ライフサイエンスコーパス: leukemia

1 pment of new approaches to monitor and treat leukemia.

2 of 3D chromatin architecture in human acute leukemia.

3 gager, blinatumomab, for acute lymphoblastic leukemia.

4 y thwarted progression of disseminated HL-60 leukemia.

5 n survivors of childhood acute lymphoblastic leukemia.

6 ated oncogenes in T cell acute lymphoblastic leukemia.

7 a) during remission, and 1 secondary myeloid leukemia.

8 nuclei from patients of acute lymphoblastic leukemia.

9 n mutations recurrent in chronic lymphocytic leukemia.

10 le, 66% were non-Hispanic White, and 36% had leukemia.

11 l treatment in childhood acute lymphoblastic leukemia.

12 is linked to diseases such as acute myeloid leukemia.

13 oping a new therapy for the treatment of MLL leukemia.

14 can alter specific 3D interactions found in leukemia.

15 sition from a healthy state to acute myeloid leukemia.

16 xPHOS supporting proliferation and growth in leukemia.

17 due to the poor prognosis of untreated acute leukemia.

18 the kinase TTK is important in acute myeloid leukemia.

19 expressed at reduced levels in human myeloid leukemia.

20 ression of Hoxa genes in order to advance to leukemia.

21 molecular regulation network in HOXA9-driven leukemia.

22 loid leukemia and a subset of acute lymphoid leukemias.

23 at is linked to the development of secondary leukemias.

24 -mutant (NPM1mut) and MLL-rearranged (MLL-r) leukemias.

25 argeted GSL modulation could help manage MDR leukemias.

26 consistently overexpressed in MLL-rearranged leukemias.

27 seen across multiple mouse and human myeloid leukemias.

28 n of FLT3, an important driver gene in acute leukemias.

29 Megakaryoblastic leukemia 1 (MKL1) promotes the regulation of essential c

30 te myeloid leukemia (AML) with mixed lineage leukemia 1 (MLL1) gene rearrangement is characterized by

31 in the murine brain requires a mixed-lineage leukemia 1 (Mll1)-dependent epigenetic memory system.

32 second cancers (control, n = 32; DC, n = 21; leukemia: 2 v 1).

33 The histone methyltransferase mixed-lineage leukemia-4 (MLL4) is a transcriptional coactivator of th

34 In a xenograft model of acute myeloid leukemia, a single injection of 10 million Jurkat cells

35 ained TFR only if an optimal balance between leukemia abundance and immunologic activation was achiev

36 orld data set from the German Study Alliance Leukemia-Acute Myeloid Leukemia (SAL-AML) registry.

37 Acute erythroid leukemia (AEL) commonly involves both myeloid and erythr

38 undergoing treatment of acute lymphoblastic leukemia (ALL) are at risk for thrombosis, caused in par

39 ive relapse formation in acute lymphoblastic leukemia (ALL) by conferring purine analog resistance.

40 omes for 90 infants with acute lymphoblastic leukemia (ALL) by providing excellent supportive care wh

41 ladelphia-positive (Ph+) acute lymphoblastic leukemia (ALL) cell growth, whereas expression of the cl

42 cellular MTXPG levels in acute lymphoblastic leukemia (ALL) cells from 388 newly diagnosed patients a

43 cure rate for childhood acute lymphoblastic leukemia (ALL) has exceeded 80% with contemporary therap

44 Relapsed acute lymphoblastic leukemia (ALL) has remained challenging to treat in chil

45 Ph(+) acute lymphoblastic leukemia (ALL) is characterized by the expression of an

46 pediatric patients with acute lymphoblastic leukemia (ALL) is efficacious, but long-term side effect

47 /refractory (r/r) B-cell acute lymphoblastic leukemia (ALL) patients.

48 ll survival of childhood acute lymphoblastic leukemia (ALL) to 90%, but its impact on long-term toxic

49 n important component of acute lymphoblastic leukemia (ALL) treatment, but is often discontinued beca

50 en with high-risk B-cell acute lymphoblastic leukemia (ALL) would also improve outcomes for those wit

51 common in patients with acute lymphoblastic leukemia (ALL), but risk differences across age groups b

52 In 5% of childhood acute lymphoblastic leukemia (ALL), the t(1,19) chromosomal translocation sp

53 most exclusively used in acute lymphoblastic leukemia (ALL), which is a very rare cancer in adults.

54 id leukemia and relapsed acute lymphoblastic leukemia (ALL).

55 o limit the prognosis of acute lymphoblastic leukemia (ALL).

