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Hui Zhang

Researcher at University of Texas MD Anderson Cancer Center

Publications -  77
Citations -  2856

Hui Zhang is an academic researcher from University of Texas MD Anderson Cancer Center. The author has contributed to research in topics: Ibrutinib & Mantle cell lymphoma. The author has an hindex of 24, co-authored 63 publications receiving 2382 citations. Previous affiliations of Hui Zhang include Sun Yat-sen University & Kunming Institute of Zoology.

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Targeting autophagy augments the anticancer activity of the histone deacetylase inhibitor SAHA to overcome Bcr-Abl-mediated drug resistance

TL;DR: It is reported that drugs that disrupt the autophagy pathway dramatically augment the antineoplastic effects of SAHA in CML cell lines and primary CML cells expressing wild-type and imatinib-resistant mutant forms of Bcr-Abl, including T315I.
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Role of mitochondria-associated hexokinase II in cancer cell death induced by 3-bromopyruvate

TL;DR: This study showed that 3-BrPA caused a covalent modification of HKII protein and directly triggered its dissociation from mitochondria, leading to a specific release of apoptosis-inducing factor (AIF) from the mitochondria to cytosol and eventual cell death.
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Autophagy inhibition enhances vorinostat-induced apoptosis via ubiquitinated protein accumulation

TL;DR: It is established that inhibition of autophagy with CQ induces ubiquitinated protein accumulation and VOR potentiates CQ‐mediated aggregate formation, superoxide generation and apoptosis and treatment with the CQ/VOR combination significantly reduced tumour burden and induced apoptosis in a colon cancer xenograft model.
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Metabolic reprogramming toward oxidative phosphorylation identifies a therapeutic target for mantle cell lymphoma

TL;DR: Genomic analyses of clinical specimens show that metabolic reprogramming toward oxidative phosphorylation (OXPHOS) and glutaminolysis is associated with therapeutic resistance to the Bruton’s tyrosine kinase inhibitor ibrutinib in mantle cell lymphoma, suggesting that targeting metabolic pathways to subvert therapeutic resistance is a clinically viable approach to treat highly refractory malignancies.