Menée sur 86 lignées cellulaires de cancer et à partir de données portant sur 3 131 échantillons tumoraux, cette étude identifie des gènes dont dépendent les cellules cancéreuses qui, en raison d'une instabilité génomique, ont par ailleurs subi une perte de gènes suppresseurs de tumeurs

Cancer Vulnerabilities Unveiled by Genomic Loss

Nijhawan, Deepak ; Zack, Travis I ; Ren, Yin ; Strickland, Matthew R ; Lamothe, Rebecca ; Schumacher, Steven E ; Tsherniak, Aviad ; Besche, Henrike C ; Rosenbluh, Joseph ; Shehata, Shyemaa ; Cowley, Glenn S ; Weir, Barbara A ; Goldberg, Alfred L ; Mesirov, Jill P ; Root, David E ; Bhatia, Sangeeta N ; Beroukhim, Rameen ; Hahn, William C

Due to genome instability, most cancers exhibit loss of regions containing tumor suppressor genes and collateral loss of other genes. To identify cancer-specific vulnerabilities that are the result of copy number losses, we performed integrated analyses of genome-wide copy number and RNAi profiles and identified 56 genes for which gene suppression specifically inhibited the proliferation of cells harboring partial copy number loss of that gene. These CYCLOPS (copy number alterations yielding [...]

Menée à partir d'échantillons de tissu tumoral et de tissu sain prélevés sur 226 patients atteints de cinq types de cancer, cette étude identifie la fréquence des mutations somatiques et germinales du génome mitochondrial selon chaque type de cancer

Spectrum of somatic mitochondrial mutations in five cancers

Larman, Tatianna C. ; DePalma, Steven R. ; Hadjipanayis, Angela G. ; The Cancer Genome Atlas Research Network ; Protopopov, Alexei ; Zhang, Jianhua ; Gabriel, Stacey B. ; Chin, Lynda ; Seidman, Christine E. ; Kucherlapati, Raju ; Seidman, J. G.

Somatic mtDNA mutations have been reported in some human tumors, but their spectrum in different malignancies and their role in cancer development remain incompletely understood. Here, we describe the breadth of somatic and inherited mutations across the mitochondrial genome by sequence analyses of paired tumor and normal tissue samples from 226 individuals with five types of cancer using whole-genome data generated by The Cancer Genome Atlas Research Network. The frequencies of deleterious [...]

Cet article passe en revue les études qui, menées à l'aide de techniques de séquençage du génome entier, mettent en évidence le rôle oncogénique des mutations structurales somatiques des chromosomes

Structural mutations in cancer: mechanistic and functional insights

Inaki, Koichiro ; Liu, Edison T.

Next-generation sequencing (NGS) has enabled the comprehensive and precise identification of many somatic structural mutations in cancer. Analyses integrating point mutation information with data on rearrangements and copy number variation have revealed a higher-order organization of the seemingly random genetic events that lead to cancer. These meta-analyses provide a more refined view of the mutational mechanisms, genomic evolution, and combinations of mutations that contribute to [...]

Cet article passe en revue les travaux récents sur le rôle de mutations d'éléments régulateurs épigénétiques dans les néoplasies myéloprolifératives, les syndromes myélodysplasiques et les leucémies myéloïdes aiguës

The role of mutations in epigenetic regulators in myeloid malignancies

Shih, Alan H. ; Abdel-Wahab, Omar ; Patel, Jay P. ; Levine, Ross L.

Recent genomic studies have identified novel recurrent somatic mutations in patients with myeloid malignancies, including myeloproliferative neoplasms (MPNs), myelodysplastic syndrome (MDS) and acute myeloid leukaemia (AML). In some cases these mutations occur in genes with known roles in regulating chromatin and/or methylation states in haematopoietic progenitors, and in other cases genetic and functional studies have elucidated a role for specific mutations in altering epigenetic patterning [...]

