ライフサイエンスコーパス: CML

1 CML in children has been considered to have the same bio

2 CML progenitors demonstrated enhanced sensitivity to Wnt

3 CML therapy based on tyrosine kinase inhibitors (TKIs) i

4 LL (RR = 1.46; 95% CI, 1.25-1.71; P <.0001), CML (RR = 1.49; 95% CI, 1.19-1.88; P = .0005), and MDS (

5 s, including primary cells explanted from 12 CML patients.

6 None of the patients experienced a CML progression.

7 ey to patients to understand the impact of a CML diagnosis on their life.

8 ort new data on the biological function of a CML-interacting partner, PRR2 (PSEUDO-RESPONSE REGULATOR

9 tic differences exist in pediatric and adult CML.

10 lder adults, and prognostic scores for adult CML do not apply to children.

11 gonist, conferred similar protection against CML.

12 d selective PORCN inhibitor, WNT974, against CML stem and progenitor cells.

13 discovery in patients almost 2 decades ago, CML LSCs have become a well-recognized exemplar of the c

14 Cell models of AML, CML, and T-ALL were potently affected by KDM1A inhibitio

15 ngerol also decreased the levels of AGEs and CML levels, via Nrf2 pathway, enhancing GSH/GSSG ratio,

16 This increased risk of AML and CML after RAI treatment was seen even in low-risk and in

17 n increased early risk of developing AML and CML but no other hematologic malignancies.

18 CaM and CML regulate a wide range of target proteins and cellula

19 Likewise, FPG and CML levels were significantly reduced in the propolis gr

20 nificantly reduces levels of HbA1c, FPG, and CML, and improves periodontal therapy outcome in people

21 at combined population dynamic modelling and CML patient biopsy genomic analysis enables patient stra

22 rs therefore of primary importance to aim at CML eradication.

23 cells and increased sCD62L plasma levels at CML diagnosis on molecular response to tyrosine kinase i

24 cells and, vice versa, low sCD62L levels at CML diagnosis were linked to superior molecular response

25 In a humanized BC CML mouse model, combined JAK2 and BCR-ABL1 inhibition p

26 In blast crisis chronic myeloid leukemia (BC CML), we show that increased JAK2 signaling and BCR-ABL1

27 4+ T cell-mediated GVL against CP-CML and BC-CML required intact leukemia MHCII; however, stem cells

28 Mouse AML and BC-CML stem cells were MHCI+ without IFN-gamma stimulation,

29 leukemia (CP-CML), but blast crisis CML (BC-CML) and acute myeloid leukemias (AML) are GVL resistant

30 udied GVL against mouse models of CP-CML, BC-CML, and AML generated by the transduction of mouse BM w

31 Here, we show that CP-CML, BC-CML, and AML stem cells upregulate MHCII in alloSCT reci

32 Importantly, IFN-gammaR-deficient BC-CML and AML were completely resistant to CD4- and CD8-me

33 IFN-gamma stimulation as a mechanism for BC-CML and AML GVL resistance, whereas independence from IF

34 e-deficient leukemias, we determined that BC-CML and AML MHC upregulation required IFN-gamma stimulat

35 ine-driven JAK-mediated signals, provided by CML cells and/or the microenvironment, antagonize MHC-II

36 CaM/CMLs decode and relay information encrypted by the secon

37 formation of N(epsilon)-carboxymethyllysine (CML) in two caseinate solutions containing: (1) glucose,

38 reactions revealed that exposure of CD34(+) CML cells to IFN-gamma or RUX significantly enhanced pro

39 ulation in CML lines and primary human CD34+ CML stem cells.

40 ere, we show that primitive (CD34(+)CD38(-)) CML cells, in contrast to corresponding normal cells, ex

41 ronic myelogenous leukemia-initiating cells (CML LICs), thereby sensitizing them to BCR-ABL tyrosine

42 I review how changing CML practices can impact HAI rates and how the financial

43 As a consequence, CML stem cells persist and cause relapse in most patient

44 chanisms that promote the survival of the CP CML LSCs and how they can be a source of new gene coding

45 own that CD4+ T cell-mediated GVL against CP-CML and BC-CML required intact leukemia MHCII; however,

46 Although CP-CML patients with T315I (63/231, 27%) had superior respo

47 bined, LDE225 + nilotinib reduced CD34(+) CP-CML cell engraftment in NSG mice and, upon administratio

48 inib, inhibited the Hh pathway in CD34(+) CP-CML cells, reducing the number and self-renewal capacity

49 at the Hh pathway is activated in CD34(+) CP-CML stem/progenitor cells.

