Author: "Gordenin, Dmitry" - Searchworks@Jio Institute Digital Library Search Results

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420 results on '"Gordenin, Dmitry"'

1. Author Correction: Comprehensive analysis of chromothripsis in 2,658 human cancers using whole-genome sequencing

Author: Cortés-Ciriano, Isidro, Lee, Jake June-Koo, Xi, Ruibin, Jain, Dhawal, Jung, Youngsook L, Yang, Lixing, Gordenin, Dmitry, Klimczak, Leszek J, Zhang, Cheng-Zhong, Pellman, David S, and Park, Peter J
Subjects: Biological Sciences, Genetics, Cancer, Biotechnology, Cancer Genomics, Human Genome, Good Health and Well Being, PCAWG Structural Variation Working Group, PCAWG Consortium, Medical and Health Sciences, Developmental Biology, Agricultural biotechnology, Bioinformatics and computational biology
Abstract: Correction to: Nature Genetics, published online 05 February 2020. In the published version of this paper, the members of the Pan-Cancer Analysis of Whole Genomes (PCAWG) Consortium were listed in the Supplementary Information; however, these members should have been included in the main paper. The original Article has been corrected to include the members and affiliations of the PCAWG Consortium in the main paper; the corrections have been made to the HTML version of the Article but not the PDF version. Additional corrections to affiliations have been made to the PDF and HTML versions of the original Article for consistency of information between the PCAWG list and the main paper.
Published: 2023

2. Comprehensive analysis of chromothripsis in 2,658 human cancers using whole-genome sequencing

Author: Cortés-Ciriano, Isidro, Lee, Jake June-Koo, Xi, Ruibin, Jain, Dhawal, Jung, Youngsook L, Yang, Lixing, Gordenin, Dmitry, Klimczak, Leszek J, Zhang, Cheng-Zhong, Pellman, David S, and Park, Peter J
Subjects: Cancer, Genetics, Human Genome, Aetiology, 2.1 Biological and endogenous factors, Good Health and Well Being, Chromothripsis, Evolution, Molecular, Genome, Human, Genomics, Humans, Mutation, Neoplasms, Whole Genome Sequencing, PCAWG Structural Variation Working Group, PCAWG Consortium, Biological Sciences, Medical and Health Sciences, Developmental Biology
Abstract: Chromothripsis is a mutational phenomenon characterized by massive, clustered genomic rearrangements that occurs in cancer and other diseases. Recent studies in selected cancer types have suggested that chromothripsis may be more common than initially inferred from low-resolution copy-number data. Here, as part of the Pan-Cancer Analysis of Whole Genomes (PCAWG) Consortium of the International Cancer Genome Consortium (ICGC) and The Cancer Genome Atlas (TCGA), we analyze patterns of chromothripsis across 2,658 tumors from 38 cancer types using whole-genome sequencing data. We find that chromothripsis events are pervasive across cancers, with a frequency of more than 50% in several cancer types. Whereas canonical chromothripsis profiles display oscillations between two copy-number states, a considerable fraction of events involve multiple chromosomes and additional structural alterations. In addition to non-homologous end joining, we detect signatures of replication-associated processes and templated insertions. Chromothripsis contributes to oncogene amplification and to inactivation of genes such as mismatch-repair-related genes. These findings show that chromothripsis is a major process that drives genome evolution in human cancer.
Published: 2020

3. The repertoire of mutational signatures in human cancer

Author: Alexandrov, Ludmil B, Kim, Jaegil, Haradhvala, Nicholas J, Huang, Mi Ni, Tian Ng, Alvin Wei, Wu, Yang, Boot, Arnoud, Covington, Kyle R, Gordenin, Dmitry A, Bergstrom, Erik N, Islam, SM Ashiqul, Lopez-Bigas, Nuria, Klimczak, Leszek J, McPherson, John R, Morganella, Sandro, Sabarinathan, Radhakrishnan, Wheeler, David A, Mustonen, Ville, Getz, Gad, Rozen, Steven G, and Stratton, Michael R
Subjects: Biological Sciences, Bioinformatics and Computational Biology, Genetics, Human Genome, Cancer Genomics, Cancer, 2.1 Biological and endogenous factors, Good Health and Well Being, Age Factors, Base Sequence, Exome, Genome, Human, Humans, Mutation, Neoplasms, Sequence Analysis, DNA, PCAWG Mutational Signatures Working Group, PCAWG Consortium, General Science & Technology
Abstract: Somatic mutations in cancer genomes are caused by multiple mutational processes, each of which generates a characteristic mutational signature1. Here, as part of the Pan-Cancer Analysis of Whole Genomes (PCAWG) Consortium2 of the International Cancer Genome Consortium (ICGC) and The Cancer Genome Atlas (TCGA), we characterized mutational signatures using 84,729,690 somatic mutations from 4,645 whole-genome and 19,184 exome sequences that encompass most types of cancer. We identified 49 single-base-substitution, 11 doublet-base-substitution, 4 clustered-base-substitution and 17 small insertion-and-deletion signatures. The substantial size of our dataset, compared with previous analyses3-15, enabled the discovery of new signatures, the separation of overlapping signatures and the decomposition of signatures into components that may represent associated-but distinct-DNA damage, repair and/or replication mechanisms. By estimating the contribution of each signature to the mutational catalogues of individual cancer genomes, we revealed associations of signatures to exogenous or endogenous exposures, as well as to defective DNA-maintenance processes. However, many signatures are of unknown cause. This analysis provides a systematic perspective on the repertoire of mutational processes that contribute to the development of human cancer.
Published: 2020

4. Infectious vaccine-derived rubella viruses emerge, persist, and evolve in cutaneous granulomas of children with primary immunodeficiencies.

Author: Perelygina, Ludmila, Chen, Min-Hsin, Suppiah, Suganthi, Adebayo, Adebola, Abernathy, Emily, Dorsey, Morna, Bercovitch, Lionel, Paris, Kenneth, White, Kevin P, Krol, Alfons, Dhossche, Julie, Torshin, Ivan Y, Saini, Natalie, Klimczak, Leszek J, Gordenin, Dmitry A, Zharkikh, Andrey, Plotkin, Stanley, Sullivan, Kathleen E, and Icenogle, Joseph
Subjects: Cell Line, Vero Cells, Skin, Animals, Humans, Rubella virus, Granuloma, Adenosine Deaminase, Immunoglobulin M, RNA-Binding Proteins, Viral Envelope Proteins, Measles-Mumps-Rubella Vaccine, Antibodies, Viral, Biopsy, Virus Shedding, Genome, Viral, Adolescent, Child, APOBEC Deaminases, Primary Immunodeficiency Diseases, Chlorocebus aethiops, Antibodies, Viral, Genome, Virology, Microbiology, Immunology, Medical Microbiology
Abstract: Rubella viruses (RV) have been found in an association with granulomas in children with primary immune deficiencies (PID). Here, we report the recovery and characterization of infectious immunodeficiency-related vaccine-derived rubella viruses (iVDRV) from diagnostic skin biopsies of four patients. Sequence evolution within PID hosts was studied by comparison of the complete genomic sequences of the iVDRVs with the genome of the vaccine virus RA27/3. The degree of divergence of each iVDRV correlated with the duration of persistence indicating continuous intrahost evolution. The evolution rates for synonymous and nonsynonymous substitutions were estimated to be 5.7 x 10-3 subs/site/year and 8.9 x 10-4 subs/site/year, respectively. Mutational spectra and signatures indicated a major role for APOBEC cytidine deaminases and a secondary role for ADAR adenosine deaminases in generating diversity of iVDRVs. The distributions of mutations across the genes and 3D hotspots for amino acid substitutions in the E1 glycoprotein identified regions that may be under positive selective pressure. Quasispecies diversity was higher in granulomas than in recovered infectious iVDRVs. Growth properties of iVDRVs were assessed in WI-38 fibroblast cultures. None of the iVDRV isolates showed complete reversion to wild type phenotype but the replicative and persistence characteristics of iVDRVs were different from those of the RA27/3 vaccine strain, making predictions of iVDRV transmissibility and teratogenicity difficult. However, detection of iVDRV RNA in nasopharyngeal specimen and poor neutralization of some iVDRV strains by sera from vaccinated persons suggests possible public health risks associated with iVDRV carriers. Detection of IgM antibody to RV in sera of two out of three patients may be a marker of virus persistence, potentially useful for identifying patients with iVDRV before development of lesions. Studies of the evolutionary dynamics of iVDRV during persistence will contribute to development of infection control strategies and antiviral therapies.
Published: 2019

5. Guidelines for DNA recombination and repair studies: Cellular assays of DNA repair pathways.

Author: Klein, Hannah L, Bačinskaja, Giedrė, Che, Jun, Cheblal, Anais, Elango, Rajula, Epshtein, Anastasiya, Fitzgerald, Devon M, Gómez-González, Belén, Khan, Sharik R, Kumar, Sandeep, Leland, Bryan A, Marie, Léa, Mei, Qian, Miné-Hattab, Judith, Piotrowska, Alicja, Polleys, Erica J, Putnam, Christopher D, Radchenko, Elina A, Saada, Anissia Ait, Sakofsky, Cynthia J, Shim, Eun Yong, Stracy, Mathew, Xia, Jun, Yan, Zhenxin, Yin, Yi, Aguilera, Andrés, Argueso, Juan Lucas, Freudenreich, Catherine H, Gasser, Susan M, Gordenin, Dmitry A, Haber, James E, Ira, Grzegorz, Jinks-Robertson, Sue, King, Megan C, Kolodner, Richard D, Kuzminov, Andrei, Lambert, Sarah Ae, Lee, Sang Eun, Miller, Kyle M, Mirkin, Sergei M, Petes, Thomas D, Rosenberg, Susan M, Rothstein, Rodney, Symington, Lorraine S, Zawadzki, Pawel, Kim, Nayun, Lisby, Michael, and Malkova, Anna
Subjects: DNA breaks, DNA repair centers, DNA resection, DSBs, Holliday junctions, R-loops, chromatin dynamics, chromosome rearrangements, crossovers, fluorescent proteins, gene amplification, gene conversion, genome instability, gross chromosome rearrangements, homologous recombination, mitotic recombination, mutagenesis, pulsed field gel electrophoresis, replication fork stalling, single-particle tracking, sister chromatid recombination, sister repetitive sequences, site-specific chromosome breaks, toxic recombination intermediates, yeast artificial chromosome
Abstract: Understanding the plasticity of genomes has been greatly aided by assays for recombination, repair and mutagenesis. These assays have been developed in microbial systems that provide the advantages of genetic and molecular reporters that can readily be manipulated. Cellular assays comprise genetic, molecular, and cytological reporters. The assays are powerful tools but each comes with its particular advantages and limitations. Here the most commonly used assays are reviewed, discussed, and presented as the guidelines for future studies.
Published: 2019

6. Molecular Evolution of Early-Onset Prostate Cancer Identifies Molecular Risk Markers and Clinical Trajectories.

Author: Gerhauser, Clarissa, Favero, Francesco, Risch, Thomas, Simon, Ronald, Feuerbach, Lars, Assenov, Yassen, Heckmann, Doreen, Sidiropoulos, Nikos, Waszak, Sebastian M, Hübschmann, Daniel, Urbanucci, Alfonso, Girma, Etsehiwot G, Kuryshev, Vladimir, Klimczak, Leszek J, Saini, Natalie, Stütz, Adrian M, Weichenhan, Dieter, Böttcher, Lisa-Marie, Toth, Reka, Hendriksen, Josephine D, Koop, Christina, Lutsik, Pavlo, Matzk, Sören, Warnatz, Hans-Jörg, Amstislavskiy, Vyacheslav, Feuerstein, Clarissa, Raeder, Benjamin, Bogatyrova, Olga, Schmitz, Eva-Maria, Hube-Magg, Claudia, Kluth, Martina, Huland, Hartwig, Graefen, Markus, Lawerenz, Chris, Henry, Gervaise H, Yamaguchi, Takafumi N, Malewska, Alicia, Meiners, Jan, Schilling, Daniela, Reisinger, Eva, Eils, Roland, Schlesner, Matthias, Strand, Douglas W, Bristow, Robert G, Boutros, Paul C, von Kalle, Christof, Gordenin, Dmitry, Sültmann, Holger, Brors, Benedikt, Sauter, Guido, Plass, Christoph, Yaspo, Marie-Laure, Korbel, Jan O, Schlomm, Thorsten, and Weischenfeldt, Joachim
Subjects: Humans, Prostatic Neoplasms, RNA-Binding Proteins, Risk Factors, Evolution, Molecular, DNA Methylation, Gene Expression Regulation, Neoplastic, Mutation, Adult, Middle Aged, Male, Transcriptome, Biomarkers, Tumor, Whole Genome Sequencing, APOBEC, cancer genomics, early-onset cancer, epigenetic risk-score, mutational processes, prostate cancer, structural variants, tumor evolution, tumor evolution prediction, Human Genome, Aging, Prevention, Cancer, Urologic Diseases, Prostate Cancer, Genetics, 4.1 Discovery and preclinical testing of markers and technologies, Aetiology, 2.1 Biological and endogenous factors, Detection, screening and diagnosis, Neurosciences, Oncology and Carcinogenesis, Oncology & Carcinogenesis
Abstract: Identifying the earliest somatic changes in prostate cancer can give important insights into tumor evolution and aids in stratifying high- from low-risk disease. We integrated whole genome, transcriptome and methylome analysis of early-onset prostate cancers (diagnosis ≤55 years). Characterization across 292 prostate cancer genomes revealed age-related genomic alterations and a clock-like enzymatic-driven mutational process contributing to the earliest mutations in prostate cancer patients. Our integrative analysis identified four molecular subgroups, including a particularly aggressive subgroup with recurrent duplications associated with increased expression of ESRP1, which we validate in 12,000 tissue microarray tumors. Finally, we combined the patterns of molecular co-occurrence and risk-based subgroup information to deconvolve the molecular and clinical trajectories of prostate cancer from single patient samples.
Published: 2018

