303 research outputs found
Lung Adenocarcinoma of Never Smokers and Smokers Harbor Differential Regions of Genetic Alteration and Exhibit Different Levels of Genomic Instability
- Author
- Adi F. Gazdar
- B Job
- B Rhead
- BA Weir
- BP Coe
- BP Coe
- BP Coe
- CA Powell
- Calum E. MacAulay
- CM Rudin
- D Chitale
- DD Bowtell
- DG Albertson
- DM Parkin
- ED Pleasance
- Emily A. Vucic
- G da Cunha Santos
- GM Newnham
- J Soh
- J Subramanian
- JM Campbell
- JM Samet
- John C. English
- Ju-Seog Lee
- Kelsie L. Thu
- M Sanchez-Cespedes
- MP Wong
- MP Wong
- P Broet
- P Broet
- Pei Wang
- PP Massion
- R Beroukhim
- Raj Chari
- Rong Fu
- S Dasgupta
- S Sun
- Stephen Lam
- W Pao
- Wan L. Lam
- Wei Zhang
- William W. Lockwood
- Ziding Feng
- Publication venue
- Public Library of Science
- Publication date
- 07/03/2012
- Field of study
Recent evidence suggests that the observed clinical distinctions between lung tumors in smokers and never smokers (NS) extend beyond specific gene mutations, such as EGFR, EML4-ALK, and KRAS, some of which have been translated into targeted therapies. However, the molecular alterations identified thus far cannot explain all of the clinical and biological disparities observed in lung tumors of NS and smokers. To this end, we performed an unbiased genome-wide, comparative study to identify novel genomic aberrations that differ between smokers and NS
Finding exclusively deleted or amplified genomic areas in lung adenocarcinomas using a novel chromosomal pattern analysis
- Author
- Publication venue
- BioMed Central
- Publication date
- 01/01/2009
- Field of study
<p>Abstract</p> <p>Background</p> <p>Genomic copy number alteration (CNA) that are recurrent across multiple samples often harbor critical genes that can drive either the initiation or the progression of cancer disease. Up to now, most researchers investigating recurrent CNAs consider separately the marginal frequencies for copy gain or loss and select the areas of interest based on arbitrary cut-off thresholds of these frequencies. In practice, these analyses ignore the interdependencies between the propensity of being deleted or amplified for a clone. In this context, a joint analysis of the copy number changes across tumor samples may bring new insights about patterns of recurrent CNAs.</p> <p>Methods</p> <p>We propose to identify patterns of recurrent CNAs across tumor samples from high-resolution comparative genomic hybridization microarrays. Clustering is achieved by modeling the copy number state (loss, no-change, gain) as a multinomial distribution with probabilities parameterized through a latent class model leading to nine patterns of recurrent CNAs. This model gives us a powerful tool to identify clones with contrasting propensity of being deleted or amplified across tumor samples. We applied this model to a homogeneous series of 65 lung adenocarcinomas.</p> <p>Results</p> <p>Our latent class model analysis identified interesting patterns of chromosomal aberrations. Our results showed that about thirty percent of the genomic clones were classified either as "exclusively" deleted or amplified recurrent CNAs and could be considered as non random chromosomal events. Most of the known oncogenes or tumor suppressor genes associated with lung adenocarcinoma were located within these areas. We also describe genomic areas of potential interest and show that an increase of the frequency of amplification in these particular areas is significantly associated with poorer survival.</p> <p>Conclusion</p> <p>Analyzing jointly deletions and amplifications through our latent class model analysis allows highlighting specific genomic areas with exclusively amplified or deleted recurrent CNAs which are good candidate for harboring oncogenes or tumor suppressor genes.</p
Integrative analyses identify modulators of response to neoadjuvant aromatase inhibitors in patients with early breast cancer
- Author
- A Mackay
- AK Dunbier
- AK Dunbier
- Alan Mackay
- Alexey Larionov
- Anita K Dunbier
- Aradhana Rani
- Ash Nerurkar
- B Weigelt
- BP Coe
- C Curtis
- C Kent
- D Generali
- DG Albertson
- DS Tan
- Elena López-Knowles
- F Kreisel
- Helen Anderson
- HW Cheung
- IE Smith
- IE Smith
- J Hicks
- J Michael Dixon
- Jorge S Reis-Filho
- JS Foster
- K Lundgren
- L Osterberg
- LA Martin
- LA Martin
- LA Martin
- Lesley-Ann Martin
- LG Leon
- Lorna Renshaw
- M Dowsett
- M Mello-Grand
- M Scaltriti
- Mitch Dowsett
- MJ Ellis
- MT Weigel
- N Turner
- P Darbre
- P Lal
- Paul M Wilkerson
- Peter Osin
- PM Wilkerson
- PM Wilkerson
- PT Simpson
- R Beroukhim
- R Duprez
- R Katz-Brull
- R Natrajan
- R Natrajan
- R Natrajan
- Ricardo Ribas
- T Miyake
- T Troiani
- TK Lam
- William R Miller
- WR Miller
- WR Miller
- WR Miller
- WR Miller
- X Huo
- Y Zhao
- Z Ghazoui
- Zara Ghazoui
- Publication venue
- 'Springer Science and Business Media LLC'
- Publication date
- 01/01/2015
- Field of study
Introduction
Aromatase inhibitors (AIs) are a vital component of estrogen receptor positive (ER+) breast cancer treatment. De novo and acquired resistance, however, is common. The aims of this study were to relate patterns of copy number aberrations to molecular and proliferative response to AIs, to study differences in the patterns of copy number aberrations between breast cancer samples pre- and post-AI neoadjuvant therapy, and to identify putative biomarkers for resistance to neoadjuvant AI therapy using an integrative analysis approach.
