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Article ; Online: Spon1+ inflammatory monocytes promote collagen remodeling and lung cancer metastasis through lipoprotein receptor 8 signaling.

Whately, Kristina M / Sengottuvel, Nisitha / Edatt, Lincy / Srivastava, Sonal / Woods, Allison T / Tsai, Yihsuan S / Porrello, Alessandro / Zimmerman, Matthew P / Chack, Aaron C / Jefferys, Stuart R / Yacovone, Gabriella / Kim, Dae Joong / Dudley, Andrew C / Amelio, Antonio L / Pecot, Chad V

JCI insight

2024 Volume 9, Issue 9

Abstract: Lung cancer is the leading cause of cancer-related deaths in the world, and non-small cell lung cancer (NSCLC) is the most common subset. We previously found that infiltration of tumor inflammatory monocytes (TIMs) into lung squamous carcinoma (LUSC) ... ...

Abstract	Lung cancer is the leading cause of cancer-related deaths in the world, and non-small cell lung cancer (NSCLC) is the most common subset. We previously found that infiltration of tumor inflammatory monocytes (TIMs) into lung squamous carcinoma (LUSC) tumors is associated with increased metastases and poor survival. To further understand how TIMs promote metastases, we compared RNA-Seq profiles of TIMs from several LUSC metastatic models with inflammatory monocytes (IMs) of non-tumor-bearing controls. We identified Spon1 as upregulated in TIMs and found that Spon1 expression in LUSC tumors corresponded with poor survival and enrichment of collagen extracellular matrix signatures. We observed SPON1+ TIMs mediate their effects directly through LRP8 on NSCLC cells, which resulted in TGF-β1 activation and robust production of fibrillar collagens. Using several orthogonal approaches, we demonstrated that SPON1+ TIMs were sufficient to promote NSCLC metastases. Additionally, we found that Spon1 loss in the host, or Lrp8 loss in cancer cells, resulted in a significant decrease of both high-density collagen matrices and metastases. Finally, we confirmed the relevance of the SPON1/LRP8/TGF-β1 axis with collagen production and survival in patients with NSCLC. Taken together, our study describes how SPON1+ TIMs promote collagen remodeling and NSCLC metastases through an LRP8/TGF-β1 signaling axis.
MeSH term(s)	Animals ; Humans ; Mice ; Carcinoma, Non-Small-Cell Lung/pathology ; Carcinoma, Non-Small-Cell Lung/metabolism ; Carcinoma, Non-Small-Cell Lung/genetics ; Carcinoma, Non-Small-Cell Lung/secondary ; Cell Line, Tumor ; Collagen/metabolism ; Extracellular Matrix Proteins/metabolism ; Extracellular Matrix Proteins/genetics ; LDL-Receptor Related Proteins/metabolism ; LDL-Receptor Related Proteins/genetics ; Lung Neoplasms/pathology ; Lung Neoplasms/metabolism ; Lung Neoplasms/secondary ; Lung Neoplasms/genetics ; Monocytes/metabolism ; Monocytes/pathology ; Neoplasm Metastasis ; Signal Transduction ; Transforming Growth Factor beta1/metabolism
Chemical Substances	Collagen (9007-34-5) ; Extracellular Matrix Proteins ; LDL-Receptor Related Proteins ; low density lipoprotein receptor-related protein 8 ; TGFB1 protein, human ; Transforming Growth Factor beta1
Language	English
Publishing date	2024-05-08
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ISSN	2379-3708
ISSN (online)	2379-3708
DOI	10.1172/jci.insight.168792
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Article ; Online: Baking a mass-spectrometry data PIE with McMC and simulated annealing: predicting protein post-translational modifications from integrated top-down and bottom-up data.

Jefferys, Stuart R / Giddings, Morgan C

Bioinformatics (Oxford, England)

2011 Volume 27, Issue 6, Page(s) 844–852

Abstract: Motivation: Post-translational modifications are vital to the function of proteins, but are hard to study, especially since several modified isoforms of a protein may be present simultaneously. Mass spectrometers are a great tool for investigating ... ...

Abstract	Motivation: Post-translational modifications are vital to the function of proteins, but are hard to study, especially since several modified isoforms of a protein may be present simultaneously. Mass spectrometers are a great tool for investigating modified proteins, but the data they provide is often incomplete, ambiguous and difficult to interpret. Combining data from multiple experimental techniques-especially bottom-up and top-down mass spectrometry-provides complementary information. When integrated with background knowledge this allows a human expert to interpret what modifications are present and where on a protein they are located. However, the process is arduous and for high-throughput applications needs to be automated. Results: This article explores a data integration methodology based on Markov chain Monte Carlo and simulated annealing. Our software, the Protein Inference Engine (the PIE) applies these algorithms using a modular approach, allowing multiple types of data to be considered simultaneously and for new data types to be added as needed. Even for complicated data representing multiple modifications and several isoforms, the PIE generates accurate modification predictions, including location. When applied to experimental data collected on the L7/L12 ribosomal protein the PIE was able to make predictions consistent with manual interpretation for several different L7/L12 isoforms using a combination of bottom-up data with experimentally identified intact masses. Availability: Software, demo projects and source can be downloaded from http://pie.giddingslab.org/
MeSH term(s)	Algorithms ; Bacterial Proteins/analysis ; Bacterial Proteins/chemistry ; Escherichia coli/chemistry ; Markov Chains ; Mass Spectrometry/methods ; Monte Carlo Method ; Protein Isoforms/analysis ; Protein Isoforms/chemistry ; Protein Processing, Post-Translational ; Proteins/analysis ; Proteins/chemistry ; Proteomics/methods ; Ribosomal Proteins/analysis ; Ribosomal Proteins/chemistry ; Software
Chemical Substances	Bacterial Proteins ; Protein Isoforms ; Proteins ; Ribosomal Proteins ; ribosomal protein L7-L12 (70815-33-7)
Language	English
Publishing date	2011-03-09
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	1422668-6
ISSN	1367-4811 ; 1367-4803
ISSN (online)	1367-4811
ISSN	1367-4803
DOI	10.1093/bioinformatics/btr027
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Article ; Online: Automated data integration and determination of posttranslational modifications with the protein inference engine.