7. Analysis of APOBEC-induced mutations in yeast strains with low levels of replicative DNA polymerases

Author: Sui, Yang, Qi, Lei, Zhang, Ke, Saini, Natalie, Klimczak, Leszek J., Sakofsky, Cynthia J., Gordenin, Dmitry A., Petes, Thomas D., and Zheng, Dao-Qiong
Published: 2020

8. Comprehensive Molecular Characterization of Muscle-Invasive Bladder Cancer

Author: Robertson, A Gordon, Kim, Jaegil, Al-Ahmadie, Hikmat, Bellmunt, Joaquim, Guo, Guangwu, Cherniack, Andrew D, Hinoue, Toshinori, Laird, Peter W, Hoadley, Katherine A, Akbani, Rehan, Castro, Mauro AA, Gibb, Ewan A, Kanchi, Rupa S, Gordenin, Dmitry A, Shukla, Sachet A, Sanchez-Vega, Francisco, Hansel, Donna E, Czerniak, Bogdan A, Reuter, Victor E, Su, Xiaoping, Carvalho, Benilton de Sa, Chagas, Vinicius S, Mungall, Karen L, Sadeghi, Sara, Pedamallu, Chandra Sekhar, Lu, Yiling, Klimczak, Leszek J, Zhang, Jiexin, Choo, Caleb, Ojesina, Akinyemi I, Bullman, Susan, Leraas, Kristen M, Lichtenberg, Tara M, Wu, Catherine J, Schultz, Nicholaus, Getz, Gad, Meyerson, Matthew, Mills, Gordon B, McConkey, David J, Network, TCGA Research, Albert, Monique, Alexopoulou, Iakovina, Ally, Adrian, Antic, Tatjana, Aron, Manju, Balasundaram, Miruna, Bartlett, John, Baylin, Stephen B, Beaver, Allison, Birol, Inanc, Boice, Lori, Bootwalla, Moiz S, Bowen, Jay, Bowlby, Reanne, Brooks, Denise, Broom, Bradley M, Bshara, Wiam, Burks, Eric, Cárcano, Flavio M, Carlsen, Rebecca, Carvalho, Benilton S, Carvalho, Andre L, Castle, Eric P, Castro, Patricia, Catto, James W, Chesla, David W, Chuah, Eric, Chudamani, Sudha, Cortessis, Victoria K, Cottingham, Sandra L, Crain, Daniel, Curley, Erin, Daneshmand, Siamak, Demchok, John A, Dhalla, Noreen, Djaladat, Hooman, Eckman, John, Egea, Sophie C, Engel, Jay, Felau, Ina, Ferguson, Martin L, Gardner, Johanna, Gastier-Foster, Julie M, Gerken, Mark, Gomez-Fernandez, Carmen R, and Harr, Jodi
Subjects: Biomedical and Clinical Sciences, Oncology and Carcinogenesis, Biotechnology, Genetics, Urologic Diseases, Cancer Genomics, Human Genome, Cancer, 2.1 Biological and endogenous factors, Aged, Cluster Analysis, DNA Methylation, Humans, MicroRNAs, Middle Aged, Muscle, Smooth, RNA, Long Noncoding, Survival Analysis, Urinary Bladder, Urinary Bladder Neoplasms, TCGA Research Network, APOBEC mutation, DNA methylation, basal mRNA subtype, lncRNA transcriptome, luminal mRNA subtype, microRNA, muscle-invasive bladder cancer, neoantigen, neuronal subtype, regulon, Biological Sciences, Medical and Health Sciences, Developmental Biology, Biological sciences, Biomedical and clinical sciences
Abstract: We report a comprehensive analysis of 412 muscle-invasive bladder cancers characterized by multiple TCGA analytical platforms. Fifty-eight genes were significantly mutated, and the overall mutational load was associated with APOBEC-signature mutagenesis. Clustering by mutation signature identified a high-mutation subset with 75% 5-year survival. mRNA expression clustering refined prior clustering analyses and identified a poor-survival "neuronal" subtype in which the majority of tumors lacked small cell or neuroendocrine histology. Clustering by mRNA, long non-coding RNA (lncRNA), and miRNA expression converged to identify subsets with differential epithelial-mesenchymal transition status, carcinoma in situ scores, histologic features, and survival. Our analyses identified 5 expression subtypes that may stratify response to different treatments.
Published: 2017

9. Genomic and evolutionary classification of lung cancer in never smokers

Author: Zhang, Tongwu, Joubert, Philippe, Ansari-Pour, Naser, Zhao, Wei, Hoang, Phuc H., Lokanga, Rachel, Moye, Aaron L., Rosenbaum, Jennifer, Gonzalez-Perez, Abel, Martínez-Jiménez, Francisco, Castro, Andrea, Muscarella, Lucia Anna, Hofman, Paul, Consonni, Dario, Pesatori, Angela C., Kebede, Michael, Li, Mengying, Gould Rothberg, Bonnie E., Peneva, Iliana, Schabath, Matthew B., Poeta, Maria Luana, Costantini, Manuela, Hirsch, Daniela, Heselmeyer-Haddad, Kerstin, Hutchinson, Amy, Olanich, Mary, Lawrence, Scott M., Lenz, Petra, Duggan, Maire, Bhawsar, Praphulla M. S., Sang, Jian, Kim, Jung, Mendoza, Laura, Saini, Natalie, Klimczak, Leszek J., Islam, S. M. Ashiqul, Otlu, Burcak, Khandekar, Azhar, Cole, Nathan, Stewart, Douglas R., Choi, Jiyeon, Brown, Kevin M., Caporaso, Neil E., Wilson, Samuel H., Pommier, Yves, Lan, Qing, Rothman, Nathaniel, Almeida, Jonas S., Carter, Hannah, Ried, Thomas, Kim, Carla F., Lopez-Bigas, Nuria, Garcia-Closas, Montserrat, Shi, Jianxin, Bossé, Yohan, Zhu, Bin, Gordenin, Dmitry A., Alexandrov, Ludmil B., Chanock, Stephen J., Wedge, David C., and Landi, Maria Teresa
Published: 2021
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10. Publisher Correction: Comprehensive analysis of chromothripsis in 2,658 human cancers using whole-genome sequencing

Author: Cortés-Ciriano, Isidro, Lee, Jake June-Koo, Xi, Ruibin, Jain, Dhawal, Jung, Youngsook L., Yang, Lixing, Gordenin, Dmitry, Klimczak, Leszek J., Zhang, Cheng-Zhong, Pellman, David S., and Park, Peter J.
Published: 2023
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11. Hypermutation in single-stranded DNA

Author: Saini, Natalie and Gordenin, Dmitry A.
Published: 2020
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12. APOBEC shapes tumor evolution and age at onset of lung cancer in smokers

Author: Zhang, Tongwu, primary, Sang, Jian, additional, Hoang, Phuc, additional, Zhao, Wei, additional, Rosenbaum, Jennifer, additional, Johnson, Kofi, additional, Klimczak, Leszek, additional, McElderry, John, additional, Klein, Alyssa, additional, Wirth, Christopher, additional, Bergstrom, Erik, additional, Diaz Gay, Marcos, additional, Vangara, Raviteja, additional, Colon-Matos, Frank, additional, Hutchinson, Amy, additional, Lawrence, Scott, additional, Cole, Nathan, additional, Zhu, Bin, additional, Przytycka, Teresa, additional, Shi, Jianxin, additional, Caporaso, Neil, additional, Homer, Robert, additional, Pesatori, Angela, additional, Consonni, Dario, additional, Imielin _ski, Marcin, additional, Chanock, Stephen, additional, Wedge, David, additional, Gordenin, Dmitry, additional, Alexandrov, Ludmil, additional, Harris, Reuben, additional, and Landi, Maria, additional
Published: 2024
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13. Author Correction: The repertoire of mutational signatures in human cancer

Author: Alexandrov, Ludmil B., Kim, Jaegil, Haradhvala, Nicholas J., Huang, Mi Ni, Tian Ng, Alvin Wei, Wu, Yang, Boot, Arnoud, Covington, Kyle R., Gordenin, Dmitry A., Bergstrom, Erik N., Islam, S. M. Ashiqul, Lopez-Bigas, Nuria, Klimczak, Leszek J., McPherson, John R., Morganella, Sandro, Sabarinathan, Radhakrishnan, Wheeler, David A., Mustonen, Ville, Getz, Gad, Rozen, Steven G., and Stratton, Michael R.
Published: 2023
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14. Somatic mutation distributions in cancer genomes vary with three-dimensional chromatin structure

Author: Akdemir, Kadir C., Le, Victoria T., Kim, Justin M., Killcoyne, Sarah, King, Devin A., Lin, Ya-Ping, Tian, Yanyan, Inoue, Akira, Amin, Samirkumar B., Robinson, Frederick S., Nimmakayalu, Manjunath, Herrera, Rafael E., Lynn, Erica J., Chan, Kin, Seth, Sahil, Klimczak, Leszek J., Gerstung, Moritz, Gordenin, Dmitry A., O’Brien, John, Li, Lei, Deribe, Yonathan Lissanu, Verhaak, Roel G., Campbell, Peter J., Fitzgerald, Rebecca, Morrison, Ashby J., Dixon, Jesse R., and Andrew Futreal, P.
Published: 2020
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15. APOBEC3-dependent kataegis and TREX1-driven chromothripsis during telomere crisis

Author: Maciejowski, John, Chatzipli, Aikaterini, Dananberg, Alexandra, Chu, Kevan, Toufektchan, Eleonore, Klimczak, Leszek J., Gordenin, Dmitry A., Campbell, Peter J., and de Lange, Titia
Published: 2020
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16. The Somatic Genomic Landscape of Chromophobe Renal Cell Carcinoma

Author: Davis, Caleb F, Ricketts, Christopher J, Wang, Min, Yang, Lixing, Cherniack, Andrew D, Shen, Hui, Buhay, Christian, Kang, Hyojin, Kim, Sang Cheol, Fahey, Catherine C, Hacker, Kathryn E, Bhanot, Gyan, Gordenin, Dmitry A, Chu, Andy, Gunaratne, Preethi H, Biehl, Michael, Seth, Sahil, Kaipparettu, Benny A, Bristow, Christopher A, Donehower, Lawrence A, Wallen, Eric M, Smith, Angela B, Tickoo, Satish K, Tamboli, Pheroze, Reuter, Victor, Schmidt, Laura S, Hsieh, James J, Choueiri, Toni K, Hakimi, A Ari, Network, The Cancer Genome Atlas Research, Creighton, Chad J, Morgan, Margaret, Wheeler, David A, Gibbs, Richard A, Signoretti, Sabina, Robertson, A Gordon, Henske, Elizabeth P, Kwiatkowski, David J, Ricketts, Christopher, Linehan, W Marston, Seiler, Michael, Rathmell, W Kimryn, Laird, Peter W, Shuch, Brian, Muzny, Donna, Chao, Hsu, Dahdouli, Mike, Xi, Liu, Kakkar, Nipun, Reid, Jeffrey G, Downs, Brittany, Drummond, Jennifer, Morton, Donna, Doddapaneni, Harsha, Lewis, Lora, English, Adam, Meng, Qingchang, Kovar, Christie, Wang, Qiaoyan, Hale, Walker, Hawes, Alicia, Kalra, Divya, Walker, Kimberly, Murray, Bradley A, Sougnez, Carrie, Saksena, Gordon, Carter, Scott L, Schumacher, Steven E, Tabak, Barbara, Zack, Travis I, Getz, Gad, Beroukhim, Rameen, Gabriel, Stacey B, Meyerson, Matthew, Ally, Adrian, Balasundaram, Miruna, Birol, Inanc, and Brooks, Denise
Subjects: Biological Sciences, Biomedical and Clinical Sciences, Bioinformatics and Computational Biology, Genetics, Oncology and Carcinogenesis, Human Genome, Biotechnology, Kidney Disease, Cancer Genomics, Rare Diseases, Cancer, 2.1 Biological and endogenous factors, 1.1 Normal biological development and functioning, Base Sequence, Carcinoma, Renal Cell, Chromosome Breakpoints, Chromosome Deletion, Chromosomes, Human, DNA Copy Number Variations, DNA Methylation, DNA Mutational Analysis, DNA, Mitochondrial, Exome, Genome, Human, Humans, Kidney Neoplasms, Molecular Sequence Data, Promoter Regions, Genetic, Telomerase, Transcriptome, The Cancer Genome Atlas Research Network, Neurosciences, Oncology & Carcinogenesis, Biochemistry and cell biology, Oncology and carcinogenesis
Abstract: We describe the landscape of somatic genomic alterations of 66 chromophobe renal cell carcinomas (ChRCCs) on the basis of multidimensional and comprehensive characterization, including mtDNA and whole-genome sequencing. The result is consistent that ChRCC originates from the distal nephron compared with other kidney cancers with more proximal origins. Combined mtDNA and gene expression analysis implicates changes in mitochondrial function as a component of the disease biology, while suggesting alternative roles for mtDNA mutations in cancers relying on oxidative phosphorylation. Genomic rearrangements lead to recurrent structural breakpoints within TERT promoter region, which correlates with highly elevated TERT expression and manifestation of kataegis, representing a mechanism of TERT upregulation in cancer distinct from previously observed amplifications and point mutations.
Published: 2014

