Page 85 - Read Online
P. 85
Page 36 Pandey et al. J Transl Genet Genom 2021;5:22-36 I http://dx.doi.org/10.20517/jtgg.2020.45
55. McGann PT, Niss O, Dong M, et al. Robust clinical and laboratory response to hydroxyurea using pharmacokinetically guided dosing for
young children with sickle cell anemia. Am J Hematol 2019;94:871-9.
56. Dayneka NL, Garg V, Jusko WJ. Comparison of four basic models of indirect pharmacodynamic responses. J Pharmacokinet Biopharm
1993;21:457-78.
57. Ma Q, Wyszynski DF, Farrell JJ, et al. Fetal hemoglobin in sickle cell anemia: genetic determinants of response to hydroxyurea.
Pharmacogenomics J 2007;7:386-94.
58. Gladwin MT, Shelhamer JH, Ognibene FP, et al. Nitric oxide donor properties of hydroxyurea in patients with sickle cell disease. Br J
Haematol 2002;116:436-44.
59. Nahavandi M, Tavakkoli F, Wyche MQ, Perlin E, Winter WP, Castro O. Nitric oxide and cyclic GMP levels in sickle cell patients
receiving hydroxyurea. Br J Haematol 2002;119:855-7.
60. Cokic VP, Andric SA, Stojilkovic SS, Noguchi CT, Schechter AN. Hydroxyurea nitrosylates and activates soluble guanylyl cyclase in
human erythroid cells. Blood 2008;111:1117-23.
61. Lou TF, Singh M, Mackie A, Li W, Pace BS. Hydroxyurea generates nitric oxide in human erythroid cells: mechanisms for gamma-globin
gene activation. Exp Biol Med (Maywood) 2009;234:1374-82.
62. Mabaera R, West RJ, Conine SJ, et al. A cell stress signaling model of fetal hemoglobin induction: what doesn’t kill red blood cells may
make them stronger. Exp Hematol 2008;36:1057-72.
63. Witt O, Monkemeyer S, Rönndahl G, et al. Induction of fetal hemoglobin expression by the histone deacetylase inhibitor apicidin. Blood
2003;101:2001-7.
64. Ramakrishnan V, Pace BS. Regulation of γ-globin gene expression involves signaling through the p38 MAPK/CREB1 pathway. Blood
Cells Mol Dis 2011;47:12-22.
65. Chou YC, Chen RL, Lai ZS, Song JS, Chao YS, Shen CK. Pharmacological Induction of Human Fetal Globin Gene in Hydroxyurea-
Resistant Primary Adult Erythroid Cells. Mol Cell Biol 2015;35:2541-53.
66. Browning DD, Windes ND, Ye RD. Activation of p38 mitogen-activated protein kinase by lipopolysaccharide in human neutrophils
requires nitric oxide-dependent cGMP accumulation. J Biol Chem 1999;274:537-42.
67. Browning DD, McShane MP, Marty C, Ye RD. Nitric oxide activation of p38 mitogen-activated protein kinase in 293T fibroblasts
requires cGMP-dependent protein kinase. J Biol Chem 2000;275:2811-6.
68. Sankaran VG, Menne TF, Xu J, et al. Human fetal hemoglobin expression is regulated by the developmental stage-specific repressor
BCL11A. Science 2008;322:1839-42.
69. Zhou D, Liu K, Sun CW, Pawlik KM, Townes TM. KLF1 regulates BCL11A expression and γ- to β-globin gene switching. Nat Genet
2010;42:742-4.
70. Xu J, Sankaran VG, Ni M, et al. Transcriptional silencing of γ-globin by BCL11A involves long-range interactions and cooperation with
SOX6. Genes Dev 2010;24:783-98.
71. Grieco AJ, Billett HH, Green NS, Driscoll MC, Bouhassira EE. Variation in Gamma-Globin Expression before and after Induction with
Hydroxyurea Associated with BCL11A, KLF1 and TAL1. PLoS One 2015;10:e0129431.
72. Almeida CB, Scheiermann C, Jang JE, et al. Hydroxyurea and a cGMP-amplifying agent have immediate benefits on acute vaso-occlusive
events in sickle cell disease mice. Blood 2012;120:2879-88.
73. Almeida CB, Souza LE, Leonardo FC, et al. Acute hemolytic vascular inflammatory processes are prevented by nitric oxide replacement
or a single dose of hydroxyurea. Blood 2015;126:711-20.