Methods
Samples from 84 patients derived from two neoadjuvant AI therapy trials were subjected to copy number profiling by microarray-based comparative genomic hybridisation (aCGH, n = 84), gene expression profiling (n = 47), matched pre- and post-AI aCGH (n = 19 pairs) and Ki67-based AI-response analysis (n = 39).
Results
Integrative analysis of these datasets identified a set of nine genes that, when amplified, were associated with a poor response to AIs, and were significantly overexpressed when amplified, including CHKA, LRP5 and SAPS3. Functional validation in vitro, using cell lines with and without amplification of these genes (SUM44, MDA-MB134-VI, T47D and MCF7) and a model of acquired AI-resistance (MCF7-LTED) identified CHKA as a gene that when amplified modulates estrogen receptor (ER)-driven proliferation, ER/estrogen response element (ERE) transactivation, expression of ER-regulated genes and phosphorylation of V-AKT murine thymoma viral oncogene homolog 1 (AKT1).
Conclusions
These data provide a rationale for investigation of the role of CHKA in further models of de novo and acquired resistance to AIs, and provide proof of concept that integrative genomic analyses can identify biologically relevant modulators of AI response
Homozygous microdeletion of exon 5 in ZNF277 in a girl with specific language impairment
- Author
- A Gregor
- AJ Iafrate
- AJ Whitehouse
- AJ Whitehouse
- Alistair T Pagnamenta
- Ann Clark
- AT Pagnamenta
- AV Molofsky
- AV Molofsky
- B Bakkaloglu
- BJ O'Roak
- BP Coe
- C Palles
- Clyde Francks
- CS Leblond
- D Malhotra
- David R Bentley
- DF Newbury
- DF Newbury
- Dianne F Newbury
- E Maestrini
- EH Cook Jr
- Elena Bacchelli
- Elena Maestrini
- Elizabeth R Hennessy
- Fabiola Ceroni
- G Conti-Ramsden
- GD Schellenberg
- Gillian Baird
- Gina Conti-Ramsden
- H Liang
- Hilary Martin
- HJ Kang
- International Molecular Genetic Study of Autism Consortium
- International Molecular Genetic Study of Autism Consortium
- J Law
- J Wincent
- J Zhang
- Jeremy Parr
- JT Glessner
- K Darvishi
- K Stromswold
- K Wang
- KA Lindgren
- KJ Livak
- L Mawhood
- LA Weiss
- LE Vissers
- M Bucan
- M Falcaro
- M Khajavi
- M Negishi
- MM Kjelgaard
- NG Riches
- Nuala H Simpson
- P Howlin
- Patrick F Bolton
- Peter Donnelly
- S Barrett
- S Berkel
- S Colella
- S Girirajan
- S Girirajan
- S Girirajan
- SC Vernes
- SE McCarthy
- Simon E Fisher
- SJ Sanders
- The SLI Consortium
- The SLI consortium (SLIC)
- Y Shao
- Publication venue
- 'Springer Science and Business Media LLC'
- Publication date
- 01/01/2014
- Field of study
Peer reviewedPublisher PD
An integrative multi-dimensional genetic and epigenetic strategy to identify aberrant genes and pathways in cancer
- Author
- A Giovane
- A Shadeo
- AN Jain
- AS Ishkanian
- B Carvalho
- B Kreike
- BP Coe
- BP Coe
- Bradley P Coe
- CD Jee
- CM Perou
- D Pils
- D Stein
- DG Albertson
- DJ Slamon
- DR Rhodes
- DS Shames
- DW Parsons
- E Hyman
- E Wang
- EA Rakha
- Emily A Vucic
- F Andre
- F Bertucci
- GS Bova
- H Yan
- J Fridlyand
- J He
- J Soh
- JC Chang
- JR Pollack
- JT Chang
- K Chin
- K Chinen
- K Jong
- K Stemke-Hale
- KE Bachman
- L Gautier
- LJ van 't Veer
- M Bibikova
- M Khojasteh
- M Lin
- M Tuna
- MC Cheang
- MJ van de Vijver
- ML Yaremko
- N Johnson
- N Turner
- O Gluz
- O Troyanskaya
- R Chari
- R Chari
