50 research outputs found
The Silent Epidemic of Exclusive University Licensing Policies on Compounds for Neglected Diseases and Beyond
- Author
- Publication venue
- Public Library of Science
- Publication date
- 01/03/2010
- Field of study
Impact of an Expanded Definition of Family History on Outcomes of Active Surveillance for Prostate Cancer
- Author
- Publication venue
- Jefferson Digital Commons
- Publication date
- 01/06/2023
- Field of study
PURPOSE: Despite family history being an established risk factor for prostate cancer, the role of a broader definition of family history inclusive of not just prostate cancer but other genetically related malignancies has not been investigated in the active surveillance population. Here, we evaluate the impact of an expanded definition of family history on active surveillance outcomes.
MATERIALS AND METHODS: Patients undergoing active surveillance for prostate cancer at Massachusetts General Hospital from 1997-2019 with detailed data available on family cancer history were identified. Primary outcome was biopsy progression-free survival, and secondary outcomes were treatment-free survival, adverse pathological features at prostatectomy, and biochemical recurrence after treatment. Statistical analyses were conducted using the Kaplan-Meier method and Cox regression.
RESULTS: Among 855 evaluable patients, 300 (35.1%) patients had any family history of prostate cancer, and 95 (11.1%) had a family history of related malignancies suggestive of a hereditary cancer syndrome. Family history of prostate cancer alone was not associated with biopsy progression, whereas family history suggestive of a hereditary cancer syndrome was associated with a significantly increased risk of biopsy progression (HR 1.43, 95%CI 1.01-2.02), independent of other known clinicopathological risk factors in multivariable analysis. Similarly, family history suggestive of a hereditary cancer syndrome was associated with significantly lower treatment-free survival (HR 1.58, 95%CI 1.14-2.18) in multivariable analysis. No significant association was found between family history and adverse features on surgical pathology or biochemical recurrence.
CONCLUSIONS: An expanded family history suggestive of a hereditary cancer syndrome is an independent predictor of biopsy progression during active surveillance. Men with such a family history may still be offered active surveillance but should be counseled regarding the higher risk of disease progression
Whole-genome sequencing reveals host factors underlying critical COVID-19
- Author
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- Weston H.
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- Whiteside J.
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- Wood H. -L.
- Wood S.
- Wood T.
- Woodford C.
- Woodruff M.
- Woods L.
- Woodyatt W.
- Woolley A. E.
- Worner R.
- Worsley L.
- Wray G.
- Wren L.
- Wright D.
- Wright J.
- Wright M.
- Wrobel N.
- Wu Y.
- Wulandari R.
- Wyllie D. H.
- Wynter I.
- Xavier K.
- Xue X.
- Yadav A.
- Yang J.
- Yassen A. M.
- Yates B.
- Ye C.
- Yun N.
- Zainy T.
- Zak A.
- Zaki A.
- Zamikula J.
- Zanella I.
- Zborowski A. C.
- Zeberg H.
- Zechner M.
- Zguro K.
- Zhang M.
- Zhao J. H.
- Zheng C.
- Zhou W.
- Zitter L.
- Zlatopolsky M.
- Zollner S.
- Zongo O.
- Zucchi P.
- Zyndorf M.
- Publication venue
- 'Springer Science and Business Media LLC'
- Publication date
- 01/01/2022
- Field of study
Critical COVID-19 is caused by immune-mediated inflammatory lung injury. Host genetic variation influences the development of illness requiring critical care1 or hospitalization2–4 after infection with SARS-CoV-2. The GenOMICC (Genetics of Mortality in Critical Care) study enables the comparison of genomes from individuals who are critically ill with those of population controls to find underlying disease mechanisms. Here we use whole-genome sequencing in 7,491 critically ill individuals compared with 48,400 controls to discover and replicate 23 independent variants that significantly predispose to critical COVID-19. We identify 16 new independent associations, including variants within genes that are involved in interferon signalling (IL10RB and PLSCR1), leucocyte differentiation (BCL11A) and blood-type antigen secretor status (FUT2). Using transcriptome-wide association and colocalization to infer the effect of gene expression on disease severity, we find evidence that implicates multiple genes—including reduced expression of a membrane flippase (ATP11A), and increased expression of a mucin (MUC1)—in critical disease. Mendelian randomization provides evidence in support of causal roles for myeloid cell adhesion molecules (SELE, ICAM5 and CD209) and the coagulation factor F8, all of which are potentially druggable targets. Our results are broadly consistent with a multi-component model of COVID-19 pathophysiology, in which at least two distinct mechanisms can predispose to life-threatening disease: failure to control viral replication; or an enhanced tendency towards pulmonary inflammation and intravascular coagulation. We show that comparison between cases of critical illness and population controls is highly efficient for the detection of therapeutically relevant mechanisms of disease
Genetic mechanisms of critical illness in COVID-19.