Jefferys, Stuart R / Giddings, Morgan C

Methods in molecular biology (Clifton, N.J.)

2011 Volume 694, Page(s) 255–290

Abstract: This chapter describes using the Protein Inference Engine (PIE) to integrate various types of data--especially top down and bottom up mass spectrometer (MS) data--to describe a protein's posttranslational modifications (PTMs). PTMs include cleavage ... ...

Abstract	This chapter describes using the Protein Inference Engine (PIE) to integrate various types of data--especially top down and bottom up mass spectrometer (MS) data--to describe a protein's posttranslational modifications (PTMs). PTMs include cleavage events such as the n-terminal loss of methionine and residue modifications like phosphorylation. Modifications are key elements in many biological processes, but are difficult to study as no single, general method adequately characterizes a protein's PTMs; manually integrating data from several MS experiments is usually required. The PIE is designed to automate this process using a guess and refine process similar to how an expert manually integrates data. The PIE repeatedly "imagines" a possible modification set, evaluates it using available data, and then tries to improve on it. After many rounds of refinement, the resulting modification set is proposed as a candidate answer. Multiple candidate answers are generated to obtain both best and near-best answers. Near-best answers are crucial in allowing for proteins with more than one supported modification pattern (isoforms) and obtaining robust results given incomplete and inconsistent data.The goal of this chapter is to walk the reader through installing and using the downloadable version of PIE, both in general and by means of a specific, detailed example. The example integrates several types of experimental and background (prior) data. It is not a "perfect-world" scenario, but has been designed to illustrate several real-world difficulties that may be encountered when trying to analyze imperfect data.
MeSH term(s)	Amino Acid Sequence ; Automatic Data Processing/methods ; Computational Biology/methods ; Mass Spectrometry ; Molecular Sequence Data ; Molecular Weight ; Peptides/chemistry ; Peptides/metabolism ; Phosphorylation ; Protein Isoforms/chemistry ; Protein Isoforms/metabolism ; Protein Processing, Post-Translational ; Proteins/chemistry ; Proteins/metabolism ; Software
Chemical Substances	Peptides ; Protein Isoforms ; Proteins
Language	English
Publishing date	2011
Publishing country	United States
Document type	Journal Article
ISSN	1940-6029
ISSN (online)	1940-6029
DOI	10.1007/978-1-60761-977-2_17
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Article ; Online: Comprehensive Viral Genotyping Reveals Prognostic Viral Phylogenetic Groups in HPV16-Associated Squamous Cell Carcinoma of the Oropharynx.

Schrank, Travis P / Landess, Lee / Stepp, Wesley H / Rehmani, Hina / Weir, William H / Lenze, Nicholas / Lal, Asim / Wu, Di / Kothari, Aditi / Hackman, Trevor G / Sheth, Siddharth / Patel, Shetal / Jefferys, Stuart R / Issaeva, Natalia / Yarbrough, Wendell G

Molecular cancer research : MCR

2022 Volume 20, Issue 10, Page(s) 1489–1501

Abstract: Human papillomavirus-positive (HPV+) squamous cell carcinoma of the oropharynx (OPSCC) is the most prevalent HPV-associated malignancy in the United States and is primarily caused by HPV subtype 16 (HPV16). Favorable treatment outcomes have led to ... ...

Abstract	Human papillomavirus-positive (HPV+) squamous cell carcinoma of the oropharynx (OPSCC) is the most prevalent HPV-associated malignancy in the United States and is primarily caused by HPV subtype 16 (HPV16). Favorable treatment outcomes have led to increasing interest in treatment deescalation to reduce treatment-related morbidity. Prognostic biomarkers are needed to identify appropriately low-risk patients for reduced treatment intensity. Targeted DNA sequencing including all HPV16 open reading frames was performed on tumors from 104 patients with HPV16+ OPSCC treated at a single center. Genotypes closely related to the HPV16-A1 reference were associated with increased numbers of somatic copy-number variants in the human genome and poor recurrence-free survival (RFS). Genotypes divergent from HPV16-A1 were associated with favorable RFS. These findings were independent of tobacco smoke exposure. Total RNA sequencing was performed on a second independent cohort of 89 HPV16+ OPSCC cases. HPV16 genotypes divergent from HPV16-A1 were again validated in this independent cohort, to be prognostic of improved RFS in patients with moderate (less than 30 pack-years) or low (no more than 10 pack-years) of tobacco smoke exposure. In summary, we show in two independent cohorts that viral sequence divergence from the HPV16-A1 reference is correlated with improved RFS in patients with moderate or low tobacco smoke exposure. Implications: HPV16 genotype is a potential biomarker that could be easily adopted to guide therapeutic decision-making related to deescalation therapy.
MeSH term(s)	Carcinoma, Squamous Cell/pathology ; Genotype ; Human papillomavirus 16/genetics ; Humans ; Oropharyngeal Neoplasms/genetics ; Papillomavirus Infections/pathology ; Phylogeny ; Prognosis ; Tobacco Smoke Pollution
Chemical Substances	Tobacco Smoke Pollution
Language	English
Publishing date	2022-06-22
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2098788-2
ISSN	1557-3125 ; 1541-7786
ISSN (online)	1557-3125
ISSN	1541-7786
DOI	10.1158/1541-7786.MCR-21-0443
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Article ; Online: Epigenomic characterization of latent HIV infection identifies latency regulating transcription factors.

Jefferys, Stuart R / Burgos, Samuel D / Peterson, Jackson J / Selitsky, Sara R / Turner, Anne-Marie W / James, Lindsey I / Tsai, Yi-Hsuan / Coffey, Alisha R / Margolis, David M / Parker, Joel / Browne, Edward P

PLoS pathogens

2021 Volume 17, Issue 2, Page(s) e1009346

Abstract: Transcriptional silencing of HIV in CD4 T cells generates a reservoir of latently infected cells that can reseed infection after interruption of therapy. As such, these cells represent the principal barrier to curing HIV infection, but little is known ... ...