- R Redon
- Raj Chari
- RC Gentleman
- S Ramaswamy
- SF Chin
- SF Chin
- SL Cooke
- T Sorlie
- T Ueki
- TL Naylor
- W Han
- Wan L Lam
- William W Lockwood
- WW Lockwood
- WW Lockwood
- Y Wang
- Publication venue
- BioMed Central
- Publication date
- 01/01/2010
- Field of study
<p>Abstract</p> <p>Background</p> <p>Genomics has substantially changed our approach to cancer research. Gene expression profiling, for example, has been utilized to delineate subtypes of cancer, and facilitated derivation of predictive and prognostic signatures. The emergence of technologies for the high resolution and genome-wide description of genetic and epigenetic features has enabled the identification of a multitude of causal DNA events in tumors. This has afforded the potential for large scale integration of genome and transcriptome data generated from a variety of technology platforms to acquire a better understanding of cancer.</p> <p>Results</p> <p>Here we show how multi-dimensional genomics data analysis would enable the deciphering of mechanisms that disrupt regulatory/signaling cascades and downstream effects. Since not all gene expression changes observed in a tumor are causal to cancer development, we demonstrate an approach based on multiple concerted disruption (MCD) analysis of genes that facilitates the rational deduction of aberrant genes and pathways, which otherwise would be overlooked in single genomic dimension investigations.</p> <p>Conclusions</p> <p>Notably, this is the first comprehensive study of breast cancer cells by parallel integrative genome wide analyses of DNA copy number, LOH, and DNA methylation status to interpret changes in gene expression pattern. Our findings demonstrate the power of a multi-dimensional approach to elucidate events which would escape conventional single dimensional analysis and as such, reduce the cohort sample size for cancer gene discovery.</p
Massively parallel sequencing of patients with intellectual disability, congenital anomalies and/or autism spectrum disorders with a targeted gene panel
- Author
- A Kakita
- AI Alvarez Retuerto
- Angeline Lai
- B Devlin
- B Meder
- BJ O'Roak
- BM Neale
- BP Coe
- Breana Cham
- C Betancur
- CS Leblond
- D Horn
- Ee-Shien Tan
- Ene-Choo Tan
- FF Hamdan
- Hao Sun
- HY Kroes
- Ivy Ng
- J Chelly
- John McPherson
- JR Lemke
- K Neveling
- LA Jolly
- Lai-Choo Ong
- M Pantaleon
- M Rehnberg
- Maggie Brett
- MH Jones
- MT Carter
- N Matsunami
- OS Latiff ZA
- Patrick Tan
- PS Tarpey
- R Gibbons
- R Sultana
- RJ Ferland
- RJ Gibbons
- S Dupont
- S Girirajan
- S Kunishima
- SJ Sanders
- Steve Rozen
- U Finckh
- VM Kalscheuer
- Z Brownstein
- Zhi Jiang Zang
- Publication venue
- 'Public Library of Science (PLoS)'
- Publication date
- 01/01/2014
- Field of study
10.1371/journal.pone.0093409PLoS ONE94-POLN
Divergent Genomic and Epigenomic Landscapes of Lung Cancer Subtypes Underscore the Selection of Different Oncogenic Pathways during Tumor Development
- Author
- A Bardelli
- A Bhattacharjee
- A Doi
- A Giangreco
- A Jemal
- A Van Den Broeck
- A Vilmar
- Adi F. Gazdar
- AH Bild
- AJ Bass
- AJ Watt
- Alfons Navarro
- AP Feinberg
- AS Ishkanian
- B Chi
- B Chi
- B Eymin
- B Lucas
- BA Weir
- BD Strahl
- BP Coe
- BP Coe
- Bradley P. Coe
- C Baldwin
- C Garnis
- C Luk
- Calum E. MacAulay
- Carmen Behrens