- Author
- A A Roger Thompson
- A Abraheem
- A Agasou
- A Ahmed
- A Ali
- A Allan
- A Altabaibeh
- A Alvaro
- A Aspinwall
- A Ayers
- A Bamford
- A Barron
- A Bashyal
- A Bellini
- A Bociek
- A Botello
- A Bowes
- A Brady
- A Brayne
- A Brown
- A Brown
- A Butler
- A Campbell
- A Carter
- A Collins
- A Cowley
- A Cowton
- A Cowton
- A Cox
- A Crew
- A Dance
- A Daniel
- A Daniels
- A Dela Rosa
- A Drummond
- A Durie
- A E Heron
- A Easthope
- A Easthope
- A Evans
- A Fofano
- A Gales
- A Ganesan
- A Gardner
- A Garg
- A Gherman
- A Gordon
- A Gratrix
- A Gulati
- A Gupta
- A Haigh
- A Haldeos
- A Harrison
- A Harvey
- A Hayes
- A Higham
- A Higham
- A Hilldrith
- A Holden
- A Hormis
- A Hutcheon
- A Javaid
- A Joseph
- A Kaliappan
- A Katary
- A Kay
- A Kayani
- A Kent
- A Kirkby
- A Knight
- A Kubisz-Pudelko
- A Kuravi
- A Lewis
- A Loveridge
- A Lyle
- A Mayer
- A McAlpine
- A McCarthy
- A McGregor
- A McGregor
- A Meikle
- A Mitchell
- A Mitra
- A Morris
- A Morrison
- A Naranjo
- A Nicholson
- A Nicholson
- A Nilsson
- A Noakes
- A Patel
- A Pickard
- A Poole
- A Price
- A Puxty
- A Quinn
- A Quinn
- A Raithatha
- A Rattray
- A Reddy
- A Reed
- A Reyes
- A Rose
- A Rose
- A Rostron
- A Roy
- A Roynon-Reed
- A S Raj
- A Salberg
- A Sanderson
- A Serrano-Ruiz
- A Solesbury
- A Sukha
- A Swain
- A Tariq
- A Thomas
- A Thomas
- A Todd
- A Tomas
- A Tridente
- A Tucci
- A Turnbull
- A Uriel
- A Ustianowski
- A Vochin
- A Vuylsteke
- A Waite
- A Walden
- A Whileman
- A Wilkinson
- A Williams
- A Williams
- A Wilson
- A Zak
- A Zaki
- Achille Iolascon
- Adam Auton
- Adam Brown
- Agnese Verzuri
- Agostino Ognibene
- Agostino Riva
- Ailsa Golightly
- Alan Maclean
- Alessandra
- Alessandra Stella
- Alessandra Vergori
- Alessia Giorli
- Alexander J Mentzer
- Alice Donati
- Alison M Meynert
- Alistair Nichol
- Ana da Silva Filipe
- Andrea Antinori
- Andrea Cossarizza
- Andrea Ganna
- Andrea Tommasi
- Andrew Rambaut
- Andrew Stenhouse
- Andy Law
- Anjali J Shastri
- Anna Canaccini
- Anna Maria Pinto
- Annarita Giliberti
- Annemarie B Docherty
- Antonella D'Arminio Monforte
- Antonia Ying Wai Ho
- Antonio Di Biagio
- Antony Symons
- Arianna Emiliozzi
- Arianna Gabrieli
- Audrey Coutts
- B Anwar
- B Attwood
- B Baines
- B Blackledge
- B Borislavova
- B Chandler
- B Charles
- B Creagh-Brown
- B David
- B Deacon
- B Deacon
- B Digby
- B Faulkner
- B Fuller
- B Gumbrill
- B Gurung
- B Hadebe
- B Hairsine
- B Hopkins
- B Johnston
- B Lenagh
- B Masunda
- B Ogg
- B Patel
- B Player
- B Purewal
- B Scholefield
- B Shelley
- B Sloan
- B Thomas
- B Wadams
- B Welsh
- B Wilkinson
- B Winter-Goodwin
- B Yates
- Baillie J Kenneth
- Barbara Rossetti
- Beale Rupert
- Beatrice Alex
- Benjamin Bach
- Bretherick Andrew D
- Bruno Frediani
- C Adams
- C Ahmed
- C Almaden-Boyle
- C Ashbrook-Raby
- C Basikolo
- C Battle
- C Beazley
- C Beith
- C Borra
- C Brandwood
- C Brantwood
- C Burnett
- C Castro Delgado
- C Clark
- C Clulow
- C Collins
- C Cruz
- C Davis
- C Demetriou
- C Dennis
- C Dexter
- C Downes
- C Dunmore
- C Eastgate
- C Eckbad
- C Finch
- C Gibson
- C Gorman
- C Hays
- C Hewitt
- C Holl
- C Howcroft
- C Humphrey
- C Jackson
- C Jardine
- C Jennings
- C Jones
- C Kaye
- C Lynch
- C Lyons
- C McCulloch
- C McParland
- C McParland
- C Murphy
- C Parmar
- C Pawley
- C Phillips
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- C Pothecary
- C Pothecary
- C Prendergast
- C Price
- C Rishton
- C Sell
- C Shovelton
- C Sicat
- C Stuart
- C Summers
- C Swan
- C Thompson
- C Thorpe
- C Tibke
- C Tierney
- C Vigurs
- C Wells
- C Whitton
- C Whyte
- C Wrey Brown
- Cameron J Fairfield
- Carmelo Piscopo
- Carmen Marciano
- Caroline Abernathy
- Carrol Gamble
- Caterina Lo Rizzo
- Catherine A Shaw
- Catherine H Weldon
- Caulfield Mark
- Ceilia Boz
- Cesira Nencioni
- Chelsea Ye
- Chiara Fallerini
- Chiara Gabbi
- Chiara Spertilli
- Chloe Donohue
- Chris Ponting
- Christoper A Green
- Cinthia E Jannes
- Clare Jackson
- Clohisey Sara
- Cristina Mussini
- D Antcliffe
- D Bakthavatsalam
- D Banach
- D Baptista
- D Bell
- D Branney
- D Brealey
- D Brealey
- D Butcher
- D Butcher
- D Childs
- D Clarke
- D Collier
- D Collier
- D Cristiano
- D Dawson
- D Donaldson
- D Duffin
- D Fottrell-Gould
- D Golden
- D Griffin
- D Hamilton
- D Hawcutt
- D Hope
- D Horner
- D Kallon
- D Kaye
- D Kelly
- D Loader
- D Lomas
- D Martin
- D McGlynn
- D McLaughlanv
- D Melia
- D Menzies
- D Mullan
- D Pogson
- D Potla
- D Potoczna
- D Purohit
- D Raynard
- D Salutous
- D Salutous
- D Scaletta
- D Shaw
- D Skinner
- D Smyth
- D Strachan
- D Tetla
- D Thornton
- D Trodd
- D Vedage
- D Walker
- D Warren
- D Williams
- D Wood
- D Wright
- Daniela Francisci
- Daniella Coker
- Danilo Tacconi
- David A van Heel
- David Bennet
- David L Robertson
- David Stuart
- Dawn Law
- Debby Bogaert
- Derek Murphy
- Domenico A Coviello
- E Abaleke
- E Allan
- E Anastasescu
- E Andrews
- E Apetri
- E B Jude
- E Beech
- E Beranova
- E Bevan
- E Black
- E Brinkworth
- E Collins
- E Combes
- E Davies
- E Dobson
- E Dooks
- E Fisher
- E Gendall
- E Goff
- E Goodwin
- E Gordon
- E Heeney
- E Horsley
- E Hughes
- E Johnson
- E Knights
- E Lee
- E London
- E Maccacari
- E Massey
- E McKenna
- E Meadows
- E Moncur
- E Morino
- E Mwaura
- E Peasgood
- E Perkins
- E Radford
- E Raith
- E Raith
- E Salciute
- E Smith
- E Smithson
- E Stoddard
- E Stones
- E Thomas
- E Tilney
- E Timlick
- E Treus Gude
- E Virgilio
- E Watson
- E Wilby
- Edoardo Conticini
- Egle Saviciute
- Elena Bargagli
- Elena Desanctis
- Elisa Benetti
- Elisa Frullanti
- Elisabetta Menatti
- Elisabetta Schiaroli
- Ellie Mcmaster
- Emma C Thomson
