L
Lesley J. Murray
Researcher at Genentech
Publications - 48
Citations - 7370
Lesley J. Murray is an academic researcher from Genentech. The author has contributed to research in topics: Haematopoiesis & CD34. The author has an hindex of 27, co-authored 48 publications receiving 7068 citations. Previous affiliations of Lesley J. Murray include Oregon Health & Science University & Novartis.
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Journal Article
In Vivo Antitumor Activity of SU11248, a Novel Tyrosine Kinase Inhibitor Targeting Vascular Endothelial Growth Factor and Platelet-derived Growth Factor Receptors Determination of a Pharmacokinetic/Pharmacodynamic Relationship
Dirk B. Mendel,A. Douglas Laird,Xiaohua Xin,Sharianne G. Louie,James G. Christensen,Guangmin Li,Randall E. Schreck,Tinya Abrams,Theresa J. Ngai,Leslie Lee,Lesley J. Murray,Jeremy P. Carver,Emily Chan,Katherine G. Moss,Joshua Ö. Haznedar,Juthamas Sukbuntherng,Robert A. Blake,Li Sun,Cho Tang,Todd W. Miller,Sheri Shirazian,Gerald Mcmahon,Julie M. Cherrington +22 more
TL;DR: The pharmacokinetic/pharmacodynamic relationship established for SU11248 in these preclinical studies has aided in the design, selection, and evaluation of dosing regimens being tested in human trials.
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SU11248 is a novel FLT3 tyrosine kinase inhibitor with potent activity in vitro and in vivo.
Anne Marie O'Farrell,Tinya Abrams,Helene A. Yuen,Theresa J. Ngai,Sharianne G. Louie,Kevin W.H. Yee,Lily Wong,Weiru Hong,Leslie Lee,Ajia Town,Beverly D. Smolich,William C. Manning,Lesley J. Murray,Michael Heinrich,Julie M. Cherrington +14 more
TL;DR: The in vivo efficacy of SU11248 (20 mg/kg/d) dramatically regresses FLT3-ITD tumors in the subcutaneous tumor xenograft model and prolongs survival in the bone marrow engraftment model, suggesting that further exploration of SU 11248 activity in AML patients is warranted.
Journal Article
SU11248 inhibits KIT and platelet-derived growth factor receptor beta in preclinical models of human small cell lung cancer.
TL;DR: It is suggested that SU11248 may have clinical potential in the treatment of SCLC via direct antitumor activity mediated via KIT as well as tumor angiogenesis via vascular endothelial growth factor receptor FLK1/KDR and PDGFRbeta.
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In vivo Antitumor Activity of MEK and Phosphatidylinositol 3-Kinase Inhibitors in Basal-Like Breast Cancer Models
Klaus P. Hoeflich,Carol O'Brien,Zachary Boyd,Guy Cavet,Steve Guerrero,Kenneth Jung,Tom Januario,Heidi Savage,Elizabeth Punnoose,Tom Truong,Wei Zhou,Leanne Berry,Lesley J. Murray,Lukas C. Amler,Marcia Belvin,Lori Friedman,Mark R. Lackner +16 more
TL;DR: The studies suggest that single-agent MEK inhibition is a promising therapeutic modality for basal-like breast cancers with intact PTEN, and also provide a basis for rational combination of MEK and PI3K inhibitors in basal- like cancers with both intact and deleted PTEN.
Journal ArticleDOI
Akt inhibition promotes autophagy and sensitizes PTEN-null tumors to lysosomotropic agents
Michael Degtyarev,Ann De Mazière,Christine Orr,Jie Lin,Brian Lee,Janet Tien,Wei Wei Prior,Suzanne van Dijk,Hong Wu,Daniel C. Gray,David Davis,Howard M. Stern,Lesley J. Murray,Klaus P. Hoeflich,Judith Klumperman,Lori Friedman,Kui Lin +16 more
TL;DR: It is shown that silencing Akt1 alone, or any combination of Akt isoforms, can suppress the growth of tumors established from phosphatase and tensin homologue–null human cancer cells, and suggests that blocking lysosomal degradation can be detrimental to cancer cell survival when autophagy is activated.