Abstract	Transcriptional silencing of HIV in CD4 T cells generates a reservoir of latently infected cells that can reseed infection after interruption of therapy. As such, these cells represent the principal barrier to curing HIV infection, but little is known about their characteristics. To further our understanding of the molecular mechanisms of latency, we characterized a primary cell model of HIV latency in which infected cells adopt heterogeneous transcriptional fates. In this model, we observed that latency is a stable, heritable state that is transmitted through cell division. Using Assay of Transposon-Accessible Chromatin sequencing (ATACseq) we found that latently infected cells exhibit greatly reduced proviral accessibility, indicating the presence of chromatin-based structural barriers to viral gene expression. By quantifying the activity of host cell transcription factors, we observe elevated activity of Forkhead and Kruppel-like factor transcription factors (TFs), and reduced activity of AP-1, RUNX and GATA TFs in latently infected cells. Interestingly, latency reversing agents with different mechanisms of action caused distinct patterns of chromatin reopening across the provirus. We observe that binding sites for the chromatin insulator CTCF are highly enriched in the differentially open chromatin of infected CD4 T cells. Furthermore, depletion of CTCF inhibited HIV latency, identifying this factor as playing a key role in the initiation or enforcement of latency. These data indicate that HIV latency develops preferentially in cells with a distinct pattern of TF activity that promotes a closed proviral structure and inhibits viral gene expression. Furthermore, these findings identify CTCF as a novel regulator of HIV latency.
MeSH term(s)	Binding Sites ; CD4-Positive T-Lymphocytes/metabolism ; CD4-Positive T-Lymphocytes/virology ; Chromatin/genetics ; Chromatin/metabolism ; Epigenomics/methods ; HIV Infections/genetics ; HIV Infections/metabolism ; HIV Infections/virology ; HIV-1/physiology ; Host-Pathogen Interactions ; Humans ; Jurkat Cells ; Transcription Factors/genetics ; Transcription Factors/metabolism ; Virus Activation ; Virus Latency
Chemical Substances	Chromatin ; Transcription Factors
Language	English
Publishing date	2021-02-26
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2205412-1
ISSN	1553-7374 ; 1553-7374
ISSN (online)	1553-7374
ISSN	1553-7374
DOI	10.1371/journal.ppat.1009346
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Article ; Online: Comprehensive Molecular Characterization of Pheochromocytoma and Paraganglioma.

Fishbein, Lauren / Leshchiner, Ignaty / Walter, Vonn / Danilova, Ludmila / Robertson, A Gordon / Johnson, Amy R / Lichtenberg, Tara M / Murray, Bradley A / Ghayee, Hans K / Else, Tobias / Ling, Shiyun / Jefferys, Stuart R / de Cubas, Aguirre A / Wenz, Brandon / Korpershoek, Esther / Amelio, Antonio L / Makowski, Liza / Rathmell, W Kimryn / Gimenez-Roqueplo, Anne-Paule /

Giordano, Thomas J / Asa, Sylvia L / Tischler, Arthur S / Pacak, Karel / Nathanson, Katherine L / Wilkerson, Matthew D

Cancer cell

2017 Volume 31, Issue 2, Page(s) 181–193

Abstract: We report a comprehensive molecular characterization of pheochromocytomas and paragangliomas (PCCs/PGLs), a rare tumor type. Multi-platform integration revealed that PCCs/PGLs are driven by diverse alterations affecting multiple genes and pathways. ... ...

Abstract	We report a comprehensive molecular characterization of pheochromocytomas and paragangliomas (PCCs/PGLs), a rare tumor type. Multi-platform integration revealed that PCCs/PGLs are driven by diverse alterations affecting multiple genes and pathways. Pathogenic germline mutations occurred in eight PCC/PGL susceptibility genes. We identified CSDE1 as a somatically mutated driver gene, complementing four known drivers (HRAS, RET, EPAS1, and NF1). We also discovered fusion genes in PCCs/PGLs, involving MAML3, BRAF, NGFR, and NF1. Integrated analysis classified PCCs/PGLs into four molecularly defined groups: a kinase signaling subtype, a pseudohypoxia subtype, a Wnt-altered subtype, driven by MAML3 and CSDE1, and a cortical admixture subtype. Correlates of metastatic PCCs/PGLs included the MAML3 fusion gene. This integrated molecular characterization provides a comprehensive foundation for developing PCC/PGL precision medicine.
MeSH term(s)	Adult ; Aged ; Aged, 80 and over ; DNA-Binding Proteins/genetics ; Female ; Gene Fusion ; Humans ; Male ; Middle Aged ; Mutation ; Nuclear Proteins/genetics ; Paraganglioma/etiology ; Paraganglioma/genetics ; Pheochromocytoma/etiology ; Pheochromocytoma/genetics ; Pol1 Transcription Initiation Complex Proteins/genetics ; Proto-Oncogene Proteins c-ret/genetics ; RNA-Binding Proteins/genetics ; Transcription Factors/genetics
Chemical Substances	CSDE1 protein, human ; DNA-Binding Proteins ; MAML3 protein, human ; Nuclear Proteins ; Pol1 Transcription Initiation Complex Proteins ; RNA-Binding Proteins ; Transcription Factors ; transcription factor UBF ; Proto-Oncogene Proteins c-ret (EC 2.7.10.1) ; RET protein, human (EC 2.7.10.1)
Language	English
Publishing date	2017-02-02
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural
ZDB-ID	2078448-X
ISSN	1878-3686 ; 1535-6108
ISSN (online)	1878-3686
ISSN	1535-6108
DOI	10.1016/j.ccell.2017.01.001
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Zs.A 5650: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (2.OG) ab Jg. 2022: Lesesaal (EG)
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Article: The Prognostic Significance of Low-Frequency Somatic Mutations in Metastatic Cutaneous Melanoma.

Zhao, Xiaobei / Little, Paul / Hoyle, Alan P / Pegna, Guillaume J / Hayward, Michele C / Ivanova, Anastasia / Parker, Joel S / Marron, David L / Soloway, Matthew G / Jo, Heejoon / Salazar, Ashley H / Papakonstantinou, Michael P / Bouchard, Deeanna M / Jefferys, Stuart R / Hoadley, Katherine A / Ollila, David W / Frank, Jill S / Thomas, Nancy E / Googe, Paul B /

Ezzell, Ashley J / Collichio, Frances A / Lee, Carrie B / Earp, H Shelton / Sharpless, Norman E / Hugo, Willy / Wilmott, James S / Quek, Camelia / Waddell, Nicola / Johansson, Peter A / Thompson, John F / Hayward, Nicholas K / Mann, Graham J / Lo, Roger S / Johnson, Douglas B / Scolyer, Richard A / Hayes, D Neil / Moschos, Stergios J

Frontiers in oncology

2019 Volume 8, Page(s) 584

Abstract: Background: ...