- Emmanuelle Marques
- Enrico Martinelli
- Esther Duncan
- Esther Merlini
- Ewen M Harrison
- F Anderson
- F Auld
- F Bibi
- F Davies
- F Farquhar
- F Fisher
- F Hurford
- F Kibutu
- F McNeela
- F Moore
- F Nasir
- F Trim
- F Wakinshaw
- F Williams
- Fabio Lena
- Fawkes Angie
- Federico Anedda
- Federico Franchi
- Ferdinando Giannattasio
- Filip Taneski
- Filippo Aucella
- Filippo Biscarini
- Floriana Valentino
- Fourman Max Head
- Francesca Andretta
- Francesca Fava
- Francesca Gatti
- Francesca Mari
- Francesca Montagnani
- Francesco Castelli
- Francesco Raimondi
- Furniss James
- G Andrew
- G Arbane
- G Bell
- G Bercades
- G Croston
- G Debreceni
- G Durrant
- G Hambrook
- G Hobden
- G Houston
- G Hughes
- G Jones
- G Lubimbi
- G Maloney
- G Martir
- G Millen
- G Mills
- G O'Connor
- G Padden
- G Randell
- G Sadera
- G Seddon
- G Sera Howe
- G Sloane
- G Subramanian
- G Tsinaslanidis
- G Turner
- G Watson
- G Wray
- Gabriella Coiro
- Gabriella Doddato
- Gail Carson
- Gardar Sveinbjornsson
- Gary Leeming
- Genni Spargi
- Georgios Pollakis
- Giacomo Zanelli
- Gian Piero Caldarelli
- Giancarlo Bosio
- Giuseppe Fiorentino
- Giuseppe Merla
- Gountouna Elvina
- Graham S Cooke
- Griffiths Fiona
- Grimes Graeme
- H Bancroft
- H Bates
- H Belfield
- H Blackman
- H Blakemore
- H Brooke
- H Button
- H Coles
- H Curgenven
- H Filipe
- H Fox
- H Golding
- H Hill
- H Holcombe
- H Houlden
- H Jeffrey
- H Kent
- H Langton
- H McGuinness
- H Meghari
- H Millward
- H Moore
- H Parker
- H Pearson
- H Prady
- H Quinn
- H Rangarajan
- H Rehman
- H Reschreiter
- H Riley
- H Sainsbury
- H Savill
- H Sturgeon
- H T-Michael
- H Tench
- H Tiveran
- H Turner
- H Whittle
- H Willis
- H Wood
- Haley Chris
- Hanning Mal
- Harrison David
- Hayley Hardwick
- Hayward Caroline
- Helen Szoor-McElhinney
- Hinds Charles
- Ho Antonia
- Horby Peter
- I Ali Mohamed Ali
- I Balagosa
- I Birkinshaw
- I Burn
- I Chadbourn
- I D Clement
- I Edmond
- I Frost
- I Hass
- I Hussain
- I Lancoma-Malcolm
- I Leadbitter
- I Nagra
- I Otahal
- I Otahal
- I Turner-Bone
- I Welters
- I White
- I Wynter
- Ilaria Meloni
- Immacolata Andolfo
- Isabella Zanella
- J Allan
- J Barker
- J Bewley
- J Biddle
- J Birch
- J Birch
- J Bradley-Potts
- J Brown
- J Bryant
- J Butler
- J Camsooksai
- J Carter
- J Caterson
- J Cebrian Suarez
- J Cockerill-Taylor
- J Cole
- J Colley
- J Cooper
- J Cupitt
- J Cuttler
- J Daglish
- J Dasgin
- J Dawson
- J Dearden
- J Deery
- J Donnachie
- J Dykes
- J Easton
- J Egan
- J Fernandez Roman
- J Finn
- J Fletcher
- J Frankham
- J Gaylard
- J Gill
- J Godden
- J Goodsell
- J Gregory
- J Greig
- J Gurasashvili
- J Hardy
- J Harris
- J Hatton
- J Hawes
- J Highgate
- J Hornsby
- J Hulme
- J Hunt
- J Hutter
- J Ingham
- J Jones
- J Jones
- J K Baillie
- J Kassam
- J Kenneth Baillie
- J Kenneth Baillie
- J Keshet-Price
- J Liew
- J Little
- J Mallinson
- J Martin
- J Matthews
- J McCormick
- J Medhora
- J Melville
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- J North
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- J Scriven
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- Janet T Scott
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- Katarzyna Hafezi
- Keating Sean
- Kenneth A Mclean
- Kirstie Morrice
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- Klenerman Paul
- Knight Julian
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- L Abel
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- L Allen
- L Armstrong
- L Barclay
- L Benham
- L Botfield
- L Bough
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- L Bunni
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- L Cagova
- L Catlow
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- L Ferguson
- L Folkes
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- L Grimmer
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- L Lennon
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- L Ma
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- L McMorrow
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- L Mew
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- L Zitter
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- Laura Bergantini
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- Laura Marsh
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- Leonardo Croci
- Lia Crotti
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- Lorenzo Salerni
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- Louise Cullum
- Louise Macgillivray
- Louise Sigfrid
- Luca Cantarini
- Luca Guidelli
- Luca Masucci
- Luisa Tavecchia
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- M Wills
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- Porteous David J
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- Stefania Mantovani
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- Stefano Rusconi
- Stella Aslibekyan
- Stephanie Roberts
- Stephen R Knight
- Summers Charlotte
- Susanna Croci
- Susanna Guerrini
- T Anderson
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- T Pogreban
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- T Samakomva
- T Smith
- T Smith
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- T Wood
- Tammy Gilchrist
- Tenesa Albert
- Teresa Filshtein-Sonmez
- Thomas M Drake
- Thushan de Silva
- Tim Walsh
- Tom Fletcher
- Tom Solomon
- Tony Wackett
- Trevor Paterson
- Tullio Trotta
- Turtle Lance
- U Poultney
- V Amin
- V Anumakonda
- V Bastion
- V Cannons
- V Crickmore
- V Gopal
- V Irvine
- V Kasipandian
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- V Linnett
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- V Page
