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Andrew W. Roberts
Researcher at Walter and Eliza Hall Institute of Medical Research
Publications - 361
Citations - 27897
Andrew W. Roberts is an academic researcher from Walter and Eliza Hall Institute of Medical Research. The author has contributed to research in topics: Venetoclax & Chronic lymphocytic leukemia. The author has an hindex of 73, co-authored 318 publications receiving 23534 citations. Previous affiliations of Andrew W. Roberts include Ludwig Institute for Cancer Research & Royal Melbourne Hospital.
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Journal ArticleDOI
ABT-199, a potent and selective BCL-2 inhibitor, achieves antitumor activity while sparing platelets
Andrew J. Souers,Joel D. Leverson,Erwin R. Boghaert,Scott L. Ackler,Nathaniel D. Catron,Jun Chen,Brian D. Dayton,Hong Ding,Sari H. Enschede,Wayne J. Fairbrother,David C.S. Huang,David C.S. Huang,Sarah G. Hymowitz,Sha Jin,Seong Lin Khaw,Seong Lin Khaw,Peter Kovar,Lloyd T. Lam,Jackie Lee,Heather Maecker,Kennan C. Marsh,Kylie D. Mason,Kylie D. Mason,Kylie D. Mason,Michael J. Mitten,Paul Nimmer,Anatol Oleksijew,Chang H. Park,Cheol-Min Park,Cheol-Min Park,Darren C. Phillips,Andrew W. Roberts,Andrew W. Roberts,Andrew W. Roberts,Deepak Sampath,John F. Seymour,John F. Seymour,Morey L. Smith,Gerard M. Sullivan,Stephen K. Tahir,Chris Tse,Michael D. Wendt,Yu Xiao,John Xue,Haichao Zhang,Rod A. Humerickhouse,Saul H. Rosenberg,Steven W. Elmore +47 more
TL;DR: The re-engineering of navitoclax is reported to create a highly potent, orally bioavailable and BCL-2–selective inhibitor, ABT-199, which inhibits the growth of BCL–dependent tumors in vivo and spares human platelets, indicating that selective pharmacological inhibition of Bcl-2 shows promise for the treatment of B CL-2-dependent hematological cancers.
Journal ArticleDOI
Targeting BCL2 with Venetoclax in Relapsed Chronic Lymphocytic Leukemia
Andrew W. Roberts,Matthew S. Davids,John M. Pagel,Brad S. Kahl,Soham D. Puvvada,John F. Gerecitano,Thomas J. Kipps,Mary Ann Anderson,Mary Ann Anderson,Jennifer R. Brown,Lori A. Gressick,Shekman Wong,Martin Dunbar,Ming Zhu,Monali Desai,Elisa Cerri,Sari H. Enschede,Rod A. Humerickhouse,William G. Wierda,John F. Seymour,John F. Seymour +20 more
TL;DR: Selective targeting of BCL2 with venetoclax had a manageable safety profile and induced substantial responses in patients with relapsed CLL or SLL, including those with poor prognostic features.
Journal ArticleDOI
The BH3 mimetic ABT-737 targets selective Bcl-2 proteins and efficiently induces apoptosis via Bak/Bax if Mcl-1 is neutralized.
Mark F. van Delft,Andrew H. Wei,Kylie D. Mason,Kylie D. Mason,Cassandra J. Vandenberg,Lin Chen,Peter E. Czabotar,Simon N. Willis,Clare L. Scott,Catherine L. Day,Suzanne Cory,Jerry M. Adams,Andrew W. Roberts,David C.S. Huang +13 more
TL;DR: It is shown that resistance reflects ABT-737's inability to target another prosurvival relative, Mcl-1, and should prove efficacious in tumors with low MCl-1 levels, or when combined with agents that inactivate Mcl -1, even to treat those tumors that overexpress Bcl-2.
Journal ArticleDOI
Programmed Anuclear Cell Death Delimits Platelet Life Span
Kylie D. Mason,Marina R. Carpinelli,Jamie I. Fletcher,Janelle E. Collinge,Adrienne A. Hilton,Sarah Ellis,Priscilla N. Kelly,Paul G Ekert,Donald Metcalf,Andrew W. Roberts,David C.S. Huang,Benjamin T. Kile,Benjamin T. Kile +12 more
TL;DR: It is shown that an intrinsic program for apoptosis controls platelet survival and dictates their life span, and this represents an important paradigm for cellular homeostasis, and has profound implications for the diagnosis and treatment of disorders that affect platelet number and function.
Journal ArticleDOI
SOCS3 negatively regulates IL-6 signaling in vivo.
Ben A. Croker,Danielle L. Krebs,Jian-Guo Zhang,Sam Wormald,Tracy A. Willson,Edouard G. Stanley,Lorraine Robb,Christopher J. Greenhalgh,Irmgard Förster,Björn E. Clausen,Nicos A. Nicola,Donald Metcalf,Douglas J. Hilton,Andrew W. Roberts,Warren S. Alexander +14 more
TL;DR: It is shown that Socs3 deficiency results in prolonged activation of signal transducer and activator of transcription 1 (STAT1) and STAT3 after IL-6 stimulation but normal activation of STAT1 after stimulation with interferon-γ (IFN-γ).