genomic hybridization: biochips to screen for genomic imbalances. Genes Chromosomes Cancer, 20: 399-407, 1997. (10.1002/(SICI)1098-2264(199712)20:4<399::AID-GCC12>3.0.CO;2-I)
Pinkel D, Segraves R, Sudar D, et al High resolution analysis of DNA copy number variation using comparative genomic hybridization to microarrays. Nat Genet, 20: 207-11, 1998. (10.1038/2524)
Albertson DG, Ylstra B, Segraves R, et al Quantitative mapping of amplicon structure by array CGH identifies CYP24 as a candidate oncogene. Nat Genet, 25: 144-6, 2000. (10.1038/75985)
Bruder CE, Hirvela C, Tapia-Paez I, et al High resolution deletion analysis of constitutional DNA from neurofibromatosis type 2 (NF2) patients using microarray-CGH. Hum Mol Genet, 10: 271-82, 2001. (10.1093/hmg/10.3.271)
Wilhelm M, Veltman JA, Olshen AB, et al Array-based comparative genomic hybridization for the differential diagnosis of renal cell cancer. Cancer Res, 62: 957-60, 2002.
Veltman JA, Fridlyand J, Pejavar S, et al Array-based comparative genomic hybridization for genome-wide screening of DNA copy number in bladder tumors. Cancer Res, 63: 2872-80, 2003.
Cheung VG, Nowak N, Jang W, et al Integration of cytogenetic landmarks into the draft sequence of the human genome. Nature (Lond), 409: 953-8, 2001.
Veltman JA, Schoenmakers EF, Eussen BH, et al High-throughput analysis of subtelomeric chromosome rearrangements by use of array-based comparative genomic hybridization. Am J Hum Genet, 70: 1269-76, 2002. (10.1086/340426)
Veltman JA, Jonkers Y, Nuijten I, et al Definition of a critical region on chromosome 18 for congenital aural atresia by array CGH. Am J Hum Genet, 72: 1578-84, 2003. (10.1086/375695)
Zafarana G, Grygalewicz B, Gillis AJ, et al 12p-amplicon structure analysis in testicular germ cell tumors of adolescents and adults by array CGH. Oncogene, 22: 7695-701, 2003. (10.1038/sj.onc.1207011)
Vissers LELM, de Vries BBA, Osoegawa K, et al Array-based comparative genomic hybridization for genome wide detection of submicroscopic chromosome abnormalities. Am J Hum Genet, 73: 1261-71, 2003. (10.1086/379977)
Pollack JR, Perou CM, Alizadeh AA, et al Genome-wide analysis of DNA copy-number changes using cDNA microarrays. Nat Genet, 23: 41-6, 1999. (10.1038/12640)
Saal LH, Troein C, Vallon-Christersson J, Gruvberger S, Borg Å, Peterson C BioArray Software Environment (BASE): a platform for comprehensive management and analysis of microarray data. Genome Biol, 3: SOFTWARE0003 2002. (10.1186/gb-2002-3-8-software0003)
Yang YH, Dudoit S, Luu P, et al Normalization for cDNA microarray data: a robust composite method addressing single and multiple slide systematic variation. Nucleic Acids Res, 30: e15 2002. (10.1093/nar/30.4.e15)
Höglund M, Johansson B, Pedersen-Bjergaard J, Marynen P, Mitelman F Molecular characterization of 12p abnormalities in hematologic malignancies deletion of KIP1, rearrangement of TEL, and amplification of. CCND2. Blood, 87: 324-30, 1996. (10.1182/blood.V87.1.324.bloodjournal871324)
Gisselsson D, Pettersson L, Höglund M, et al Chromosomal breakage-fusion-bridge events cause genetic intratumor heterogeneity. Proc Natl Acad Sci USA, 97: 5357-62, 2000. (10.1073/pnas.090013497)
Nishiwaki T, Daigo Y, Kawasoe T, Nakamura Y Isolation and mutational analysis of a novel human cDNA, DEC1 (deleted in esophageal cancer 1), derived from the tumor suppressor locus in 9q32. Genes Chromosomes Cancer, 27: 169-76, 2000. (10.1002/(SICI)1098-2264(200002)27:2<169::AID-GCC8>3.0.CO;2-M)
Höglund M, Säll T, Heim S, Mitelman F, Mandahl N, Fadl-Elmula I Identification of cytogenetic subgroups and karyotypic pathways in transitional cell carcinoma. Cancer Res, 61: 8241-6, 2001.
Höglund M, Gisselsson D, Hansen GB, Säll T, Mitelman F, Nilbert M Dissecting karyotypic patterns in colorectal tumors: two distinct but overlapping pathways in the adenoma-carcinoma transition. Cancer Res, 62: 5939-46, 2002.
Höglund M, Gisselsson D, Hansen GB, Säll T, Mitelman F Ovarian carcinoma develops through multiple modes of chromosomal evolution. Cancer Res, 63: 3378-85, 2003.
Armengol G, Knuutila S, Lluis F, Capella G, Miro R, Caballin MR DNA copy number changes and evaluation of MYC, IGF1R, and FES amplification in xenografts of pancreatic adenocarcinoma. Cancer Genet Cytogenet, 116: 133-41, 2000. (10.1016/S0165-4608(99)00118-1)
Mahlamäki EH, Bärlund M, Tanner M, et al Frequent amplification of 8q24, 11q, 17q, and 20q-specific genes in pancreatic cancer. Genes Chromosomes Cancer, 35: 353-8, 2002. (10.1002/gcc.10122)
Mostert MC, Verkerk AJMH, van den Pol M, et al Identification of the critical region of 12p over-representation in testicular germ cell tumors of adolescents and adults. Oncogene, 16: 2617-27, 1998. (10.1038/sj.onc.1201787)
Zafarana G, Gillis AJ, van Gurp RJ, et al Coamplification of DAD-R, SOX5, and EKI1 in human testicular seminomas, with specific overexpression of DAD-R, correlates with reduced levels of apoptosis and earlier clinical manifestation. Cancer Res, 62: 1822-31, 2002.
Ebert M, Yokoyama M, Friess H, Buchler MW, Korc M Coexpression of the c-met proto-oncogene and hepatocyte growth factor in human pancreatic cancer. Cancer Res, 54: 5775-8, 1994.
Cheng JQ, Ruggeri B, Klein WM, et al Amplification of AKT2 in human pancreatic cancer cells and inhibition of AKT2 expression and tumorigenecity by antisense RNA. Proc Natl Acad Sci USA, 93: 3636-41, 1996. (10.1073/pnas.93.8.3636)
Hahn SA, Seymour AB, Hoque ATMS, et al Allelotype of pancreatic adenocarcinoma using xenograft enrichment. Cancer Res, 55: 4670-5, 1995.
Jin Y, Höglund M, Jin C, et al FISH characterization of head and neck carcinomas reveals that amplification of band 11q13 is associated with deletion of distal 11q. Genes Chromosomes Cancer, 22: 312-20, 1998. (10.1002/(SICI)1098-2264(199808)22:4<312::AID-GCC7>3.0.CO;2-Y)