17. Chromosomal Site-Specific Double-Strand Breaks Are Efficiently Targeted for Repair by Oligonucleotides in Yeast

Author: Storici, Francesca, Durham, Christopher L., Gordenin, Dmitry A., and Resnick, Michael A.
Published: 2003

18. Genomic Subtypes of Non-invasive Bladder Cancer with Distinct Metabolic Profile and Female Gender Bias in KDM6A Mutation Frequency

Author: Hurst, Carolyn D., Alder, Olivia, Platt, Fiona M., Droop, Alastair, Stead, Lucy F., Burns, Julie E., Burghel, George J., Jain, Sunjay, Klimczak, Leszek J., Lindsay, Helen, Roulson, Jo-An, Taylor, Claire F., Thygesen, Helene, Cameron, Angus J., Ridley, Anne J., Mott, Helen R., Gordenin, Dmitry A., and Knowles, Margaret A.
Published: 2017
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19. Comprehensive Molecular Characterization of Muscle-Invasive Bladder Cancer

Author: Akbani, Rehan, Al-Ahmadie, Hikmat, Albert, Monique, Alexopoulou, Iakovina, Ally, Adrian, Antic, Tatjana, Aron, Manju, Balasundaram, Miruna, Bartlett, John, Baylin, Stephen B., Beaver, Allison, Bellmunt, Joaquim, Birol, Inanc, Boice, Lori, Bootwalla, Moiz S., Bowen, Jay, Bowlby, Reanne, Brooks, Denise, Broom, Bradley M., Bshara, Wiam, Bullman, Susan, Burks, Eric, Cárcano, Flavio M., Carlsen, Rebecca, Carvalho, Benilton S., Carvalho, Andre L., Castle, Eric P., Castro, Mauro A.A., Castro, Patricia, Catto, James W., Chagas, Vinicius S., Cherniack, Andrew D., Chesla, David W., Choo, Caleb, Chuah, Eric, Chudamani, Sudha, Cortessis, Victoria K., Cottingham, Sandra L., Crain, Daniel, Curley, Erin, Czerniak, Bogdan A., Daneshmand, Siamak, Demchok, John A., Dhalla, Noreen, Djaladat, Hooman, Eckman, John, Egea, Sophie C., Engel, Jay, Felau, Ina, Ferguson, Martin L., Gardner, Johanna, Gastier-Foster, Julie M., Gerken, Mark, Getz, Gad, Gibb, Ewan A., Gomez-Fernandez, Carmen R., Gordenin, Dmitry A., Guo, Guangwu, Hansel, Donna E., Harr, Jodi, Hartmann, Arndt, Herbert, Lynn M., Hinoue, Toshinori, Ho, Thai H., Hoadley, Katherine A., Holt, Robert A., Hutter, Carolyn M., Jones, Steven J.M., Jorda, Merce, Kahnoski, Richard J., Kanchi, Rupa S., Kasaian, Katayoon, Kim, Jaegil, Klimczak, Leszek J., Kwiatkowski, David J., Lai, Phillip H., Laird, Peter W., Lane, Brian R., Leraas, Kristen M., Lerner, Seth P., Lichtenberg, Tara M., Liu, Jia, Lolla, Laxmi, Lotan, Yair, Lu, Yiling, Lucchesi, Fabiano R., Ma, Yussanne, Machado, Roberto D., Maglinte, Dennis T., Mallery, David, Marra, Marco A., Martin, Sue E., Mayo, Michael, McConkey, David J., Meraney, Anoop, Meyerson, Matthew, Mills, Gordon B., Moinzadeh, Alireza, Moore, Richard A., Mora Pinero, Edna M., Morris, Scott, Morrison, Carl, Mungall, Karen L., Mungall, Andrew J., Myers, Jerome B., Naresh, Rashi, O'Donnell, Peter H., Ojesina, Akinyemi I., Parekh, Dipen J., Parfitt, Jeremy, Paulauskis, Joseph D., Sekhar Pedamallu, Chandra, Penny, Robert J., Pihl, Todd, Porten, Sima, Quintero-Aguilo, Mario E., Ramirez, Nilsa C., Rathmell, W. Kimryn, Reuter, Victor E., Rieger-Christ, Kimberly, Robertson, A. Gordon, Sadeghi, Sara, Saller, Charles, Salner, Andrew, Sanchez-Vega, Francisco, Sandusky, George, Scapulatempo-Neto, Cristovam, Schein, Jacqueline E., Schuckman, Anne K., Schultz, Nikolaus, Shelton, Candace, Shelton, Troy, Shukla, Sachet A., Simko, Jeff, Singh, Parminder, Sipahimalani, Payal, Smith, Norm D., Sofia, Heidi J., Sorcini, Andrea, Stanton, Melissa L., Steinberg, Gary D., Stoehr, Robert, Su, Xiaoping, Sullivan, Travis, Sun, Qiang, Tam, Angela, Tarnuzzer, Roy, Tarvin, Katherine, Taubert, Helge, Thiessen, Nina, Thorne, Leigh, Tse, Kane, Tucker, Kelinda, Van Den Berg, David J., van Kessel, Kim E., Wach, Sven, Wan, Yunhu, Wang, Zhining, Weinstein, John N., Weisenberger, Daniel J., Wise, Lisa, Wong, Tina, Wu, Ye, Wu, Catherine J., Yang, Liming, Zach, Leigh Anne, Zenklusen, Jean C., Zhang, Jiashan (Julia), Zhang, Jiexin, Zmuda, Erik, Zwarthoff, Ellen C., de Sa Carvalho, Benilton, Pedamallu, Chandra Sekhar, and Schultz, Nicholaus
Published: 2017
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20. APOBEC3B cytidine deaminase targets the non-transcribed strand of tRNA genes in yeast

Author: Saini, Natalie, Roberts, Steven A., Sterling, Joan F., Malc, Ewa P., Mieczkowski, Piotr A., and Gordenin, Dmitry A.
Published: 2017
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21. The 3′→5′ Exonuclease of DNA Polymerase δ can Substitute for the 5′ Flap Endonuclease Rad27/Fen1 in Processing Okazaki Fragments and Preventing Genome Instability

Author: Jin, Yong Hwan, Obert, Robyn, Kunkel, Thomas A., Resnick, Michael A., and Gordenin, Dmitry A.
Published: 2001

22. Mutator Phenotypes of Yeast Strains Heterozygous for Mutations in the MSH2 Gene

Author: Drotschmann, Karin, Clark, Alan B., Tran, Hiep T., Resnick, Michael A., Gordenin, Dmitry A., and Kunkel, Thomas A.
Published: 1999

23. Glycidamide-induced hypermutation in yeast single-stranded DNA reveals a ubiquitous clock-like mutational motif in humans

Author: Hudson, Kathleen M, primary, Klimczak, Leszek J, additional, Sterling, Joan F, additional, Burkholder, Adam B, additional, Kazanov, Marat D, additional, Saini, Natalie, additional, Mieczkowski, Piotr A, additional, and Gordenin, Dmitry A, additional
Published: 2023
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24. Changes in metabolic landscapes shape divergent but distinct mutational signatures and cytotoxic consequences of redox stress

Author: Degtyareva, Natalya P, primary, Placentra, Victoria C, additional, Gabel, Scott A, additional, Klimczak, Leszek J, additional, Gordenin, Dmitry A, additional, Wagner, Brett A, additional, Buettner, Garry R, additional, Mueller, Geoffrey A, additional, Smirnova, Tatyana I, additional, and Doetsch, Paul W, additional
Published: 2023
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25. Abstract 1166: APOBEC deaminases compete with tobacco smoking mutagenesis and affect age at onset of lung cancer

Author: Zhang, Tongwu, primary, Sang, Jian, additional, Hoang, Phuc H., additional, Zhao, Wei, additional, Rosenbaum, Jennifer, additional, Klimczak, Leszek J., additional, McElderry, John, additional, Klein, Alyssa, additional, Wirth, Christopher, additional, Bergstrom, Erik N., additional, Díaz-Gay, Marcos, additional, Vangara, Raviteja, additional, Hutchinson, Amy, additional, Lawrence, Scott M., additional, Cole, Nathan, additional, Zhu, Bin, additional, Przytycka, Teresa M., additional, Shi, Jianxin, additional, Caporaso, Neil E., additional, Homer, Robert, additional, Pesatori, Angela C., additional, Consonni, Dario, additional, Chanock, Stephen J., additional, Wedge, David C., additional, Gordenin, Dmitry A., additional, Alexandrov, Ludmil B., additional, Harris, Reuben S., additional, and Landi, Maria Teresa, additional
Published: 2023
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26. Integrated genomic and molecular characterization of cervical cancer