Menée sur 147 échantillons tumoraux prélevés sur des patients atteints d'un mélanome, cette étude de séquençage des exons identifie des mutations somatiques du gène RAC1 en association avec une exposition aux rayonnements ultra-violets

Exome sequencing identifies recurrent somatic RAC1 mutations in melanoma

Krauthammer, Michael ; Kong, Yong ; Ha, Byung Hak ; Evans, Perry ; Bacchiocchi, Antonella ; McCusker, James P. ; Cheng, Elaine ; Davis, Matthew J. ; Goh, Gerald ; Choi, Murim ; Ariyan, Stephan ; Narayan, Deepak ; Dutton-Regester, Ken ; Capatana, Ana ; Holman, Edna C. ; Bosenberg, Marcus ; Sznol, Mario ; Kluger, Harriet M. ; Brash, Douglas E. ; Stern, David F. ; Materin, Miguel A. ; Lo, Roger S. ; Mane, Shrikant ; Ma, Shuangge ; Kidd, Kenneth K. ; Hayward, Nicholas K. ; Lifton, Richard P. ; Schlessinger, Joseph ; Boggon, Titus J. ; Halaban, Ruth

We characterized the mutational landscape of melanoma, the form of skin cancer with the highest mortality rate, by sequencing the exomes of 147 melanomas. Sun-exposed melanomas had markedly more ultraviolet (UV)-like C>T somatic mutations compared to sun-shielded acral, mucosal and uveal melanomas. Among the newly identified cancer genes was PPP6C, encoding a serine/threonine phosphatase, which harbored mutations that clustered in the active site in 12% of sun-exposed melanomas, exclusively in [...]

Menée sur 70 paires d'échantillons de tissu tumoral et de tissu sain prélevés sur des patients atteints d'un cancer du côlon, cette étude identifie des fusions de gènes de la famille des R-spondines associées à une activation de la signalisation Wnt et à la tumorigenèse

Recurrent R-spondin fusions in colon cancer

Seshagiri, Somasekar ; Stawiski, Eric W. ; Durinck, Steffen ; Modrusan, Zora ; Storm, Elaine E. ; Conboy, Caitlin B. ; Chaudhuri, Subhra ; Guan, Yinghui ; Janakiraman, Vasantharajan ; Jaiswal, Bijay S. ; Guillory, Joseph ; Ha, Connie ; Dijkgraaf, Gerrit J. P. ; Stinson, Jeremy ; Gnad, Florian ; Huntley, Melanie A. ; Degenhardt, Jeremiah D. ; Haverty, Peter M. ; Bourgon, Richard ; Wang, Weiru ; Koeppen, Hartmut ; Gentleman, Robert ; Starr, Timothy K. ; Zhang, Zemin ; Largaespada, David A. ; Wu, Thomas D. ; de Sauvage, Frederic J.

Identifying and understanding changes in cancer genomes is essential for the development of targeted therapeutics. Here we analyse systematically more than 70 pairs of primary human colon tumours by applying next-generation sequencing to characterize their exomes, transcriptomes and copy-number alterations. We have identified 36,303 protein-altering somatic changes that include several new recurrent mutations in the Wnt pathway gene TCF7L2, chromatin-remodelling genes such as TET2 and TET3 and [...]

Cette étude évalue la faisabilité d'un dispositif permettant de mettre en évidence des fusions de télomères dans les tissus de tumeurs du sein

Telomere fusions in early human breast carcinoma

Tanaka, Hiromi ; Abe, Satoshi ; Huda, Nazmul ; Tu, LiRen ; Beam, Matthew J. ; Grimes, Brenda ; Gilley, David

Several lines of evidence suggest that defects in telomere maintenance play a significant role in the initiation of genomic instability during carcinogenesis. Although the general concept of defective telomere maintenance initiating genomic instability has been acknowledged, there remains a critical gap in the direct evidence of telomere dysfunction in human solid tumors. To address this topic, we devised a multiplex PCR-based assay, termed TAR (telomere-associated repeat) fusion PCR, to detect [...]

Menée sur 97 échantillons tumoraux prélevés sur des patients atteints d'un glioblastome multiforme, cette étude identifie la présence d'une fusion des gènes FGFR et TACC dans 3% des tumeurs

Transforming Fusions of FGFR and TACC Genes in Human Glioblastoma

Singh, Devendra ; Chan, Joseph Minhow ; Zoppoli, Pietro ; Niola, Francesco ; Sullivan, Ryan ; Castano, Angelica ; Liu, Eric Minwei ; Reichel, Jonathan ; Porrati, Paola ; Pellegatta, Serena ; Qiu, Kunlong ; Gao, Zhibo ; Ceccarelli, Michele ; Riccardi, Riccardo ; Brat, Daniel J. ; Guha, Abhijit ; Aldape, Ken ; Golfinos, John G. ; Zagzag, David ; Mikkelsen, Tom ; Finocchiaro, Gaetano ; Lasorella, Anna ; Rabadan, Raul ; Iavarone, Antonio

The brain tumor glioblastoma multiforme (GBM) is among the most lethal forms of human cancer. Here, we report that a small subset of GBMs (3.1%; 3 of 97 tumors examined) harbor oncogenic chromosomal translocations that fuse in-frame the tyrosine kinase coding domains of fibroblast growth factor receptor (FGFR) genes (FGFR1 or FGFR3) to the transforming acidic coiled-coil (TACC) coding domains of TACC1 or TACC3, respectively. The FGFR-TACC fusion protein displays oncogenic activity when [...]