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- V Parris
- V Pristopan
- V Ratnam
- V Rivers
- V Sarathy
- V Thomas
- V Thwaites
- V Tuckey
- V Turner
- V Wagstaff
- V Waugh
- Valentina Anemoli
- Vanessa Sancho-Shimizu
- Victoria Shaw
- Vitart Veronique
- W Harrison
- W Khaliq
- W Khaliq
- W McCormick
- W Woodyatt
- Walker Susan
- Walsh Timothy
- Wang Bo
- Wei Shen Lim
- Wendy S Barclay
- William A Paxton
- William Greenhalf
- Wilson James F
- Wrobel Nicola
- Wu Yang
- X Qiu
- Y Baird
- Y Choudhury
- Y Hussain
- Y Jackson
- Y Thirlwall
- Yang Jian
- Yang Zhijian
- Z Alldis
- Z Belagodu
- Z Bradshaw
- Z Coton
- Z Daly
- Z Farzad
- Z Fernandez
- Z Garland
- Z Maqsood
- Z Omar
- Z Prime
- Z Scott
- Zechner Marie
- Zhai Ranran
- Zheng Chenqing
- Publication venue
- Nature
- Publication date
- 01/01/2020
- Field of study
Host-mediated lung inflammation is present1, and drives mortality2, in the critical illness caused by coronavirus disease 2019 (COVID-19). Host genetic variants associated with critical illness may identify mechanistic targets for therapeutic development3. Here we report the results of the GenOMICC (Genetics Of Mortality In Critical Care) genome-wide association study in 2,244 critically ill patients with COVID-19 from 208 UK intensive care units. We have identified and replicated the following new genome-wide significant associations: on chromosome 12q24.13 (rs10735079, P = 1.65 × 10-8) in a gene cluster that encodes antiviral restriction enzyme activators (OAS1, OAS2 and OAS3); on chromosome 19p13.2 (rs74956615, P = 2.3 × 10-8) near the gene that encodes tyrosine kinase 2 (TYK2); on chromosome 19p13.3 (rs2109069, P = 3.98 × 10-12) within the gene that encodes dipeptidyl peptidase 9 (DPP9); and on chromosome 21q22.1 (rs2236757, P = 4.99 × 10-8) in the interferon receptor gene IFNAR2. We identified potential targets for repurposing of licensed medications: using Mendelian randomization, we found evidence that low expression of IFNAR2, or high expression of TYK2, are associated with life-threatening disease; and transcriptome-wide association in lung tissue revealed that high expression of the monocyte-macrophage chemotactic receptor CCR2 is associated with severe COVID-19. Our results identify robust genetic signals relating to key host antiviral defence mechanisms and mediators of inflammatory organ damage in COVID-19. Both mechanisms may be amenable to targeted treatment with existing drugs. However, large-scale randomized clinical trials will be essential before any change to clinical practice
Common, low-frequency, rare, and ultra-rare coding variants contribute to COVID-19 severity
- Author
- A. Abraheem
- A. Agasou
- A. Ahmed
- A. Ali
- A. Allan
- A. Altabaibeh
- A. Alvaro
- A. Aspinwall
- A. Ayers
- A. Bamford
- A. Barron
- A. Bashyal
- A. Bellini
- A. Bociek
- A. Botello
- A. Bowes
- A. Brady
- A. Brayne
- A. Brown
- A. Brown
- A. Butler
- A. Carter
- A. Collins
- A. Cowley
- A. Cowton
- A. Cowton
- A. Cox
- A. Crew
- A. Dance
- A. Daniel
- A. Daniels
- A. Dela Rosa
- A. Drummond
- A. Durie
- A. E. Heron
- A. Easthope
- A. Easthorpe
- A. Evans.
- A. Fofano
- A. Gales
- A. Ganesan
- A. Gardner
- A. Garg
- A. Gherman
- A. Gordon
- A. Gratrix
- A. Gulati
- A. Gupta
- A. Haigh
- A. Haldeos
- A. Harrison
- A. Harvey
- A. Hayes
- A. Higham
- A. Higham
- A. Hilldrith
- A. Holden
- A. Hormis
- A. Hutcheon
- A. Javaid
- A. Joseph
- A. Kaliappan
- A. Katary
- A. Kay
- A. Kayani
- A. Kent
- A. Kirkby
- A. Knight
- A. Kubisz-Pudelko
- A. Kuravi
- A. Lewis
- A. Loveridge
- A. Lyle
- A. Mayer
- A. McAlpine
- A. McCarthy
- A. McGregor
- A. McGregor
- A. Meikle
- A. Mitchell
- A. Mitra
- A. Morris
- A. Morrison
- A. Naranjo
- A. Nicholson
- A. Nicholson
- A. Noakes
- A. Patel
- A. Pickard
- A. Price
- A. Puxty
- A. Quinn
- A. Quinn
- A. Raithatha
- A. Rattray
- A. Reddy
- A. Reed
- A. Reyes
- A. Rose
- A. Rose
- A. Rostron
- A. Roy
- A. Roynon-Reed
- A. S. Raj
- A. Salberg
- A. Sanderson
- A. Serrano-Ruiz
- A. Solesbury
- A. Sukha
- A. Swain
- A. Tariq
- A. Thomas
- A. Thomas
- A. Todd
- A. Tomas
- A. Tridente
- A. Tucci
- A. Turnbull
- A. Uriel
- A. Ustianowski
- A. Vochin
- A. Vuylsteke
- A. Waite
- A. Walden
- A. Whileman
- A. Wilkinson
- A. Williams
- A. Williams
- A. Wilson
- A. Zak
- A. Zaki
- Achille Iolascon
- Adam Brown
- Adam Krętowski
- Adriana Roży
- Agnese Verzuri
- Agnieszka Adamek
- Agnieszka Bielska
- Agostino Ognibene
- Agostino Riva
- Ailsa Golightly
- Alan Maclean
- Albert Tenesa
- Aleksandra Berkan-Kawinska
- Aleksandra Jezela-Stanek
- Aleksandra Starosz
- Alessandra Guarnaccia
- Alessandra Renieri &
- Alessandra Stella
- Alessandra Vergori
- Alessandro Pancrazzi
- Alessia Giorli
- Alice Donati
- Alison Meynert
- Alistair Nichol
- Anders Larsson
- Andrea Antinori
- Andrea Cossarizza
- Andrea Gabbuti
- Andrea Tommasi
- Andrew D. Bretherick
- Andrew Law
- Andrew Stenhouse
- Andrzej Eljaszewicz
- Andrzej Horban
- Andy Law
- Angelica Pagliazzi
- Angie Fawkes
- Anke Hinney
- Anna Canaccini
- Anna Kruk
- Anna Maria Pinto
- Anna Moniuszko-Malinowska
- Anna Parfieniuk-Kowerda
- Anna Piekarska
- Anna Szałkowska
- Annarita Giliberti
- Anne Richmond
- Antonella D. ’Arminio Monforte
- Antonella Vincenti
- Antonia Ho
- Antonio Di Biagio
- Antonio Perrella
- Arianna Emiliozzi
- Arianna Gabrieli
- Arsalin Azzadin
- Asma Al Thani &
- Athanasios Kousathanas
- Audrey Coutts
- Axel Schmidt
- Axel Schmidt
- B. Anwar
- B. Attwood
- B. Baines
- B. Blackledge
- B. Borislavova
- B. Chandler
- B. Charles
- B. Creagh-Brown
- B. David
- B. Deacon
- B. Deacon
- B. Digby
- B. Faulkner
- B. Fuller