56 activity in B-precursor acute lymphoblastic leukemia (ALL).

57 UP98) are recurrently found in acute myeloid leukemia (AML) and are associated with poor prognosis.

58 Here we report a cohort of 86 acute myeloid leukemia (AML) and myelodysplastic syndrome (MDS) famili

59 ted with an aggressive form of acute myeloid leukemia (AML) and poor survival rate.

60 metabolic enzymes required for acute myeloid leukemia (AML) cell growth.

61 Primary acute myeloid leukemia (AML) cells harvested from patients with NPM1mu

62 the influence of NOD2 in human acute myeloid leukemia (AML) cells, demonstrating that IFN-gamma treat

63 ed detailed genetic studies in acute myeloid leukemia (AML) cells.

64 ts most suitable for intensive acute myeloid leukemia (AML) chemotherapy.

65 criptome that are required for acute myeloid leukemia (AML) development.

66 We show that human acute myeloid leukemia (AML) expresses CD83 and that myeloid leukemia

67 Patients with acute myeloid leukemia (AML) harboring FLT3 internal tandem duplicatio

68 ment of relapsed or refractory acute myeloid leukemia (AML) has presented challenges for hematologist

69 ectives regarding treatment of acute myeloid leukemia (AML) include achieving complete remission (CR)

70 s used in the treatment of acute myelogenous leukemia (AML) inhibit the activity of the mammalian top

71 Acute myeloid leukemia (AML) is a cancer derived from the myeloid line

72 Acute myeloid leukemia (AML) is a deadly hematologic malignancy with p

73 Acute myeloid leukemia (AML) is a systemic, heterogeneous hematologic

74 Acute myeloid leukemia (AML) is an attractive system for investigating

75 Acute myeloid leukemia (AML) is characterised by a series of genetic a

76 s they age, but progression to acute myeloid leukemia (AML) is rare.

77 Epigenetic reprogramming in Acute Myeloid Leukemia (AML) leads to the aberrant activation of super

78 Using acute myeloid leukemia (AML) mouse models, we show AML blasts release

79 hown that the highly prevalent acute myeloid leukemia (AML) mutation, Arg882His, in DNMT3A disrupts i

80 Using acute myelogenous leukemia (AML) patient-derived xenograft (PDX) models of

81 marrow cells derived from six acute myeloid leukemia (AML) patients and treated with the nucleoside

82 ested MASQ in a pilot study in acute myeloid leukemia (AML) patients who entered complete remission.

83 Acute myeloid leukemia (AML) represents the most common acute leukemia

84 ically relevant event in human acute myeloid leukemia (AML) that contributes to impaired differentiat

85 -independence in patients with acute myeloid leukemia (AML) treated with the isocitrate dehydrogenase

86 ment failure for patients with acute myeloid leukemia (AML) who undergo allogeneic stem cell transpla

87 Acute myeloid leukemia (AML) with mixed lineage leukemia 1 (MLL1) gene

88 High CD33 expression in acute myeloid leukemia (AML) with mutated NPM1 provides a rationale fo

89 However, in acute myeloid leukemia (AML), ALKBH5 was reported to be frequently del

90 during leukemogenesis of human acute myeloid leukemia (AML), and ALKBH5 is required for maintaining l

91 odysplastic Syndrome (MDS) and Acute Myeloid Leukemia (AML), and the most common mutation is a missen

92 es, we present our results for acute myeloid leukemia (AML), breast cancer and prostate cancer.

93 patients with newly diagnosed acute myeloid leukemia (AML), immediate treatment start is recommended

94 ke CBFB-MYH11 are prevalent in acute myeloid leukemia (AML), often necessary for leukemogenesis, pers

95 toclax has an emerging role in acute myeloid leukemia (AML), with promising response rates in combina

96 nt-naive elderly patients with acute myeloid leukemia (AML).

97 ol determine aggressiveness of acute myeloid leukemia (AML).

98 iated with a poor prognosis in acute myeloid leukemia (AML).

99 uent chromosome aberrations in acute myeloid leukemia (AML).

100 ession and promotes relapse in acute myeloid leukemia (AML).

101 resulted in the development of acute myeloid leukemia (AML).

102 methylation of its promoter in acute myeloid leukemia (AML).

103 x1 in a mouse model of inv(16) acute myeloid leukemia (AML).

104 eatment of IDH1-mutant (mIDH1) acute myeloid leukemia (AML).

105 over-expressed and mutated in acute myeloid leukemia (AML).

106 ious outcomes in patients with acute myeloid leukemia (AML).