- CJ Langer
- CM Croce
- DF Lee
- E Felip
- E Hyman
- ES Lee
- F Barlesi
- F de Fraipont
- F Orzan
- G Scagliotti
- G Sozzi
- G Sozzi
- G Tonon
- H Kim
- H Yamamoto
- HH Yang
- I Petersen
- I Petersen
- Ian M. Wilson
- IC Wang
- Ignacio I. Wistuba
- J Geradts
- J Lamb
- J Pei
- JA Gollob
- John D. Minna
- John English
- John Yee
- JR Pollack
- JS Kim
- K Grigo
- K Jong
- KA Olaussen
- KA Olaussen
- Kelsie L. Thu
- L Cheng
- LA Garraway
- LA Garraway
- Larissa A. Pikor
- LM Solis
- Luisa M. Solis
- M Esteller
- M Esteller
- M Higashiyama
- M Hussain
- M Khojasteh
- M Sato
- Maria I. Nunez
- MD Wilkerson
- Ming-Sound Tsao
- MJ Hoffmann
- MP Coleman
- Nevin Murray
- NL Guo
- NL Lazarevich
- NL Lazarevich
- P Broet
- P Yuan
- R Chari
- R Maruyama
- RA Irizarry
- Raj Chari
- RD Morin
- RK Thomas
- RS Herbst
- S Sel
- S Sun
- S Toyooka
- S Toyooka
- SH Choi
- SK Watson
- SM Sy
- Stephen Lam
- T Hillemacher
- T Vaissiere
- TP Dang
- TS Mok
- Wan L. Lam
- WD Travis
- WD Travis
- WD Travis
- William W. Lockwood
- WW Lockwood
- WW Lockwood
- WW Lockwood
- Y Tomizawa
- Y Zhao
- ZL Wu
- Publication venue
- Public Library of Science
- Publication date
- 01/01/2012
- Field of study
For therapeutic purposes, non-small cell lung cancer (NSCLC) has traditionally been regarded as a single disease. However, recent evidence suggest that the two major subtypes of NSCLC, adenocarcinoma (AC) and squamous cell carcinoma (SqCC) respond differently to both molecular targeted and new generation chemotherapies. Therefore, identifying the molecular differences between these tumor types may impact novel treatment strategy. We performed the first large-scale analysis of 261 primary NSCLC tumors (169 AC and 92 SqCC), integrating genome-wide DNA copy number, methylation and gene expression profiles to identify subtype-specific molecular alterations relevant to new agent design and choice of therapy. Comparison of AC and SqCC genomic and epigenomic landscapes revealed 778 altered genes with corresponding expression changes that are selected during tumor development in a subtype-specific manner. Analysis of >200 additional NSCLCs confirmed that these genes are responsible for driving the differential development and resulting phenotypes of AC and SqCC. Importantly, we identified key oncogenic pathways disrupted in each subtype that likely serve as the basis for their differential tumor biology and clinical outcomes. Downregulation of HNF4α target genes was the most common pathway specific to AC, while SqCC demonstrated disruption of numerous histone modifying enzymes as well as the transcription factor E2F1. In silico screening of candidate therapeutic compounds using subtype-specific pathway components identified HDAC and PI3K inhibitors as potential treatments tailored to lung SqCC. Together, our findings suggest that AC and SqCC develop through distinct pathogenetic pathways that have significant implication in our approach to the clinical management of NSCLC
Jet energy measurement with the ATLAS detector in proton-proton collisions at root s=7 TeV
- Author
- Aad G
- Abbott B
- Abdallah J
- Abdelalim AA
- Abdesselam A
- Abdinov O
- Abi B
- Abolins M
- Abramowicz H
- Abreu H
- Acerbi E
- Acharya BS
- Adams DL
- Addy TN
- Adelman J
- Aderholz M
- Adomeit S
- Adragna P
- Adye T
- Aefsky S
