P
Paul A. Beavis
Researcher at Peter MacCallum Cancer Centre
Publications - 83
Citations - 7585
Paul A. Beavis is an academic researcher from Peter MacCallum Cancer Centre. The author has contributed to research in topics: Immunotherapy & T cell. The author has an hindex of 31, co-authored 71 publications receiving 4991 citations. Previous affiliations of Paul A. Beavis include University of Oxford & Imperial College London.
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Journal ArticleDOI
Single-cell profiling of breast cancer T cells reveals a tissue-resident memory subset associated with improved prognosis
Peter Savas,Balaji Virassamy,Chengzhong Ye,Agus Salim,Agus Salim,Christopher P. Mintoff,Franco Caramia,Roberto Salgado,David J Byrne,Zhi Ling Teo,Zhi Ling Teo,Sathana Dushyanthen,Ann Byrne,Lironne Wein,Stephen J Luen,Catherine Poliness,Sophie Nightingale,Anita S Skandarajah,Anita S Skandarajah,David E. Gyorki,Chantel M Thornton,Paul A. Beavis,Paul A. Beavis,Stephen B. Fox,Phillip K. Darcy,Phillip K. Darcy,Terence P. Speed,Terence P. Speed,Laura K. Mackay,Paul J Neeson,Paul J Neeson,Sherene Loi,Sherene Loi +32 more
TL;DR: Detailed, high-dimensional characterization of T cells in breast cancer reveals activated TRM population and a gene signature associated with improved prognosis and suggest that CD8+ TRM cells contribute to BC immunosurveillance and are the key targets of modulation by immune checkpoint inhibition.
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Anti-PD-1 Antibody Therapy Potently Enhances the Eradication of Established Tumors By Gene-Modified T Cells
Liza B John,Christel Devaud,Connie P.M. Duong,Carmen S M Yong,Paul A. Beavis,Nicole M. Haynes,Melvyn T. Chow,Mark J. Smyth,Michael H. Kershaw,Phillip K. Darcy +9 more
TL;DR: This study shows that specifically blocking PD-1 immunosuppression can potently enhance CAR T-cell therapy that has significant implications for potentially improving therapeutic outcomes of this approach in patients with cancer.
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CMTM6 maintains the expression of PD-L1 and regulates anti-tumour immunity
Marian L. Burr,Marian L. Burr,Marian L. Burr,Christina E. Sparbier,Yih-Chih Chan,James C Williamson,Katherine Woods,Paul A. Beavis,Paul A. Beavis,Enid Y.N. Lam,Enid Y.N. Lam,Melissa A. Henderson,Melissa A. Henderson,Charles C. Bell,Charles C. Bell,Sabine Stolzenburg,Omer Gilan,Omer Gilan,Stuart Bloor,Tahereh Noori,David W. Morgens,Michael C. Bassik,Paul J Neeson,Paul J Neeson,Andreas Behren,Phillip K. Darcy,Phillip K. Darcy,Sarah-Jane Dawson,Sarah-Jane Dawson,Ilia Voskoboinik,Ilia Voskoboinik,Joseph A. Trapani,Joseph A. Trapani,Jonathan Cebon,Paul J. Lehner,Mark A. Dawson +35 more
TL;DR: Insight is provided into the biology of PD-L1 regulation, a previously unrecognized master regulator of this critical immune checkpoint is identified, and a potential therapeutic target to overcome immune evasion by tumour cells is highlighted.
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RAS/MAPK activation is associated with reduced tumor-infiltrating lymphocytes in triple-negative breast cancer: therapeutic cooperation between MEK and PD-1/PD-L1 immune checkpoint inhibitors
Sherene Loi,Sherene Loi,Sathana Dushyanthen,Paul A. Beavis,Roberto Salgado,Carsten Denkert,Peter Savas,Susan E. Combs,David L. Rimm,Jennifer M. Giltnane,Monica V. Estrada,Violeta Sanchez,Melinda E. Sanders,Rebecca S. Cook,Mark A. Pilkinton,Simon Mallal,Kai Wang,Vincent A. Miller,Philip J. Stephens,Roman Yelensky,Franco Doimi,Henry L. Gomez,Sergey Ryzhov,Phillip K. Darcy,Phillip K. Darcy,Carlos L. Arteaga,Justin M. Balko +26 more
TL;DR: The possibility that Ras–MAPK pathway activation promotes immune-evasion in TNBC is suggested, and clinical trials combining MEK- and PD-L1–targeted therapies are support, and Ras/MAPK activation and MHC expression may be predictive biomarkers of response to immune checkpoint inhibitors.
Journal ArticleDOI
CD73 promotes anthracycline resistance and poor prognosis in triple negative breast cancer
Sherene Loi,Sandra Pommey,Benjamin Haibe-Kains,Paul A. Beavis,Phillip K. Darcy,Phillip K. Darcy,Mark J. Smyth,John Stagg +7 more
TL;DR: Using mouse models of breast cancer, it is demonstrated that CD73 overexpression in tumor cells conferred chemoresistance to doxorubicin, a commonly used anthracycline, by suppressing adaptive antitumor immune responses via activation of A2A adenosine receptors.