Abstract	Background:
Language	English
Publishing date	2019-01-04
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2649216-7
ISSN	2234-943X
ISSN	2234-943X
DOI	10.3389/fonc.2018.00584
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Article: Comprehensive and Integrated Genomic Characterization of Adult Soft Tissue Sarcomas

Abeshouse, Adam / Adebamowo, Clement / Adebamowo, Sally N / Akbani, Rehan / Akeredolu, Teniola / Ally, Adrian / Anderson, Matthew L / Anur, Pavana / Appelbaum, Elizabeth L / Armenia, Joshua / Auman, J. Todd / Bailey, Matthew H / Baker, Laurence / Balasundaram, Miruna / Balu, Saianand / Barthel, Floris P / Bartlett, John / Baylin, Stephen B / Behera, Madhusmita /

Belyaev, Dmitry / Bennett, Joesph / Benz, Christopher / Beroukhim, Rameen / Birrer, Michael / Bocklage, Thèrése / Bodenheimer, Tom / Boice, Lori / Bootwalla, Moiz S / Bowen, Jay / Bowlby, Reanne / Boyd, Jeff / Brohl, Andrew S / Brooks, Denise / Byers, Lauren / Carlsen, Rebecca / Castro, Patricia / Chen, Hsiao-Wei / Cherniack, Andrew D / Chibon, Fréderic / Chin, Lynda / Cho, Juok / Chuah, Eric / Chudamani, Sudha / Cibulskis, Carrie / Cooper, Lee A.D / Cope, Leslie / Cordes, Matthew G / Crain, Daniel / Curley, Erin / Danilova, Ludmila / Dao, Fanny / Davis, Ian J / Davis, Lara E / Defreitas, Timothy / Delman, Keith / Demchok, John A / Demetri, George D / Demicco, Elizabeth G / Dhalla, Noreen / Diao, Lixia / Ding, Li / DiSaia, Phil / Dottino, Peter / Doyle, Leona A / Drill, Esther / Dubina, Michael / Eschbacher, Jennifer / Fedosenko, Konstantin / Felau, Ina / Ferguson, Martin L / Frazer, Scott / Fronick, Catrina C / Fulidou, Victoria / Fulton, Lucinda A / Fulton, Robert S / Gabriel, Stacey B / Gao, Jianjiong / Gao, Qingsong / Gardner, Johanna / Gastier-Foster, Julie M / Gay, Carl M / Gehlenborg, Nils / Gerken, Mark / Getz, Gad / Godwin, Andrew K / Godwin, Eryn M / Gordienko, Elena / Grilley-Olson, Juneko E / Gutman, David A / Gutmann, David H / Hayes, D. Neil / Hegde, Apurva M / Heiman, David I / Heins, Zachary / Helsel, Carmen / Hepperla, Austin J / Higgins, Kelly / Hoadley, Katherine A / Hobensack, Shital / Holt, Robert A / Hoon, Dave B / Hornick, Jason L / Hoyle, Alan P / Hu, Xin / Huang, Mei / Hutter, Carolyn M / Iacocca, Mary / Ingram, Davis R / Ittmann, Michael / Iype, Lisa / Jefferys, Stuart R / Jones, Kevin B / Jones, Corbin D / Jones, Steven J.M / Kalir, Tamara / Karlan, Beth Y / Karseladze, Apollon / Kasaian, Katayoon / Kim, Jaegil / Kundra, Ritika / Kuo, Hanluen / Ladanyi, Marc / Lai, Phillip H / Laird, Peter W / Larsson, Erik / Lawrence, Michael S / Lazar, Alexander J / Lee, Sanghoon / Lee, Darlene / Lehmann, Kjong-Van / Leraas, Kristen M / Lester, Jenny / Levine, Douglas A / Li, Irene / Lichtenberg, Tara M / Lin, Pei / Liu, Jia / Liu, Wenbin / Liu, Eric Minwei / Lolla, Laxmi / Lu, Yiling / Ma, Yussanne / Madan, Rashna / Maglinte, Dennis T / Magliocco, Anthony / Maki, Robert G / Mallery, David / Manikhas, Georgy / Mardis, Elaine R / Mariamidze, Armaz / Marra, Marco A / Martignetti, John A / Martinez, Cathleen / Mayo, Michael / McLellan, Michael D / Meier, Sam / Meng, Shaowu / Meyerson, Matthew / Mieczkowski, Piotr A / Miller, Christopher A / Mills, Gordon B / Moore, Richard A / Morris, Scott / Mose, Lisle E / Mozgovoy, Evgeny / Mungall, Andrew J / Mungall, Karen / Nalisnik, Michael / Naresh, Rashi / Newton, Yulia / Noble, Michael S / Novak, Janet E / Ochoa, Angelica / Olvera, Narciso / Owonikoko, Taofeek K / Paklina, Oxana / Parfitt, Jeremy / Parker, Joel S / Pastore, Alessandro / Paulauskis, Joseph / Penny, Robert / Pereira, Elena / Perou, Charles M / Perou, Amy H / Pihl, Todd / Pollock, Raphael E / Potapova, Olga / Radenbaugh, Amie J / Ramalingam, Suresh S / Ramirez, Nilsa C / Rathmell, W. Kimryn / Raut, Chandrajit P / Riedel, Richard F / Reilly, Colleen / Reynolds, Sheila M / Roach, Jeffrey / Robertson, A. Gordon / Roszik, Jason / Rubin, Brian P / Sadeghi, Sara / Saksena, Gordon / Salner, Andrew / Sanchez-Vega, Francisco / Sander, Chris / Schein, Jacqueline E / Schmidt, Heather K / Schultz, Nikolaus / Schumacher, Steven E / Sekhon, Harman / Senbabaoglu, Yasin / Setdikova, Galiya / Shelton, Candace / Shelton, Troy / Shen, Ronglai / Shi, Yan / Shih, Juliann / Shmulevich, Ilya / Sica, Gabriel L / Simons, Janae V / Singer, Samuel / Sipahimalani, Payal / Skelly, Tara / Socci, Nicholas / Sofia, Heidi J / Soloway, Matthew G / Spellman, Paul / Sun, Qiang / Swanson, Patricia / Tam, Angela / Tan, Donghui / Tarnuzzer, Roy / Thiessen, Nina / Thompson, Eric / Thorne, Leigh B / Tong, Pan / Torres, Keila E / van de Rijn, Matt / Van Den Berg, David J / Van Tine, Brian A / Veluvolu, Umadevi / Verhaak, Roel / Voet, Doug / Voronina, Olga / Wan, Yunhu / Wang, Zhining / Wang, Jing / Weinstein, John N / Weisenberger, Daniel J / Wilkerson, Matthew D / Wilson, Richard K / Wise, Lisa / Wong, Tina / Wong, Winghing / Wrangle, John / Wu, Ye / Wyczalkowski, Matthew / Yang, Liming / Yau, Christina / Yellapantula, Venkata / Zenklusen, Jean C / Zhang, Jiashan (Julia) / Zhang, Hailei / Zhang, Hongxin / Zmuda, Erik

