Array-based comparative genomic hybridization identifies localized DNA amplifications and homozygous deletions in pancreatic cancer

Neoplasia

Volumn 7, Issue 6, 2005, Pages 556-562

  Bashyam, Murali D ^a,b   Bair, Ryan ^a   Kim, Young H ^a   Wang, Pei ^c   Hernandez Boussard, Tina ^c   Karikari, Collins A ^d   Tibshirani, Robert ^c   Maitra, Anirban ^d   Pollack, Jonathan R ^a  

^a STANFORD UNIVERSITY SCHOOL OF MEDICINE   (United States)

^b Center for DNA Fingerprinting and Diagnostics   (India)

^c STANFORD UNIVERSITY   (United States)

^d JOHNS HOPKINS UNIVERSITY SCHOOL OF MEDICINE   (United States)

Author keywords

Array CGH; Comparative genomic hybridization; DNA amplification; Expression profiling; Pancreatic cancer

Indexed keywords

AMPLICON; ANKRD3 GENE; ARTICLE; BIRC2 GENE; BIRC3 GENE; CANCER GROWTH; CANCER INCIDENCE; CHUK GENE; COMPARATIVE GENOMIC HYBRIDIZATION; CONTROLLED STUDY; DKK3 GENE; DNA MICROARRAY; GENE AMPLIFICATION; GENE DELETION; GENE IDENTIFICATION; HUMAN; HUMAN CELL; ONCOGENE; PANCREAS CANCER; POLYMERASE CHAIN REACTION; PRDM15 GENE; PRIORITY JOURNAL; SMURF1 GENE; TGFB3 GENE; TNC GENE; TNFSF15 GENE; TRRAP GENE; TUMOR SUPPRESSOR GENE; TUSC3 GENE; UNITED STATES;

EID: 22044450542     PISSN: 15228002     EISSN: None     Source Type: Journal    
DOI: 10.1593/neo.04586     Document Type: Article

References (48)

