Wei Wei Li
Memorial Sloan Kettering Cancer Center
18 Papers
295 Citations
Wei Wei Li is an academic researcher from Memorial Sloan Kettering Cancer Center. The author has contributed to research in topics: Trimetrexate & Antifolate. The author has an hindex of 13, co-authored 17 publications.
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Papers
•Journal Article
Sequence-dependent Enhancement of Cytotoxicity Produced by Ecteinascidin 743 (ET-743) with Doxorubicin or Paclitaxel in Soft Tissue Sarcoma Cells
TL;DR: The cytotoxicity resulting from combining ET-743 with three other antineoplastic agents: doxorubicin (DXR), trimetrexate, and paclitaxel in different administration schedules in two soft tissue sarcoma cell lines was examined in vitro.
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Resistance Mechanisms to Methotrexate in Tumors
TL;DR: In blasts from patients with acute lymphocytic leukemia, resistance mechanisms found are decreased uptake and increased dihydrofolate reductase (DHFR) activity, due to an increased rate of transcription of this gene, stimulated by an increase in levels of free E2F, not sequestered by hypophosphorylated retinoblastoma protein.
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Molecular mechanisms of resistance to antifolates, a review.
Debabrata Banerjee,Emine A. Ercikan-Abali,Mark Waltham,Barbara Schnieders,Daniel Hochhauser,Wei Wei Li,Jianguo Fan,Richard Gorlick,Erdem Goker,Joseph R. Bertino +9 more
TL;DR: Cloning of the human folylpolyglutamate synthase gene and the reduced folate transport gene have been reported recently and should facilitate the identification of the molecular basis of these resistant phenotypes.
Increased Activity of γ-Glutamyl Hydrolase in Human Sarcoma Cell Lines: A Novel Mechanism of Intrinsic Resistance to Methotrexate (MTX)
TL;DR: GGH activity was measured and found increased levels of this enzyme in MTX resistant soft tissue sarcoma cell lines and no appreciable difference of FPGS activity was observed between MTX-resistant and sensitive cells.
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Leucovorin Enhances Chtotoxicity of Trimetrexate/Fluorouracil, But Not Methotrexate/Fluorouracil, in CCRF-CEM Cells
TL;DR: The hypothesis that the lack of additional cell kill when high-dose LV is added to the MTX/5-FU combination may be due to competition of MTX with LV for cellular uptake and/or competition ofMTX or its polyglutamates with polyglUTamylation of reduced folates is supported.
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