Cell. 2017 Nov. 02, v. 171, no. 4

2017

Abstract: Sarcomas are a broad family of mesenchymal malignancies exhibiting remarkable histologic diversity. We describe the multi-platform molecular landscape of 206 adult soft tissue sarcomas representing 6 major types. Along with novel insights into the ... ...

Institution	The Cancer Genome Atlas Research Network
Abstract	Sarcomas are a broad family of mesenchymal malignancies exhibiting remarkable histologic diversity. We describe the multi-platform molecular landscape of 206 adult soft tissue sarcomas representing 6 major types. Along with novel insights into the biology of individual sarcoma types, we report three overarching findings: (1) unlike most epithelial malignancies, these sarcomas (excepting synovial sarcoma) are characterized predominantly by copy-number changes, with low mutational loads and only a few genes (TP53, ATRX, RB1) highly recurrently mutated across sarcoma types; (2) within sarcoma types, genomic and regulomic diversity of driver pathways defines molecular subtypes associated with patient outcome; and (3) the immune microenvironment, inferred from DNA methylation and mRNA profiles, associates with outcome and may inform clinical trials of immune checkpoint inhibitors. Overall, this large-scale analysis reveals previously unappreciated sarcoma-type-specific changes in copy number, methylation, RNA, and protein, providing insights into refining sarcoma therapy and relationships to other cancer types.
Keywords	DNA methylation ; adults ; clinical trials ; epithelium ; genes ; genomics ; histology ; messenger RNA ; patients ; sarcoma ; therapeutics
Language	English
Dates of publication	2017-1102
Size	p. 950-965.e28.
Publishing place	Elsevier Inc.
Document type	Article
ZDB-ID	187009-9
ISSN	1097-4172 ; 0092-8674
ISSN (online)	1097-4172
ISSN	0092-8674
DOI	10.1016/j.cell.2017.10.014
Database	NAL-Catalogue (AGRICOLA)

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Article ; Online: Comprehensive Molecular Characterization of Papillary Renal-Cell Carcinoma.

Linehan, W Marston / Spellman, Paul T / Ricketts, Christopher J / Creighton, Chad J / Fei, Suzanne S / Davis, Caleb / Wheeler, David A / Murray, Bradley A / Schmidt, Laura / Vocke, Cathy D / Peto, Myron / Al Mamun, Abu Amar M / Shinbrot, Eve / Sethi, Anurag / Brooks, Samira / Rathmell, W Kimryn / Brooks, Angela N / Hoadley, Katherine A / Robertson, A Gordon /