50 hereas IFN-gammaR/IFNAR1 double-deficient CP-CML was fully GVL sensitive.

51 In contrast, for CP-CML patients without T315I, the inferior responses previ

52 to elucidate the role of Hh signaling in CP-CML and determine if inhibition of Hh signaling, through

53 rapeutic strategy to improve responses in CP-CML by targeting both stem and progenitor cells.

54 h chronic phase chronic myeloid leukemia (CP-CML) are treated with tyrosine kinase inhibitors (TKIs).

55 ronic phase chronic myelogenous leukemia (CP-CML), but blast crisis CML (BC-CML) and acute myeloid le

56 e, we studied GVL against mouse models of CP-CML, BC-CML, and AML generated by the transduction of mo

57 including 231 patients in chronic phase (CP-CML).

58 ereas independence from IFN-gamma renders CP-CML more GVL sensitive, even with a lower-level alloimmu

59 SMO), was an effective strategy to target CP-CML LSC.

60 Here, we show that CP-CML, BC-CML, and AML stem cells upregulate MHCII in allo

61 n required IFN-gamma stimulation, whereas CP-CML MHC upregulation was independent of both the IFN-gam

62 nd prognostic impact of 598 patients with CP-CML treated on clinical trials with various TKIs.

63 logenous leukemia (CP-CML), but blast crisis CML (BC-CML) and acute myeloid leukemias (AML) are GVL r

64 also marks a fraction of human blast crisis CML and acute myeloid leukemia (AML) cells with similar

65 not only is activated in human blast crisis CML and de novo acute myeloid leukaemia, but also predic

66 and impairs the propagation of blast crisis CML both in vitro and in vivo.

67 tion through BCAA production in blast crisis CML cells.

68 ng protein that is required for blast crisis CML.

69 eradicate CML LSCs may be a strategy to cure CML.

70 elapse, and additional approaches to deplete CML LSC are needed to enhance the possibility of discont

71 sducedGab2(-/-)bone marrow failed to develop CML-like myeloproliferative neoplasia.

72 domly assigned patients with newly diagnosed CML in the chronic phase to receive either imatinib or i

73 Patients with newly diagnosed CML-CP were randomly assigned to receive dasatinib 100 m

74 a murine model of retroviral BCR-ABL-driven CML and impaired the in vivo self-renewal capacity of tr

75 Identifying therapeutic targets to eradicate CML LSCs may be a strategy to cure CML.

76 d to complete disease control and eradicated CML xenograft tumours without recurrence after the cessa

77 protein translation, selectively eradicates CML LSCs both in vitro and in a xenotransplantation mode

78 LTHSCs and suggest that high MPL-expressing CML stem cells are potential targets for therapy.

79 supports the implementation of ELISA in food CML/AGEs screening.

80 identified a molecular network critical for CML LSC survival and propose that simultaneously targeti

81 CL6 expression was shown to be essential for CML stem cell survival and self-renewal during imatinib

82 mal residual disease and are responsible for CML relapse following discontinuation of treatment.

83 ing signals from Tyr177 to PI3K and SHP2 for CML pathogenesis, whereas only the GAB2-SHP2 pathway is

84 hibitors could provide effective therapy for CML.

85 ture-initiating cells (LTC-ICs) in LSCs from CML patients.

86 Patients recorded as having CML in the Swedish Cancer Registry from 1973 to 2013 wer

87 ficiently antagonized Wnt signaling in human CML CD34(+) cells, and in combination with the TKI nilot

88 verexpression of PRMT5 was observed in human CML LSCs.

89 lso inhibited long-term engraftment of human CML CD34+ cells in immunodeficient mice.

90 colony or cluster-forming capacity of human CML stem cells in the absence or presence of IM, respect

91 etely blocked the cluster formation of human CML stem cells.

92 and in a xenotransplantation model of human CML.

93 tial prognostic impact of individual ACAs in CML is unknown, and a classification system to reflect s

94 conclusion, the Hh pathway is deregulated in CML stem and progenitor cells.

95 transactivator (CIITA) are downregulated in CML compared with non-CML stem/progenitor cells in a BCR

96 L-1 strategies to enhance LSC elimination in CML.

97 nodrug could upregulate FRbeta expression in CML cancer cells and xenograft tumor model, facilitating

98 zed if IFNgamma modulates BCL6 expression in CML cells.

