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Chromothripsis is a common mechanism driving genomic rearrangements in primary and metastatic colorectal cancer

Wigard P Kloosterman1, Marlous Hoogstraat12, Oscar Paling2, Masoumeh Tavakoli-Yaraki1, Ivo Renkens1, Joost S Vermaat2, Markus J van Roosmalen1, Stef van Lieshout12, Isaac J Nijman3, Wijnand Roessingh2, Ruben van 't Slot1, José van de Belt1, Victor Guryev3, Marco Koudijs2, Emile Voest2 and Edwin Cuppen13*

Author Affiliations

1 Department of Medical Genetics, University Medical Center Utrecht, Universiteitsweg 100, Utrecht, 3584 CG, The Netherlands

2 Department of Medical Oncology, University Medical Center Utrecht, Universiteitsweg 100, Utrecht, 3584 CG, The Netherlands

3 Hubrecht Institute KNAW and University Medical Center Utrecht, Uppsalalaan 8, Utrecht, 3584 CT, The Netherlands

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Genome Biology 2011, 12:R103  doi:10.1186/gb-2011-12-10-r103

Published: 19 October 2011

Additional files

Additional file 1:

A flow-diagram of the procedure for detecting tumor-specific rearrangements.

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Additional file 2:

Mean insert sizes of mate-pair libraries.

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Additional file 3:

Table with SOLiD sequencing statistics of mate-pair libraries from tumor samples and healthy tissues.

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Additional file 4:

Table with all tumor-specific structural rearrangements identified by mate-pair sequencing in the four patients.

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Additional file 5:

Size distribution of tumor-specific deletions in four patients.

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Additional file 6:

Three examples of clusters of rearrangements in colorectal tumor genomes.

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Additional file 7:

Copy number changes coinciding with breakpoints of rearrangement clusters.

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Additional file 8:

Log R ratios and B allele frequencies for chromosomes affected by chromothripsis.

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Additional file 9:

PCR gel of genomic rearrangements within clusters on chromosomes 17 and 21 and chromosomes 3 and 6.

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Additional file 10:

Table indicating the presence of complex rearrangement clusters in primary and metastatic tumors.

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Additional file 11:

Sequence characteristics of tumor-specific fusion points.

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Additional file 12:

Hotspots of rearrangements in PARK2 and MACROD2.

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