Page 375 - Williams Hematology ( PDFDrive )
P. 375
350 Part V: Therapeutic Principles Chapter 22: Pharmacology and Toxicity of Antineoplastic Drugs 351
196. Chen GQ, Shi XG, Tang W, et al: Use of arsenic trioxide (As2O3) in the treatment of 225. Wyspiańska BS, Bannister AJ, Barbieri I, et al: BET protein inhibition shows efficacy
acute promyelocytic leukemia (APL): I. As2O3 exerts dose-dependent dual effects on against JAK2V617F-driven neoplasms. Leukemia 28:88–97, 2014.
APL cells. Blood 89:3345–3353, 1997. 226. Delmore JE, Issa GC, Lemieux ME, et al: BET bromodomain inhibition as a therapeu-
197. Gupta A, Lawrence AT, Krishnan K, et al: Current concepts in the mechanisms and tic strategy to target c-Myc. Cell. 146(6):904–17, 2011. (http://www.ncbi.nlm.nih.gov/
management of drug-induced QT prolongation and torsade de pointes. Am Heart J pubmed/21889194) Last accessed June 2015.
153:891–899, 2007. 227. Fiskus W, Sharma S, Qi J, et al: Highly active combination of BRD4 antagonist and
198. Shen ZX, Chen GQ, Ni JH, et al: Use of arsenic trioxide (As2O3) in the treatment of histone deacetylase inhibitor against human acute myelogenous leukemia cells. Mol
acute promyelocytic leukemia (APL): II. Clinical efficacy and pharmacokinetics in Cancer Ther 13:1142–1154, 2014.
relapsed patients. Blood 89:3354–3360, 1997. 228. Stewart HJ, Horne GA, Bastow S, Chevassut TJ: BRD4 associates with p53 in
199. Dawson MA, Kouzarides T: Cancer epigenetics: From mechanism to therapy. Cell DNMT3A-mutated leukemia cells and is implicated in apoptosis by the bromodomain
150:12–27, 2012. inhibitor JQ1. Cancer Med 2:826–835, 2013.
200. Silverman LR, Demakos EP, Peterson BL, et al: Randomized controlled trial of azaciti- 229. Zhao Y, Yang CY, Wang S: The making of I-BET762, a BET bromodomain inhibitor
dine in patients with the myelodysplastic syndrome: A study of the cancer and leukemia now in clinical development. J Med Chem 56:7498–7500, 2013.
group B. J Clin Oncol 20:2429–2440, 2002. 230. Druker BJ: Perspectives on the development of a molecularly targeted agent. Cancer
201. Fenaux P, Mufti GJ, Hellstrom-Lindberg E, et al: Efficacy of azacitidine compared with Cell 1:31–36, 2002.
that of conventional care regimens in the treatment of higher-risk myelodysplastic syn- 231. Druker BJ, Guilhot F, O’Brien SG, et al: Five-year follow-up of patients receiving ima-
dromes: A randomised, open-label, phase III study. Lancet Oncol 10:223–232, 2009. tinib for chronic myeloid leukemia. N Engl J Med 355:2408–2417, 2006.
202. Kantarjian H, Issa JP, Rosenfeld CS, et al: Decitabine improves patient outcomes in 232. O’Brien SG, Guilhot F, Larson RA, et al: Imatinib compared with interferon and low-
myelodysplastic syndromes: Results of a phase III randomized study. Cancer 106:1794– dose cytarabine for newly diagnosed chronic-phase chronic myeloid leukemia. N Engl
1803, 2006. J Med 348:994–1004, 2003.
203. Lübbert M, Suciu S, Baila L, et al: Low-dose decitabine versus best supportive care in 233. Cortes J, Lipton JH, Rea D, et al: Phase 2 study of subcutaneous omacetaxine mepesuc-
elderly patients with intermediate- or high-risk myelodysplastic syndrome (MDS) inel- cinate after TKI failure in patients with chronic-phase CML with T315I mutation. Blood
igible for intensive chemotherapy: Final results of the randomized phase III study of the 120:2573–2580, 2012.
European Organisation for Research and Treatment of Cancer Leukemia Group and 234. Heinrich MC, Griffith DJ, Druker BJ, et al: Inhibition of c-kit receptor tyrosine kinase
the German MDS Study Group. J Clin Oncol 29:1987–1996, 2011. activity by STI 571, a selective tyrosine kinase inhibitor. Blood 96:925–932, 2000.
204. Lee YG, Kim I, Yoon SS, et al: Comparative analysis between azacitidine and decitabine 235. Demetri GD, von Mehren M, Blanke CD, et al: Efficacy and safety of imatinib mesylate
for the treatment of myelodysplastic syndromes. Br J Haematol 161:339–347, 2013. in advanced gastrointestinal stromal tumors. N Engl J Med 347:472–480, 2002.