99 Inhibition of MPL expression in CML LTHSCs reduced THPO-induced JAK/STAT signaling and l

100 embers of the BCL2 and BIRC gene families in CML cells, including the long isoform of MCL1, which pro

101 ell-extrinsic disruption of hematopoiesis in CML associated with clinical outcome.

102 , direct upregulation of BCL6 by IFNgamma in CML cells.

103 ed in an upregulation of CIITA and MHC-II in CML stem/progenitor cells; however, the extent of IFN-ga

104 de novel insights into the role of IL1RAP in CML and a strong rationale for the development of an IL1

105 ytokine interleukin-1 (IL-1) is increased in CML bone marrow.

106 n on CD4(+)/CD8(+) T cells were increased in CML patients at diagnosis.

107 overexpression of inflammatory mediators in CML LSC, suggesting that blocking IL-1 signaling could m

108 T5 abrogated the Wnt/beta-catenin pathway in CML CD34+ cells by depleting dishevelled homolog 3 (DVL3

109 eneity within the putative LSC population in CML at diagnosis and demonstrate differences in response

110 tein arginine methyltransferase 5 (PRMT5) in CML cells.

111 to TKIs is a significant clinical problem in CML, and TKI therapy is much less effective against Ph(+

112 at interferon gamma (IFNgamma) production in CML patients might have a central role in the response t

113 effector and suppressor immune responses in CML patients at diagnosis (n = 21), on TKI (imatinib, ni

114 s of patient-specific treatment responses in CML, we predict that after one year of targeted treatmen

115 agonist (IL-1RA) inhibited IL-1 signaling in CML LSC and inhibited growth of CML LSC.

116 roviding an innovative therapeutic target in CML.

117 um supplementation as an adjuvant therapy in CML.

118 ment induced remarkable BCL6 upregulation in CML lines and primary human CD34+ CML stem cells.

119 ner, we searched for such vulnerabilities in CML LSCs.

120 FZD4 knockdown inhibited CML progenitor growth.

121 y and increased CyPG levels, which inhibited CML progression.

122 ces in the clinical microbiology laboratory (CML) provide more-precise and -sensitive tests, altering

123 Participants consumed less CML, CEL, and MG-H1 during the low-AGE dietary period th

124 Chronic myeloid leukaemia (CML) arises after transformation of a haemopoietic stem

125 ally required for chronic myeloid leukaemia (CML) in humans and in mouse models of CML.

126 Chronic myeloid leukaemia (CML) is driven by the activity of the BCR-ABL1 fusion on

127 hronic phase (CP) chronic myeloid leukaemia (CML).

128 e specific to chronic myelogeneous leukemia (CML).

129 Chronic myelogenous leukemia (CML) in children is relatively rare.

130 ties (ACAs) in chronic myelogenous leukemia (CML) is generally associated with decreased response to

131 e treatment of chronic myelogenous leukemia (CML) largely depends on the eradication of CML leukemic

132 ual disease in chronic myelogenous leukemia (CML) may be relevant for long-term control or cure of CM

133 Chronic myelogenous leukemia (CML) results from transformation of a long-term hematopo

134 n to alleviate chronic myelogenous leukemia (CML) via the elimination of leukemia stem cells (LSCs) i

135 Treatment of chronic myelogenous leukemia (CML) with BCR-ABL tyrosine kinase inhibitors (TKI) fails

136 used to treat chronic myelogenous leukemia (CML).

137 and relapse of chronic myelogenous leukemia (CML).

138 rs (GISTs) and chronic myelogenous leukemia (CML).

139 gnancies including chronic myeloid leukemia (CML) and myelodysplastic syndromes (MDS) either sensitiv

140 ive progression of chronic myeloid leukemia (CML) and tyrosine kinase inhibitor resistance through po

141 BL) transcripts in chronic myeloid leukemia (CML) are e13a2 (b2a2) and e14a2 (b3a2).

142 Using chronic myeloid leukemia (CML) as a paradigm for hierarchical disease evolution we

143 positive (FRbeta+) chronic myeloid leukemia (CML) cells, resulting in more intracellular accumulation

144 ad perception that chronic myeloid leukemia (CML) has become another chronic disease, where lifelong

145 (TKI) treatment of chronic myeloid leukemia (CML) has limited efficacy against leukemia stem cells (L

146 s of patients with chronic myeloid leukemia (CML) in chronic phase (CP) treated with dasatinib or ima