- B. Gumbrill
- B. Gurung
- B. Hadebe
- B. Hairsine
- B. Hopkins
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- B. Masunda
- B. Ogg
- B. Patel
- B. Player
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- B. Shelley
- B. Sloan
- B. Thomas
- B. Wadams
- B. Welsh
- B. Wilkinson
- B. Winter-Goodwin
- B. Yates
- Barbara Rossetti
- Barbara Shih
- Barbara Sobala-Szczygiel
- Beata Puzanowska
- Benedetta Romanin
- Björn Jensen
- Bo Wang
- Brent Richards
- Bruno Frediani
- C. Adams
- C. Ahmed
- C. Almaden-Boyle
- C. Ashbrook-Raby
- C. Basikolo
- C. Battle
- C. Beazley
- C. Beith
- C. Borra
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- C. Clark
- C. Clulow
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- C. Gibson
- C. Gorman
- C. Hays
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- C. Jennings
- C. Jones
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- C. Lynch
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- C. McCulloch
- C. McParland
- C. McParland
- C. Murphy
- C. Parmar
- C. Pawley
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- C. Phillips
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- C. Pothecary
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- C. Price
- C. Rishton
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- C. Summers
- C. Swan
- C. Thompson
- C. Thorpe
- C. Tibke
- C. Tierney
- C. Vigurs
- C. Wells
- C. Whitton
- C. Whyte
- C. Wrey Brown
- Carlo Maj
- Carmelo Piscopo
- Caroline Abernathy
- Caterina Lo Rizzo
- Ce Dunmore
- Cecilia Costa
- Ceilia Boz
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- Chadi Saad
- Charles Hinds
- Charlotte Summers
- Chenqing Zheng
- Chiara Barbieri
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- Chiara Spertilli Raffaelli
- Chris P. Ponting
- Chris Ponting
- Christian Herr
- Christof Winter
- Christoph D. Spinner
- Clark D. Russell
- Claudia Suardi
- Claudio Ferri
- Clemens M. Wendtner
- Cristina Mussini
- D. Antcliffe
- D. Bakthavatsalam
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- D. Baptista
- D. Bell
- D. Branney
- D. Brealey
- D. Brealey
- D. Butcher
- D. Butcher
- D. Childs
- D. Clarke
- D. Collier
- D. Collier
- D. Cristiano
- D. Dawson
- D. Donaldson
- D. Duffin
- D. Golden
- D. Griffin
- D. Hawcutt
- D. Hope
- D. Horner
- D. Kallon
- D. Kaye
- D. Kelly
- D. Loader
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- D. Martin
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- D. Melia
- D. Menzies
- D. Mullan
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- D. Salutous
- D. Salutous
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- D. Shaw
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- D. Thornton
- D. Trodd
- D. Vedage
- D. Walker
- D. Warren
- D. Williams
- D. Wood
- D. Wright
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- Danilo Tacconi
- Danny McAuley
- David Bennett
- David Harrison
- David Maslove
- Davide Grassi
- Davide Romani
- Dawn Law
- Diana Alaverdian
- Diana Martonik
- Diego Ripamonti
- Domenico A. Coviello
- Dorota Pasko
- Dorota Zarębska-Michaluk
- E. Abaleke
- E. Allan
- E. Anastasescu
- E. Andrews
- E. Apetri
- E. Beech
- E. Beranova
- E. Bevan
- E. Black
- E. Brinkworth
- E. Collins
- E. Combes
- E. Davies
- E. Dobson
- E. Dooks
- E. Fisher
- E. Gendall
- E. Goff
- E. Goodwin
- E. Gordon
- E. Heeney
- E. Horsley
- E. Hughes
- E. Johnson
- E. Jude
- E. Knights
- E. Lee
- E. London
- E. Maccacari
- E. Massey
- E. McKenna
- E. Meadows
- E. Moncur
- E. Morino
- E. Mwaura
- E. Peasgood
- E. Perkins
- E. Radford
- E. Raith
- E. Salciute L. Grauslyte
- E. Smith
- E. Smithson
- E. Stoddard
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- E. Thomas
- E. Tilney
- E. Timlick
- E. Treus Gude
- E. Virgilio
- E. Watson
- E. Wilby
- E. Wraith
- Edoardo Conticini
- Elena Andreucci
- Elena Bargagli
- Elena Desanctis
- Elisa Benetti
- Elisa Frullanti
- Elisabetta Menatti
- Elisabetta Schiaroli
- Ellie Mcmaster
- Elvina Gountouna
- Emanuele Catena
- Enrico Cabri
- Enrico Martinelli
- Erika Fiorentini
- Erola Pairo-Castineira
- Erola Pairo-Castineira
- Esther Duncan
- Eugenia Quiros-Roldan
- Eva C. Schulte
- Eva C. Schulte
- F. Anderson
- F. Auld
- F. Bibi
- F. Davies
- F. Farquhar
- F. Fisher
- F. Hurford
- F. Kibutu
- F. McNeela
- F. Moore
- F. Nasir
- F. Trim
- F. Wakinshaw
- F. Williams
- Fabian Brand
- Fabio Lena
- Faisal Almalki
- Federica Gaia Miraglia
- Federico Anedda
- Federico Franchi
- Ferdinando Giannattasio
- Filip Taneski
- Filippo Aucella
- Filippo Biscarini
- Fiona Griffiths
- Floriana Valentino
- Francesca Andretta
- Francesca Ariani
- Francesca Colombo
- Francesca Fava
- Francesca Gatti
- Francesca Mari
- Francesca Minnai
- Francesca Montagnani
- Francesca Vichi
- Francesco Bianchi
- Francesco Brancati
- Francesco Castelli
- Francesco Menichetti
- Francesco Paciosi
- Francesco Raimondi
- Francesco Vladimiro Segala
- Francis P. Crawley
- Franco Maggiolo
- Franco Marinangeli
- G. Andrew
- G. Arbane
- G. Bell
- G. Bercades
- G. Croston
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- G. Durrant
- G. Hambrook
- G. Hobden
- G. Houston
- G. Hughes
- G. Jones
- G. Lubimbi
- G. Maloney
- G. Martir
- G. Millen
- G. Mills
- G. O’Connor
- G. Randell
- G. Sadera
- G. Seddon
- G. Sera Howe
- G. Sloane
- G. Subramanian
- G. Tsinaslanidis
- G. Turner
- G. Watson
- G. Wray
- Gabriela Sokołowska
- Gabriella Coiro
- Gabriella Doddato
- Gabriella Maria Squeo
- GEN-COVID Multicenter Study
- Genni Spargi
- GenOMICC Consortium
- Giada Beligni
- Gian Piero Caldarelli
- Gianfranco Parati
- Giovanna Morelli
- Giulia Gori
- Giuseppe Fiorentino
- Giuseppe Merla