1. Jemal A, Tiwari RC, Murray T, Ghafoor A, Samuels A, Ward E, Feuer EJ, and Thun MJ (2004). Cancer statistics, 2004. CA Cancer J Clin 54, 8-29.
2. Bardeesy N and DePinho RA (2002). Pancreatic cancer biology and genetics. Nat Rev Cancer 2, 897-909.
3. Yamada H, Sakamoto H, Taira M, Nishimura S, Shimosato Y, Terada M, and Sugimura T (1986). Amplifications of both c-Ki-ras with a point mutation and c-myc in a primary pancreatic cancer and its metastatic tumors in lymph nodes. Jpn J Cancer Res 77, 370-375.
4. Solinas-Toldo S, Wallrapp C, Muller-Pillasch F, Bentz M, Gress T, and Lichter P (1996). Mapping of chromosomal imbalances in pancreatic carcinoma by comparative genomic hybridization. Cancer Res 56, 3803-3807.
5. Kamb A, Gruis NA, Weaver-Feldhaus J, Liu Q, Harshman K, Tavtigian SV, Stocken E, Day RS, Johnson BE, and Skolnick MH (1994). A cell cycle regulator potentially involved in genesis of many tumor types. Science 264, 436-440.
6. Hahn SA, Schutte M, Hoque AT, Moskaluk CA, da Costa LT, Rozenblum E, Weinstein CL, Fischer A, Yeo CJ, Hruban RH, et al. (1996). DPC4, a candidate tumor suppressor gene at human chromosome 18q21.1. Science 271, 350-353.
7. Kallioniemi A, Kallioniemi OP, Sudar D, Rutovitz D, Gray JW, Waldman F, and Pinkel D (1992). Comparative genomic hybridization for molecular cytogenetic analysis of solid tumors. Science 258, 818-821.
8. Pinkel D, Segraves R, Sudar D, Clark S, Poole I, Kowbel D, Collins C, Kuo WL, Chen C, Zhai Y, et al. (1998). High resolution analysis of DNA copy number variation using comparative genomic hybridization to microarrays. Nat Genet 20, 207-211.
9. Pollack JR, Perou CM, Alizadeh AA, Eisen MB, Pergamenschikov A, Williams CF, Jeffrey SS, Botstein D, and Brown PO (1999). Genomewide analysis of DNA copy-number changes using cDNA micro-arrays. Nat Genet 23, 41-46.
10. Lucito R, West J, Reiner A, Alexander J, Esposito D, Mishra B, Powers S, Norton L, and Wigler M (2000). Detecting gene copy number fluctuations in tumor cells by microarray analysis of genomic representations. Genome Res 10, 1726-1736.
11. Schuler GD (1997). Pieces of the puzzle: expressed sequence tags and the catalog of human genes. J Mol Med 75, 694-698.
12. Poilack JR, Sorlie T, Perou CM, Rees CA, Jeffrey SS, Lonning PE, Tibshirani R, Botstein D, Borresen-Dale AL, and Brown PO (2002). Microarray analysis reveals a major direct role of DNA copy number alteration in the transcriptional program of human breast tumors. Proc Natl Acad Sci USA 99, 12963-12968.
13. Lapointe J, Li C, Higgins JP, van de Rijn M, Bair E, Montgomery K, Ferrari M, Egevad L, Rayford W, Bergerheim U, et al. (2004). Gene expression profiling identifies clinically relevant subtypes of prostate cancer. Proc Natl Acad Sci USA 101, 811-816.
14. Gollub J, Ball CA, Binkley G, Demeter J, Finkelstein DB, Hebert JM, Hernandez-Boussard T, Jin H, Kaloper M, Matese JC, et al. (2003). The Stanford Microarray Database: data access and quality assessment tools. Nucleic Acids Res 31, 94-96.
15. Wang P, Kim Y, Pollack J, Narasimhan B, and Tibshirani R (2005). A method for calling gains and losses in array CGH data. Biostatistics 6, 45-58.
16. Mahlamaki EH, Hoglund M, Gorunova L, Karhu R, Dawiskiba S, Andren-Sandberg A, Kallioniemi OP, and Johansson B (1997). 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, 383-391.
17. Curtis LJ, Li Y, Gerbault-Seureau M, Kuick R, Dutrillaux AM, Goubin G, Fawcett J, Cram S, Dutrillaux B, Hanash S, et al. (1998). Amplification of DNA sequences from chromosome 19q13.1 in human pancreatic cell lines. Genomics 53, 42-55.
18. Ghadimi BM, Schrock E, Walker RL, Wangsa D, Jauho A, Meltzer PS, and Ried T (1999). Specific chromosomal aberrations and amplification of the AIB1 nuclear receptor coactivator gene in pancreatic carcinomas. Am J Pathol 154, 525-536.
19. Schleger C, Arens N, Zentgraf H, Bleyl U, and Verbeke C (2000). Identification of frequent chromosomal aberrations in ductal adenocarcinoma of the pancreas by comparative genomic hybridization (CGH). J Pathol 191, 27-32.
20. Harada T, Okita K, Shiraishi K, Kusano N, Furuya T, Oga A, Kawauchi S, Kondoh S, and Sasaki K (2002). Detection of genetic alterations in pancreatic cancers by comparative genomic hybridization coupled with tissue microdissection and degenerate oiigonucleotide primed polymerase chain reaction. Oncology 62, 251-258.
21. Peiper M, Nagoshi M, Patel D, Fletcher JA, Goedegebuure PS, and Eberlein TJ (1997). Human pancreatic cancer cells (MPanc-96) recognized by autologous tumor-infiltrating lymphocytes after in vitro as well as in vivo tumor expansion. Int J Cancer 71, 993-999.
22. Chen WH, Horoszewicz JS, Leong SS, Shimano T, Penetrante R, Sanders WH, Berjian R, Douglass HO, Martin EW, and Chu TM (1982). Human pancreatic adenocarcinoma: in vitro and in vivo morphology of a new tumor line established from ascites. In Vitro 18, 24-34.
23. Heidenblad M, Jonson T, Mahlamaki EH, Gorunova L, Karhu R, Johansson B, and Hoglund M (2002). 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, 211-223.
24. Cheng JQ, Ruggeri B, Klein WM, Sonoda G, Altomare DA, Watson DK, and Testa JR (1996). Amplification of AKT2 in human pancreatic cells and inhibition of AKT2 expression and tumorigenicity by antisense RNA. Proc Natl Acad Sci USA 93, 3636-3641.