147 Chronic myeloid leukemia (CML) is a hematopoietic stem cell (HSC)-driven neoplasia

148 Chronic myeloid leukemia (CML) is caused by the acquisition of the tyrosine kinase

149 Chronic myeloid leukemia (CML) is currently treated with tyrosine kinase inhibitor

150 n in chronic phase chronic myeloid leukemia (CML) patients at diagnosis and following conventional ty

151 ecular response in chronic myeloid leukemia (CML) patients on tyrosine kinase inhibitor (TKI) therapy

152 f highly quiescent chronic myeloid leukemia (CML) SCs that is enriched following therapy with tyrosin

153 from patients with chronic myeloid leukemia (CML) throughout the disease course, revealing heterogene

154 ificantly affected chronic myeloid leukemia (CML) treatment, transforming the life expectancy of pati

155 b in patients with chronic myeloid leukemia (CML) was interrupted due to an important increase of vas

156 d in patients with chronic myeloid leukemia (CML) who have had undetectable minimal residual disease

157 beneficiaries with chronic myeloid leukemia (CML) with and without cost-sharing subsidies.

158 Treatment of chronic myeloid leukemia (CML) with imatinib mesylate and other second- and/or thi

159 el of blast crisis chronic myeloid leukemia (CML), adipose-resident LSCs exhibit a pro-inflammatory p

160 for patients with chronic myeloid leukemia (CML), but continuous administration of these drugs may e

161 ged the outcome of chronic myeloid leukemia (CML), turning a life-threatening disease into a chronic

162 gnancies including chronic myeloid leukemia (CML), where BCL6 expression was shown to be essential fo

163 ept in the case of chronic myeloid leukemia (CML), wherein our model recapitulated the clinical histo

164 highly aggressive chronic myeloid leukemia (CML)-blast phase-like disease in mice compared with less

165 iesis resembling a chronic myeloid leukemia (CML)-like disease manifesting in "lymphoid blast crisis.

166 discontinuation in chronic myeloid leukemia (CML).

167 reatic cancer, and chronic myeloid leukemia (CML).

168 t of patients with chronic myeloid leukemia (CML).

169 pies used to treat chronic myeloid leukemia (CML).

170 for patients with chronic myeloid leukemia (CML).

171 ced mouse model of chronic myeloid leukemia (CML).

172 2.82; P = .01) and chronic myeloid leukemia (CML; hazard ratio, 3.44; 95% CI, 1.87 to 6.36; P < .001)

173 n (CaM) and closely related calmodulin-like (CML) polypeptides are principal sensors of Ca(2+) signal

174 Calmodulin-like (CML) proteins are major EF-hand-containing, calcium (Ca(

175 ted by Calmodulin (CaM) and calmodulin-like (CML) proteins is critical to plant immunity.

176 (FPG), serum N(euro)-(carboxymethyl) lysine (CML), and periodontal parameters (secondary outcomes).

177 ibition of N(epsilon)-(carboxymethyl)lysine (CML) formation.

178 f AGEs and N(epsilon)-(carboxymethyl)lysine (CML) found to be predominantly higher in the diabetic po

179 N(epsilon)-(carboxymethyl)lysine (CML), N(epsilon)-(1-carboxyethyl)lysine (CEL) and N(delt

180 urinary AGEs N(euro)-(carboxymethyl)lysine (CML), N(euro)-(carboxyethyl)lysin (CEL), and methylglyox

181 N(epsilon)-carboxymethyl-lysine (CML) is measured in food, but there is a controversy con

182 leukaemic stem cells (LSCs), which maintain CML.

183 disease in mice compared with less malignant CML-chronic phase-like disease from BCR-ABL1-Abl1(+/+) c

184 now time to change our approach for the many CML patients who have achieved a stable deep molecular r

185 +)CD4(+)/CD8(+) T cells persisted in pre-MMR CML patients on TKI.

186 obtained by ELISA performed with monoclonal CML-antibody (beta=0.98, p<0.0001) whereas My Bio Source

187 In both solutions, more CML was formed at 130 degrees C than at 120 degrees C.

188 esponsible for disease propagation, and most CML patients require continued TKI treatment to maintain

189 Moreover, in a murine CML model, ACF decreased leukemia development and reduce

190 nd activity of LSCs in a pre-clinical murine CML model and a xenograft model of transplanted CML pati

191 ted significantly less-severe effects on non-CML hematopoietic cells in vitro and in vivo.