- Aguilar-Saavedra JA
- Aharrouche M
- Ahlen SP
- Ahles F
- Ahmad A
- Ahsan M
- Aielli G
- Akdogana T
- Akesson TPA
- Akimoto G
- Akimov AV
- Akiyama A
- Aktas A
- Alam MA
- Alam MS
- Albert J
- Albrand S
- Aleksa M
- Aleksandrov IN
- Alessandria F
- Alexa C
- Alexander G
- Alexandre G
- Alexopoulos T
- Alhroob M
- Aliev M
- Alimonti G
- Alison J
- Aliyev M
- Allport PP
- Allwood-Spiers SE
- Almenar CC
- Almond J
- Aloisio A
- Alon R
- Alonso A
- Alviggi MG
- Amako K
- Amaral P
- Amelung C
- Ammosov VV
- Amorim A
- Amoros G
- Amram N
- Anastopoulos C
- Ancu LS
- Andari N
- Andeen T
- Anders CF
- Anders G
- Anderson KJ
- Andreazza A
- Andrei V
- Andrieux M-L
- Anduaga XS
- Angerami A
- Anghinolfi F
- Anh TV
- Anjos N
- Annovi A
- Antonaki A
- Antonelli M
- Antonov A
- Antos J
- Anulli F
- Aoun S
- Apolle R
- Arabidze G
- Aracena I
- Arai Y
- Aranda CP
- Arce ATH
- Archambault JP
- Arfaoui S
- Arguin J-F
- Arik E
- Arik M
- Armbruster AJ
- Arnaez O
- Arnault C
- Artamonov A
- Artoni G
- Arutinov D
- Asai S
- Asfandiyarov R
- Ask S
- Asman B
- Asner D
- Asquith L
- Assamagan K
- Astbury A
- Astvatsatourov A
- Atoian G
- Aubert B
- Auge E
- Augsten K
- Aurousseau M
- Austin N
- Avolio G
- Avramidou R
- Axen D
- Ay C
- Azuelos G
- Azuma Y
- Baak MA
- Baccaglioni G
- Bacci C
- Bach AM
- Bachacou H
- Bachas K
- Bachy G
- Backes M
- Backhaus M
- Badescu E
- Bagnaia P
- Bahinipati S
- Bai Y
- Bailey DC
- Bain T
- Baines JT
- Baker MD
- Baker OK
- Baker S
- Banas E
- Banerjee P
- Banerjee S
- Banfi D
- Bangert A
- Bansal V
- Bansil HS
- Barajas CAC
- Barak L
- Baranov SP
- Barashkou A
- Barber T
- Barberio EL
- Barberis D
- Barbero M
- Bardin DY
- Barillari T
- Barisonzi M
- Barklow T
- Barlow N
- Barnett BM
- Barnett RM
- Baroncelli A
- Barone G
- Barr AJ
- Barreiro F
- Barrera CO
- Barrillon P
- Bartoldus R
- Barton AE
- Bartsch D
- Bartsch V
- Bates RL
- Batkova L
- Batley JR
- Battaglia A
- Battistin M
- Battistoni G
- Bauer F
- Bawa HS
- Beare B
- Beau T
- Beauchemin PH
- Beccherle R
- Bechtle P
- Beck GA
- Beck HP
- Beckingham M
- Becks KH
- Beddall A
- Beddall AJ
- Bedikian S
- Bednyakov VA
- Bee CP
- Begel M
- Behera PK
- Beimforde M
- Belanger-Champagne C
- Belenguer MJ
- Bell PJ
- Bell WH
- Bella G
- Bella LA
- Bellagamba L
- Bellina F
- Bellomo M
- Belloni A
- Beloborodova O
- Belotskiy K
- Beltramello O
- Ben Ami S
- Benary O
- Benchekroun D
- Benchouk C
- Bendel M
- Benekos N
- Benhammou Y
- Benjamin DP
- Benoit M
- Bensinger JR
- Benslama K
- Bentvelsen S
- Beretta M
- Berge D
- Berger N
- Berghaus F
- Berglund E
- Beringer J
- Bernardet K
- Bernat P
- Bernhard R
- Bernius C
- Berry T
- Bertin A
- Bertinelli F
- Bertolucci F
- Besana MI
- Besson N
- Bethke S
- Bhimji W
- Bianchi RM
- Bianco M
- Biebel O
- Bieniek SP
- Bierwagen K
- Biesiada J
- Biglietti M
- Bilokon H
- Bindi M
- Binet S
- Bingul A
- Bini C
- Biscarat C
- Bitenc U
- Black KM
- Blair RE
- Blanchard J-B
- Blanchot G
- Blazek T
- Blocker C
- Blocki J
- Blondel A
- Blum W
- Blumenschein U
- Bobbink GJ
- Bobrovnikov VB
- Bocchetta SS
- Bocci A
- Boddy CR
- Boehler M
- Boek J
- Boelaert N
- Boeriu OEV
- Boeser S
- Bogaerts JA
- Bogdanchikov A
- Bogouch A
- Bohm C
- Boisvert V
- Bold T
- Boldea V
- Bolnet NM
- Bona M
- Bondarenko VG
- Bondioli M
- Boonekamp M
- Boorman G
- Booth CN
- Bordoni S
- Borer C
