Assembly of microarrays for genome-wide measurement of DNA copy number

Snijders, Antoine M.; Nowak, Norma J.; Segraves, Richard; Blackwood, Stephanie; Brown, Nils; Conroy, Jeffrey M.; Hamilton, Greg; Hindle, Anna Katherine; Huey, Bing; Kimura, Karen; Law, Sindy; Myambo, Ken; Palmer, Joel E.; Ylstra, Bauke; Yue, Jingzhu Pearl; Gray, Joe W.; Jain, Ajay N.; Pinkel, Daniel; Albertson, Donna G.

doi:10.1038/ng754

Cited by 821 publications

(737 citation statements)

References 7 publications

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“…The hybridization reactions were applied to arrays, which were incubated under cover slips for 48-72 h at 371C. Slides were washed (Snijders et al, 2001) and scanned using an Agilent Microarray scanner (Agilent Technologies, Santa Clara, CA, USA). Identification of individual spots on scanned arrays was performed with Gene Pix Pro 4.0 (Axon Instruments, Wheatherford, TX, USA), and the quantified data matrix was loaded into BioArray Software Environment (BASE) (Saal et al, 2002).…”

Section: Arraycghmentioning

confidence: 99%

Genomic profiling of malignant melanoma using tiling-resolution arrayCGH

et al. 2007

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Malignant melanoma is an aggressive, heterogeneous disease where new biomarkers for diagnosis and clinical outcome are needed. We searched for chromosomal aberrations that characterize its pathogenesis using 47 different melanoma cell lines and tiling-resolution bacterial artificial chromosome-arrays for comparative genomic hybridization. Major melanoma genes, including BRAF, NRAS, CDKN2A, TP53, CTNNB1, CDK4 and PTEN, were examined for mutations. Distinct copy number alterations were detected, including loss or gain of whole chromosomes but also minute amplifications and homozygous deletions. Most common overlapping regions with losses were mapped to 9p24.3-q13, 10 and 11q14.1-qter, whereas copy number gains were most frequent on chromosomes 1q, 7, 17q and 20q. Amplifications were delineated to oncogenes such as MITF (3p14), CCND1 (11q13), MDM2 (12q15), CCNE1 (19q12) and NOTCH2 (1p12). Frequent findings of homozygous deletions on 9p21 and 10q23 confirmed the importance of CDKN2A and PTEN. Pair-wise comparisons revealed distinct sets of alterations, for example, mutually exclusive mutations in BRAF and NRAS, mutual mutations in BRAF and PTEN, concomitant chromosome 7 gain and 10 loss and concomitant chromosome 15q22.2-q26.3 gain and 20 gain. Moreover, alterations of the various melanoma genes were associated with distinct chromosomal imbalances suggestive of specific genomic programs in melanoma development.

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Section: Arraycghmentioning

confidence: 99%

Genomic profiling of malignant melanoma using tiling-resolution arrayCGH

et al. 2007

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“…Amplification of BAC clone DNA was performed by ligation-mediated polymerase chain reaction (PCR) according to Snijders et al (2001), followed by purification with Montage PCR s m96 filter plates (Millipore BV, Amsterdam, the Netherlands). This DNA was spotted at a concentration of 10 mg/ml in 150 mM sodium phosphate buffer, pH 8.5) on CodeLinkt microscopic glass slides (Amersham Bioscience, Roosendaal, The Netherlands), using a Spot Array 72 robot (Perkin-Elmer Life Sciences, Zaventum, Belgium).…”

Section: Microarray Cghmentioning

confidence: 99%

Genome-wide DNA copy number alterations in head and neck squamous cell carcinomas with or without oncogene-expressing human papillomavirus

et al. 2005

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Oncogene-expressing human papillomavirus type 16 (HPV16) is found in a subset of head and neck squamous cell carcinomas (HNSCC). HPV16 drives carcinogenesis by inactivating p53 and pRb with the viral oncoproteins E6 and E7, paralleled by a low level of mutations in TP53 and allelic loss at 3p, 9p, and 17p, genetic changes frequently found in HNSCCs of nonviral etiology. We hypothesize that two pathways to HNSCC exist: one determined by HPV16 and the other by environmental carcinogens. To define the critical genetic events in these two pathways, we now present a detailed genome analysis of HNSCC with and without HPV16 involvement by employing high-resolution microarray comparative genomic hybridization. Four regions showed alterations in HPV-negative tumors that were absent in HPV-positive tumors: losses at 3p11.2-26.3, 5q11.2-35.2, and 9p21.1-24, and gains/amplifications at 11q12.1-13.4. Also, HPV16-negative tumors demonstrated loss at 18q12.1-23, in contrast to gain in HPV16-positive tumors. Seven regions were altered at high frequency (>33%) in both groups: gains at 3q22.2-qter, 5p15.2-pter, 8p11.2-qter, 9q22-34.1, and 20p-20q, and losses at 11q14.1-qter and 13q11-33. These data show that HNSCC arising by environmental carcinogens are characterized by genetic alterations that differ from those observed in HPV16-induced HNSCC, and most likely occur early in carcinogenesis. A number of genetic changes are shared in both tumor groups and can be considered crucial in the later stages of HNSCC progression.

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“…Array-based CGH (aCGH), using large-insert genomic clones, offers a high-resolution analysis of copy number alterations (CNA) that can be directly related to sequence information (Snijders et al, 2001). This approach has been widely applied to the study of the malignant genome, including the characterization of CNA in a range of hematological malignancies (MartinezRamirez et al, 2005;Nakashima et al, 2005;RubioMoscardo et al, 2005;Hosoya et al, 2006;Horsley et al, 2006;Paulsson et al, 2006;Rucker et al, 2006, Tyybakinoja et al, 2006van Vlierberghe et al, 2006).…”

Section: Introductionmentioning

confidence: 99%