192 nificantly lower than when compared with non-CML CD34(+) cells.

193 ) are downregulated in CML compared with non-CML stem/progenitor cells in a BCR-ABL kinase-independen

194 Occurrence of AML but not CML in patients with WDTC was associated with shorter me

195 FIC, the presence of significant amounts of CML and enhanced browning were observed, along with incr

196 ays and HPLC-ESI-ITMS/MS for the analysis of CML in several food items.

197 cing the number and self-renewal capacity of CML LSC in vitro.

198 be relevant for long-term control or cure of CML.

199 Small differences of CML concentrations in food items prepared by different c

200 work we mathematically model the dynamics of CML response to combination therapy and analyze the impa

201 relation (0.853-0.990) with effectiveness of CML inhibition, except in the case of samples with FA.

202 (CML) largely depends on the eradication of CML leukemic stem cells (LSCs).

203 ggressive strategies, such as eradication of CML stem cells with limited duration and intensive regim

204 entially lead to the complete eradication of CML stem cells.

205 o assist in the detection and eradication of CML stem/progenitor cells.

206 multiple therapies based on the evolution of CML according to our ordinary differential equation mode

207 avine (ACF) decreased survival and growth of CML cells.

208 signaling in CML LSC and inhibited growth of CML LSC.

209 e disease course, revealing heterogeneity of CML-SCs, including the identification of a subgroup of C

210 ulted in significantly greater inhibition of CML LSC compared with TKI alone.

211 upplemented with PCs contained low levels of CML, this process may adversely affect bread flavor, red

212 IL-1 signaling contributes to maintenance of CML LSC following TKI treatment and that IL-1 blockade w

213 lator of LSC survival, on the maintenance of CML stem cell potential.

214 nd complementary to conventional measures of CML disease burden and prognosis.

215 Using a genetic strategy and mouse models of CML and B-ALL, we show here that GAB2 is essential for m

216 aemia (CML) in humans and in mouse models of CML.

217 methods showed the same decreasing order of CML concentration: beef, bacon>chicken > fish>dairy prod

218 not TKIs, targets the stem cell potential of CML cells, including primary cells explanted from 12 CML

219 roliferation and colony-forming potential of CML stem and progenitor cells and reduced their growth i

220 from the BMM contributes to preservation of CML LSC following TKI treatment.

221 BCAT1 is upregulated during progression of CML and promotes BCAA production in leukaemia cells by a

222 with CML and life-years lost as a result of CML between 1973 and 2013 in Sweden.

223 average, lose < 3 life-years as a result of CML.

224 -initiating capacity and drug sensitivity of CML LTHSCs and suggest that high MPL-expressing CML stem

225 function and vascular damage in the serum of CML patients who were treated with dasatinib, compared w

226 ion, which was also present in a subclone of CML-SCs during the chronic phase in a patient who subseq

227 ncluding the identification of a subgroup of CML-SCs with a distinct molecular signature that selecti

228 upplemented diets, alleviate the symptoms of CML through their ability to activate the nuclear hormon

229 etion and signaling and enhance targeting of CML stem cells while sparing their normal counterparts.

230 emerged from chronic phase or at the time of CML diagnosis.

231 -line therapy for the long-term treatment of CML-CP.

232 d identification of novel target proteins of CMLs deserve special attention.

233 and improves therapeutic efficacy of ATO on CML and xenograft tumor model.

234 fore, we recommend further investigations on CML-like BCR-ABL1-positive ALL.

235 tor type 1 and has been found upregulated on CML stem cells.

236 lood and marrow transplantation in pediatric CML is currently indicated only for recurrent progressiv

237 phase, no progression toward advanced phase CML occurred, and all relapsing patients regained MMR an

238 ce transplanted with chronic and blast phase CML cells resulted in therapeutic effects mediated by mu

239 In vitro treatment of immature chronic phase CML cells with TKI alone, or in combination with interfe

240 udy involved 481 patients with chronic phase CML expressing various BCR-ABL transcripts.

241 when emerging in patients with chronic-phase CML across various TKIs.

242 Studies in patients with chronic-phase CML have shown that around 50% of patients who achieve a

243 nilotinib-naive patients with chronic-phase CML.

244 ase inhibitor therapy in early chronic-phase CML.

245 , as a novel therapeutic approach to prevent CML relapse and, in combination with TKIs, enhance induc

246 enotransplanted with patient-derived primary CML cells.

