R
Richard D. Baird
Researcher at University of Cambridge
Publications - 108
Citations - 6236
Richard D. Baird is an academic researcher from University of Cambridge. The author has contributed to research in topics: Breast cancer & Cancer. The author has an hindex of 25, co-authored 90 publications receiving 4562 citations. Previous affiliations of Richard D. Baird include Institute of Cancer Research & The Royal Marsden NHS Foundation Trust.
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Journal ArticleDOI
Liquid biopsies come of age: towards implementation of circulating tumour DNA
Jonathan C. M. Wan,Charles E. Massie,Javier Garcia-Corbacho,Florent Mouliere,James D. Brenton,Carlos Caldas,Simon Pacey,Richard D. Baird,Nitzan Rosenfeld +8 more
TL;DR: The field is now in an exciting transitional period in which ctDNA analysis is beginning to be applied clinically, although there is still much to learn about the biology of cell-free DNA.
Journal ArticleDOI
Enhanced detection of circulating tumor DNA by fragment size analysis
Florent Mouliere,Dineika Chandrananda,Anna M. Piskorz,Elizabeth Moore,Elizabeth Moore,James Morris,Lise Barlebo Ahlborn,Richard Mair,Teodora Goranova,Francesco Marass,Katrin Heider,Jonathan C. M. Wan,Anna Supernat,Anna Supernat,Irena Hudecova,Ioannis Gounaris,Ioannis Gounaris,Susana Ros,Mercedes Jimenez-Linan,Javier Garcia-Corbacho,Keval M. Patel,Olga Østrup,Suzanne Murphy,Matthew D. Eldridge,Davina Gale,Grant D. Stewart,Grant D. Stewart,Johanna Burge,Wendy N. Cooper,Michiel S. van der Heijden,Charles E. Massie,Colin Watts,Pippa Corrie,Simon Pacey,Simon Pacey,Kevin M. Brindle,Richard D. Baird,Morten Mau-Sørensen,Christine Parkinson,Christopher Smith,James D. Brenton,Nitzan Rosenfeld +41 more
TL;DR: Fragment size analysis and selective sequencing of specific fragment sizes can boost ctDNA detection and could complement or provide an alternative to deeper sequencing of cfDNA.
Journal ArticleDOI
First-in-Man Clinical Trial of the Oral Pan-AKT Inhibitor MK-2206 in Patients With Advanced Solid Tumors
Timothy A. Yap,Li Yan,Amita Patnaik,Ivy Fearen,David Olmos,Kyriakos P. Papadopoulos,Richard D. Baird,Liliana Delgado,Adekemi Taylor,Lisa Lupinacci,Ruth Riisnaes,Lorna Pope,Simon P. Heaton,George Thomas,Michelle D. Garrett,Daniel M. Sullivan,Johann S. de Bono,Anthony W. Tolcher +17 more
TL;DR: MK-2206 was well tolerated, with evidence of AKT signaling blockade, and Rational combination trials are ongoing to maximize clinical benefit with this therapeutic strategy.
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The poly(ADP-ribose) polymerase inhibitor niraparib (MK4827) in BRCA mutation carriers and patients with sporadic cancer: a phase 1 dose-escalation trial
Shahneen Sandhu,Shahneen Sandhu,William R. Schelman,George Wilding,Victor Moreno,Richard D. Baird,Susana Miranda,Lucy Hylands,Ruth Riisnaes,Martin Forster,Aurelius Omlin,Nathan Kreischer,Khin Thway,Heidrun Gevensleben,L. Sun,John W. Loughney,Manash Shankar Chatterjee,Carlo Toniatti,Carlo Toniatti,Christopher L. Carpenter,Robert Iannone,Stan B. Kaye,Johann S. de Bono,Robert M Wenham +23 more
TL;DR: Niraparib (MK4827) as mentioned in this paper is an oral potent, selective PARP-1/PARP-2 inhibitor that induces synthetic lethality in preclinical tumour models with loss of BRCA and PTEN function.
Journal ArticleDOI
A Biobank of Breast Cancer Explants with Preserved Intra-tumor Heterogeneity to Screen Anticancer Compounds.
Alejandra Bruna,Oscar M. Rueda,Wendy Greenwood,Ankita Sati Batra,Maurizio Callari,R N Batra,Katherine Pogrebniak,José Luis Sandoval,John W. Cassidy,Ana Tufegdzic-Vidakovic,Stephen John Sammut,Linda Jones,Linda Jones,Elena Provenzano,Richard D. Baird,Richard D. Baird,Peter Eirew,James Hadfield,Matthew D. Eldridge,Anne McLaren-Douglas,Andrew Barthorpe,Howard Lightfoot,Mark J. O'Connor,Joe W. Gray,Javier Cortes,José Baselga,Elisabetta Marangoni,Alana L. Welm,Samuel Aparicio,Violeta Serra,Mathew J. Garnett,Carlos Caldas,Carlos Caldas +32 more
TL;DR: A large collection of breast cancer patient-derived tumor xenografts (PDTXs) are created, in which the morphological and molecular characteristics of the originating tumor are preserved through passaging in the mouse, and the intra-tumor genomic clonal architecture present in the originating breast cancers was mostly preserved.