Gene-expression patterns in drug-resistant acute lymphoblastic leukemia cells and response to treatment.
By Amy Holleman, M. Cheok, M. D. den Boer, Wenjian Yang, A. Veerman, K. Kazemier, Deqing Pei, Cheng Cheng, Ching-Hon Pui, Mary V. Relling and 3 more. New England Journal of Medicine, 2004
623 citations recorded by the source corpus.
Subfields: Hematology, Public Health, Environmental and Occupational Health
View Paper: https://www.semanticscholar.org/paper/76c5ed1e2dd7c7bcf986c2ca49e05f5bdfd987ab
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- Yusuke Nakamura
- Ryuji Hamamoto
- M. Eichelbaum
- Magnus Ingelman-Sundberg
- M. Mutonga
- K. Tamura
- G. Malnassy
- Houda Alachkar
Citations in the corpus
- Targeting Suppressor of Variegation 3-9 Homologue 2 (SUV39H2) in Acute Lymphoblastic Leukemia (ALL) (2015, background): “Therefore, a better understanding of the pathogenesis and the basis of chemoresistance is critically important to further improve the prognosis of these high-risk leukemias [11,12].”
- Pharmacogenomics and individualized drug therapy. (2006, methodology): “The various strategies now being used include genome-wide haplotype mapping (1), gene expression analyses (109, 110), and proteomic methods, as well as “candidate gene” approaches based on known pharmacokinetic (111) and pharmacodynamic (67) factors.”
- Deriving chemosensitivity from cell lines: Forensic bioinformatics and reproducible research in high-throughput biology (2009, neutral): “These Gene Expression Omnibus (GEO) data sets, which derive from a study on acute lymphocytic leukemia (ALL) by Holleman et al. (2004), give gene profiles for samples from 94 patients sensitive to daunorubicin (in the same chemical family as doxorubicin) and 28 resistant.”