Dates

Type	When
Created	19 years, 11 months ago (Sept. 20, 2005, 6:38 p.m.)
Deposited	3 years, 2 months ago (June 16, 2022, 5:08 p.m.)
Indexed	3 months, 3 weeks ago (May 15, 2025, 1:10 p.m.)
Issued	21 years, 4 months ago (May 1, 2004)
Published	21 years, 4 months ago (May 1, 2004)
Published Online	21 years, 4 months ago (May 3, 2004)
Published Print	21 years, 4 months ago (May 1, 2004)

Funders 0

None

BibTeX

@article{Heidenblad_2004, title={Genome-Wide Array-Based Comparative Genomic Hybridization Reveals Multiple Amplification Targets and Novel Homozygous Deletions in Pancreatic Carcinoma Cell Lines}, volume={64}, ISSN={1538-7445}, url={http://dx.doi.org/10.1158/0008-5472.can-03-3159}, DOI={10.1158/0008-5472.can-03-3159}, number={9}, journal={Cancer Research}, publisher={American Association for Cancer Research (AACR)}, author={Heidenblad, Markus and Schoenmakers, Eric F. P. M. and Jonson, Tord and Gorunova, Ludmila and Veltman, Joris A. and van Kessel, Ad Geurts and Höglund, Mattias}, year={2004}, month=may, pages={3052–3059} }

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