- Giusy Tiseo
- Graeme Grimes
- Guillaume Butler-Laporte
- Guillaume Butler-Laporte
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- H. Tench
- H. Tiveran
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- Wadha Al-Muftah
- WES/WGS Working Group Within the HGI
- Wiktoria Izdebska
- Wilna Oosthuyzen
- X. Qiu
- Xia Shen
- Y. Baird
- Y. Choudhury
- Y. Hussain
- Y. Jackson
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- Yanara Marincevic-Zuniga
- Yang Wu
- Yaser Al-Sarraj
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- Z. Farzad
- Z. Fernandez
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- Z. Omar
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- Z. Scott
- Zhijian Yang
- Publication venue
- Publication date
- 01/01/2022
- Field of study
The combined impact of common and rare exonic variants in COVID-19 host genetics is currently insufficiently understood. Here, common and rare variants from whole-exome sequencing data of about 4000 SARS-CoV-2-positive individuals were used to define an interpretable machine-learning model for predicting COVID-19 severity. First, variants were converted into separate sets of Boolean features, depending on the absence or the presence of variants in each gene. An ensemble of LASSO logistic regression models was used to identify the most informative Boolean features with respect to the genetic bases of severity. The Boolean features selected by these logistic models were combined into an Integrated PolyGenic Score that offers a synthetic and interpretable index for describing the contribution of host genetics in COVID-19 severity, as demonstrated through testing in several independent cohorts. Selected features belong to ultra-rare, rare, low-frequency, and common variants, including those in linkage disequilibrium with known GWAS loci. Noteworthily, around one quarter of the selected genes are sex-specific. Pathway analysis of the selected genes associated with COVID-19 severity reflected the multi-organ nature of the disease. The proposed model might provide useful information for developing diagnostics and therapeutics, while also being able to guide bedside disease management. © 2021, The Author(s)
The impact of surgical delay on resectability of colorectal cancer: An international prospective cohort study
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- Abadia M
- Abassy J
- Abate E
- Abbott Tom EF
- Abdelaal Samir A
- Abdeldayem H
- Abdelkabir M
- Abdelsamed A
- Abdulwahed E
- Abiyere H
- Abou Chaar MK
- Abukhalaf SA
- Abukhalaf Sadi
- Adamina Michel
- Ademuyiwa Adesoji
- Ademuyiwa Adesoji O
- Adeyeye A
- Adisa Adewale
- Afzal MF
- Agarwal Arnav
- Aggarwal M
- Agnes A
- Agostini C
- Agrawal A
- Agrawal N
- Agresta F
- Aguiar Junior S
- Ahmed A
- Ahmed K
- Ahmed Nafees R
- Ahmed Z
- Ahn JH
- Aime A
- Akhtar N
- Akkulak Murat
- Akrivou D
- Al Abdallah M
- Al Riyami S
- Al Sayed M
- Al-Masri M
- Al-Najjar H
- Al-Slaibi I
- Alaa S
- Alakaloko Felix
- Alameer Ehab
- Alamri Alex
- Alawneh F
- Albertsmeier M
- Albertsmeier Markus
- Alderson Derek
- Aldokali N
- Alemanno G
- Alfieri S
- Algallai M
- Ali AA
- Alkadiki Ghadah Z
- Almaadany Faraj S
- Almeida AC
- Almeida-Reis R
- Almezghwi H
- Almond Max
- Alrahawy M
- Alser Osaid
- Alshaar Muhammad
- Alshareea E
- Alshareef K
- Alshryda Sattar
- Alsoufi A
- Altamirano Riquoir C
- Altomare DF
- Altomi I
- Alurralde C
- Alvarez MR
- Alvi A
- Alwarfly S
- AlZAEDE S
- Alzeerelhouseini IAH
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- Sundar Sudha
- Susztak N
- Sutherland A
- Swinson B
- Syed WAS
- Syllaios A
- Szubota I
- Tabiri Stephen
- Tactuk N
- Taddei A
- Taibi A
- Talaat M
- Tamini N
- Tammaro P
- Tan JA
- Tanzanu M
- Tartaglia D
- Tasis N
- Tavares F
- Tawheed A
- Teh C
- Teixeira J
- Teixeira M
- Testa V
- Thanapal MR
- Thekinkattil Dinesh
- Theodosopoulos T
- Thian A
- Tirloni L
- Tirotta Fabio
- Tojal A
- Tolani MA
- Tom K
- Tonini V
- Tooulias A
- Townen Philip
- Townend D
- Townend Philip
- Travaglio E
- Tribillon E
- Tropeano FP
- Tsiaoussis I
- Tsoulfas G
- Tsoulfas Georgios
- Tucci R
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- Umar A
- Urbani A
- Usai A
- Uzunoglu FG
- Vaccarella G
- Vale R
- Valenzuela J
- Vallance Abigail
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- Van den Eynde R
- van der Plas Willemijn
- Van Heinsbergen M
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- Van Ramshorst G
- van Ramshorst Gabrielle H
- Varghese Chris
- Vasey C
- Vassiliu P
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- Vaz-Pereira R
- Veetil Kannummal S
- Vendrame C
- Venskutonis D
- Vergari R
- Vernon L
- Vescio G
- Vezakis A
- Vidya Raghavan
- Vieira A
- Vieira B
- Vignali A
- Vignotto C
- Vilar-Compte D
- Vimalachandran Dale
- Vimalchandra Dale
- Violante T
- Vishnoi JR
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- Volpin E
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- Vovola F
- Waldron A
- Walker P
- Walkes K
- Wani R
- Waqar SH
- Warren Oliver J
- Watson E
- Wedderburn Duane
- Weitz J
- Welsch T
- Werner J
- Whelan M
- Wilkins Alex
- Willaert W
- Wimmer A
- Winter D
- Winter Stuart C
- Wong MP
- Wood M
- Wrigh Naomi
- Wullschleger M
- Xavier R
- Xenaki S
- Xynos E
- Yadev I
- Yang W
- Ye G
- Yezzaji H
- Yiallourou A
- Yousof EA
- Yunus Mohd MF
- Yurttas C
- Zakaria AD
- Zakaria Z
- Zambon M
- Zanus G
- Zatecky J
- Zelic M
- Zerbib P
- Zervas K
- Zese M
- Zhang H
- Zizzo M
- Zmora O
- Zografos C
- Zonta S
- Zourntou S
- Publication venue
- 'Royal College of Obstetricians & Gynaecologists (RCOG)'
- Publication date
- 01/06/2022
- Field of study