Author: Burk, Robert D., Chen, Zigui, Saller, Charles, Tarvin, Katherine, Carvalho, Andre L., Scapulatempo-Neto, Cristovam, Silveira, Henrique C., Fregnani, Jos H., Creighton, Chad J., Anderson, Matthew L., Castro, Patricia, Wang, Sophia S., Yau, Christina, Benz, Christopher, Robertson, A. Gordon, Mungall, Karen, Lim, Lynette, Bowlby, Reanne, Sadeghi, Sara, Brooks, Denise, Sipahimalani, Payal, Mar, Richard, Ally, Adrian, Clarke, Amanda, Mungall, Andrew J., Tam, Angela, Lee, Darlene, Chuah, Eric, Schein, Jacqueline E., Tse, Kane, Kasaian, Katayoon, Ma, Yussanne, Marra, Marco A., Mayo, Michael, Balasundaram, Miruna, Thiessen, Nina, Dhalla, Noreen, Carlsen, Rebecca, Moore, Richard A., Holt, Robert A., Jones, Steven J. M., Wong, Tina, Pantazi, Angeliki, Parfenov, Michael, Kucherlapati, Raju, Hadjipanayis, Angela, Seidman, Jonathan, Kucherlapati, Melanie, Ren, Xiaojia, Xu, Andrew W., Yang, Lixing, Park, Peter J., Lee, Semin, Rabeno, Brenda, Huelsenbeck-Dill, Lori, Borowsky, Mark, Cadungog, Mark, Iacocca, Mary, Petrelli, Nicholas, Swanson, Patricia, Ojesina, Akinyemi I., Le, Xuan, Sandusky, George, Adebamowo, Sally N., Akeredolu, Teniola, Adebamowo, Clement, Reynolds, Sheila M., Shmulevich, Ilya, Shelton, Candace, Crain, Daniel, Mallery, David, Curley, Erin, Gardner, Johanna, Penny, Robert, Morris, Scott, Shelton, Troy, Liu, Jia, Lolla, Laxmi, Chudamani, Sudha, Wu, Ye, Birrer, Michael, McLellan, Michael D., Bailey, Matthew H., Miller, Christopher A., Wyczalkowski, Matthew A., Fulton, Robert S., Fronick, Catrina C., Lu, Charles, Mardis, Elaine R., Appelbaum, Elizabeth L., Schmidt, Heather K., Fulton, Lucinda A., Cordes, Matthew G., Li, Tiandao, Ding, Li, Wilson, Richard K., Rader, Janet S., Behmaram, Behnaz, Uyar, Denise, Bradley, William, Wrangle, John, Pastore, Alessandro, Levine, Douglas A., Dao, Fanny, Gao, Jianjiong, Schultz, Nikolaus, Sander, Chris, Ladanyi, Marc, Einstein, Mark, Teeter, Randall, Benz, Stephen, Wentzensen, Nicolas, Felau, Ina, Zenklusen, Jean C., Bodelon, Clara, Demchok, John A., Yang, Liming, Sheth, Margi, Ferguson, Martin L., Tarnuzzer, Roy, Yang, Hannah, Schiffman, Mark, Zhang, Jiashan, Wang, Zhining, Davidsen, Tanja, Olaniyan, Olayinka, Hutter, Carolyn M., Sofia, Heidi J., Gordenin, Dmitry A., Chan, Kin, Roberts, Steven A., Klimczak, Leszek J., Van Waes, Carter, Chen, Zhong, Saleh, Anthony D., Cheng, Hui, Parfitt, Jeremy, Bartlett, John, Albert, Monique, Arnaout, Angel, Sekhon, Harman, Gilbert, Sebastien, Peto, Myron, Myers, Jerome, Harr, Jodi, Eckman, John, Bergsten, Julie, Tucker, Kelinda, Zach, Leigh Anne, Karlan, Beth Y., Lester, Jenny, Orsulic, Sandra, Sun, Qiang, Naresh, Rashi, Pihl, Todd, Wan, Yunhu, Zaren, Howard, Sapp, Jennifer, Miller, Judy, Drwiega, Paul, Murray, Bradley A., Zhang, Hailei, Cherniack, Andrew D., Sougnez, Carrie, Pedamallu, Chandra Sekhar, Lichtenstein, Lee, Meyerson, Matthew, Noble, Michael S., Heiman, David I., Voet, Doug, Getz, Gad, Saksena, Gordon, Kim, Jaegil, Shih, Juliann, Cho, Juok, Lawrence, Michael S., Gehlenborg, Nils, Lin, Pei, Beroukhim, Rameen, Frazer, Scott, Gabriel, Stacey B., Schumacher, Steven E., Leraas, Kristen M., Lichtenberg, Tara M., Zmuda, Erik, Bowen, Jay, Frick, Jessica, Gastier-Foster, Julie M., Wise, Lisa, Gerken, Mark, Ramirez, Nilsa C., Danilova, Ludmila, Cope, Leslie, Baylin, Stephen B., Salvesen, Helga B., Vellano, Christopher P., Ju, Zhenlin, Diao, Lixia, Zhao, Hao, Chong, Zechen, Ryan, Michael C., Martinez-Ledesma, Emmanuel, Verhaak, Roeland G., Averett Byers, Lauren, Yuan, Yuan, Chen, Ken, Ling, Shiyun, Mills, Gordon B., Lu, Yiling, Akbani, Rehan, Seth, Sahil, Liang, Han, Wang, Jing, Han, Leng, Weinstein, John N., Bristow, Christopher A., Zhang, Wei, Mahadeshwar, Harshad S., Sun, Huandong, Tang, Jiabin, Zhang, Jianhua, Song, Xingzhi, Protopopov, Alexei, Shaw, Kenna R. Mills, Chin, Lynda, Olabode, Oluwole, DiSaia, Philip, Radenbaugh, Amie, Haussler, David, Zhu, Jingchun, Stuart, Josh, Chalise, Prabhakar, Koestler, Devin, Fridley, Brooke L., Godwin, Andrew K., Madan, Rashna, Ciriello, Giovanni, Martinez, Cathleen, Higgins, Kelly, Bocklage, Therese, Auman, J. Todd, Perou, Charles M., Tan, Donghui, Parker, Joel S., Hoadley, Katherine A., Wilkerson, Matthew D., Mieczkowski, Piotr A., Skelly, Tara, Veluvolu, Umadevi, Hayes, D. Neil, Rathmell, W. Kimryn, Hoyle, Alan P., Simons, Janae V., Wu, Junyuan, Mose, Lisle E., Soloway, Matthew G., Balu, Saianand, Meng, Shaowu, Jefferys, Stuart R., Bodenheimer, Tom, Shi, Yan, Roach, Jeffrey, Thorne, Leigh B., Boice, Lori, Huang, Mei, Jones, Corbin D., Zuna, Rosemary, Walker, Joan, Gunderson, Camille, Snowbarger, Carie, Brown, David, Moxley, Katherine, Moore, Kathleen, Andrade, Kelsi, Landrum, Lisa, Mannel, Robert, McMeekin, Scott, Johnson, Starla, Nelson, Tina, Elishaev, Esther, Dhir, Rajiv, Edwards, Robert, Bhargava, Rohit, Tiezzi, Daniel G., Andrade, Jurandyr M., Noushmehr, Houtan, Gilberto Carlotti, Carlos, Jr, Tirapelli, Daniela Pretti da Cunha, Weisenberger, Daniel J., Van Den Berg, David J., Maglinte, Dennis T., Bootwalla, Moiz S., Lai, Phillip H., Triche, Timothy, Jr, Swisher, Elizabeth M., Agnew, Kathy J., Shelley, Carl Simon, Laird, Peter W., Schwarz, Julie, Grigsby, Perry, and Mutch, David
Subjects: Care and treatment, Genetic aspects, Causes of, Health aspects, Cervical cancer -- Genetic aspects -- Care and treatment -- Causes of, Gene mutation -- Health aspects
Abstract: Author(s): The Cancer Genome Atlas Research Network; Albert Einstein College of Medicine; Robert D. Burk [1]; Zigui Chen [1]; Analytical Biological Services; Charles Saller [2]; Katherine Tarvin [2]; Barretos Cancer [...], Cervical cancer remains one of the leading causes of cancer-related deaths worldwide. Here we report the extensive molecular characterization of 228 primary cervical cancers, one of the largest comprehensive genomic studies of cervical cancer to date. We observed notable APOBEC mutagenesis patterns and identified SHKBP1, ERBB3, CASP8, HLA-A and TGFBR2 as novel significantly mutated genes in cervical cancer. We also discovered amplifications in immune targets CD274 (also known as PD-L1) and PDCD1LG2 (also known as PD-L2), and the BCAR4 long non-coding RNA, which has been associated with response to lapatinib. Integration of human papilloma virus (HPV) was observed in all HPV18-related samples and 76% of HPV16-related samples, and was associated with structural aberrations and increased target-gene expression. We identified a unique set of endometrial-like cervical cancers, comprised predominantly of HPV-negative tumours with relatively high frequencies of KRAS, ARID1A and PTEN mutations. Integrative clustering of 178 samples identified keratin-low squamous, keratin-high squamous and adenocarcinoma-rich subgroups. These molecular analyses reveal new potential therapeutic targets for cervical cancers.
Published: 2017
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27. Hypermutability Associated with Double-Strand Break Repair

Author: Gordenin, Dmitry A., Mothersill, Carmel E., editor, Korogodina, Victoria, editor, and Seymour, Colin B., editor
Published: 2012
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28. A deep learning system accurately classifies primary and metastatic cancers using passenger mutation patterns

Author: Jiao, Wei, Atwal, Gurnit, Polak, Paz, Karlic, Rosa, Cuppen, Edwin, Al-Shahrour, Fatima, Bailey, Peter J, Biankin, Andrew V, Boutros, Paul C, Campbell, Peter J, Chang, David K, Cooke, Susanna L, Deshpande, Vikram, Faltas, Bishoy M, Faquin, William C, Garraway, Levi, Getz, Gad, Grimmond, Sean M, Haider, Syed, Hoadley, Katherine A, Kaiser, Vera B, Kato, Mamoru, Kübler, Kirsten, Lazar, Alexander J, Li, Constance H, Louis, David N, Margolin, Adam, Martin, Sancha, Nahal-Bose, Hardeep K, Nielsen, G Petur, Nik-Zainal, Serena, Omberg, Larsson, P’ng, Christine, Perry, Marc D, Rheinbay, Esther, Rubin, Mark A, Semple, Colin A, Sgroi, Dennis C, Shibata, Tatsuhiro, Siebert, Reiner, Smith, Jaclyn, Stein, Lincoln D, Stobbe, Miranda D, Sun, Ren X, Thai, Kevin, Wright, Derek W, Wu, Chin-Lee, Yuan, Ke, Zhang, Junjun, Danyi, Alexandra, de Ridder, Jeroen, van Herpen, Carla, Lolkema, Martijn P, Steeghs, Neeltje, Morris, Quaid D, Aaltonen, Lauri A, Abascal, Federico, Abeshouse, Adam, Aburatani, Hiroyuki, Adams, David J, Agrawal, Nishant, Ahn, Keun Soo, Ahn, Sung-Min, Aikata, Hiroshi, Akbani, Rehan, Akdemir, Kadir C, Al-Ahmadie, Hikmat, Al-Sedairy, Sultan T, Alawi, Malik, Albert, Monique, Aldape, Kenneth, Alexandrov, Ludmil B, Ally, Adrian, Alsop, Kathryn, Alvarez, Eva G, Amary, Fernanda, Amin, Samirkumar B, Aminou, Brice, Ammerpohl, Ole, Anderson, Matthew J, Ang, Yeng, Antonello, Davide, Anur, Pavana, Aparicio, Samuel, Appelbaum, Elizabeth L, Arai, Yasuhito, Aretz, Axel, Arihiro, Koji, Ariizumi, Shun-ichi, Armenia, Joshua, Arnould, Laurent, Asa, Sylvia, Assenov, Yassen, Aukema, Sietse, Auman, J Todd, Aure, Miriam RR, Awadalla, Philip, Aymerich, Marta, Bader, Gary D, Baez-Ortega, Adrian, Bailey, Matthew H, Balasundaram, Miruna, Balu, Saianand, Bandopadhayay, Pratiti, Banks, Rosamonde E, Barbi, Stefano, Barbour, Andrew P, Barenboim, Jonathan, Barnholtz-Sloan, Jill, Barr, Hugh, Barrera, Elisabet, Bartlett, John, Bartolome, Javier, Bassi, Claudio, Bathe, Oliver F, Baumhoer, Daniel, Bavi, Prashant, Baylin, Stephen B, Bazant, Wojciech, Beardsmore, Duncan, Beck, Timothy A, Behjati, Sam, Behren, Andreas, Niu, Beifang, Bell, Cindy, Beltran, Sergi, Benz, Christopher, Berchuck, Andrew, Bergmann, Anke K, Bergstrom, Erik N, Berman, Benjamin P, Berney, Daniel M, Bernhart, Stephan H, Beroukhim, Rameen, Berrios, Mario, Bersani, Samantha, Bertl, Johanna, Betancourt, Miguel, Bhandari, Vinayak, Bhosle, Shriram G, Bieg, Matthias, Bigner, Darell, Binder, Hans, Birney, Ewan, Birrer, Michael, Biswas, Nidhan K, Bjerkehagen, Bodil, Bodenheimer, Tom, Boice, Lori, Bonizzato, Giada, De Bono, Johann S, Boot, Arnoud, Bootwalla, Moiz S, Borg, Ake, Borkhardt, Arndt, Boroevich, Keith A, Borozan, Ivan, Borst, Christoph, Bosenberg, Marcus, Bosio, Mattia, Boultwood, Jacqueline, Bourque, Guillaume, Bova, G Steven, Bowen, David T, Bowlby, Reanne, Bowtell, David DL, Boyault, Sandrine, Boyce, Rich, Boyd, Jeffrey, Brazma, Alvis, Brennan, Paul, Brewer, Daniel S, Brinkman, Arie B, Bristow, 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Jeong, Karaszi, Katalin, Karlan, Beth, Karlić, Rosa, Karsch, Dennis, Kasaian, Katayoon, Kassahn, Karin S, Katai, Hitoshi, Katoh, Hiroto, Kawakami, Yoshiiku, Kay, Jonathan D, Kazakoff, Stephen H, Kazanov, Marat D, Keays, Maria, Kebebew, Electron, Kefford, Richard F, Kellis, Manolis, Kench, James G, Kennedy, Catherine J, Kerssemakers, Jules NA, Khoo, David, Khoo, Vincent, Khuntikeo, Narong, Khurana, Ekta, Kilpinen, Helena, Kim, Hark Kyun, Kim, Hyung-Lae, Kim, Hyung-Yong, Kim, Hyunghwan, Kim, Jaegil, Kim, Jihoon, Kim, Jong K, Kim, Youngwook, King, Tari A, Klapper, Wolfram, Kleinheinz, Kortine, Klimczak, Leszek J, Knappskog, Stian, Kneba, Michael, Knoppers, Bartha M, Koh, Youngil, Komorowski, Jan, Komura, Daisuke, Komura, Mitsuhiro, Kong, Gu, Kool, Marcel, Korbel, Jan O, Korchina, Viktoriya, Korshunov, Andrey, Koscher, Michael, Koster, Roelof, Kote-Jarai, Zsofia, Koures, Antonios, Kovacevic, Milena, Kremeyer, Barbara, Kretzmer, Helene, Kreuz, Markus, Krishnamurthy, Savitri, Kube, Dieter, 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Xiao, Xiao, Xing, Rui, Xiong, Heng, Xu, Qinying, Xu, Yanxun, Xue, Hong, Yachida, Shinichi, Yakneen, Sergei, Yamaguchi, Rui, Yamaguchi, Takafumi N, Yamamoto, Masakazu, Yamamoto, Shogo, Yamaue, Hiroki, Yang, Fan, Yang, Huanming, Yang, Jean Y, Yang, Liming, Yang, Lixing, Yang, Shanlin, Yang, Tsun-Po, Yang, Yang, Yao, Xiaotong, Yaspo, Marie-Laure, Yates, Lucy, Yau, Christina, Ye, Chen, Ye, Kai, Yellapantula, Venkata D, Yoon, Christopher J, Yoon, Sung-Soo, Yousif, Fouad, Yu, Jun, Yu, Kaixian, Yu, Willie, Yu, Yingyan, Yuan, Yuan, Yuen, Denis, Yung, Christina K, Zaikova, Olga, Zamora, Jorge, Zapatka, Marc, Zenklusen, Jean C, Zenz, Thorsten, Zeps, Nikolajs, Zhang, Cheng-Zhong, Zhang, Fan, Zhang, Hailei, Zhang, Hongwei, Zhang, Hongxin, Zhang, Jiashan, Zhang, Jing, Zhang, Xiuqing, Zhang, Xuanping, Zhang, Yan, Zhang, Zemin, Zhao, Zhongming, Zheng, Liangtao, Zheng, Xiuqing, Zhou, Wanding, Zhou, Yong, Zhu, Bin, Zhu, Hongtu, Zhu, Jingchun, Zhu, Shida, Zou, Lihua, Zou, Xueqing, deFazio, Anna, van As, Nicholas, van Deurzen, Carolien HM, van de Vijver, Marc J, Veer, L van’t, and von Mering, Christian
Subjects: Human Biology & Physiology, Ecology,Evolution & Ethology, Tumour Biology, Genetics & Genomics, Structural Biology & Biophysics, Computational & Systems Biology
Abstract: In cancer, the primary tumour’s organ of origin and histopathology are the strongest determinants of its clinical behaviour, but in 3% of cases a patient presents with a metastatic tumour and no obvious primary. Here, as part of the ICGC/TCGA Pan-Cancer Analysis of Whole Genomes (PCAWG) Consortium, we train a deep learning classifier to predict cancer type based on patterns of somatic passenger mutations detected in whole genome sequencing (WGS) of 2606 tumours representing 24 common cancer types produced by the PCAWG Consortium. Our classifier achieves an accuracy of 91% on held-out tumor samples and 88% and 83% respectively on independent primary and metastatic samples, roughly double the accuracy of trained pathologists when presented with a metastatic tumour without knowledge of the primary. Surprisingly, adding information on driver mutations reduced accuracy. Our results have clinical applicability, underscore how patterns of somatic passenger mutations encode the state of the cell of origin, and can inform future strategies to detect the source of circulating tumour DNA.
Published: 2023
Full Text: View/download PDF

