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

[1]  N. Munshi,et al.  Chromothripsis identifies a rare and aggressive entity among newly diagnosed multiple myeloma patients. , 2011, Blood.

[2]  Markus J. van Roosmalen,et al.  Chromothripsis as a mechanism driving complex de novo structural rearrangements in the germline. , 2011, Human molecular genetics.

[3]  Chee Seng Chan,et al.  Comprehensive long-span paired-end-tag mapping reveals characteristic patterns of structural variations in epithelial cancer genomes. , 2011, Genome research.

[4]  Hidenori Ojima,et al.  High-resolution characterization of a hepatocellular carcinoma genome , 2011, Nature Genetics.

[5]  M. Stratton Exploring the Genomes of Cancer Cells: Progress and Promise , 2011, Science.

[6]  Jim McDermott,et al.  Harnessing our opportunity to make primary care sustainable. , 2011, The New England journal of medicine.

[7]  Michael R Stratton,et al.  Genomics and the continuum of cancer care. , 2011, The New England journal of medicine.

[8]  N. Carter,et al.  Massive Genomic Rearrangement Acquired in a Single Catastrophic Event during Cancer Development , 2011, Cell.

[9]  Y. Pekarsky,et al.  Common Fragile Site Tumor Suppressor Genes and Corresponding Mouse Models of Cancer , 2010, Journal of biomedicine & biotechnology.

[10]  Eric S. Lander,et al.  The genomic complexity of primary human prostate cancer , 2010, Nature.

[11]  Edwin Cuppen,et al.  Mutation discovery by targeted genomic enrichment of multiplexed barcoded samples , 2010, Nature Methods.

[12]  Andrew Menzies,et al.  The patterns and dynamics of genomic instability in metastatic pancreatic cancer , 2010, Nature.

[13]  M. Nowak,et al.  Distant Metastasis Occurs Late during the Genetic Evolution of Pancreatic Cancer , 2010, Nature.

[14]  D. Adams,et al.  PARK2 deletions occur frequently in sporadic colorectal cancer and accelerate adenoma development in Apc mutant mice , 2010, Proceedings of the National Academy of Sciences.

[15]  M. Lieber,et al.  The mechanism of double-strand DNA break repair by the nonhomologous DNA end-joining pathway. , 2010, Annual review of biochemistry.

[16]  Joshua F. McMichael,et al.  Genome Remodeling in a Basal-like Breast Cancer Metastasis and Xenograft , 2010, Nature.

[17]  M. Jasin,et al.  Alternative end-joining is suppressed by the canonical NHEJ component Xrcc4/ligase IV during chromosomal translocation formation , 2010, Nature Structural &Molecular Biology.

[18]  Francisco M. De La Vega,et al.  Development of Personalized Tumor Biomarkers Using Massively Parallel Sequencing , 2010, Science Translational Medicine.

[19]  Edwin Cuppen,et al.  Accurate SNP and mutation detection by targeted custom microarray-based genomic enrichment of short-fragment sequencing libraries , 2010, Nucleic acids research.

[20]  M. Stratton,et al.  A census of amplified and overexpressed human cancer genes , 2010, Nature Reviews Cancer.

[21]  R. DePinho,et al.  Telomeres and telomerase in cancer. , 2010, Carcinogenesis.

[22]  A. Børresen-Dale,et al.  COMPLEX LANDSCAPES OF SOMATIC REARRANGEMENT IN HUMAN BREAST CANCER GENOMES , 2009, Nature.

[23]  M. Bertagnolli,et al.  Molecular origins of cancer: Molecular basis of colorectal cancer. , 2009, The New England journal of medicine.

[24]  Paul Medvedev,et al.  Computational methods for discovering structural variation with next-generation sequencing , 2009, Nature Methods.

[25]  Ryan D. Morin,et al.  Mutational evolution in a lobular breast tumour profiled at single nucleotide resolution , 2009, Nature.

[26]  Steven J. M. Jones,et al.  Circos: an information aesthetic for comparative genomics. , 2009, Genome research.

[27]  Richard Durbin,et al.  Sequence analysis Fast and accurate short read alignment with Burrows – Wheeler transform , 2009 .

[28]  C. Klein,et al.  Parallel progression of primary tumours and metastases , 2009, Nature Reviews Cancer.

[29]  J. Iovanna,et al.  ArgBP2-dependent signaling regulates pancreatic cell migration, adhesion, and tumorigenicity. , 2008, Cancer research.

[30]  Antony V. Cox,et al.  Identification of somatically acquired rearrangements in cancer using genome-wide massively parallel paired-end sequencing , 2008, Nature Genetics.

[31]  Randal L. Croshaw,et al.  Somatic mutations to CSMD1 in colorectal adenocarcinomas , 2008, Cancer biology & therapy.

[32]  Martin A. Nowak,et al.  Comparative lesion sequencing provides insights into tumor evolution , 2008, Proceedings of the National Academy of Sciences.

[33]  A. Sparks,et al.  The Genomic Landscapes of Human Breast and Colorectal Cancers , 2007, Science.

[34]  R. Kucherlapati,et al.  Tumor progression in Apc1638N mice with Exo1 and Fen1 deficiencies , 2007, Oncogene.

[35]  Andrew Menzies,et al.  Architectures of somatic genomic rearrangement in human cancer amplicons at sequence-level resolution. , 2007, Genome research.

[36]  E. Birney,et al.  Patterns of somatic mutation in human cancer genomes , 2007, Nature.

[37]  David I. Smith,et al.  Large common fragile site genes and cancer. , 2007, Seminars in cancer biology.

[38]  G. Parmigiani,et al.  The Consensus Coding Sequences of Human Breast and Colorectal Cancers , 2006, Science.

[39]  S. Knuutila,et al.  Manifestation, mechanisms and mysteries of gene amplifications. , 2006, Cancer letters.

[40]  A. Rowan,et al.  Missense mutations in fumarate hydratase in multiple cutaneous and uterine leiomyomatosis and renal cell cancer. , 2005, The Journal of molecular diagnostics : JMD.

[41]  L. Chin,et al.  Telomere dysfunction provokes regional amplification and deletion in cancer genomes. , 2002, Cancer cell.