Brooks, Denise / Bowlby, Reanne / Sadeghi, Sara / Shen, Hui / Weisenberger, Daniel J / Bootwalla, Moiz / Baylin, Stephen B / Laird, Peter W / Cherniack, Andrew D / Saksena, Gordon / Haake, Scott / Li, Jun / Liang, Han / Lu, Yiling / Mills, Gordon B / Akbani, Rehan / Leiserson, Mark D M / Raphael, Benjamin J / Anur, Pavana / Bottaro, Donald / Albiges, Laurence / Barnabas, Nandita / Choueiri, Toni K / Czerniak, Bogdan / Godwin, Andrew K / Hakimi, A Ari / Ho, Thai H / Hsieh, James / Ittmann, Michael / Kim, William Y / Krishnan, Bhavani / Merino, Maria J / Mills Shaw, Kenna R / Reuter, Victor E / Reznik, Ed / Shelley, Carl S / Shuch, Brian / Signoretti, Sabina / Srinivasan, Ramaprasad / Tamboli, Pheroze / Thomas, George / Tickoo, Satish / Burnett, Kenneth / Crain, Daniel / Gardner, Johanna / Lau, Kevin / Mallery, David / Morris, Scott / Paulauskis, Joseph D / Penny, Robert J / Shelton, Candace / Shelton, W Troy / Sherman, Mark / Thompson, Eric / Yena, Peggy / Avedon, Melissa T / Bowen, Jay / Gastier-Foster, Julie M / Gerken, Mark / Leraas, Kristen M / Lichtenberg, Tara M / Ramirez, Nilsa C / Santos, Tracie / Wise, Lisa / Zmuda, Erik / Demchok, John A / Felau, Ina / Hutter, Carolyn M / Sheth, Margi / Sofia, Heidi J / Tarnuzzer, Roy / Wang, Zhining / Yang, Liming / Zenklusen, Jean C / Zhang, Jiashan / Ayala, Brenda / Baboud, Julien / Chudamani, Sudha / Liu, Jia / Lolla, Laxmi / Naresh, Rashi / Pihl, Todd / Sun, Qiang / Wan, Yunhu / Wu, Ye / Ally, Adrian / Balasundaram, Miruna / Balu, Saianand / Beroukhim, Rameen / Bodenheimer, Tom / Buhay, Christian / Butterfield, Yaron S N / Carlsen, Rebecca / Carter, Scott L / Chao, Hsu / Chuah, Eric / Clarke, Amanda / Covington, Kyle R / Dahdouli, Mahmoud / Dewal, Ninad / Dhalla, Noreen / Doddapaneni, Harsha V / Drummond, Jennifer A / Gabriel, Stacey B / Gibbs, Richard A / Guin, Ranabir / Hale, Walker / Hawes, Alicia / Hayes, D Neil / Holt, Robert A / Hoyle, Alan P / Jefferys, Stuart R / Jones, Steven J M / Jones, Corbin D / Kalra, Divya / Kovar, Christie / Lewis, Lora / Li, Jie / Ma, Yussanne / Marra, Marco A / Mayo, Michael / Meng, Shaowu / Meyerson, Matthew / Mieczkowski, Piotr A / Moore, Richard A / Morton, Donna / Mose, Lisle E / Mungall, Andrew J / Muzny, Donna / Parker, Joel S / Perou, Charles M / Roach, Jeffrey / Schein, Jacqueline E / Schumacher, Steven E / Shi, Yan / Simons, Janae V / Sipahimalani, Payal / Skelly, Tara / Soloway, Matthew G / Sougnez, Carrie / Tam, Angela / Tan, Donghui / Thiessen, Nina / Veluvolu, Umadevi / Wang, Min / Wilkerson, Matthew D / Wong, Tina / Wu, Junyuan / Xi, Liu / Zhou, Jane / Bedford, Jason / Chen, Fengju / Fu, Yao / Gerstein, Mark / Haussler, David / Kasaian, Katayoon / Lai, Phillip / Ling, Shiyun / Radenbaugh, Amie / Van Den Berg, David / Weinstein, John N / Zhu, Jingchun / Albert, Monique / Alexopoulou, Iakovina / Andersen, Jeremiah J / Auman, J Todd / Bartlett, John / Bastacky, Sheldon / Bergsten, Julie / Blute, Michael L / Boice, Lori / Bollag, Roni J / Boyd, Jeff / Castle, Erik / Chen, Ying-Bei / Cheville, John C / Curley, Erin / Davies, Benjamin / DeVolk, April / Dhir, Rajiv / Dike, Laura / Eckman, John / Engel, Jay / Harr, Jodi / Hrebinko, Ronald / Huang, Mei / Huelsenbeck-Dill, Lori / Iacocca, Mary / Jacobs, Bruce / Lobis, Michael / Maranchie, Jodi K / McMeekin, Scott / Myers, Jerome / Nelson, Joel / Parfitt, Jeremy / Parwani, Anil / Petrelli, Nicholas / Rabeno, Brenda / Roy, Somak / Salner, Andrew L / Slaton, Joel / Stanton, Melissa / Thompson, R Houston / Thorne, Leigh / Tucker, Kelinda / Weinberger, Paul M / Winemiller, Cynthia / Zach, Leigh Anne / Zuna, Rosemary

The New England journal of medicine

2016 Volume 374, Issue 2, Page(s) 135–145

Abstract: Background: Papillary renal-cell carcinoma, which accounts for 15 to 20% of renal-cell carcinomas, is a heterogeneous disease that consists of various types of renal cancer, including tumors with indolent, multifocal presentation and solitary tumors ... ...

Abstract	Background: Papillary renal-cell carcinoma, which accounts for 15 to 20% of renal-cell carcinomas, is a heterogeneous disease that consists of various types of renal cancer, including tumors with indolent, multifocal presentation and solitary tumors with an aggressive, highly lethal phenotype. Little is known about the genetic basis of sporadic papillary renal-cell carcinoma, and no effective forms of therapy for advanced disease exist. Methods: We performed comprehensive molecular characterization of 161 primary papillary renal-cell carcinomas, using whole-exome sequencing, copy-number analysis, messenger RNA and microRNA sequencing, DNA-methylation analysis, and proteomic analysis. Results: Type 1 and type 2 papillary renal-cell carcinomas were shown to be different types of renal cancer characterized by specific genetic alterations, with type 2 further classified into three individual subgroups on the basis of molecular differences associated with patient survival. Type 1 tumors were associated with MET alterations, whereas type 2 tumors were characterized by CDKN2A silencing, SETD2 mutations, TFE3 fusions, and increased expression of the NRF2-antioxidant response element (ARE) pathway. A CpG island methylator phenotype (CIMP) was observed in a distinct subgroup of type 2 papillary renal-cell carcinomas that was characterized by poor survival and mutation of the gene encoding fumarate hydratase (FH). Conclusions: Type 1 and type 2 papillary renal-cell carcinomas were shown to be clinically and biologically distinct. Alterations in the MET pathway were associated with type 1, and activation of the NRF2-ARE pathway was associated with type 2; CDKN2A loss and CIMP in type 2 conveyed a poor prognosis. Furthermore, type 2 papillary renal-cell carcinoma consisted of at least three subtypes based on molecular and phenotypic features. (Funded by the National Institutes of Health.).
MeSH term(s)	Carcinoma, Papillary/genetics ; Carcinoma, Papillary/metabolism ; CpG Islands/physiology ; DNA Methylation ; Humans ; Kidney Neoplasms/genetics ; Kidney Neoplasms/metabolism ; MicroRNAs/chemistry ; Mutation ; NF-E2-Related Factor 2/genetics ; NF-E2-Related Factor 2/metabolism ; Phenotype ; Proto-Oncogene Proteins c-met/chemistry ; Proto-Oncogene Proteins c-met/genetics ; Proto-Oncogene Proteins c-met/metabolism ; RNA, Messenger/chemistry ; RNA, Neoplasm/chemistry ; Sequence Analysis, RNA ; Signal Transduction/physiology
Chemical Substances	MicroRNAs ; NF-E2-Related Factor 2 ; NFE2L2 protein, human ; RNA, Messenger ; RNA, Neoplasm ; MET protein, human (EC 2.7.10.1) ; Proto-Oncogene Proteins c-met (EC 2.7.10.1)
Language	English
Publishing date	2016-01-14
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	207154-x
ISSN	1533-4406 ; 0028-4793
ISSN (online)	1533-4406
ISSN	0028-4793
DOI	10.1056/NEJMoa1505917
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: Perspective on Oncogenic Processes at the End of the Beginning of Cancer Genomics