29. Combined burden and functional impact tests for cancer driver discovery using DriverPower

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Michael S, Lee, Donghoon, Lehmann, Kjong-Van, Li, Shantao, Li, Xiaotong, Lin, Ziao, Liu, Eric Minwei, Lochovsky, Lucas, Lou, Shaoke, Madsen, Tobias, Marchal, Kathleen, Martincorena, Iñigo, Martinez-Fundichely, Alexander, Maruvka, Yosef E, McGillivray, Patrick D, Meyerson, William, Muiños, Ferran, Mularoni, Loris, Nakagawa, Hidewaki, Nielsen, Morten Muhlig, Paczkowska, Marta, Park, Keunchil, Park, Kiejung, Pedersen, Jakob Skou, Pons, Tirso, Pulido-Tamayo, Sergio, Raphael, Benjamin J, Reimand, Jüri, Reyes-Salazar, Iker, Reyna, Matthew A, Rheinbay, Esther, Rubin, Mark A, Rubio-Perez, Carlota, Sahinalp, S Cenk, Saksena, Gordon, Salichos, Leonidas, Sander, Chris, Schumacher, Steven E, Shackleton, Mark, Shapira, Ofer, Shen, Ciyue, Shrestha, Raunak, Sidiropoulos, Nikos, Sieverling, Lina, Sinnott-Armstrong, Nasa, Stein, Lincoln D, Stuart, Joshua M, Tamborero, David, Tiao, Grace, Tsunoda, Tatsuhiko, Umer, Husen M, Uusküla-Reimand, Liis, Valencia, Alfonso, Vazquez, Miguel, Verbeke, Lieven PC, 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Subjects: Human Biology & Physiology, Ecology,Evolution & Ethology, Tumour Biology, Genetics & Genomics, Structural Biology & Biophysics, Computational & Systems Biology
Abstract: The discovery of driver mutations is one of the key motivations for cancer genome sequencing. Here, as part of the ICGC/TCGA Pan-Cancer Analysis of Whole Genomes (PCAWG) Consortium, which aggregated whole genome sequencing data from 2658 cancers across 38 tumour types, we describe DriverPower, a software package that uses mutational burden and functional impact evidence to identify driver mutations in coding and non-coding sites within cancer whole genomes. Using a total of 1373 genomic features derived from public sources, DriverPower’s background mutation model explains up to 93% of the regional variance in the mutation rate across multiple tumour types. By incorporating functional impact scores, we are able to further increase the accuracy of driver discovery. Testing across a collection of 2583 cancer genomes from the PCAWG project, DriverPower identifies 217 coding and 95 non-coding driver candidates. Comparing to six published methods used by the PCAWG Drivers and Functional Interpretation Working Group, DriverPower has the highest F1 score for both coding and non-coding driver discovery. This demonstrates that DriverPower is an effective framework for computational driver discovery.
Published: 2023
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30. Integrative pathway enrichment analysis of multivariate omics data

Author: Paczkowska, Marta, Barenboim, Jonathan, Sintupisut, Nardnisa, Fox, Natalie S, Zhu, Helen, Abd-Rabbo, Diala, Mee, Miles W, Boutros, Paul C, Abascal, Federico, Amin, Samirkumar B, Bader, Gary D, Beroukhim, Rameen, Bertl, Johanna, Boroevich, Keith A, Brunak, Søren, Campbell, Peter J, Carlevaro-Fita, Joana, Chakravarty, Dimple, Chan, Calvin Wing Yiu, Chen, Ken, Choi, Jung Kyoon, Deu-Pons, Jordi, Dhingra, Priyanka, Diamanti, Klev, Feuerbach, Lars, Fink, J Lynn, Fonseca, Nuno A, Frigola, Joan, Gambacorti-Passerini, Carlo, Garsed, Dale W, Gerstein, Mark, Getz, Gad, Gonzalez-Perez, Abel, Guo, Qianyun, Gut, Ivo G, Haan, David, Hamilton, Mark P, Haradhvala, Nicholas J, Harmanci, Arif O, Helmy, Mohamed, Herrmann, Carl, Hess, Julian M, Hobolth, Asger, Hodzic, Ermin, Hong, Chen, Hornshøj, Henrik, Isaev, Keren, Izarzugaza, Jose MG, Johnson, Rory, Johnson, Todd A, Juul, Malene, Juul, Randi Istrup, Kahles, Andre, Kahraman, Abdullah, Kellis, Manolis, Khurana, Ekta, Kim, Jaegil, Kim, Jong K, Kim, Youngwook, Komorowski, Jan, Korbel, Jan O, Kumar, Sushant, Lanzós, Andrés, Lawrence, Michael S, Lee, Donghoon, Lehmann, Kjong-Van, Li, Shantao, Li, Xiaotong, Lin, Ziao, Liu, Eric Minwei, Lochovsky, Lucas, Lou, Shaoke, Madsen, Tobias, Marchal, Kathleen, Martincorena, Iñigo, Martinez-Fundichely, Alexander, Maruvka, Yosef E, McGillivray, Patrick D, Meyerson, William, Muiños, Ferran, Mularoni, Loris, Nakagawa, Hidewaki, Nielsen, Morten Muhlig, Park, Keunchil, Park, Kiejung, Pedersen, Jakob Skou, Pich, Oriol, Pons, Tirso, Pulido-Tamayo, Sergio, Raphael, Benjamin J, Reyes-Salazar, Iker, Reyna, Matthew A, Rheinbay, Esther, Rubin, Mark A, Rubio-Perez, Carlota, Sabarinathan, Radhakrishnan, Sahinalp, S Cenk, Saksena, Gordon, Salichos, Leonidas, Sander, Chris, Schumacher, Steven E, Shackleton, Mark, Shapira, Ofer, Shen, Ciyue, Shrestha, Raunak, Shuai, Shimin, Sidiropoulos, Nikos, Sieverling, Lina, Sinnott-Armstrong, Nasa, Stein, Lincoln D, Stuart, Joshua M, Tamborero, David, Tiao, Grace, 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Qian, Xiao, Xiao, Xing, Rui, Xiong, Heng, Xu, Qinying, Xu, Yanxun, Xue, Hong, Yachida, Shinichi, Yakneen, Sergei, Yamaguchi, Rui, Yamaguchi, Takafumi N, Yamamoto, Masakazu, Yamamoto, Shogo, Yamaue, Hiroki, Yang, Fan, Yang, Huanming, Yang, Jean Y, Yang, Liming, Yang, Lixing, Yang, Shanlin, Yang, Tsun-Po, Yang, Yang, Yao, Xiaotong, Yaspo, Marie-Laure, Yates, Lucy, Yau, Christina, Ye, Chen, Ye, Kai, Yellapantula, Venkata D, Yoon, Christopher J, Yoon, Sung-Soo, Yousif, Fouad, Yu, Kaixian, Yu, Willie, Yu, Yingyan, Yuan, Ke, Yuan, Yuan, Yuen, Denis, Yung, Christina K, Zaikova, Olga, Zamora, Jorge, Zapatka, Marc, Zenklusen, Jean C, Zenz, Thorsten, Zeps, Nikolajs, Zhang, Cheng-Zhong, Zhang, Fan, Zhang, Hailei, Zhang, Hongwei, Zhang, Hongxin, Zhang, Jiashan, Zhang, Junjun, Zhang, Xiuqing, Zhang, Zemin, Zheng, Liangtao, Zheng, Xiuqing, Zhou, Wanding, Zhou, Yong, Zhu, Bin, Zhu, Hongtu, Zhu, Jingchun, Zhu, Shida, Zou, Xueqing, deFazio, Anna, van As, Nicholas, van Deurzen, Carolien HM, van de Vijver, Marc J, and Veer, L van’t
Subjects: Human Biology & Physiology, Ecology,Evolution & Ethology, Tumour Biology, Genetics & Genomics, Structural Biology & Biophysics, Computational & Systems Biology
Abstract: Multi-omics datasets represent distinct aspects of the central dogma of molecular biology. Such high-dimensional molecular profiles pose challenges to data interpretation and hypothesis generation. ActivePathways is an integrative method that discovers significantly enriched pathways across multiple datasets using statistical data fusion, rationalizes contributing evidence and highlights associated genes. As part of the ICGC/TCGA Pan-Cancer Analysis of Whole Genomes (PCAWG) Consortium, which aggregated whole genome sequencing data from 2658 cancers across 38 tumor types, we integrated genes with coding and non-coding mutations and revealed frequently mutated pathways and additional cancer genes with infrequent mutations. We also analyzed prognostic molecular pathways by integrating genomic and transcriptomic features of 1780 breast cancers and highlighted associations with immune response and anti-apoptotic signaling. Integration of ChIP-seq and RNA-seq data for master regulators of the Hippo pathway across normal human tissues identified processes of tissue regeneration and stem cell regulation. ActivePathways is a versatile method that improves systems-level understanding of cellular organization in health and disease through integration of multiple molecular datasets and pathway annotations.
Published: 2023
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31. Pathway and network analysis of more than 2500 whole cancer genomes