205. Khan H, Vale C, Bhagat T, Verma A: Role of DNA methylation in the pathogenesis and
treatment of myelodysplastic syndromes. Semin Hematol 50:16–37, 2013. 236. Cools J, DeAngelo DJ, Gotlib J, et al: A tyrosine kinase created by fusion of the PDG-
206. Campbell RM, Tummino PJ: Cancer epigenetics drug discovery and development: The FRA and FIP1L1 genes as a therapeutic target of imatinib in idiopathic hypereosinophilic
challenge of hitting the mark. J Clin Invest 124:64–69, 2014. syndrome. N Engl J Med 348:1201–1214, 2003.
207. Navada SC, Steinmann J, Lübbert M, Silverman LR: Clinical development of demethy- 237. Magnusson MK, Meade KE, Nakamura R, et al: Activity of STI571 in chronic myelo-
lating agents in hematology. J Clin Invest 124:40–46, 2014. monocytic leukemia with a platelet-derived growth factor beta receptor fusion onco-
208. West AC, Johnstone RW: New and emerging HDAC inhibitors for cancer treatment. J gene. Blood 100:1088–1091, 2002.
Clin Invest 124:30–39, 2014. 237A. Passamonti F: PDGFREB disease: Right diagnosis to prolong survival. Blood. 123:
209. Duan H, Heckman CA, Boxer LM: Histone deacetylase inhibitors down-regulate bcl-2 3526–8. 2014.
expression and induce apoptosis in t(14;18) lymphomas. Mol Cell Biol 25:1608–1619, 238. Sirvent N, Maire G, Pedeutour F: Genetics of dermatofibrosarcoma protuberans family
2005. of tumors: From ring chromosomes to tyrosine kinase inhibitor treatment. Genes Chro-
210. Luo J, Su F, Chen D, et al: Deacetylation of p53 modulates its effect on cell growth and mosomes Cancer 37:1–19, 2003.
apoptosis. Nature 408:377–381, 2000. 239. Shah NP, Tran C, Lee FY, et al: Overriding imatinib resistance with a novel ABL kinase
211. Heideman MR, Wilting RH, Yanover E, et al: Dosage-dependent tumor suppression by inhibitor. Science 305:399–401, 2004.
histone deacetylases 1 and 2 through regulation of c-Myc collaborating genes and p53 240. Weisberg E, Manley PW, Breitenstein W, et al: Characterization of AMN107, a selective
function. Blood 121:2038–2050, 2013. inhibitor of native and mutant Bcr-Abl. Cancer Cell 7:129–141, 2005.
212. McGraw AL: Romidepsin for the treatment of T-cell lymphomas. Am J Health Syst 241. O’Hare T, Walters DK, Stoffregen EP, et al: In vitro activity of Bcr-Abl inhibitors
Pharm 70:1115–1122, 2013. AMN107 and BMS-354825 against clinically relevant imatinib-resistant Abl kinase
213. Mann BS, Johnson JR, Cohen MH, et al: FDA approval summary: Vorinostat for treat- domain mutants. Cancer Res 65:4500–4505, 2005.
ment of advanced primary cutaneous T-cell lymphoma. Oncologist 12:1247–1252, 2007. 242. Wisniewski D, Lambek CL, Liu C, et al: Characterization of potent inhibitors of the
214. Piekarz RL, Frye R, Turner M, et al: Phase II multi-institutional trial of the histone Bcr-Abl and the c-kit receptor tyrosine kinases. Cancer Res 62:4244–4255, 2002.
deacetylase inhibitor romidepsin as monotherapy for patients with cutaneous T-cell 243. Khorashad JS, Kelley TW, Szankasi P, et al: BCR-ABL1 compound mutations in
lymphoma. J Clin Oncol 27:5410–5417, 2009. tyrosine kinase inhibitor-resistant CML: Frequency and clonal relationships. Blood
215. Piekarz RL, Frye R, Turner M, et al: Phase 2 trial of romidepsin in patients with periph- 121:489–498, 2013.
eral T-cell lymphoma. Blood 117:5827–5834, 2011. 244. Soverini S, Colarossi S, Gnani A, et al: Contribution of ABL kinase domain muta-
216. Coiffier B, Pro B, Prince HM, et al: Romidepsin for the treatment of relapsed/refractory tions to imatinib resistance in different subsets of Philadelphia-positive patients: By
peripheral T-cell lymphoma: Pivotal study update demonstrates durable responses. J the GIMEMA Working Party on Chronic Myeloid Leukemia. Clin Cancer Res 12:
Hematol Oncol 7:11, 2014. 7374–7379, 2006.