247 tional assays, we demonstrate that primitive CML cells rely on upregulated oxidative metabolism for t

248 s and existence of an autocrine loop promote CML-primitive cells' TKI resistance.

249 PCs were found to significantly reduce CML (31.77%-87.56%), even at the lowest concentration, w

250 (+)-Catechin reduced CML levels the most, probably due to its structure-antio

251 n IL1RAP antibody therapy to target residual CML stem cells.

252 on with ICG-001 can eliminate drug-resistant CML LICs without deleterious effects to the normal endog

253 Since CML appeared to be thermally unstable under the current

254 , drug resistance remains a problem for some CML patients.

255 Recent trials demonstrate that some CML patients who have achieved stable deep molecular res

256 f this PGE1-EP4 pathway specifically targets CML LSCs and that the combination of PGE1/misoprostol wi

257 At both heating temperatures, CML concentration in lactose-caseinate solution was high

258 We recently showed that CML LSCs depend on Tcf1 and Lef1 factors for self-renewa

259 Strong evidence now shows that CML LSCs are resistant to the effects of TKIs and persis

260 Modelling results suggested that CML was not formed from oxidation of the reducing sugars

261 , but these do not effectively eliminate the CML stem cells.

262 were 54 arterial and 20 venous events in the CML cohort, corresponding to relative risks of 1.5 (95%

263 A8, uncovering a possible involvement of the CML protein family in the modulation of plant-autoinhibi

264 Additionally, cell surface expression of the CML stem cell markers CD25, CD26, and IL1RAP is high in

265 s expose a considerable heterogeneity of the CML stem cell population and propose a Lin(-)CD34(+)CD38

266 kinase activity of BCR-ABL1 have transformed CML from a once-fatal disease to a manageable one for th

267 Treatment of transgenic CML mice in vivo with NIL in combination with WNT974 sig

268 n vivo self-renewal capacity of transplanted CML LSCs.

269 model and a xenograft model of transplanted CML patient CD34(+) stem/progenitor cells.

270 BCL6, we demonstrated that in an IM-treated CML line the antiapoptotic effect of IFNgamma was indepe

271 poptotic effect of IFNgamma in an IM-treated CML line.

272 h IL-1RA enhances elimination of TKI-treated CML LSC.

273 IITA and MHC-II significantly increased when CML stem/progenitor cells were treated with the JAK1/2 i

274 This is the first study in which CML formation was linked to available information on the

275 sion Only 68% of Medicare beneficiaries with CML initiated TKI therapy within 6 months of diagnosis.

276 active growth, morbidities in children with CML may be distinct from those in adults and require car

277 Because children with CML may receive tyrosine kinase inhibitor (TKI) therapy

278 o were treated with dasatinib, compared with CML patients treated with imatinib.

279 Results Among 393 individuals diagnosed with CML from 2007 to 2011, 68% initiated TKI treatment withi

280 ta, we identified individuals diagnosed with CML from 2007 to 2011.

281 of therapy among individuals diagnosed with CML.

282 CD34(-)) cells derived from individuals with CML, and we compared the signature of these cells with t

283 alysis of nonleukemic SCs from patients with CML also provided new insights into cell-extrinsic disru

284 ffected the life expectancy of patients with CML and life-years lost as a result of CML between 1973

285 linical development testing in patients with CML and Philadelphia chromosome-positive (Ph(+)) acute l

286 uted to the life expectancy in patients with CML approaching that of the general population today.

287 Results T cells of patients with CML at diagnosis expressed low l-selectin (CD62L) levels

288 f vascular occlusive events in patients with CML treated by new generations of TKIs and provide an ov

289 us vascular events was seen in patients with CML treated with a TKI.

290 A total of 2,662 patients with CML were diagnosed between 1973 and 2013.

291 than 10 years of follow-up in patients with CML who were treated with imatinib as initial therapy.

292 , the increasing prevalence of patients with CML will have a great effect on future health care costs

293 tion with tigecycline to treat patients with CML with minimal residual disease.

294 spectively discontinued in 100 patients with CML with UMRD sustained for at least 2 years.

295 re also present in LTHSCs from patients with CML, and patient LTHSCs with high MPL expression had red

296 oved the clinical outcomes for patients with CML, with over 80% of patients treated with imatinib sur

297 treated and imatinib-resistant patients with CML.

298 overall survival at 1 year in patients with CML.

299 .78) compared with imatinib in patients with CML.

300 kinase inhibitor (TKI) used in patients with CML.