P
Philip L. Lorenzi
Researcher at University of Texas MD Anderson Cancer Center
Publications - 128
Citations - 22127
Philip L. Lorenzi is an academic researcher from University of Texas MD Anderson Cancer Center. The author has contributed to research in topics: Medicine & Biology. The author has an hindex of 37, co-authored 96 publications receiving 17665 citations. Previous affiliations of Philip L. Lorenzi include University of Michigan & Loyola University Chicago.
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Journal ArticleDOI
Cancer: Discrepancies in drug sensitivity
TL;DR: Although the gene expression data are largely concordant between them, the reported drug-sensitivity measures and subsequently their association with genomic features are highly discordant and the authors call for standardization of drug-response measurements, to aid the discovery of robust biomarkers and mechanisms of drug response and hence progress in personalized cancer medicine.
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Coordinate phosphorylation of multiple residues on single AKT1 and AKT2 molecules
Huifang Guo,Meng Gao,Yiling Lu,Jiyong Liang,Philip L. Lorenzi,Shanshan Bai,David H. Hawke,Jie Li,Turgut Dogruluk,Kenneth L. Scott,Eric Jonasch,Gordon B. Mills,Zhiyong Ding +12 more
TL;DR: NIA technology provides an ability to characterize coordinate phosphorylation of individual AKT molecules providing important information about AKT isoform-specific phosphorylated, which is required for optimal development and implementation of drugs targeting aberrant AKT activation.
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EWS-FLI1 reprograms the metabolism of Ewing sarcoma cells via positive regulation of glutamine import and serine-glycine biosynthesis.
Nirmalya Sen,Allison M. Cross,Philip L. Lorenzi,Javed Khan,Berkley E. Gryder,Suntae Kim,Natasha J. Caplen +6 more
TL;DR: It is demonstrated that EWS‐FLI1 reprograms the metabolism of EWS cells and that serine‐glycine metabolism or glutamine uptake are potential targetable vulnerabilities in this tumor type.
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Targeted metabolomic analysis of amino acid response to L-asparaginase in adherent cells
TL;DR: This study provides new insight into L-ASP’s mechanism of action, and the optimized analytical method can be extended, with only slight modification, to other metabolically active amino acids, related compounds, and a range of cultured cell types.
Journal ArticleDOI
Targeting MCL-1 dysregulates cell metabolism and leukemia-stroma interactions and resensitizes acute myeloid leukemia to BCL-2 inhibition.
Bing Z. Carter,Po Yee Mak,Wenjing Tao,Marc O. Warmoes,Philip L. Lorenzi,Duncan Mak,Vivian Ruvolo,Lin Tan,Justin Cidado,Lisa Drew,Michael Andreeff +10 more
TL;DR: In this paper, the authors showed that co-targeting MCL-1 and BCL-2 improves the efficacy of venetoclax/decitabine-resistant acute myeloid leukemia.