Cette étude met en évidence le rôle joué par la kinase PKM2 dans la régulation épigénétique de la tumorigenèse via la phosphorylation de l'histone H3

PKM2 Phosphorylates Histone H3 and Promotes Gene Transcription and Tumorigenesis

Yang, Weiwei ; Xia, Yan ; Hawke, David ; Li, Xinjian ; Liang, Ji ; Xing, Dongming ; Aldape, Kenneth ; Hunter, Tony ; Alfred Yung, W. K. ; Lu, Zhimin

Tumor-specific pyruvate kinase M2 (PKM2) is essential for the Warburg effect. In addition to its well-established role in aerobic glycolysis, PKM2 directly regulates gene transcription. However, the mechanism underlying this nonmetabolic function of PKM2 remains elusive. We show here that PKM2 directly binds to histone H3 and phosphorylates histone H3 at T11 upon EGF receptor activation. This phosphorylation is required for the dissociation of HDAC3 from the CCND1 and MYC promoter regions and [...]

Cet article passe en revue les travaux récents sur le rôle du réseau des micro-ARNs régulés par p53 dans la tumorigenèse

MicroRNAs in the p53 network: micromanagement of tumour suppression

Hermeking, Heiko

In recent years, microRNAs (miRNAs) have been identified as mediators of tumour suppression and stress responses exerted by the p53 tumour suppressor. p53-regulated miRNAs contribute to tumour suppression by controlling the expression of central components of multiple processes, including cell cycle progression, epithelial–mesenchymal transition, stemness, metabolism, cell survival and angiogenesis. The expression and activity of p53 itself is also under the control of miRNAs. Finally, genetic [...]

Menée à l'aide d'un modèle murin, cette étude suggère que la délétion du gène BAP1 chez l'adulte est susceptible d'induire un syndrome myélodysplasique

Loss of the Tumor Suppressor BAP1 Causes Myeloid Transformation

Dey, Anwesha ; Seshasayee, Dhaya ; Noubade, Rajkumar ; French, Dorothy M. ; Liu, Jinfeng ; Chaurushiya, Mira S. ; Kirkpatrick, Donald S. ; Pham, Victoria C. ; Lill, Jennie R. ; Bakalarski, Corey E. ; Wu, Jiansheng ; Phu, Lilian ; Katavolos, Paula ; LaFave, Lindsay M. ; Abdel-Wahab, Omar ; Modrusan, Zora ; Seshagiri, Somasekar ; Dong, Ken ; Lin, Zhonghua ; Balazs, Mercedesz ; Suriben, Rowena ; Newton, Kim ; Hymowitz, Sarah ; Garcia-Manero, Guillermo ; Martin, Flavius ; Levine, Ross L. ; Dixit, Vishva M.

Deubiquitinating enzyme BAP1 is mutated in a hereditary cancer syndrome with increased risk of mesothelioma and uveal melanoma. Somatic BAP1 mutations occur in various malignancies. We show that mouse Bap1 gene deletion is lethal during embryogenesis, but systemic or hematopoietic-restricted deletion in adults recapitulates features of human myelodysplastic syndrome (MDS). Knock-in mice expressing BAP1 with a 3xFlag tag revealed that BAP1 interacts with HCF-1, OGT, and the polycomb group [...]