25. Albertson DG, Ylstra B, Segraves R, Collins C, Dairkee SH, Kowbel D, Kuo WL, Gray JW, and Pinkel D (2000). Quantitative mapping of amplicon structure by array CGH identifies CYP24 as a candidate oncogene. Nat Genet 25, 144-146.
26. Ebisawa T, Fukuchi M, Murakami G, Chiba T, Tanaka K, Imamura T, and Miyazono K (2001). Smurf1 interacts with transforming growth factor-beta type I receptor through Smad7 and induces receptor degradation. J Biol Chem 276, 12477-12480.
27. Welch MD (1999). The world according to Arp: regulation of actin nucleation by the Arp2/3 complex. Trends Cell Biol 9, 423-427.
28. McMahon SB, Van Buskirk HA, Dugan KA, Copeland TD, and Cole MD (1998). The novel ATM-related protein TRRAP is an essential cofactor for the c-Myc and E2F oncoproteins. Cell 94, 363-374.
29. Liston P, Fong WG, and Korneluk RG (2003). The inhibitors of apoptosis: there is more to life than Bcl2. Oncogene 22, 8568-8580.
30. Shi Y and Massague J (2003). Mechanisms of TGF-beta signaling from cell membrane to the nucleus. Cell 113, 685-700.
31. Hilgers W, Song JJ, Haye M, Hruban RR, Kern SE, and Fearon ER (2000). Homozygous deletions inactivate DCC, but not MADH4/DPC4/SMAD4, in a subset of pancreatic and biliary cancers. Genes Chromosomes Cancer 27, 353-357.
32. MacGrogan D, Levy A, Bova GS, Isaacs WB, and Bookstein R (1996). Structure and methylation-associated silencing of a gene within a homozygously deleted region of human chromosome band 8p22. Genomics 35, 55-65.
33. Chiquet-Ehrismann R and Chiquet M (2003). Tenascins: regulation and putative functions during pathological stress. J Pathol 200, 488-499.
34. Zhai Y, Ni J, Jiang GW, Lu J, King L, Lincoln C, Carter KC, Janat F, Kozak D, Xu S, et al. (1999). VEGI, a novel cytokine of the tumor necrosis factor family, is an angiogenesis inhibitor that suppresses the growth of colon carcinomas in vivo. FASEB J 13, 181-189.
35. Regnier CH, Song HY, Gao X, Goeddel DV, Cao Z, and Rothe M (1997). Identification and characterization of an IkappaB kinase. Cell 90, 373-383.
36. Krupnik VE, Sharp JD, Jiang C, Robison K, Chickering TW, Amaravadi L, Brown DE, Guyot D, Mays G, Leiby K, et al. (1999). Functional and structural diversity of the human Dickkopf gene family. Gene 238, 301-313.
37. Hoang BH, Kubo T, Healey JH, Yang R, Nathan SS, Kolb EA, Mazza B, Meyers PA, and Gorlick R (2004). Dickkopf 3 inhibits invasion and motility of Saos-2 osteosarcoma cells by modulating the Wnt-beta-catenin pathway. Cancer Res 64, 2734-2739.
38. Schneider R, Bannister AJ, and Kouzarides T (2002). Unsafe SETs: histone lysine methyltransferases and cancer. Trends Biochem Sci 27, 396-402.
39. Meylan E, Martinen F, Thome M, Gschwendt M, and Tschopp J (2002). RIP4 (DIK/PKK), a novel member of the RIP kinase family, activates NF-kappa B and is processed during apoptosis. EMBO Rep 3, 1201-1208.
40. Tirado CA, Sandberg AA, and Stone JF (1999). Identification of a novel amplicon at 1q31 in pancreatic cancer cell lines. Cancer Genet Cytogenet 113, 110-114.
41. Kallioniemi OP, Kallioniemi A, Piper J, Isola J, Waldman FM, Gray JW, and Pinkel D (1994). Optimizing comparative genomic hybridization for analysis of DNA sequence copy number changes in solid tumors. Genes Chromosomes Cancer 10, 231-243.
42. Holzmann K, Kohlhammer H, Schwaenen C, Wessendorf S, Kestler HA, Schwoerer A, Rau B, Radlwimmer B, Dohner H, Lichter P, et al. (2004). Genomic DNA-chip hybridization reveals a higher incidence of genomic amplifications in pancreatic cancer than conventional comparative genomic hybridization and leads to the identification of novel candidate genes. Cancer Res 64, 4428-4433.
43. Aguirre AJ, Brennan C, Bailey G, Sinha R, Feng B, Leo C, Zhang Y, Zhang J, Gans JD, Bardeesy N, et al. (2004). High-resolution characterization of the pancreatic adenocarcinoma genome. Proc Natl Acad Sci USA 101, 9067-9072.
44. Heidenblad M, Schoenmakers EF, Jonson T, Gorunova L, Veltman JA, van Kessel AG, and Hoglund M (2004). Genome-wide array-based comparative genomic hybridization reveals multiple amplification targets and novel homozygous deletions in pancreatic carcinoma cell lines. Cancer Res 64, 3052-3059.
45. Subramanian G, Schwarz RE, Higgins L, McEnroe G, Chakravarty S, Dugar S, and Reiss M (2004). Targeting endogenous transforming growth factor beta receptor signaling in SMAD4-deficient human pancreatic carcinoma cells inhibits their invasive phenotype 1. Cancer Res 64, 5200-5211.
46. Kucharczak J, Simmons MJ, Fan Y, and Gelinas C (2003). To be, or not to be: NF-kappaB is the answer-role of Rel/NF-kappaB in the regulation of apoptosis. Oncogens 22, 8961-8982.
47. Karim R, Tse G, Putti T, Scolyer R, and Lee S (2004). The significance of the Wnt pathway in the pathology of human cancers. Pathology 36, 120-128.
48. Caca K, Kolligs FT, Ji X, Hayes M, Qian J, Yahanda A, Rimm DL, Costa J, and Fearon ER (1999). Beta- and gamma-catenin mutations, but not E-cadherin inactivation, underlie T-cell factor/lymphoid enhancer factor transcriptional deregulation in gastric and pancreatic cancer. Cell Growth Differ 10, 369-376.