AIM: The SARS-CoV-2 pandemic has provided a unique opportunity to explore the impact of surgical delays on cancer resectability. This study aimed to compare resectability for colorectal cancer patients undergoing delayed versus non-delayed surgery. METHODS: This was an international prospective cohort study of consecutive colorectal cancer patients with a decision for curative surgery (January-April 2020). Surgical delay was defined as an operation taking place more than 4 weeks after treatment decision, in a patient who did not receive neoadjuvant therapy. A subgroup analysis explored the effects of delay in elective patients only. The impact of longer delays was explored in a sensitivity analysis. The primary outcome was complete resection, defined as curative resection with an R0 margin. RESULTS: Overall, 5453 patients from 304 hospitals in 47 countries were included, of whom 6.6% (358/5453) did not receive their planned operation. Of the 4304 operated patients without neoadjuvant therapy, 40.5% (1744/4304) were delayed beyond 4 weeks. Delayed patients were more likely to be older, men, more comorbid, have higher body mass index and have rectal cancer and early stage disease. Delayed patients had higher unadjusted rates of complete resection (93.7% vs. 91.9%, P = 0.032) and lower rates of emergency surgery (4.5% vs. 22.5%, P < 0.001). After adjustment, delay was not associated with a lower rate of complete resection (OR 1.18, 95% CI 0.90-1.55, P = 0.224), which was consistent in elective patients only (OR 0.94, 95% CI 0.69-1.27, P = 0.672). Longer delays were not associated with poorer outcomes. CONCLUSION: One in 15 colorectal cancer patients did not receive their planned operation during the first wave of COVID-19. Surgical delay did not appear to compromise resectability, raising the hypothesis that any reduction in long-term survival attributable to delays is likely to be due to micro-metastatic disease
Oncogenic Signaling Pathways in The Cancer Genome Atlas
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- A. Abeshouse
- A. Ally
- A. Antenucci
- A. Arnaout
- A. Berchuck
- A. Bergeron
- A. Bossler
- A. Boussioutas
- A. Breggia
- A. Burnette
- A. Chen
- A. Clipca
- A. Davis
- A. De Rienzo
- A. De Rose
- A. Fehrenbach
- A. Gillis
- A. Gimenez-Roqueplo
- A. Gopalan
- A. Haddad
- A. Hartmann
- A. Iavarone
- A. Jimeno
- A. Kastl
- A. Kendler
- A. Kibel
- A. Korkut
- A. Longatto-Filho
- A. Luna
- A. Luna
- A. Malykh
- A. Mariamidze
- A. Mes-Masson
- A. Noss
- A. Ochoa
- A. Ochoa
- A. Perin
- A. Piché
- A. Pickens
- A. Rao
- A. Sankarankuty
- A. Secord
- A. Sepulveda
- A. Shabunin
- A. Sharp
- A. Sood
- A. Spillane
- A. Tam
- A. Tischler
- A. Tsao
- A. Unterberg
- A. Vicha
- A. von Deimling
- A.C. Berger
- A.C. de Carvalho
- A.D. Cherniack
- A.D. Cherniack
- A.D. Tward
- A.E. Sloan
- A.G. Robertson
- A.H. Berger
- A.H. Bryce
- A.H. Perou
- A.J. Kovatich
- A.J. Lazar
- A.J. Lazar
- A.J. Mungall
- A.K. Godwin
- A.L. Carvalho
- A.L. Guillermo
- A.M. Hegde
- A.M.A. Gonzalez
- A.P. Hoyle
- A.R. Metwalli
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- L. Xuan
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- L. Zhang
- L.A. Donehower
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- L.A. Zach
- L.E. Mose
- L.N. Kwong
- L.S. Schmidt
- M. Albert
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- T.A. Chan
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- U. Dogrusoz
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- V. Lyadov
- V. Reuter
- V. Thorsson
- W. Barrett
- W. Eijckenboom
- W. Hale
- W. Kycler
- W. Liang
- W. Liu
- W. Oosterhuis
- W. Urba
- W. Ye
- W. Zhang
- W. Zhou
- W. Zhou
- W.E. Grizzle
- W.G. Richards
- W.J. Edenfield
- W.K. Chatila
- W.K. Chatila
- W.K. Rathmell
- W.M. Linehan
- X. Liu
- X. Liu
- X. Sastre
- Y. Han
- Y. Liu
- Y. Shi
- Y. Sun
- Y. Tang
- Y. Wan
- Y. Wolinsky
- Y. Xiao
- Z. Heins
- Z. Wang
- Z.J. Heins
- Publication venue
- 'Elsevier BV'
- Publication date
- 05/04/2018
- Field of study
Genetic alterations in signaling pathways that control cell-cycle progression, apoptosis, and cell growth are common hallmarks of cancer, but the extent, mechanisms, and co-occurrence of alterations in these pathways differ between individual tumors and tumor types. Using mutations, copy-number changes, mRNA expression, gene fusions and DNA methylation in 9,125 tumors profiled by The Cancer Genome Atlas (TCGA), we analyzed the mechanisms and patterns of somatic alterations in ten canonical pathways: cell cycle, Hippo, Myc, Notch, Nrf2, PI-3-Kinase/Akt, RTK-RAS, TGFb signaling, p53 and beta-catenin/Wnt. We charted the detailed landscape of pathway alterations in 33 cancer types, stratified into 64 subtypes, and identified patterns of co-occurrence and mutual exclusivity. Eighty-nine percent of tumors had at least one driver alteration in these one alteration potentially targetable by currently available drugs. Thirty percent of tumors had multiple targetable alterations, indicating opportunities for combination therapy
Whole-genome sequencing reveals host factors underlying critical COVID-19
- Author
- Abd Elghafar M.S.
- Abdel-Aziz M.
- Abdelrazik M.
- Abdollahi H.
- Abdullah T.
- Abecasis G.R.
- Abecasis G.R.
- Abedalthagafi M.
- Abel L.
- Abernathy C.
- Abraheem A.
- Abul-Husn N.S.
- Acquilini D.
- Adams C.
- Adams E.L.
- Adams K.
- Adamsara A.
- Adanini O.
- Adeleye O.
- Adra D.
- Afilalo J.
- Afilalo M.
- Afolabi D.
- Afrasiabi Z.
- Agasou A.
- Agrawal S.
- Agüero D.
- Ahmad N.
- Ahmadi S.
- Ahmed A.
- Ahmed C.
- Akeroyd L.
- Akhtar M.N.
- Akinkugbe O.
- Aksentijevich A.
- Al Harthi F.
