J
Jia-Nan Gong
Researcher at Walter and Eliza Hall Institute of Medical Research
Publications - 29
Citations - 2843
Jia-Nan Gong is an academic researcher from Walter and Eliza Hall Institute of Medical Research. The author has contributed to research in topics: Venetoclax & Leukemia. The author has an hindex of 20, co-authored 29 publications receiving 2146 citations. Previous affiliations of Jia-Nan Gong include Peking Union Medical College & University of Melbourne.
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Journal ArticleDOI
The MCL1 inhibitor S63845 is tolerable and effective in diverse cancer models
András Kotschy,Szlávik Zoltán,James A. H. Murray,James Edward Paul Davidson,Ana Leticia Maragno,Gaëtane Le Toumelin-Braizat,Maïa Chanrion,Gemma L. Kelly,Gemma L. Kelly,Jia-Nan Gong,Jia-Nan Gong,Donia M Moujalled,Alain Bruno,Csékei Márton,Attila Paczal,Zoltán B. Szabó,Szabolcs Sipos,Gabor Radics,Proszenyák Ágnes,Balázs Bálint,Levente Ondi,Gábor Blasko,Alan P. Robertson,Allan E. Surgenor,Pawel Dokurno,Chen I-Jen,Natalia Matassova,Julia Smith,C. Pedder,Chris Graham,Aurélie Studeny,Gaëlle Lysiak-Auvity,Anne-Marie Girard,Fabienne Gravé,David J. Segal,David J. Segal,Chris D. Riffkin,Chris D. Riffkin,Giovanna Pomilio,Laura C. A. Galbraith,Laura C. A. Galbraith,Brandon J. Aubrey,Brandon J. Aubrey,Brandon J. Aubrey,Margs S. Brennan,Margs S. Brennan,Marco J Herold,Marco J Herold,Catherine Chang,Catherine Chang,Ghislaine Guasconi,Nicolas Cauquil,Fabien Melchiore,Nolwen Guigal-Stephan,Brian Lockhart,Frédéric Colland,John A. Hickman,Andrew W. Roberts,David C.S. Huang,David C.S. Huang,Andrew H. Wei,Andrew H. Wei,Andreas Strasser,Andreas Strasser,Guillaume Lessene,Guillaume Lessene,Olivier Geneste +66 more
TL;DR: It is demonstrated that S63845 potently kills MCL1-dependent cancer cells, including multiple myeloma, leukaemia and lymphoma cells, by activating the BAX/BAK-dependent mitochondrial apoptotic pathway.
Journal ArticleDOI
AMG 176, a Selective MCL1 Inhibitor, Is Effective in Hematologic Cancer Models Alone and in Combination with Established Therapies.
Sean Caenepeel,Sean P. Brown,Brian Belmontes,Gordon Moody,Kathleen S. Keegan,Danny Chui,Douglas A. Whittington,Xin Huang,Leszek Poppe,Alan C. Cheng,Mario G. Cardozo,Jonathan B. Houze,Yunxiao Li,Brian Lucas,Nick A. Paras,Xianghong Wang,Joshua Taygerly,Marc Vimolratana,Manuel Zancanella,Liusheng Zhu,Elaina Cajulis,Tao Osgood,Jan Sun,Leah J. Damon,Regina K. Egan,Patricia Greninger,Joseph McClanaghan,Jia-Nan Gong,Jia-Nan Gong,Donia M Moujalled,Giovanna Pomilio,Pedro J. Beltran,Cyril H. Benes,Andrew W. Roberts,David C.S. Huang,David C.S. Huang,Andrew H. Wei,Jude Canon,Angela Coxon,Paul E. Hughes +39 more
TL;DR: AMG 176 is a potent, selective, and orally bioavailable MCL1 inhibitor that induces a rapid commitment to apoptosis in models of hematologic malignancies and the synergistic combination of AMG 176 and venetoclax is synergistic in acute myeloid leukemia (AML) tumor models and in primary patient samples at tolerated doses.
Journal ArticleDOI
Acquisition of the Recurrent Gly101Val Mutation in BCL2 Confers Resistance to Venetoclax in Patients with Progressive Chronic Lymphocytic Leukemia.
Piers Blombery,Piers Blombery,Mary Ann Anderson,Mary Ann Anderson,Mary Ann Anderson,Jia-Nan Gong,Jia-Nan Gong,Rachel Thijssen,Rachel Thijssen,Richard W Birkinshaw,Richard W Birkinshaw,Ella R. Thompson,Ella R. Thompson,Charis E Teh,Charis E Teh,Tamia Nguyen,Tamia Nguyen,Zhen Xu,Christoffer Flensburg,Thomas E Lew,Ian J. Majewski,Daniel H.D. Gray,Daniel H.D. Gray,David Westerman,David Westerman,Constantine S. Tam,Constantine S. Tam,John F. Seymour,John F. Seymour,Peter E. Czabotar,Peter E. Czabotar,David C.S. Huang,David C.S. Huang,Andrew W. Roberts +33 more
TL;DR: The first description of an acquired point mutation in BCL2 arising recurrently and exclusively in venetoclax-treated patients is provided, providing new insights into the pathobiology of venetclax resistance and provides a potential biomarker of impending clinical relapse.
Journal ArticleDOI
MicroRNA-29a and microRNA-142-3p are regulators of myeloid differentiation and acute myeloid leukemia
Xiaoshuang Wang,Jia-Nan Gong,Jia Yu,Fang Wang,Xin-Hua Zhang,Xiao-Lin Yin,Zhen-Qing Tan,Zi-Mian Luo,Gui-Hua Yang,Chao Shen,Jun-Wu Zhang +10 more
TL;DR: It is demonstrated that enforced expression of either miR-29a orMiR-142-3p in hematopoietic stem/progenitor cells from healthy controls and acute myeloid leukemia patients down-regulated expression of their targets and promoted myeloids differentiation.
Journal ArticleDOI
Synergistic action of the MCL-1 inhibitor S63845 with current therapies in preclinical models of triple-negative and HER2-amplified breast cancer.
Delphine Merino,Delphine Merino,James R. Whittle,James R. Whittle,James R. Whittle,François Vaillant,François Vaillant,Antonin Serrano,Antonin Serrano,Jia-Nan Gong,Jia-Nan Gong,Göknur Giner,Göknur Giner,Ana Leticia Maragno,Maïa Chanrion,Emilie Schneider,Bhupinder Pal,Bhupinder Pal,Xiang Li,Xiang Li,Grant Dewson,Grant Dewson,Julius Gräsel,Julius Gräsel,Kevin H. Liu,Kevin H. Liu,Najoua Lalaoui,Najoua Lalaoui,David J. Segal,David J. Segal,Marco J Herold,Marco J Herold,David C.S. Huang,David C.S. Huang,Gordon K. Smyth,Gordon K. Smyth,Olivier Geneste,Guillaume Lessene,Guillaume Lessene,Jane E. Visvader,Jane E. Visvader,Geoffrey J. Lindeman +41 more
TL;DR: The MCL-1 inhibitor S63845 is effective in combination with conventional therapy for targeting triple-negative and HER2-amplified breast cancer and a protein that can promote treatment resistance is identified, which may help predict which patients are more likely to benefit from the new treatment.