Author: Reyna, Matthew A, Haan, David, Paczkowska, Marta, Verbeke, Lieven PC, Vazquez, Miguel, Kahraman, Abdullah, Pulido-Tamayo, Sergio, Barenboim, Jonathan, Wadi, Lina, Dhingra, Priyanka, Shrestha, Raunak, Getz, Gad, Lawrence, Michael S, Pedersen, Jakob Skou, Rubin, Mark A, Wheeler, David A, Brunak, Søren, Izarzugaza, Jose MG, Khurana, Ekta, Marchal, Kathleen, von Mering, Christian, Sahinalp, S Cenk, Valencia, Alfonso, Abascal, Federico, Amin, Samirkumar B, Bader, Gary D, Bandopadhayay, Pratiti, Beroukhim, Rameen, Bertl, Johanna, Boroevich, Keith A, Busanovich, John, Campbell, Peter J, Carlevaro-Fita, Joana, Chakravarty, Dimple, Chan, Calvin Wing Yiu, Chen, Ken, Choi, Jung Kyoon, Deu-Pons, Jordi, Diamanti, Klev, Feuerbach, Lars, Fink, J Lynn, Fonseca, Nuno A, Frigola, Joan, Gambacorti-Passerini, Carlo, Garsed, Dale W, Gerstein, Mark, Guo, Qianyun, Gut, Ivo G, Hamilton, Mark P, Haradhvala, Nicholas J, Harmanci, Arif O, Helmy, Mohamed, Herrmann, Carl, Hess, Julian M, Hobolth, Asger, Hodzic, Ermin, Hong, Chen, Hornshøj, Henrik, Isaev, Keren, Johnson, Rory, Johnson, Todd A, Juul, Malene, Juul, Randi Istrup, Kahles, Andre, Kellis, Manolis, Kim, Jaegil, Kim, Jong K, Kim, Youngwook, Komorowski, Jan, Korbel, Jan O, Kumar, Sushant, Lanzós, Andrés, Larsson, Erik, Lee, Donghoon, Lehmann, Kjong-Van, Li, Shantao, Li, Xiaotong, Lin, Ziao, Liu, Eric Minwei, Lochovsky, Lucas, Lou, Shaoke, Madsen, Tobias, Martincorena, Iñigo, Martinez-Fundichely, Alexander, Maruvka, Yosef E, McGillivray, Patrick D, Meyerson, William, Muiños, Ferran, Mularoni, Loris, Nakagawa, Hidewaki, Nielsen, Morten Muhlig, Park, Keunchil, Park, Kiejung, Pons, Tirso, Reyes-Salazar, Iker, Rheinbay, Esther, Rubio-Perez, Carlota, Saksena, Gordon, Salichos, Leonidas, Sander, Chris, Schumacher, Steven E, Shackleton, Mark, Shapira, Ofer, Shen, Ciyue, Shuai, Shimin, Sidiropoulos, Nikos, Sieverling, Lina, Sinnott-Armstrong, Nasa, Stein, Lincoln D, Tamborero, David, Tiao, Grace, Tsunoda, Tatsuhiko, Umer, Husen M, 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Subjects: Human Biology & Physiology, Ecology,Evolution & Ethology, Tumour Biology, Genetics & Genomics, Structural Biology & Biophysics, Computational & Systems Biology
Abstract: The catalog of cancer driver mutations in protein-coding genes has greatly expanded in the past decade. However, non-coding cancer driver mutations are less well-characterized and only a handful of recurrent non-coding mutations, most notably TERT promoter mutations, have been reported. Here, as part of the ICGC/TCGA Pan-Cancer Analysis of Whole Genomes (PCAWG) Consortium, which aggregated whole genome sequencing data from 2658 cancer across 38 tumor types, we perform multi-faceted pathway and network analyses of non-coding mutations across 2583 whole cancer genomes from 27 tumor types compiled by the ICGC/TCGA PCAWG project that was motivated by the success of pathway and network analyses in prioritizing rare mutations in protein-coding genes. While few non-coding genomic elements are recurrently mutated in this cohort, we identify 93 genes harboring non-coding mutations that cluster into several modules of interacting proteins. Among these are promoter mutations associated with reduced mRNA expression in TP53, TLE4, and TCF4. We find that biological processes had variable proportions of coding and non-coding mutations, with chromatin remodeling and proliferation pathways altered primarily by coding mutations, while developmental pathways, including Wnt and Notch, altered by both coding and non-coding mutations. RNA splicing is primarily altered by non-coding mutations in this cohort, and samples containing non-coding mutations in well-known RNA splicing factors exhibit similar gene expression signatures as samples with coding mutations in these genes. These analyses contribute a new repertoire of possible cancer genes and mechanisms that are altered by non-coding mutations and offer insights into additional cancer vulnerabilities that can be investigated for potential therapeutic treatments.
Published: 2023
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32. Divergent mutational processes distinguish hypoxic and normoxic tumours

Author: Bhandari, Vinayak, Li, Constance H, Bristow, Robert G, Boutros, Paul C, Aaltonen, Lauri A, Abascal, Federico, Abeshouse, Adam, Aburatani, Hiroyuki, Adams, David J, Agrawal, Nishant, Ahn, Keun Soo, Ahn, Sung-Min, Aikata, Hiroshi, Akbani, Rehan, Akdemir, Kadir C, Al-Ahmadie, Hikmat, Al-Sedairy, Sultan T, Al-Shahrour, Fatima, Alawi, Malik, Albert, Monique, Aldape, Kenneth, Alexandrov, Ludmil B, Ally, Adrian, Alsop, Kathryn, Alvarez, Eva G, Amary, Fernanda, Amin, Samirkumar B, Aminou, Brice, Ammerpohl, Ole, Anderson, Matthew J, Ang, Yeng, Antonello, Davide, Anur, Pavana, Aparicio, Samuel, Appelbaum, Elizabeth L, Arai, Yasuhito, Aretz, Axel, Arihiro, Koji, Ariizumi, Shun-ichi, Armenia, Joshua, Arnould, Laurent, Asa, Sylvia, Assenov, Yassen, Atwal, Gurnit, Aukema, Sietse, Auman, J Todd, Aure, Miriam RR, Awadalla, Philip, Aymerich, Marta, Bader, Gary D, Baez-Ortega, Adrian, Bailey, Matthew H, Bailey, Peter J, Balasundaram, Miruna, Balu, Saianand, Bandopadhayay, Pratiti, Banks, Rosamonde E, Barbi, Stefano, Barbour, Andrew P, Barenboim, Jonathan, Barnholtz-Sloan, Jill, Barr, Hugh, Barrera, Elisabet, Bartlett, John, Bartolome, Javier, Bassi, Claudio, Bathe, Oliver F, Baumhoer, Daniel, Bavi, Prashant, Baylin, Stephen B, Bazant, Wojciech, Beardsmore, Duncan, Beck, Timothy A, Behjati, Sam, Behren, Andreas, Niu, Beifang, Bell, Cindy, Beltran, Sergi, Benz, Christopher, Berchuck, Andrew, Bergmann, Anke K, Bergstrom, Erik N, Berman, Benjamin P, Berney, Daniel M, Bernhart, Stephan H, Beroukhim, Rameen, Berrios, Mario, Bersani, Samantha, Bertl, Johanna, Betancourt, Miguel, Bhosle, Shriram G, Biankin, Andrew V, Bieg, Matthias, Bigner, Darell, Binder, Hans, Birney, Ewan, Birrer, Michael, Biswas, Nidhan K, Bjerkehagen, Bodil, Bodenheimer, Tom, Boice, Lori, Bonizzato, Giada, De Bono, Johann S, Boot, Arnoud, Bootwalla, Moiz S, Borg, Ake, Borkhardt, Arndt, Boroevich, Keith A, Borozan, Ivan, Borst, Christoph, Bosenberg, Marcus, Bosio, Mattia, Boultwood, Jacqueline, Bourque, 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Masakazu, Yamamoto, Shogo, Yamaue, Hiroki, Yang, Fan, Yang, Huanming, Yang, Jean Y, Yang, Liming, Yang, Lixing, Yang, Shanlin, Yang, Tsun-Po, Yang, Yang, Yao, Xiaotong, Yaspo, Marie-Laure, Yates, Lucy, Yau, Christina, Ye, Chen, Ye, Kai, Yellapantula, Venkata D, Yoon, Christopher J, Yoon, Sung-Soo, Yousif, Fouad, Yu, Jun, Yu, Kaixian, Yu, Willie, Yu, Yingyan, Yuan, Ke, Yuan, Yuan, Yuen, Denis, Yung, Christina K, Zaikova, Olga, Zamora, Jorge, Zapatka, Marc, Zenklusen, Jean C, Zenz, Thorsten, Zeps, Nikolajs, Zhang, Cheng-Zhong, Zhang, Fan, Zhang, Hailei, Zhang, Hongwei, Zhang, Hongxin, Zhang, Jiashan, Zhang, Jing, Zhang, Junjun, Zhang, Xiuqing, Zhang, Xuanping, Zhang, Yan, Zhang, Zemin, Zhao, Zhongming, Zheng, Liangtao, Zheng, Xiuqing, Zhou, Wanding, Zhou, Yong, Zhu, Bin, Zhu, Hongtu, Zhu, Jingchun, Zhu, Shida, Zou, Lihua, Zou, Xueqing, deFazio, Anna, van As, Nicholas, van Deurzen, Carolien HM, van de Vijver, Marc J, Veer, L van’t, and von Mering, Christian
Subjects: Human Biology & Physiology, Ecology,Evolution & Ethology, Tumour Biology, Genetics & Genomics, Structural Biology & Biophysics, Computational & Systems Biology
Abstract: Many primary tumours have low levels of molecular oxygen (hypoxia), and hypoxic tumours respond poorly to therapy. Pan-cancer molecular hallmarks of tumour hypoxia remain poorly understood, with limited comprehension of its associations with specific mutational processes, non-coding driver genes and evolutionary features. Here, as part of the ICGC/TCGA Pan-Cancer Analysis of Whole Genomes (PCAWG) Consortium, which aggregated whole genome sequencing data from 2658 cancers across 38 tumour types, we quantify hypoxia in 1188 tumours spanning 27 cancer types. Elevated hypoxia associates with increased mutational load across cancer types, irrespective of underlying mutational class. The proportion of mutations attributed to several mutational signatures of unknown aetiology directly associates with the level of hypoxia, suggesting underlying mutational processes for these signatures. At the gene level, driver mutations in TP53, MYC and PTEN are enriched in hypoxic tumours, and mutations in PTEN interact with hypoxia to direct tumour evolutionary trajectories. Overall, hypoxia plays a critical role in shaping the genomic and evolutionary landscapes of cancer.
Published: 2023
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33. Genomic footprints of activated telomere maintenance mechanisms in cancer

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Nakagawa, Hidewaki, Navarro, Fabio CP, Ossowski, Stephan, Pearson, John V, Puiggròs, Montserrat, Rippe, Karsten, Roberts, Nicola D, Roberts, Steven A, Rodriguez-Martin, Bernardo, Schumacher, Steven E, Scully, Ralph, Shackleton, Mark, Sidiropoulos, Nikos, Stewart, Chip, Torrents, David, MC Tubio, Jose, Villasante, Izar, Waddell, Nicola, Wala, Jeremiah A, Weischenfeldt, Joachim, Yang, Lixing, Yao, Xiaotong, Yoon, Sung-Soo, Zamora, Jorge, Zhang, Cheng-Zhong, Aaltonen, Lauri A, Abascal, Federico, Abeshouse, Adam, Aburatani, Hiroyuki, Adams, David J, Agrawal, Nishant, Ahn, Keun Soo, Ahn, Sung-Min, Aikata, Hiroshi, Akbani, Rehan, Al-Ahmadie, Hikmat, Al-Sedairy, Sultan T, Al-Shahrour, Fatima, Alawi, Malik, Albert, Monique, Aldape, Kenneth, Alexandrov, Ludmil B, Ally, Adrian, Alsop, Kathryn, Amary, Fernanda, Amin, Samirkumar B, Aminou, Brice, Ammerpohl, Ole, Anderson, Matthew J, Ang, Yeng, Antonello, Davide, Anur, Pavana, Aparicio, Samuel, Appelbaum, Elizabeth L, Arai, Yasuhito, Aretz, Axel, 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Christian
Subjects: Human Biology & Physiology, Ecology,Evolution & Ethology, Tumour Biology, Genetics & Genomics, Structural Biology & Biophysics, Computational & Systems Biology
Abstract: Cancers require telomere maintenance mechanisms for unlimited replicative potential. They achieve this through TERT activation or alternative telomere lengthening associated with ATRX or DAXX loss. Here, as part of the ICGC/TCGA Pan-Cancer Analysis of Whole Genomes (PCAWG) Consortium, we dissect whole-genome sequencing data of over 2500 matched tumor-control samples from 36 different tumor types aggregated within the ICGC/TCGA Pan-Cancer Analysis of Whole Genomes (PCAWG) Consortium to characterize the genomic footprints of these mechanisms. While the telomere content of tumors with ATRX or DAXX mutations (ATRX/DAXXtrunc) is increased, tumors with TERT modifications show a moderate decrease of telomere content. One quarter of all tumor samples contain somatic integrations of telomeric sequences into non-telomeric DNA. This fraction is increased to 80% prevalence in ATRX/DAXXtrunc tumors, which carry an aberrant telomere variant repeat (TVR) distribution as another genomic marker. The latter feature includes enrichment or depletion of the previously undescribed singleton TVRs TTCGGG and TTTGGG, respectively. Our systematic analysis provides new insight into the recurrent genomic alterations associated with telomere maintenance mechanisms in cancer.
Published: 2023
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34. The Somatic Genomic Landscape of Chromophobe Renal Cell Carcinoma