Ding, Li / Bailey, Matthew H. / Porta-Pardo, Eduard / Thorsson, Vesteinn / Colaprico, Antonio / Bertrand, Denis / Gibbs, David L. / Weerasinghe, Amila / Huang, Kuan-lin / Tokheim, Collin / Cortés-Ciriano, Isidro / Jayasinghe, Reyka / Chen, Feng / Yu, Lihua / Sun, Sam / Olsen, Catharina / Kim, Jaegil / Taylor, Alison M. / Cherniack, Andrew D. /

Akbani, Rehan / Suphavilai, Chayaporn / Nagarajan, Niranjan / Stuart, Joshua M. / Mills, Gordon B. / Wyczalkowski, Matthew A. / Vincent, Benjamin G. / Hutter, Carolyn M. / Zenklusen, Jean Claude / Hoadley, Katherine A. / Wendl, Michael C. / Shmulevich, llya / Lazar, Alexander / Wheeler, David A. / Getz, Gad / Caesar-Johnson, Samantha J. / Demchok, John A. / Felau, Ina / Kasapi, Melpomeni / Ferguson, Martin L. / Sofia, Heidi J. / Tarnuzzer, Roy / Wang, Zhining / Yang, Liming / Zenklusen, Jean C. / Zhang, Jiashan (Julia) / Chudamani, Sudha / Liu, Jia / Lolla, Laxmi / Naresh, Rashi / Pihl, Todd / Sun, Qiang / Wan, Yunhu / Wu, Ye / Cho, Juok / DeFreitas, Timothy / Frazer, Scott / Gehlenborg, Nils / Heiman, David I. / Lawrence, Michael S. / Lin, Pei / Meier, Samuel A. / Noble, Michael S. / Saksena, Gordon / Voet, Doug / Zhang, Hailei / Bernard, Brady / Chambwe, Nyasha / Dhankani, Varsha / Knijnenburg, Theo / Kramer, Roger / Leinonen, Kalle / Liu, Yuexin / Miller, Michael / Reynolds, Sheila / Shmulevich, Ilya / Zhang, Wei / Broom, Bradley M. / Hegde, Apurva M. / Ju, Zhenlin / Kanchi, Rupa S. / Korkut, Anil / Li, Jun / Liang, Han / Ling, Shiyun / Liu, Wenbin / Lu, Yiling / Ng, Kwok-Shing / Rao, Arvind / Ryan, Michael / Wang, Jing / Weinstein, John N. / Zhang, Jiexin / Abeshouse, Adam / Armenia, Joshua / Chakravarty, Debyani / Chatila, Walid K. / de Bruijn, Ino / Gao, Jianjiong / Gross, Benjamin E. / Heins, Zachary J. / Kundra, Ritika / La, Konnor / Ladanyi, Marc / Luna, Augustin / Nissan, Moriah G. / Ochoa, Angelica / Phillips, Sarah M. / Reznik, Ed / Sanchez-Vega, Francisco / Sander, Chris / Schultz, Nikolaus / Sheridan, Robert / Sumer, S. Onur / Sun, Yichao / Taylor, Barry S. / Wang, Jioajiao / Zhang, Hongxin / Anur, Pavana / Peto, Myron / Spellman, Paul / Benz, Christopher / Wong, Christopher K. / Yau, Christina / Hayes, D. Neil / Parker, Joel S. / Wilkerson, Matthew D. / Ally, Adrian / Balasundaram, Miruna / Bowlby, Reanne / Brooks, Denise / Carlsen, Rebecca / Chuah, Eric / Dhalla, Noreen / Holt, Robert / Jones, Steven J.M. / Kasaian, Katayoon / Lee, Darlene / Ma, Yussanne / Marra, Marco A. / Mayo, Michael / Moore, Richard A. / Mungall, Andrew J. / Mungall, Karen / Robertson, A. Gordon / Sadeghi, Sara / Schein, Jacqueline E. / Sipahimalani, Payal / Tam, Angela / Thiessen, Nina / Tse, Kane / Wong, Tina / Berger, Ashton C. / Beroukhim, Rameen / Cibulskis, Carrie / Gabriel, Stacey B. / Gao, Galen F. / Ha, Gavin / Meyerson, Matthew / Schumacher, Steven E. / Shih, Juliann / Kucherlapati, Melanie H. / Kucherlapati, Raju S. / Baylin, Stephen / Cope, Leslie / Danilova, Ludmila / Bootwalla, Moiz S. / Lai, Phillip H. / Maglinte, Dennis T. / Van Den Berg, David J. / Weisenberger, Daniel J. / Auman, J. Todd / Balu, Saianand / Bodenheimer, Thomas / Fan, Cheng / Hoyle, Alan P. / Jefferys, Stuart R. / Jones, Corbin D. / Meng, Shaowu / Mieczkowski, Piotr A. / Mose, Lisle E. / Perou, Amy H. / Perou, Charles M. / Roach, Jeffrey / Shi, Yan / Simons, Janae V. / Skelly, Tara / Soloway, Matthew G. / Tan, Donghui / Veluvolu, Umadevi / Fan, Huihui / Hinoue, Toshinori / Laird, Peter W. / Shen, Hui / Zhou, Wanding / Bellair, Michelle / Chang, Kyle / Covington, Kyle / Creighton, Chad J. / Dinh, Huyen / Doddapaneni, HarshaVardhan / Donehower, Lawrence A. / Drummond, Jennifer / Gibbs, Richard / Glenn, Robert / Hale, Walker / Han, Yi / Hu, Jianhong / Korchina, Viktoriya / Lee, Sandra / Lewis, Lora / Li, Wei / Liu, Xiuping / Morgan, Margaret / Morton, Donna / Muzny, Donna / Santibanez, Jireh / Sheth, Margi / Shinbrot, Eve / Wang, Linghua / Wang, Min / Xi, Liu / Zhao, Fengmei / Hess, Julian / Appelbaum, Elizabeth L. / Bailey, Matthew / Cordes, Matthew G. / Fronick, Catrina C. / Fulton, Lucinda A. / Fulton, Robert S. / Kandoth, Cyriac / Mardis, Elaine R. / McLellan, Michael D. / Miller, Christopher A. / Schmidt, Heather K. / Wilson, Richard K. / Crain, Daniel / Curley, Erin / Gardner, Johanna / Lau, Kevin / Mallery, David / Morris, Scott / Paulauskis, Joseph / Penny, Robert / Shelton, Candace / Shelton, Troy / Sherman, Mark / Thompson, Eric / Yena, Peggy / Bowen, Jay / Gastier-Foster, Julie M. / Gerken, Mark / Leraas, Kristen M. / Lichtenberg, Tara M. / Ramirez, Nilsa C. / Wise, Lisa / Zmuda, Erik / Corcoran, Niall / Costello, Tony / Hovens, Christopher / Carvalho, Andre L. / de Carvalho, Ana C. / Fregnani, José H. / Filho, Adhemar Longatto / Reis, Rui M. / Scapulatempo-Neto, Cristovam / Silveira, Henrique C.S. / Vidal, Daniel O. / Burnette, Andrew / Eschbacher, Jennifer / Hermes, Beth / Noss, Ardene / Singh, Rosy / Anderson, Matthew L. / Castro, Patricia D. / Ittmann, Michael / Huntsman, David / Kohl, Bernard / Lệ Xuân / Thorp, Richard / Andry, Chris / Duffy, Elizabeth R. / Lyadov, Vladimir / Paklina, Oxana / Setdikova, Galiya / Shabunin, Alexey / Tavobilov, Mikhail / McPherson, Christopher / Warnick, Ronald / Berkowitz, Ross / Cramer, Daniel / Feltmate, Colleen / Horowitz, Neil / Kibel, Adam / Muto, Michael / Raut, Chandrajit P. / Malykh, Andrei / Barnholtz-Sloan, Jill S. / Barrett, Wendi / Devine, Karen / Fulop, Jordonna / Ostrom, Quinn T. / Shimmel, Kristen / Wolinsky, Yingli / Sloan, Andrew E. / De Rose, Agostino / Giuliante, Felice / Goodman, Marc / Karlan, Beth Y. / Hagedorn, C. H. / Eckman, John / Harr, Jodi / Myers, Jerome / Tucker, Kelinda / Zach, Leigh Anne / Deyarmin, Brenda / Hu, Hai / Kvecher, Leonid / Larson, Caroline / Mural, Richard J. / Somiari, Stella / Vicha, Ales / Zelinka, Tomas / Bennett, Joseph / Iacocca, Mary / Rabeno, Brenda / Swanson, Patricia / Latour, Mathieu / Lacombe, Louis / Têtu, Bernard / Bergeron, Alain / McGraw, Mary / Staugaitis, Susan M. / Chabot, John / Hibshoosh, Hanina / Sepulveda, Antonia / Su, Tao / Wang, Timothy / Potapova, Olga / Voronina, Olga / Desjardins, Laurence / Mariani, Odette / Roman-Roman, Sergio / Sastre, Xavier / Stern, Marc-Henri / Cheng, Feixiong / Signoretti, Sabina / Berchuck, Andrew / Bigner, Darell / Lipp, Eric / Marks, Jeffrey / McCall, Shannon / McLendon, Roger / Secord, Angeles / Sharp, Alexis / Behera, Madhusmita / Brat, Daniel J. / Chen, Amy / Delman, Keith / Force, Seth / Khuri, Fadlo / Magliocca, Kelly / Maithel, Shishir / Olson, Jeffrey J. / Owonikoko, Taofeek / Pickens, Alan / Ramalingam, Suresh / Shin, Dong M. / Sica, Gabriel / Van Meir, Erwin G. / Zhang, Hongzheng / Eijckenboom, Wil / Gillis, Ad / Korpershoek, Esther / Looijenga, Leendert / Oosterhuis, Wolter / Stoop, Hans / van Kessel, Kim E. / Zwarthoff, Ellen C. / Calatozzolo, Chiara / Cuppini, Lucia / Cuzzubbo, Stefania / DiMeco, Francesco / Finocchiaro, Gaetano / Mattei, Luca / Perin, Alessandro / Pollo, Bianca / Chen, Chu / Houck, John / Lohavanichbutr, Pawadee / Hartmann, Arndt / Stoehr, Christine / Stoehr, Robert / Taubert, Helge / Wach, Sven / Wullich, Bernd / Kycler, Witold / Murawa, Dawid / Wiznerowicz, Maciej / Chung, Ki / Edenfield, W. 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Cell. 2018 Apr. 05, v. 173, no. 2 p.305-320.e10

