An Unbiased Oncology Compound Screen to Identify Novel Combination Strategies
暂无分享,去创建一个
Yair Benita | J. O'neil | I. Feldman | R. Cristescu | A. Loboda | Melissa Chenard | Brian S. Roberts | Yaping Liu | Jing Li | A. Kral | S. Lejnine | W. Arthur | B. Haines | C. Winter | Theresa Zhang | A. Bloecher | S. Shumway | Mélissa Chénard | M. Chénard
[1] Combination chemotherapy of acute leukemia and Hodgkin's disease. , 1972, JAMA.
[2] Tobias Schmelzle,et al. TOR, a Central Controller of Cell Growth , 2000, Cell.
[3] J. Raleigh,et al. The G(2) DNA damage checkpoint targets both Wee1 and Cdc25. , 2000, Journal of cell science.
[4] J. Lehár,et al. Systematic discovery of multicomponent therapeutics , 2003, Proceedings of the National Academy of Sciences of the United States of America.
[5] N. Sonenberg,et al. Upstream and downstream of mTOR. , 2004, Genes & development.
[6] L. Rozamus,et al. Structure-based design of AP23573, a phosphorus-containing analog of rapamycin for anti-tumor therapy. , 2004 .
[7] L. Cantley,et al. Ras, PI(3)K and mTOR signalling controls tumour cell growth , 2006, Nature.
[8] A. Harris,et al. Phase I Study of the Poly(ADP-Ribose) Polymerase Inhibitor, AG014699, in Combination with Temozolomide in Patients with Advanced Solid Tumors , 2008, Clinical Cancer Research.
[9] Tsuyoshi Arai,et al. Small-molecule inhibition of Wee1 kinase by MK-1775 selectively sensitizes p53-deficient tumor cells to DNA-damaging agents , 2009, Molecular Cancer Therapeutics.
[10] C. Paweletz,et al. A gene expression signature of RAS pathway dependence predicts response to PI3K and RAS pathway inhibitors and expands the population of RAS pathway activated tumors , 2010, BMC Medical Genomics.
[11] T. Helleday,et al. Regulators of cyclin-dependent kinases are crucial for maintaining genome integrity in S phase , 2010, The Journal of cell biology.
[12] R. Medema,et al. Wee1 controls genomic stability during replication by regulating the Mus81-Eme1 endonuclease , 2011, The Journal of cell biology.
[13] S. Ramaswamy,et al. Systematic identification of genomic markers of drug sensitivity in cancer cells , 2012, Nature.
[14] B. Al-Lazikani,et al. Combinatorial drug therapy for cancer in the post-genomic era , 2012, Nature Biotechnology.
[15] Adam A. Margolin,et al. The Cancer Cell Line Encyclopedia enables predictive modeling of anticancer drug sensitivity , 2012, Nature.
[16] Karin J Jensen,et al. Synthetic Lethal Screening with Small-Molecule Inhibitors Provides a Pathway to Rational Combination Therapies for Melanoma , 2012, Molecular Cancer Therapeutics.
[17] S. Chandarlapaty,et al. Relief of profound feedback inhibition of mitogenic signaling by RAF inhibitors attenuates their activity in BRAFV600E melanomas. , 2012, Cancer cell.
[18] Unique functions of CHK1 and WEE1 underlie synergistic anti-tumor activity upon pharmacologic inhibition , 2012, Cancer Cell International.
[19] Paul Workman,et al. Genome-based cancer therapeutics: targets, kinase drug resistance and future strategies for precision oncology. , 2013, Current opinion in pharmacology.
[20] Yair Benita,et al. Preclinical Evaluation of the WEE1 Inhibitor MK-1775 as Single-Agent Anticancer Therapy , 2013, Molecular Cancer Therapeutics.
[21] M. Held,et al. Genotype-selective combination therapies for melanoma identified by high-throughput drug screening. , 2013, Cancer discovery.
[22] R. Plummer,et al. Phase 1 dose-escalation study of the PARP inhibitor CEP-9722 as monotherapy or in combination with temozolomide in patients with solid tumors , 2014, Cancer Chemotherapy and Pharmacology.
[23] S. Peters,et al. Dramatic response of vemurafenib-induced cutaneous lesions upon switch to dual BRAF/MEK inhibition in a metastatic melanoma patient. , 2014, Melanoma research.
[24] Andrew P. Hodges,et al. Identification of Drug Combinations Containing Imatinib for Treatment of BCR-ABL+ Leukemias , 2014, PloS one.
[25] N. Gray,et al. Identification of Wee1 as a novel therapeutic target for mutant RAS-driven acute leukemia and other malignancies , 2014, Leukemia.