Menée à l'aide d'un modèle murin et d'échantillons prélevés sur des patients atteints d'une leucémie myéloïde, cette étude identifie des groupes de gènes dont l'expression est associée à la régulation et la croissance des cellules souches leucémiques

Gene Sets Identified with Oncogene Cooperativity Analysis Regulate In Vivo Growth and Survival of Leukemia Stem Cells

Ashton, John M ; Balys, Marlene ; Neering, Sarah J ; Hassane, Duane C ; Cowley, Glenn ; Root, David E ; Miller, Peter G ; Ebert, Benjamin L ; McMurray, Helene R ; Land, Hartmut ; Jordan, Craig T

Leukemia stem cells (LSCs) represent a biologically distinct subpopulation of myeloid leukemias, with reduced cell cycle activity and increased resistance to therapeutic challenge. To better characterize key properties of LSCs, we employed a strategy based on identification of genes synergistically dysregulated by cooperating oncogenes. We hypothesized that such genes, termed cooperation response genes (CRGs), would represent regulators of LSC growth and survival. Using both a primary mouse [...]

Menée in vitro, cette étude montre que la tristétrapoline joue un rôle de suppresseur de tumeurs dans les lymphomes induits par l'oncoprotéine Myc

Tristetraprolin Impairs Myc-Induced Lymphoma and Abolishes the Malignant State

Rounbehler, Robert J ; Fallahi, Mohammad ; Yang, Chunying ; Steeves, Meredith A ; Li, Weimin ; Doherty, Joanne R ; Schaub, Franz X ; Sanduja, Sandhya ; Dixon, Dan A ; Blackshear, Perry J ; Cleveland, John L

Myc oncoproteins directly regulate transcription by binding to target genes, yet this only explains a fraction of the genes affected by Myc. mRNA turnover is controlled via AU-binding proteins (AUBPs) that recognize AU-rich elements (AREs) found within many transcripts. Analyses of precancerous and malignant Myc-expressing B cells revealed that Myc regulates hundreds of ARE-containing (ARED) genes and select AUBPs. Notably, Myc directly suppresses transcription of Tristetraprolin (TTP/ZFP36), [...]

Menée à l'aide d'un modèle murin, cette étude montre que la mutation L597V du gène BRAF, en association avec une mutation du gène RAS, est susceptible d'induire un mélanome et suggère qu'un traitement à l'aide d'inhibiteurs de BRAF, comme le vemurafenib, activerait paradoxalement la croissance tumorale

The intermediate-activity L597VBRAF mutant acts as an epistatic modifier of oncogenic RAS by enhancing signaling through the RAF/MEK/ERK pathway

Andreadi, Catherine ; Cheung, Lai-Kay ; Giblett, Susan ; Patel, Bipin ; Jin, Hong ; Mercer, Kathryn ; Kamata, Tamihiro ; Lee, Pearl ; Williams, Alexander ; McMahon, Martin ; Marais, Richard ; Pritchard, Catrin

L597VBRAF mutations are acquired somatically in human cancer samples and are frequently coincident with RAS mutations. Germline L597VBRAF mutations are also found in several autosomal dominant developmental conditions known as RASopathies, raising the important question of how the same mutation can contribute to both pathologies. Using a conditional knock-in mouse model, we show that endogenous expression of L597VBraf leads to approximately twofold elevated Braf kinase activity and weak [...]

Menée in vitro et in vivo, cette étude met en évidence le rôle joué par MUC1, une protéine transmembranaire, dans la régulation du métabolisme des cellules cancéreuses du pancréas

MUC1 mucin stabilizes and activates hypoxia-inducible factor 1 alpha to regulate metabolism in pancreatic cancer

Chaika, Nina V. ; Gebregiworgis, Teklab ; Lewallen, Michelle E. ; Purohit, Vinee ; Radhakrishnan, Prakash ; Liu, Xiang ; Zhang, Bo ; Mehla, Kamiya ; Brown, Roger B. ; Caffrey, Thomas ; Yu, Fang ; Johnson, Keith R. ; Powers, Robert ; Hollingsworth, Michael A. ; Singh, Pankaj K.

Aberrant glucose metabolism is one of the hallmarks of cancer that facilitates cancer cell survival and proliferation. Here, we demonstrate that MUC1, a large, type I transmembrane protein that is overexpressed in several carcinomas including pancreatic adenocarcinoma, modulates cancer cell metabolism to facilitate growth properties of cancer cells. MUC1 occupies the promoter elements of multiple genes directly involved in glucose metabolism and regulates their expression. Furthermore, MUC1 [...]