- Borisov A
- Borissov G
- Borjanovic I
- Borroni S
- Bos K
- Boscherini D
- Bosman M
- Boterenbrood H
- Botterill D
- Bouchami J
- Boudreau J
- Bouhova-Thacker EV
- Bourdarios C
- Bousson N
- Boveia A
- Boyd J
- Boyko IR
- Bozhko NI
- Bozovic-Jelisavcic I
- Bracinik J
- Braem A
- Branchini P
- Brandenburg GW
- Brandt A
- Brandt G
- Brandt O
- Bratzler U
- Brau B
- Brau JE
- Braun HM
- Brelier B
- Bremer J
- Brenner R
- Bressler S
- Breton D
- Britton D
- Brochu FM
- Brock I
- Brock R
- Brodbeck TJ
- Brodet E
- Broggi F
- Bromberg C
- Brooijmans G
- Brooks WK
- Brown G
- Brown H
- Bruncko D
- Bruneliere R
- Brunet S
- Bruni A
- Bruni G
- Bruschi M
- BScher V
- Buanes T
- Bucci F
- Buchanan J
- Buchanan NJ
- Buchholz P
- Buckingham RM
- Buckley AG
- Buda SI
- Budagov IA
- Budick B
- Bueso XP
- Bugge L
- Buira-Clark D
- Bulekov O
- Bunse M
- Buran T
- Burckhart H
- Burdin S
- Burgess T
- Burke S
- Busato E
- Bussey P
- Buszello CP
- Butin F
- Butler B
- Butler JM
- Buttar CM
- Butterworth JM
- Buttinger W
- Caballero J
- Caforio D
- Cakir IT
- Cakir O
- Calafiura P
- Calderini G
- Calfayan P
- Calkins R
- Caloba LP
- Caloi R
- Calvet D
- Calvet S
- Camarri P
- Cambiaghi M
- Cameron D
- Camilocci ES
- Campana S
- Campanelli M
- Canale V
- Canelli F
- Canepaa A
- Cantero J
- Capasso L
- Caprini I
- Caprini M
- Capriotti D
- Capua M
- Caputo R
- Caramarcu C
- Cardarelli R
- Carli T
- Carlino G
- Carminati L
- Caron B
- Caron S
- Carter AA
- Carter JR
- Carvalho J
- Casadei D
- Casado MP
- Cascella M
- Caso C
- Castaneda-Miranda E
- Castanheira MTD
- Castillo LRF
- Castro NF
- Cataldi G
- Cataneo F
- Catinaccio A
- Catmore JR
- Cattai A
- Cattani G
- Caughron S
- Cauz D
- Cavalcanti TP
- Cavalleri P
- Cavalli D
- Cavalli-Sforza M
- Cavasinni V
- Ceradini F
- Cerqueira AS
- Cerri A
- Cerrito L
- Cerutti F
- Cetin SA
- Cevenini F
- Chafaq A
- Chakraborty D
- Chan K
- Chapleau B
- Chapman JD
- Chapman JW
- Chareyre E
- Charlton DG
- Chavda V
- Cheatham S
- Chekanov S
- Chekulaev SV
- Chelkov GA
- Chelstowska MA
- Chen C
- Chen H
- Chen S
- Chen T
- Chen X
- Cheng S
- Cheong ALF
- Cheplakov A
- Chepurnov VF
- Chernyatin V
- Cheu E
- Cheung SL
- Chevalier L
- Chiefari G
- Chikovani L
- Childers JT
- Chilingarov A
- Chiodini G
- Chizhov MV
- Choudalakis G
- Chouridou S
- Christidi IA
- Christov A
- Chromek-Burckhart D
- Chu ML
- Chudoba J
- Ciapetti G
- Ciba K
- Ciftci AK
- Ciftci R
- Cinca D
- Cindro V
- Ciobotaru MD
- Cioccaa C
- Ciocio A
- Cirilli M
- Citterio M
- Ciubancan M
- Clark A
- Clark PJ
- Cleland W
- Clemens JC
- Clement B
- Clement C
- Clifft RW
- Coadou Y
- Cobal M
- Coccaro A
- Cochran J
- Codina EP
- Coe P
- Cogan JG
- Coggeshall J
- Cogneras E
- Cojocaru CD
- Colas J
- Colijn AP
- Collaboration ATLAS
- Collard C
- Collins NJ
- Collins-Tooth C
- Collot J
- Colon G
- Coniavitis E
- Conidi MC
- Consonni M
- Consorti V
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- Yildizb HD
- Yilmaz M
- Yoosootiniya R
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- Zajacova Z
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- Zarzhitsky P
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- Zenonos Z
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- Zhemchugov A
- Zheng S
- Zhong J
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- Zhu CG
- Zhu H
