H
Hongliang Zong
Researcher at Cornell University
Publications - 20
Citations - 1370
Hongliang Zong is an academic researcher from Cornell University. The author has contributed to research in topics: Leukemia & Stem cell. The author has an hindex of 13, co-authored 20 publications receiving 1082 citations. Previous affiliations of Hongliang Zong include Boston Medical Center.
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Journal ArticleDOI
Pharmacologic Inhibition of the Menin-MLL Interaction Blocks Progression of MLL Leukemia In Vivo.
Dmitry Borkin,Shihan He,Hongzhi Miao,Katarzyna Kempińska,Jonathan Pollock,Jennifer Chase,Trupta Purohit,Bhavna Malik,Ting Zhao,Jingya Wang,Bo Wen,Hongliang Zong,Morgan Jones,Gwenn Danet-Desnoyers,Monica L. Guzman,Moshe Talpaz,Dale L. Bixby,Duxin Sun,Jay L. Hess,Andrew G. Muntean,Ivan Maillard,Tomasz Cierpicki,Jolanta Grembecka +22 more
TL;DR: In this article, the authors report the development of highly potent and orally bioavailable small-molecule inhibitors of the menin-MLL interaction, MI-463 and MI-503, and show their profound effects in mixed lineage leukemia cells and substantial survival benefit in mouse models of MLL leukemia.
Journal ArticleDOI
Affinity-based proteomics reveal cancer-specific networks coordinated by Hsp90
Kamalika Moulick,James H. Ahn,Hongliang Zong,Anna Rodina,Leandro Cerchietti,Gomes-Dagama Erica M,Eloisi Caldas-Lopes,Kristin Beebe,Fabiana Perna,Katerina Hatzi,Ly P. Vu,Xinyang Zhao,Danuta Zatorska,Tony Taldone,Peter Smith-Jones,Mary L. Alpaugh,Steven S. Gross,Nagavarakishore Pillarsetty,Thomas Ku,Jason S. Lewis,Steven M. Larson,Ross L. Levine,Hediye Erdjument-Bromage,Monica L. Guzman,Stephen D. Nimer,Ari Melnick,Len Neckers,Gabriela Chiosis +27 more
TL;DR: This work uses PU-H71 affinity capture to design a proteomic approach that, when combined with bioinformatic pathway analysis, identifies dysregulated signaling networks and key oncoproteins in chronic myeloid leukemia and shows that this method can provide global insights into the biology of individual tumors, including primary patient specimens.
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The epichaperome is an integrated chaperome network that facilitates tumour survival
Anna Rodina,Tai Wang,Pengrong Yan,Erica DaGama Gomes,Mark Dunphy,Nagavarakishore Pillarsetty,John Koren,John F. Gerecitano,Tony Taldone,Hongliang Zong,Eloisi Caldas-Lopes,Mary L. Alpaugh,Adriana D. Corben,Matthew Riolo,Brad Beattie,Christina Pressl,Radu I Peter,Chao Xu,Robert Trondl,Hardik J. Patel,Fumiko Shimizu,Alexander Bolaender,Chenghua Yang,Palak Panchal,Mohammad F. Farooq,Sarah Kishinevsky,Shanu Modi,Oscar Lin,Feixia Chu,Sujata Patil,Hediye Erdjument-Bromage,Pat Zanzonico,Clifford A. Hudis,Lorenz Studer,Gail J. Roboz,Ethel Cesarman,Leandro Cerchietti,Ross L. Levine,Ari Melnick,Steven M. Larson,Jason S. Lewis,Monica L. Guzman,Gabriela Chiosis,Gabriela Chiosis +43 more
TL;DR: It is found that under conditions of stress, such as malignant transformation fuelled by MYC, the chaperome becomes biochemically ‘rewired’ to form a network of stable, survival-facilitating, high-molecular-weight complexes.
Journal ArticleDOI
FDA-approved ferumoxytol displays anti-leukaemia efficacy against cells with low ferroportin levels.
Vicenta Trujillo-Alonso,Edwin C. Pratt,Edwin C. Pratt,Hongliang Zong,Andres Lara-Martinez,Charalambos Kaittanis,Mohamed O. Rabie,Valerie A. Longo,Michael W. Becker,Gail J. Roboz,Jan Grimm,Jan Grimm,Monica L. Guzman +12 more
TL;DR: Administration of the clinically approved iron oxide nanoparticle drug ferumoxytol in vitro results in an anti-leukaemia effect and in vivo extended overall survival in part due to the low expression of the iron export protein ferroportin.
Journal ArticleDOI
A small-molecule inhibitor of the aberrant transcription factor CBFβ-SMMHC delays leukemia in mice
Anuradha Illendula,John Anto Pulikkan,Hongliang Zong,Jolanta Grembecka,Liting Xue,Siddhartha Sen,Yunpeng Zhou,Adam Boulton,Aravinda Kuntimaddi,Yan Gao,Roger A. Rajewski,Monica L. Guzman,Lucio H. Castilla,John H. Bushweller +13 more
TL;DR: The development of a protein-protein interaction inhibitor, AI-10-49, that selectively binds to CBFβ-SMMHC and disrupts its binding to RUNX1 is reported, suggesting that direct inhibition of the oncogenic CBF β-sMMHC fusion protein may be an effective therapeutic approach for inv(16) AML and they provide support for transcription factor targeted therapy in other cancers.