Menée sur un modèle murin, cette étude met en évidence un mécanisme par lequel une inflammation est susceptible d'induire une modification du microbiote intestinal favorisant la tumorigenèse

Intestinal Inflammation Targets Cancer-Inducing Activity of the Microbiota

Arthur, Janelle C. ; Perez-Chanona, Ernesto ; Mühlbauer, Marcus ; Tomkovich, Sarah ; Uronis, Joshua M. ; Fan, Ting-Jia ; Campbell, Barry J. ; Abujamel, Turki ; Dogan, Belgin ; Rogers, Arlin B. ; Rhodes, Jonathan M. ; Stintzi, Alain ; Simpson, Kenneth W. ; Hansen, Jonathan J. ; Keku, Temitope O. ; Fodor, Anthony A. ; Jobin, Christian

Inflammation alters host physiology to promote cancer, as seen in colitis-associated colorectal cancer (CRC). Here, we identify the intestinal microbiota as a target of inflammation that impacts the progression of CRC. High-throughput sequencing revealed that inflammation modifies gut microbial composition in colitis-susceptible interleukin-10–deficient (Il10−/−) mice. Monocolonization with the commensal Escherichia coli NC101 promoted invasive carcinoma in azoxymethane (AOM)–treated Il10−/− [...]

Menée in vitro et in vivo, cette étude suggère que, dans le contexte d'un cancer de la thyroïde, la protéine STAT3 exerce paradoxalement une régulation négative de la croissance tumorale

STAT3 negatively regulates thyroid tumorigenesis

Couto, Joana Pinto ; Daly, Laura ; Almeida, Ana ; Knauf, Jeffrey A. ; Fagin, James A. ; Sobrinho-Simões, Manuel ; Lima, Jorge ; Máximo, Valdemar ; Soares, Paula ; Lyden, David ; Bromberg, Jacqueline F.

Although tyrosine-phosphorylated or activated STAT3 (pY-STAT3) is a well-described mediator of tumorigenesis, its role in thyroid cancer has not been investigated. We observed that 63 of 110 (57%) human primary papillary thyroid carcinoma (PTC) cases expressed nuclear pY-STAT3 in tumor cells, preferentially in association with the tumor stroma. An inverse relationship between pY-STAT3 expression with tumor size and the presence of distant metastases was observed. Using human thyroid [...]

Menée à l'aide d'un modèle microfluidique tridimensionnel, cette étude met en évidence le rôle joué par des facteurs de l'endothélium pour réguler l'intravasion des cellules tumorales

Three-dimensional microfluidic model for tumor cell intravasation and endothelial barrier function

Zervantonakis, Ioannis K. ; Hughes-Alford, Shannon K. ; Charest, Joseph L. ; Condeelis, John S. ; Gertler, Frank B. ; Kamm, Roger D.

Entry of tumor cells into the blood stream is a critical step in cancer metastasis. Although significant progress has been made in visualizing tumor cell motility in vivo, the underlying mechanism of cancer cell intravasation remains largely unknown. We developed a microfluidic-based assay to recreate the tumor-vascular interface in three-dimensions, allowing for high resolution, real-time imaging, and precise quantification of endothelial barrier function. Studies are aimed at testing the [...]

Menée in vitro, cette étude identifie un mécanisme par lequel le facteur de transcription HSF1, un régulateur de la réponse au choc thermique, favorise le processus métastatique dans les cancers du poumon, du côlon et du sein

HSF1 Drives a Transcriptional Program Distinct from Heat Shock to Support Highly Malignant Human Cancers

Mendillo, Marc L ; Santagata, Sandro ; Koeva, Martina ; Bell, George W ; Hu, Rong ; Tamimi, Rulla M ; Fraenkel, Ernest ; Ince, Tan A ; Whitesell, Luke ; Lindquist, Susan

Heat-Shock Factor 1 (HSF1), master regulator of the heat-shock response, facilitates malignant transformation, cancer cell survival, and proliferation in model systems. The common assumption is that these effects are mediated through regulation of heat-shock protein (HSP) expression. However, the transcriptional network that HSF1 coordinates directly in malignancy and its relationship to the heat-shock response have never been defined. By comparing cells with high and low malignant potential [...]

Menée in vitro et in vivo, cette étude met en évidence un mécanisme par lequel la protéine YAP, en interaction avec le facteur de transcription TEAD, favorise la progression du cancer et le processus métastatique dans les cancers du sein et les mélanomes

The Hippo pathway target, YAP, promotes metastasis through its TEAD-interaction domain

Lamar, John M. ; Stern, Patrick ; Liu, Hui ; Schindler, Jeffrey W. ; Jiang, Zhi-Gang ; Hynes, Richard O.