- Al Mutairi A.
- Al-Afghani H.
- Al-Awdah L.
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- Venturelli S.
- Vergori A.
- Verlander M.
- Verma A.
- Verma A.
- Verma S.S.
- Vertue M.
- Verula J.
- Verzuri A.
- Vigurs C.
- Villalonga J.M.
- Vincent R.
- Vincenti A.
- Virgilio E.
- Vitart V.
- Vizcaychipi M.P.
- Vochin A.
- Voide C.
- von Frenckell C.
- von Hohenstaufen K.A.
- Vonk J.M.
- Vulesevic B.
- Vuylsteke A.
- Wackett T.
- Wadams B.
- Waddington N.
- Wagstaff V.
- Wain L.V.
- Waite A.A.C.
- Wakefield P.
- Wakinshaw F.
- Waldron J.
- Walker D.
- Walker R.
- Walker S.
- Walker S.
- Walker S.
- Wall A.
- Walsh T.
- Walsh T.
- Walters R.K.
- Walton O.
- Wang B.
- Wang J.
- Wang X.
- Wanying Z.
- Ward G.
- Ward L.
- Ward M.
- Warden S.
- Warmerdam R.
- Warren D.
- Wassall H.
- Wasson C.
- Watkins C.
- Watson E.
- Watson G.
- Watson J.
- Watters M.
- Waugh V.
- Weaver J.
- Webster A.
- Webster D.
- Webster K.
- Wei S.
- Weiss S.T.
- Weldon C.H.
- Wells C.
- Welters I.D.
- Weston H.
- Whileman A.
- Whitbread J.
- White D.
- White I.
- White K.
- White M.
- White N.
- White N.
- Whiteley S.
- Whiteside J.
- Whittle H.
- Whitton C.
- Whyte C.
- Wicks S.J.
- Wilby E.
- Wilcox L.
- Wilcox R.
- Wild H.
- Wild L.
- Wild L.
- Wilding L.
- Wiles M.
- Wilkins J.
- Wilkinson A.
- Wilkinson B.
- Willer C.
- Williams A.
- Williams A.
- Williams A.
- Williams A.T.
- Williams D.
- Williams E.
- Williams F.
- Williams G.
- Williams H.
- Williams K.
- Williams M.
- Williams P.
- Williams S.
- Williams T.
- Willis C.
- Willis H.
- Wills M.
- Willson J.
- Wilson A.
- Wilson D.J.
- Wilson J.
- Wilson J.F.
- Wilson J.F.
- Winnard S.
- Winter-Goodwin B.
- Wolf-Roberts R.
- Wolford B.
- Wong J.
- Wood D.
- Wood H.-L.
- Wood S.
- Wood T.
- Woodford C.
- Woodruff M.
- Woods L.
- Woodyatt W.
- Woolley A.E.
- Worner R.
- Worsley L.
- Wray G.
- Wren L.
- Wrey Brown C.
- Wright D.
- Wright J.
- Wright M.
- Wrobel N.
- Wu Y.
- Wulandari R.
- Wyllie D.H.
- Wynter I.
- Xavier K.
- Xue X.
- Yadav A.
- Yang J.
- Yassen A.M.
- Yates B.
- Ye C.
- Yun N.
- Zainy T.
- Zak A.
- Zaki A.
- Zamikula J.
- Zanella I.
- Zborowski A.C.
- Zeberg H.
- Zechner M.
- Zechner M.
- Zguro K.
- Zhang M.
- Zhao J.H.
- Zheng C.
- Zhou W.
- Zitter L.
- Zlatopolsky M.
- Zongo O.
- Zucchi P.
- Zyndorf M.
- Zöllner S.
- Åsvold B.O.
- Publication venue
- Springer Science and Business Media LLC
- Publication date
- 07/07/2022
- Field of study
Critical COVID-19 is caused by immune-mediated inflammatory lung injury. Host genetic variation influences the development of illness requiring critical care1 or hospitalization2,3,4 after infection with SARS-CoV-2. The GenOMICC (Genetics of Mortality in Critical Care) study enables the comparison of genomes from individuals who are critically ill with those of population controls to find underlying disease mechanisms. Here we use whole-genome sequencing in 7,491 critically ill individuals compared with 48,400 controls to discover and replicate 23 independent variants that significantly predispose to critical COVID-19. We identify 16 new independent associations, including variants within genes that are involved in interferon signalling (IL10RB and PLSCR1), leucocyte differentiation (BCL11A) and blood-type antigen secretor status (FUT2). Using transcriptome-wide association and colocalization to infer the effect of gene expression on disease severity, we find evidence that implicates multiple genes—including reduced expression of a membrane flippase (ATP11A), and increased expression of a mucin (MUC1)—in critical disease. Mendelian randomization provides evidence in support of causal roles for myeloid cell adhesion molecules (SELE, ICAM5 and CD209) and the coagulation factor F8, all of which are potentially druggable targets. Our results are broadly consistent with a multi-component model of COVID-19 pathophysiology, in which at least two distinct mechanisms can predispose to life-threatening disease: failure to control viral replication; or an enhanced tendency towards pulmonary inflammation and intravascular coagulation. We show that comparison between cases of critical illness and population controls is highly efficient for the detection of therapeutically relevant mechanisms of disease
The SAGA Histone Deubiquitinase Module Controls Yeast Replicative Lifespan via Sir2 Interaction
- Author
- Publication venue
- 'Elsevier BV'
- Publication date
- 01/07/2014
- Field of study
We have analyzed the yeast replicative lifespan of a large number of open reading frame (ORF) deletions. Here, we report that strains lacking genes SGF73, SGF11, and UBP8 encoding SAGA/SLIK complex histone deubiquitinase module (DUBm) components are exceptionally long lived. Strains lacking other SAGA/SALSA components, including the acetyltransferase encoded by GCN5, are not long lived; however, these genes are required for the lifespan extension observed in DUBm deletions. Moreover, the SIR2-encoded histone deacetylase is required, and we document both a genetic and physical interaction between DUBm and Sir2. A series of studies assessing Sir2-dependent functions lead us to propose that DUBm strains are exceptionally long lived because they promote multiple prolongevity events, including reduced rDNA recombination and altered silencing of telomere-proximal genes. Given that ataxin-7, the human Sgf73 ortholog, causes the neurodegenerative disease spinocerebellar ataxia type 7, our findings indicate that the genetic and epigenetic interactions between DUBm and SIR2 will be relevant to neurodegeneration and aging
Network Scale-Up Correction Factors for Population Size Estimation of People Who Inject Drugs and Female Sex Workers in Iran
- Author
- Publication venue
- 'Public Library of Science (PLoS)'
- Publication date
- Field of study