Author: Creighton, Chad J., Davis, Caleb F., Morgan, Margaret, Gunaratne, Preethi H., Donehower, Lawrence A., Kaipparettu, Benny A., Wheeler, David A., Gibbs, Richard A., Signoretti, Sabina, Cherniack, Andrew D., Robertson, A. Gordon, Chu, Andy, Choueiri, Toni K., Henske, Elizabeth P., Kwiatkowski, David J., Reuter, Victor, Hsieh, James J., Hakimi, A. Ari, Tickoo, Satish K., Ricketts, Christopher, Linehan, W. Marston, Schmidt, Laura S., Gordenin, Dmitry A., Bhanot, Gyan, Seiler, Michael, Tamboli, Pheroze, Rathmell, W. Kimryn, Fahey, Catherine C., Hacker, Kathryn E., Smith, Angela B., Wallen, Eric M., Shen, Hui, Laird, Peter W., Shuch, Brian, Muzny, Donna, Buhay, Christian, Wang, Min, Chao, Hsu, Dahdouli, Mike, Xi, Liu, Kakkar, Nipun, Reid, Jeffrey G., Downs, Brittany, Drummond, Jennifer, Morton, Donna, Doddapaneni, Harsha, Lewis, Lora, English, Adam, Meng, Qingchang, Kovar, Christie, Wang, Qiaoyan, Hale, Walker, Hawes, Alicia, Kalra, Divya, Walker, Kimberly, Murray, Bradley A., Sougnez, Carrie, Saksena, Gordon, Carter, Scott L., Schumacher, Steven E., Tabak, Barbara, Zack, Travis I., Getz, Gad, Beroukhim, Rameen, Gabriel, Stacey B., Meyerson, Matthew, Ally, Adrian, Balasundaram, Miruna, Birol, Inanc, Brooks, Denise, Butterfield, Yaron S.N., Chuah, Eric, Clarke, Amanda, Dhalla, Noreen, Guin, Ranabir, Holt, Robert A., Kasaian, Katayoon, Lee, Darlene, Li, Haiyan I., Lim, Emilia, Ma, Yussanne, Mayo, Michael, Moore, Richard A., Mungall, Andrew J., Schein, Jacqueline E., Sipahimalani, Payal, Tam, Angela, Thiessen, Nina, Wong, Tina, Jones, Steven J.M., Marra, Marco A., Auman, J. Todd, Tan, Donghui, Meng, Shaowu, Jones, Corbin D., Hoadley, Katherine A., Mieczkowski, Piotr A., Mose, Lisle E., Jefferys, Stuart R., Roach, Jeffrey, Veluvolu, Umadevi, Wilkerson, Matthew D., Waring, Scot, Buda, Elizabeth, Wu, Junyuan, Bodenheimer, Tom, Hoyle, Alan P., Simons, Janae V., Soloway, Mathew G., Balu, Saianand, Parker, Joel S., Hayes, D. Neil, Perou, Charles M., Weisenberger, Daniel J., Bootwalla, Moiz S., Triche, Timothy, Jr., Lai, Phillip H., Van Den Berg, David J., Baylin, Stephen B., Chen, Fengju, Coarfa, Cristian, Noble, Michael S., DiCara, Daniel, Zhang, Hailei, Cho, Juok, Heiman, David I., Gehlenborg, Nils, Voet, Doug, Lin, Pei, Frazer, Scott, Stojanov, Petar, Liu, Yingchun, Zou, Lihua, Kim, Jaegil, Lawrence, Michael S., Chin, Lynda, Yang, Lixing, Seth, Sahil, Bristow, Christopher A., Protopopov, Alexei, Song, Xingzhi, Zhang, Jianhua, Pantazi, Angeliki, Hadjipanayis, Angela, Lee, Eunjung, Luquette, Lovelace J., Lee, Semin, Parfenov, Michael, Santoso, Netty, Seidman, Jonathan, Xu, Andrew W., Kucherlapati, Raju, Park, Peter J., Kang, Hyojin, Lee, Junehawk, Roberts, Steven A., Klimczak, Leszek J., Fargo, David, Lang, Martin, Choi, Yoon-La, Kim, Sang Cheol, Lee, June-Koo, Park, Woong-Yang, Wang, Wenyi, Fan, Yu, Ahn, Jaeil, Akbani, Rehan, Weinstein, John N., Haussler, David, Ma, Singer, Radenbaugh, Amie, Zhul, Jingchun, Biehl, Michael, Lichtenberg, Tara M., Zmuda, Erik, Black, Aaron D., Hanf, Benjamin, Ramirez, Nilsa C., Wise, Lisa, Bowen, Jay, Leraas, Kristen M., Hall, Tracy M., Gastier-Foster, Julie M., Kaelin, William G., Thorne, Leigh, Boice, Lori, Huang, Mei, Vocke, Cathy, Peterson, James, Worrell, Robert, Merino, Maria, Czerniak, Bogdan A., Aldape, Kenneth D., Wood, Christopher G., Spellman, Paul T., Atkins, Michael B., Cheville, John, Thompson, R. Houston, Jensen, Mark A., Pihl, Todd, Wan, Yunhu, Ayala, Brenda, Baboud, Julien, Velaga, Sudhakar, Walton, Jessica, Liu, Jia, Chudamani, Sudha, Wu, Ye, Sheth, Margi, Mills Shaw, Kenna R., Demchok, John A., Davidsen, Tanja, Yang, Liming, Wang, Zhining, Tarnuzzer, Roy W., Zhang, Jiashan, Eley, Greg, Felau, Ina, Zenklusen, Jean Claude, Hutter, Carolyn M., Guyer, Mark S., Ozenberger, Bradley A., Sofia, Heidi J., and Ricketts, Christopher J.
Published: 2014
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35. Break-Induced Replication Is a Source of Mutation Clusters Underlying Kataegis

Author: Sakofsky, Cynthia J., Roberts, Steven A., Malc, Ewa, Mieczkowski, Piotr A., Resnick, Michael A., Gordenin, Dmitry A., and Malkova, Anna
Published: 2014
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36. The choice of nucleotide inserted opposite abasic sites formed within chromosomal DNA reveals the polymerase activities participating in translesion DNA synthesis

Author: Chan, Kin, Resnick, Michael A., and Gordenin, Dmitry A.
Published: 2013
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37. Comprehensive analysis of chromothripsis in 2,658 human cancers using whole-genome sequencing

Author: Xi, Ruibin, Jain, Dhawal, Jung, Youngsook L., Yang, Lixing, Gordenin, Dmitry, Pellman, David S., Akdemir, Kadir C., Alvarez, Eva G., Baez-Ortega, Adrian, Beroukhim, Rameen, Boutros, Paul C., Bowtell, David D. L., Brors, Benedikt, Burns, Kathleen H., Campbell, Peter J., Chan, Kin, Chen, Ken, Cortés-Ciriano, Isidro, Dueso-Barroso, Ana, Dunford, Andrew J., Edwards, Paul A., Estivill, Xavier, Etemadmoghadam, Dariush, Feuerbach, Lars, Fink, J. Lynn, Frenkel-Morgenstern, Milana, Garsed, Dale W., Gerstein, Mark, Gordenin, Dmitry A., Haan, David, Haber, James E., Hess, Julian M., Hutter, Barbara, Imielinski, Marcin, Jones, David T. W., Ju, Young Seok, Kazanov, Marat D., Klimczak, Leszek J., Koh, Youngil, Korbel, Jan O., Kumar, Kiran, Lee, Eunjung Alice, Lee, Jake June-Koo, Li, Yilong, Lynch, Andy G., Macintyre, Geoff, Markowetz, Florian, Martincorena, Iñigo, Martinez-Fundichely, Alexander, Miyano, Satoru, Nakagawa, Hidewaki, Navarro, Fabio C. P., Ossowski, Stephan, Park, Peter J., Pearson, John V., Puiggròs, Montserrat, Rippe, Karsten, Roberts, Nicola D., Roberts, Steven A., Rodriguez-Martin, Bernardo, Schumacher, Steven E., Scully, Ralph, Shackleton, Mark, Sidiropoulos, Nikos, Sieverling, Lina, Stewart, Chip, Torrents, David, Tubio, Jose M. C., Villasante, Izar, Waddell, Nicola, Wala, Jeremiah A., Weischenfeldt, Joachim, Yao, Xiaotong, Yoon, Sung-Soo, Zamora, Jorge, Zhang, Cheng-Zhong, Cortés-Ciriano, Isidro [0000-0002-2036-494X], Lee, Jake June-Koo [0000-0003-1348-4094], Xi, Ruibin [0000-0001-7545-7361], Gordenin, Dmitry [0000-0002-8399-1836], Klimczak, Leszek J. [0000-0003-3048-2576], Zhang, Cheng-Zhong [0000-0001-8825-7158], Park, Peter J. [0000-0001-9378-960X], and Apollo - University of Cambridge Repository
Subjects: 631/67, 45, analysis, 631/208/212, 45/23, 631/114
Abstract: Funder: Ludwig Center at Harvard, Funder: National Cancer Institute: K22CA193848, Funder: US National Institutes of Health Intramural Research Program Project Z1AES103266, Chromothripsis is a mutational phenomenon characterized by massive, clustered genomic rearrangements that occurs in cancer and other diseases. Recent studies in selected cancer types have suggested that chromothripsis may be more common than initially inferred from low-resolution copy-number data. Here, as part of the Pan-Cancer Analysis of Whole Genomes (PCAWG) Consortium of the International Cancer Genome Consortium (ICGC) and The Cancer Genome Atlas (TCGA), we analyze patterns of chromothripsis across 2,658 tumors from 38 cancer types using whole-genome sequencing data. We find that chromothripsis events are pervasive across cancers, with a frequency of more than 50% in several cancer types. Whereas canonical chromothripsis profiles display oscillations between two copy-number states, a considerable fraction of events involve multiple chromosomes and additional structural alterations. In addition to non-homologous end joining, we detect signatures of replication-associated processes and templated insertions. Chromothripsis contributes to oncogene amplification and to inactivation of genes such as mismatch-repair-related genes. These findings show that chromothripsis is a major process that drives genome evolution in human cancer.
Published: 2021
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38. An APOBEC3A hypermutation signature is distinguishable from the signature of background mutagenesis by APOBEC3B in human cancers

Author: Chan, Kin, Roberts, Steven A, Klimczak, Leszek J, Sterling, Joan F, Saini, Natalie, Malc, Ewa P, Kim, Jaegil, Kwiatkowski, David J, Fargo, David C, Mieczkowski, Piotr A, Getz, Gad, and Gordenin, Dmitry A
Published: 2015
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39. Clustered Mutations in Yeast and in Human Cancers Can Arise from Damaged Long Single-Strand DNA Regions

Author: Roberts, Steven A., Sterling, Joan, Thompson, Cole, Harris, Shawn, Mav, Deepak, Shah, Ruchir, Klimczak, Leszek J., Kryukov, Gregory V., Malc, Ewa, Mieczkowski, Piotr A., Resnick, Michael A., and Gordenin, Dmitry A.
Published: 2012
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40. RAD53 is limiting in double-strand break repair and in protection against toxicity associated with ribonucleotide reductase inhibition

Author: Covo, Shay, Westmoreland, James W., Reddy, Amit K., Gordenin, Dmitry A., and Resnick, Michael A.
Published: 2012
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41. Genome-wide model for the normal eukaryotic DNA replication fork

Author: Larrea, Andres A., Lujan, Scott A., McElhinny, Stephanie A. Nick, Mieczkowski, Piotr A., Resnick, Michael A., Gordenin, Dmitry A., and Kunkel, Thomas A.
Published: 2010
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42. A single-strand specific lesion drives MMS-induced hyper-mutability at a double-strand break in yeast

Author: Yang, Yong, Gordenin, Dmitry A., and Resnick, Michael A.
Published: 2010
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43. Flexibility of Eukaryotic Okazaki Fragment Maturation through Regulated Strand Displacement Synthesis

Author: Stith, Carrie M., Sterling, Joan, Resnick, Michael A., Gordenin, Dmitry A., and Burgers, Peter M.
Published: 2008
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44. Division of Labor at the Eukaryotic Replication Fork

Author: Nick McElhinny, Stephanie A., Gordenin, Dmitry A., Stith, Carrie M., Burgers, Peter M.J., and Kunkel, Thomas A.
Published: 2008
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45. Clustered and genome-wide transient mutagenesis in human cancers: Hypermutation without permanent mutators or loss of fitness