The transcriptional coactivator Yes-associated protein (YAP) is a major regulator of organ size and proliferation in vertebrates. As such, YAP can act as an oncogene in several tissue types if its activity is increased aberrantly. Although no activating mutations in the yap1 gene have been identified in human cancer, yap1 is located on the 11q22 amplicon, which is amplified in several human tumors. In addition, mutations or epigenetic silencing of members of the Hippo pathway, which represses [...]

Menée à l'aide d'un modèle murin de leucémie myélogène chronique, cette étude montre que la formation de pièges neutrophiliques extracellulaires contribue à une thrombose associée au cancer

Cancers predispose neutrophils to release extracellular DNA traps that contribute to cancer-associated thrombosis

Demers, Mélanie ; Krause, Daniela S. ; Schatzberg, Daphne ; Martinod, Kimberly ; Voorhees, Jaymie R. ; Fuchs, Tobias A. ; Scadden, David T. ; Wagner, Denisa D.

Cancer-associated thrombosis often lacks a clear etiology. However, it is linked to a poor prognosis and represents the second-leading cause of death in cancer patients. Recent studies have shown that chromatin released into blood, through the generation of neutrophil extracellular traps (NETs), is procoagulant and prothrombotic. Using a murine model of chronic myelogenous leukemia, we show that malignant and nonmalignant neutrophils are more prone to NET formation. This increased sensitivity [...]

Menée à l'aide de modèles murins, cette étude met en évidence un mécanisme par lequel la protéine Coco, un inhibiteur endogène de la signalisation BMP, régule la formation de métastases pulmonaires d'un cancer du sein

The BMP Inhibitor Coco Reactivates Breast Cancer Cells at Lung Metastatic Sites

Gao, Hua ; Chakraborty, Goutam ; Lee-Lim, Ai Ping ; Mo, Qianxing ; Decker, Markus ; Vonica, Alin ; Shen, Ronglai ; Brogi, Edi ; Brivanlou, Ali H ; Giancotti, Filippo G

The mechanistic underpinnings of metastatic dormancy and reactivation are poorly understood. A gain-of-function cDNA screen reveals that Coco, a secreted antagonist of TGF-² ligands, induces dormant breast cancer cells to undergo reactivation in the lung. Mechanistic studies indicate that Coco exerts this effect by blocking lung-derived BMP ligands. Whereas Coco enhances the manifestation of traits associated with cancer stem cells, BMP signaling suppresses it. Coco induces a discrete gene [...]

Menée sur 99 tumeurs primitives non métastatiques et 101 tumeurs primitives métastatiques de carcinome épidermoïde de la tête et du cou, cette étude met en évidence le rôle joué par l'intégrine bêta1 dans le processus métastatique

The Pivotal Role of Integrin beta 1 in Metastasis of Head and Neck Squamous Cell Carcinoma

Wang, Dongsheng ; Muller, Susan ; Amin, A.R.M. Ruhul ; Huang, Donghai ; Su, Ling ; Hu, Zhongliang ; Rahman, Mohammad A. ; Nannapaneni, Sreenivas ; Koenig, Lydia ; Chen, Zhengjia ; Tighiouart, Mourad ; Shin, Dong M. ; Chen, Zhuo Georgia

Purpose:To understand the prognostic value of integrin beta1 expression in squamous cell carcinoma of the head and neck (HNSCC) and the mechanism underlying its association with metastatic HNSCC. Experimental Design:Archival HNSCC tissues including 99 non-metastatic primary tumors and 101 metastatic primary tumors were examined for the association of integrin beta1 expression with metastasis and disease prognosis by appropriate statistical methods. Fluorescence activated cell sorting was used [...]

Cet article passe en revue les enjeux associés à l'analyse, l'interprétation, la reproductibilité et l'accessibilité des données produites par des instruments de séquençage de prochaine génération

Next-generation sequencing data interpretation: enhancing reproducibility and accessibility

Nekrutenko, Anton ; Taylor, James

Areas of life sciences research that were previously distant from each other in ideology, analysis practices and toolkits, such as microbial ecology and personalized medicine, have all embraced techniques that rely on next-generation sequencing instruments. Yet the capacity to generate the data greatly outpaces our ability to analyse it. Existing sequencing technologies are more mature and accessible than the methodologies that are available for individual researchers to move, store, analyse [...]