217. Ramalingam SS, Kummar S, Sarantopoulos J, et al: Phase I study of vorinostat in 245. Soverini S, Hochhaus A, Nicolini FE, et al: BCR-ABL kinase domain mutation anal-
patients with advanced solid tumors and hepatic dysfunction: A National Cancer Insti- ysis in chronic myeloid leukemia patients treated with tyrosine kinase inhibitors:
tute Organ Dysfunction Working Group study. J Clin Oncol 28:4507–4512, 2010. Recommendations from an expert panel on behalf of European LeukemiaNet. Blood
218. Iwamoto M, Friedman EJ, Sandhu P, et al: Clinical pharmacology profile of vorinostat, 118:1208–1215, 2011.
a histone deacetylase inhibitor. Cancer Chemother Pharmacol 72:493–508, 2013. 246. Cortes JE, Kim DW, Pinilla-Ibarz J, et al: A phase 2 trial of ponatinib in Philadelphia
219. Wong NS, Seah EZh, Wang LZ, et al: Impact of UDP-gluconoryltransferase 2B17 geno- chromosome–positive leukemias. N Engl J Med 369:1783–1796, 2013.
type on vorinostat metabolism and clinical outcomes in Asian women with breast can- 247. Takayama N, Sato N, O’Brien SG, et al: Imatinib mesylate has limited activity against
cer. Pharmacogenet Genomics 21:760–768, 2011. the central nervous system involvement of Philadelphia chromosome-positive acute
220. Wang F, Travins J, DeLaBarre B, et al: Targeted inhibition of mutant IDH2 in leukemia lymphoblastic leukaemia due to poor penetration into cerebrospinal fluid. Br J Haema-
cells induces cellular differentiation. Science 340:622–626, 2013. tol 119:106–108, 2002.
220A. Stein E, Tallman M, Pollyea D et al: Clinical safety and activity in a phase I trial of 248. Gambacorti-Passerini C, Zucchetti M, Russo D, et al: Alpha1 acid glycoprotein binds
AG-221, a first in class, potent inhibitor of the IDH2-mutant protein, in patients with to imatinib (STI571) and substantially alters its pharmacokinetics in chronic myeloid
IDH2 mutant positive advanced hematologic malignancies [abstract]. In: Proceedings leukemia patients. Clin Cancer Res 9:625–632, 2003.
of the 105th Annual Meeting of the American Association for Cancer Research; 2014 249. Shah NP, Nicoll JM, Nagar B, et al: Multiple BCR-ABL kinase domain mutations con-
Apr 5-9; San Diego (CA: AACR; 2014. Abstract nr CT103). fer polyclonal resistance to the tyrosine kinase inhibitor imatinib (STI571) in chronic
221. Daigle SR, Olhava EJ, Therkelsen CA, et al: Potent inhibition of DOT1L as treatment of phase and blast crisis chronic myeloid leukemia. Cancer Cell 2:117–125, 2002.
MLL-fusion leukemia. Blood 122:1017–1025, 2013. 250. O’Hare T, Eide CA, Deininger MW: Bcr-Abl kinase domain mutations, drug resistance,
222. Fathi AT, Sadrzadeh H, Borger DR, et al: Prospective serial evaluation of 2-hydroxyglu- and the road to a cure for chronic myeloid leukemia. Blood 110:2242–2249, 2007.
tarate, during treatment of newly diagnosed acute myeloid leukemia, to assess disease 251. Corbin AS, La Rosée P, Stoffregen EP, et al: Several Bcr-Abl kinase domain mutants
activity and therapeutic response. Blood 120:4649–4652, 2012. associated with imatinib mesylate resistance remain sensitive to imatinib. Blood
223. McCabe MT, Ott HM, Ganji G, et al: EZH2 inhibition as a therapeutic strategy for 101:4611–4614, 2003.
lymphoma with EZH2-activating mutations. Nature 492:108–112, 2012. 252. Branford S, Rudzki Z, Walsh S, et al: Detection of BCR-ABL mutations in patients with
224. Knutson SK, Kawano S, Minoshima Y, et al: Selective inhibition of EZH2 by EPZ-6438 CML treated with imatinib is virtually always accompanied by clinical resistance, and
leads to potent antitumor activity in EZH2-mutant non-Hodgkin lymphoma. Mol Can- mutations in the ATP phosphate-binding loop (P-loop) are associated with a poor
cer Ther 13:842–854, 2014. prognosis. Blood 102:276–283, 2003.
Kaushansky_chapter 22_p0313-0352.indd 350 9/18/15 10:26 PM