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- Zhuang X
- Zhuravlov V
- Zieminska D
- Zimmermann R
- Zimmermann S
- Zimmermann S
- Zinonos Z
- Ziolkowski M
- Zitoun R
- Zivkovic L
- Zmouchko VV
- Zobernig G
- Zoccoli A
- Zolnierowski Y
- Zsenei A
- Zutshi V
- Zwalinski L
- Publication venue
- 'Springer Science and Business Media LLC'
- Publication date
- 01/03/2013
- Field of study
The jet energy scale and its systematic uncertainty are determined for jets measured with the ATLAS detector at the LHC in proton-proton collision data at a centre-of-mass energy of √s = 7TeV corresponding to an integrated luminosity of 38 pb-1. Jets are reconstructed with the anti-kt algorithm with distance parameters R=0. 4 or R=0. 6. Jet energy and angle corrections are determined from Monte Carlo simulations to calibrate jets with transverse momenta pT≥20 GeV and pseudorapidities {pipe}η{pipe}<4. 5. The jet energy systematic uncertainty is estimated using the single isolated hadron response measured in situ and in test-beams, exploiting the transverse momentum balance between central and forward jets in events with dijet topologies and studying systematic variations in Monte Carlo simulations. The jet energy uncertainty is less than 2. 5 % in the central calorimeter region ({pipe}η{pipe}<0. 8) for jets with 60≤pT<800 GeV, and is maximally 14 % for pT<30 GeV in the most forward region 3. 2≤{pipe}η{pipe}<4. 5. The jet energy is validated for jet transverse momenta up to 1 TeV to the level of a few percent using several in situ techniques by comparing a well-known reference such as the recoiling photon pT, the sum of the transverse momenta of tracks associated to the jet, or a system of low-pT jets recoiling against a high-pT jet. More sophisticated jet calibration schemes are presented based on calorimeter cell energy density weighting or hadronic properties of jets, aiming for an improved jet energy resolution and a reduced flavour dependence of the jet response. The systematic uncertainty of the jet energy determined from a combination of in situ techniques is consistent with the one derived from single hadron response measurements over a wide kinematic range. The nominal corrections and uncertainties are derived for isolated jets in an inclusive sample of high-pT jets. Special cases such as event topologies with close-by jets, or selections of samples with an enhanced content of jets originating from light quarks, heavy quarks or gluons are also discussed and the corresponding uncertainties are determined. © 2013 CERN for the benefit of the ATLAS collaboration
Measurement of the inclusive and dijet cross-sections of b-jets in pp collisions at sqrt(s) = 7 TeV with the ATLAS detector
- Author
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- Abdallah J
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- Abdesselam A
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- Publication venue
- 'Springer Science and Business Media LLC'
- Publication date
- 31/12/2010
- Field of study
The inclusive and dijet production cross-sections have been measured for jets
containing b-hadrons (b-jets) in proton-proton collisions at a centre-of-mass
energy of sqrt(s) = 7 TeV, using the ATLAS detector at the LHC. The
measurements use data corresponding to an integrated luminosity of 34 pb^-1.