2018

Abstract: The Cancer Genome Atlas (TCGA) has catalyzed systematic characterization of diverse genomic alterations underlying human cancers. At this historic junction marking the completion of genomic characterization of over 11,000 tumors from 33 cancer types, we ... ...

Institution	The Cancer Genome Atlas Research Network
Abstract	The Cancer Genome Atlas (TCGA) has catalyzed systematic characterization of diverse genomic alterations underlying human cancers. At this historic junction marking the completion of genomic characterization of over 11,000 tumors from 33 cancer types, we present our current understanding of the molecular processes governing oncogenesis. We illustrate our insights into cancer through synthesis of the findings of the TCGA PanCancer Atlas project on three facets of oncogenesis: (1) somatic driver mutations, germline pathogenic variants, and their interactions in the tumor; (2) the influence of the tumor genome and epigenome on transcriptome and proteome; and (3) the relationship between tumor and the microenvironment, including implications for drugs targeting driver events and immunotherapies. These results will anchor future characterization of rare and common tumor types, primary and relapsed tumors, and cancers across ancestry groups and will guide the deployment of clinical genomic sequencing.
Keywords	ancestry ; carcinogenesis ; epigenome ; genomics ; germ cells ; humans ; neoplasms ; proteome ; transcriptome ; oncogenic process ; TCGA ; omics ; cancer ; cancer genomics
Language	English
Dates of publication	2018-0405
Size	p. 305-320.e10.
Publishing place	Elsevier Inc.
Document type	Article ; Online
Note	NAL-AP-2-clean ; Resource is Open Access
ZDB-ID	187009-9
ISSN	1097-4172 ; 0092-8674
ISSN (online)	1097-4172
ISSN	0092-8674
DOI	10.1016/j.cell.2018.03.033
Database	NAL-Catalogue (AGRICOLA)

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