Author: Roberts, Steven A. and Gordenin, Dmitry A.
Published: 2014
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46. Comprehensive molecular characterization of urothelial bladder carcinoma

Author: Weinstein, John N., Akbani, Rehan, Broom, Bradley M., Wang, Wenyi, Verhaak, Roeland G. W., McConkey, David, Lerner, Seth, Morgan, Margaret, Creighton, Chad J., Smith, Carolyn, Kwiatkowski, David J., Cherniack, Andrew D., Kim, Jaegil, Pedamallu, Chandra Sekhar, Noble, Michael S., Al-Ahmadie, Hikmat A., Reuter, Victor E., Rosenberg, Jonathan E., Bajorin, Dean F., Bochner, Bernard H., Solit, David B., Koppie, Theresa, Robinson, Brian, Gordenin, Dmitry A., Fargo, David, Klimczak, Leszek J., Roberts, Steven A., Au, Jessie, Laird, Peter W., Hinoue, Toshinori, Schultz, Nikolaus, Ramirez, Ricardo, Hansel, Donna, Hoadley, Katherine A., Kim, William Y., Damrauer, Jeffrey S., Baylin, Stephen B., Mungall, Andrew J., Robertson, Gordon A., Chu., Andy, Sougnez, Carrie, Cibulskis, Kristian, Lichtenstein, Lee, Sivachenko, Andrey, Stewart, Chip, Lawrence, Michael S., Getz, Gad, Lander, Eric, Gabriel., Stacey B., Donehower, Lawrence, Carter, Scott L., Saksena, Gordon, Schumacher, Steven E., Freeman, Samuel S., Jung, Joonil, Bhatt, Ami S., Pugh, Trevor, Beroukhim, Rameen, Gabriel, Stacey B., Meyerson, Matthew, Chu, Andy, Ally, Adrian, Balasundaram, Miruna, Butterfield, Yaron S. N., Dhalla, Noreen, Hirst, Carrie, Holt, Robert A., Jones, Steven J. M., Lee, Darlene, Li, Haiyan I., Marra, Marco A., Mayo, Michael, Moore, Richard A., Schein, Jacqueline E., Sipahimalani, Payal, Tam, Angela, Thiessen, Nina, Wong, Tina, Wye, Natasja, Bowlby, Reanne, Chuah, Eric, Guin, Ranabir, Shen, Hui, Bootwalla, Moiz S., Jr, Timothy Triche, Lai, Phillip H., Van Den Berg, David J., Weisenberger, Daniel J., Balu, Saianand, Bodenheimer, Tom, Damrauer Alan P. Hoyle, Jeffrey S., Jefferys, Stuart R., Meng, Shaowu, Mose, Lisle E., Simons, Janae V., Soloway, Mathew G., Wu, Junyuan, Parker, Joel S., Hayes, Neil D., Roach, Jeffrey, Buda, Elizabeth, Jones, Corbin D., Mieczkowski, Piotr A., Tan, Donghui, Veluvolu, Umadevi, Waring, Scot, Auman, Todd J., Perou, Charles M., Wilkerson, Matthew D., Santoso, Netty, Parfenov, Michael, Ren, Xiaojia, Pantazi, Angeliki, Hadjipanayis, Angela, Seidman, Jonathan, Kucherlapati, Raju, Lee, Semin, Yang, Lixing, Park, Peter J., Xu, Andrew Wei, Protopopov, Alexei, Zhang, Jianhua, Bristow, Christopher, Mahadeshwar, Harshad S., Seth, Sahil, Song, Xingzhi, Tang, Jiabin, Zeng, Dong, Chin, Lynda, Guo, Charles, Casasent, Tod D., Liu, Wenbin, Ju, Zhenlin, Motter, Thomas, Peng, Bo, Ryan, Michael, Su, Xiaoping, Yang, Ji-Yeon, Lorenzi, Philip L., Yao, Hui, Zhang, Nianxiang, Zhang, Jiexin, Mills, Gordon B., Cho, Juok, DiCara, Daniel, Frazer, Scott, Gehlenborg, Nils, Heiman, David I., Lin, Pei, Liu, Yingchun, Stojanov, Petar, Voet, Doug, Zhang, Hailei, Zou, Lihua, Bernard, Brady, Kreisberg, Dick, Reynolds, Sheila, Rovira, Hector, Shmulevich, Ilya, Gao, Jianjiong, Jacobsen, Anders, Aksoy, Arman B., Antipin, Yevgeniy, Ciriello, Giovanni, Dresdner, Gideon, Gross, Benjamin, Lee, William, Reva, Boris, Shen, Ronglai, Sinha, Rileen, Sumer, Onur S., Weinhold, Nils, Ladanyi, Marc, Sander, Chris, Benz, Christopher, Carlin, Daniel, Haussler, David, Ng, Sam, Paull, Evan O., Stuart, Joshua, Zhu, Jing, Liu, Yuexin, Zhang, Wei, Taylor, Barry S., Lichtenberg, Tara M., Zmuda, Erik, Barr, Thomas, Black, Aaron D., George, Myra, Hanf, Benjamin, Helsel, Carmen, McAllister, Cynthia, Ramirez, Nilsa C., Tabler, Teresa R., Weaver, Stephanie, Wise, Lisa, Bowen, Jay, Gastier-Foster, Julie M., Jian, Weiguo, Tello, Sebrina, Ittman, Michael, Castro, Patricia, McClenden, Whitney D., Gibbs, Richard, Saller, Charles, Tarvin, Katherine, DiPiero, Jennifer M., Owens, Jennifer, Bollag, Roni, Li, Qiang, Weinberger, Paul, Czerwinski, Christine, Huelsenbeck-Dill, Lori, Iacocca, Mary, Petrelli, Nicholas, Rabeno, Brenda, Swanson, Pat, Shelton, Troy, Curley, Erin, Gardner, Johanna, Mallery, David, Penny, Robert, Van Bang, Nguyen, Thi Hanh, Phan, Kohl, Bernard, Van Le, Xuan, Duc Phu, Bui, Thorp, Richard, Tien, Nguyen Viet, Vinh, Le Quang, Sandusky, George, Burks, Eric, Christ, Kimberly, Gee, Jason, Holway, Antonia, Moinzadeh, Alireza, Sorcini, Andrea, Sullivan, Travis, Garcia-Grossman, Ilana R., Regazzi, Ashley M., Boice, Lori, Rathmell, Wendy Kimryn, Thorne, Leigh, Bastacky, Sheldon, Davies, Benjamin, Dhir, Rajiv, Gingrich, Jeffrey, Hrebinko, Ronald, Maranchie, Jodi, Nelson, Joel, Parwani, Anil, Bshara, Wiam, Gaudioso, Carmelo, Morrison, Carl, Alexopoulou, Vina, Bartlett, John, Engel, Jay, Kodeeswaran, Sugy, Antic, Tatjana, O’Donnell, Peter H., Smith, Norm D., Steinberg, Gary D., Egea, Sophie, Gomez-Fernandez, Carmen, Herbert, Lynn, Jorda, Merce, Soloway, Mark, Beaver, Allison, Carter, Suzie, Kapur, Payal, Lewis, Cheryl, Lotan, Yair, Bondaruk, Jolanta, Czerniak, Bogdan, Skinner, Eila, Aldape, Kenneth, Jensen, Mark A., Kahn, Ari B., Pihl, Todd D., Pot, David A., Srinivasan, Deepak, Wan, Yunhu, Ferguson, Martin L., Zenklusen, Jean Claude, Davidsen, Tanja, Demchok, John A., Mills Shaw, Kenna R., Sheth, Margi, Tarnuzzer, Roy, Wang, Zhining, Yang, Liming, Hutter, Carolyn, Ozenberger, Bradley A., Sofia, Heidi J., and Eley, Greg
Published: 2014
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47. Abstract 865: Genomic and evolutionary classification of lung cancer in never smokers from the Sherlock-Lungstudy

Author: Zhang, Tongwu, primary, Alexandrov, Ludmil B., additional, Zhao, Wei, additional, Sang, Jian, additional, Shi, Jianxin, additional, Zhu, Bin, additional, Gordenin, Dmitry A., additional, Garcia-Closas, Montserrat, additional, Lan, Qing, additional, Rothman, Nathaniel, additional, Chanock, Stephen J., additional, Wedge, David C., additional, and Landi, Maria Teresa, additional
Published: 2021
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48. From RNA World to SARS-CoV-2: The Edited Story of RNA Viral Evolution

Author: Kockler, Zachary W., primary and Gordenin, Dmitry A., additional
Published: 2021
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49. Disruption of chromatin folding domains by somatic genomic rearrangements in human cancer

Author: Akdemir, Kadir C., Le, Victoria T., Chandran, Sahaana, Li, Yilong, Verhaak, Roel G., Beroukhim, Rameen, Campbell, Peter J., Chin, Lynda, Dixon, Jesse R., Futreal, P. Andrew, Alvarez, Eva G., Baez-Ortega, Adrian, Boutros, Paul C., Bowtell, David D.L., Brors, Benedikt, Burns, Kathleen H., Chan, Kin, Chen, Ken, Cortés-Ciriano, Isidro, Dueso-Barroso, Ana, Dunford, Andrew J., Edwards, Paul A., Estivill, Xavier, Etemadmoghadam, Dariush, Feuerbach, Lars, Fink, J. Lynn, Frenkel-Morgenstern, Milana, Garsed, Dale W., Gerstein, Mark, Gordenin, Dmitry A., Haan, David, Haber, James E., Hess, Julian M., Hutter, Barbara, Imielinski, Marcin, Jones, David T.W., Ju, Young Seok, Kazanov, Marat D., Klimczak, Leszek J., Koh, Youngil, Korbel, Jan O., Kumar, Kiran, Lee, Eunjung Alice, Lee, Jake June Koo, Sidiropoulos, Nikos, Weischenfeldt, Joachim, Futreal, P Andrew [0000-0001-8663-2671], Apollo - University of Cambridge Repository, University of St Andrews. School of Medicine, University of St Andrews. Statistics, University of St Andrews. Sir James Mackenzie Institute for Early Diagnosis, and University of St Andrews. Cellular Medicine Division
Subjects: QH301 Biology, Genoma humà, Genome, Medical and Health Sciences, Cromatina, chemistry.chemical_compound, 0302 clinical medicine, Neoplasms, 2.1 Biological and endogenous factors, Aetiology, Cancer, Regulation of gene expression, Gene Rearrangement, 0303 health sciences, Women's cancers Radboud Institute for Molecular Life Sciences [Radboudumc 17], 3rd-DAS, Biological Sciences, Chromatin, Women's cancers Radboud Institute for Health Sciences [Radboudumc 17], Gene Expression Regulation, Neoplastic, 030220 oncology & carcinogenesis, PCAWG Structural Variation Working Group, Human, Biotechnology, Genomic Structural Variation, QH426 Genetics, Computational biology, Biology, Article, RC0254, QH301, 03 medical and health sciences, SDG 3 - Good Health and Well-being, Genetics, Humans, Data mining, QH426, Gene, Tumors, 030304 developmental biology, Neoplastic, RC0254 Neoplasms. Tumors. Oncology (including Cancer), Genome, Human, Human Genome, PCAWG Consortium, Gene rearrangement, Human genetics, Reordenament genètic, chemistry, Gene Expression Regulation, Gene expression, Genètica, DNA, Developmental Biology
Abstract: Chromatin is folded into successive layers to organize linear DNA. Genes within the same topologically associating domains (TADs) demonstrate similar expression and histone-modification profiles, and boundaries separating different domains have important roles in reinforcing the stability of these features. Indeed, domain disruptions in human cancers can lead to misregulation of gene expression. However, the frequency of domain disruptions in human cancers remains unclear. Here, as part of the Pan-Cancer Analysis of Whole Genomes (PCAWG) Consortium of the International Cancer Genome Consortium (ICGC) and The Cancer Genome Atlas (TCGA), which aggregated whole-genome sequencing data from 2,658 cancers across 38 tumor types, we analyzed 288,457 somatic structural variations (SVs) to understand the distributions and effects of SVs across TADs. Notably, SVs can lead to the fusion of discrete TADs, and complex rearrangements markedly change chromatin folding maps in the cancer genomes. Notably, only 14% of the boundary deletions resulted in a change in expression in nearby genes of more than twofold., A pan-cancer genomic analysis reports the effects of structural variations on chromatin domains (TADs). Most TAD disruptions do not result in appreciable changes in expression of nearby genes.
Published: 2020
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50. Oxidative stress-induced mutagenesis in single-strand DNA occurs primarily at cytosines and is DNA polymerase zeta-dependent only for adenines and guanines

Author: Degtyareva, Natalya P., Heyburn, Lanier, Sterling, Joan, Resnick, Michael A., Gordenin, Dmitry A., and Doetsch, Paul W.
Published: 2013
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