The b-jets are identified using either a lifetime-based method, where secondary
decay vertices of b-hadrons in jets are reconstructed using information from
the tracking detectors, or a muon-based method where the presence of a muon is
used to identify semileptonic decays of b-hadrons inside jets. The inclusive
b-jet cross-section is measured as a function of transverse momentum in the
range 20 < pT < 400 GeV and rapidity in the range |y| < 2.1. The bbbar-dijet
cross-section is measured as a function of the dijet invariant mass in the
range 110 < m_jj < 760 GeV, the azimuthal angle difference between the two jets
and the angular variable chi in two dijet mass regions. The results are
compared with next-to-leading-order QCD predictions. Good agreement is observed
between the measured cross-sections and the predictions obtained using POWHEG +
Pythia. MC@NLO + Herwig shows good agreement with the measured bbbar-dijet
cross-section. However, it does not reproduce the measured inclusive
cross-section well, particularly for central b-jets with large transverse
momenta.Comment: 10 pages plus author list (21 pages total), 8 figures, 1 table, final
version published in European Physical Journal
Measurement of the production cross section for W-bosons in association with jets in pp collisions at s=7 TeV with the ATLAS detector
- Author
- Adomeit S
- Adragna P
- Adye T
- Aefsky S
- Aguilar-Saavedra J
- Aharrouche M
- Ahmad A
- Alam M
- Albrand S
- Aleksa M
- Aleksandrov I
- Aleppo M
- Alessandria F
- Alexa C
- Alexander G
- Alexandre G
- Alexopoulos T
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- Aliev M
- Alimonti G
- Alison J
- Aliyev M
- Allport P
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- Almond J
- Aloisio A
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- Amako K
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- Amorós G
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- Vinogradov V
- Virchaux M
- Viret S
- Virzi J
- Vitale A
- Vitells O
- Vivarelli I
- Vives Vaque F
- Vlachos S
- Vlasak M
- Vlasov N
- Vogel A
- Vokac P
- Volpi M
- Volpini G
- von der Schmitt H
- von Loeben J
- von Radziewski H
- von Toerne E
- Vorobel V
- Vorobiev A
- Vorwerk V
- Vos M
- Voss R
- Voss T
- Vossebeld J
- Vovenko A
- Vranjes Milosavljevic M
- Vranjes N
- Vrba V
- Vreeswijk M
- Vu Anh T
- Vuillermet R
- Vukotic I
- Wagner P
- Wagner W
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- Wakabayashi J
- Walbersloh J
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- Waller P
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- Warburton A
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- Warsinsky M
- Watkins P
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- Watts G
- Watts S
- Waugh A
- Waugh B
- Weber J
- Weber M
- Weber M
- Weber P
- Weidberg A
- Weingarten J
- Weiser C
- Wellenstein H
- Wells P
- Wen M
- Wenaus T
- Wendler S
- Weng Z
- Wengler T
- Wenig S
- Wermes N
- Werner M
- Werner P
- Werth M
- Wessels M
- Whalen K
- Wheeler-Ellis S
- Whitaker S
- White A
- White M
- White S
- Whitehead S
- Whiteson D
- Whittington D
- Wicek F
- Wicke D
- Wickens F
- Wiedenmann W
- Wielers M
- Wienemann P
- Wiglesworth C
- Wiik L
- Wildauer A
- Wildt M
- Wilhelm I
- Wilkens H
- Will J
- Williams E
- Williams H
- Willis W
- Willocq S
- Wilson A
- Wilson J
- Wilson M
- Wingerter-Seez I
- Winkelmann S
- Winklmeier F
- Wittgen M
- Wolter M
- Wolters H
- Wooden G
- Wosiek B
- Wotschack J
- Woudstra M
- Wraight K
- Wright C
- Wrona B
- Wu S
- Wu X
- Wu Y
- Wulf E
- Wunstorf R
- Wynne B
- Xaplanteris L
- Xella S
- Xie S
- Xie Y
- Xu C
- Xu D
- Xu G
- Yabsley B
- Yamada M
- Yamamoto A
- Yamamoto K
- Yamamoto S
- Yamamura T
- Yamaoka J
- Yamazaki T
- Yamazaki Y
- Yan Z
- Yang H
- Yang U
- Yang Y
- Yang Z
- Yanush S
- Yao W
- Yao Y
- Yasu Y
- Ye J
- Ye S
- Yilmaz M
- Yoosoofmiya R
- Yorita K
- Yoshida R
- Young C
- Youssef S
- Yu D
- Yu J
- Yuan L
- Yurkewicz A
- Zaets V
- Zaidan R
- Zaitsev A
- Zajacova Z
- Zalite Y
- Zanello L
- Zarzhitsky P
- Zaytsev A
- Zdrazil M
- Zeitnitz C
- Zeller M
- Zema P
- Zemla A
- Zendler C
- Zenin A
- Zenin O
- Zenonos Z
- Zenz S
- Zerwas D
- Zevi della Porta G
- Zhan Z
- Zhang D
- Zhang H
- Zhang J
- Zhang X
- Zhang Z
- Zhao L
- Zhao T
- Zhao Z
- Zhemchugov A
- Zheng S
- Zhong J
- Zhou B
- Zhou N
- Zhou Y
- Zhu C
- Zhu H
- Zhu Y
- Zhuang X
- Zhuravlov V
- Zieminska D
- Zilka B
- Zimmermann R
- Zimmermann S
- Ziolkowski M
- Zitoun R
- Zivkovic L
- Zmouchko V
- Zobernig G
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- Zolnierowski Y
- Zsenei A
- zur Nedden M
- Zutshi V
- Zwalinski L
- ¿eni¿ T
- Åsman B
- Øye O
- Publication venue
- Publication date
- 01/01/2011
- Field of study
- …