107 Secondary acute myeloid leukemias (AMLs) evolving from an antecedent myeloprolif

108 kemia (AML) represents the most common acute leukemia among adults.

109 driver oncogene that causes chronic myeloid leukemia and a subset of acute lymphoid leukemias.

110 r a new therapeutic target in MLL-rearranged leukemia and act as further validation of a burgeoning p

111 With optimal, holistic management of leukemia and all other conditions afflicting them, patie

112 etastatic cancers, such as acute myelogenous leukemia and breast cancer.

113 strategy for patients with NPM1mut or MLL-r leukemia and concurrent FLT3 mutation.

114 ential element in the progression of myeloid leukemia and could be an attractive target for the treat

115 nctions of selected deubiquitinases in acute leukemia and efforts to target these enzymes with the ai

116 s were used to identify cancer stem cells in leukemia and gliomas.

117 nowledge related to altered UPR signaling in leukemia and highlight possible strategies for exploitin

118 olymorphism array results from acute myeloid leukemia and prostate cancer datasets available on TCGA.

119 ing intensive chemotherapy for acute myeloid leukemia and relapsed acute lymphoblastic leukemia (ALL)

120 In vivo, Fas-4-1BB ACT eradicated leukemia and significantly improved survival in the aggr

121 arnib reduced cell viability in these T-cell leukemia and TCL cell lines, induced apoptosis and modif

122 as a potential therapeutic option in T-cell leukemia and TCL.

123 iagnosed with precursor B-cell lymphoblastic leukemia and underwent transplantation of hematopoietic

124 iagnosed with precursor B-cell lymphoblastic leukemia and underwent transplantation of hematopoietic

125 ogeneity is a common feature of many myeloid leukemias and a significant reason for treatment failure

126 oding the tyrosine kinase FLT3 occur in both leukemias and are particularly common in the NPM1mut sub

127 TPN11 mutations drive oncogenesis in several leukemias and cause developmental disorders with increas

128 the treatment of B-cell disorders including leukemias and lymphomas.

129 acute myeloid leukemia, chronic lymphocytic leukemia, and a variety of solid tumors.

130 marker of treatment response with MI-3454 in leukemia, and demonstrated that this compound is well to

131 scular dystrophy (FSHD), acute lymphoblastic leukemia, and sarcomas.

132 diseases, including developmental disorders, leukemia, and solid tumors.

133 ed model to study the crosstalk among HSPCs, leukemia, and their MSC niche, and a molecular mechanism

134 Acute promyeloid leukemia (APL) is characterized by the oncogenic fusion

135 Leukemias are routinely sub-typed for risk/outcome predi

136 ysplastic syndrome with progression to acute leukemia associated with acquisition of additional drive

137 Although acquisition of leukemia-associated somatic mutations by 1 or more hemat

138 A subset of B cell acute lymphoblastic leukemia (B-ALL) patients will relapse and succumb to th

139 in patients with B cell acute lymphoblastic leukemia (B-ALL), making B-ALL an excellent model for st

140 g Msi2-reporter blast crisis chronic myeloid leukemia (bcCML) and identify several adhesion molecules

141 12.2 in B-cell precursor acute lymphoblastic leukemia (BCP-ALL) eliminate the boundary of a topologic

142 ociated with insertional mutagenesis causing leukemia, because the viral enhancer induced transactiva

143 cytes from patients with chronic lymphocytic leukemia being treated with ibrutinib.

144 tly emerged as novel players in the field of leukemia biology.

145 l transduction of B-cell acute lymphoblastic leukemia blasts during CART19 manufacturing can lead to

146 t, CD36(High) LSCs were unable to transplant leukemia but were highly proliferative.

147 ved treatment of pediatric acute lymphocytic leukemia, can consistently achieve curative outcomes in

148 NFAT-DsRed rat basophil leukemia cell attachment and retention during washing st

149 6 18S rRNA 2'-O-methylation is essential for leukemia cell growth and survival.

150 onfirmed by a second in vivo model using the leukemia cell line NALM6.

151 ukemia (AML) expresses CD83 and that myeloid leukemia cell lines are readily killed by CD83 CAR T cel

152 y low cytotoxicity as a single agent against leukemia cell lines, it augmented the apoptosis inductio

153 presses cell growth by inducing apoptosis in leukemia cell lines.

154 treatment with an EZH2 inhibitor in several leukemia cell lines.

155 reveals that the spatiotemporal dynamics of leukemia cells are critically dependent on syndecan sign

156 fficiency of pseudodiploid mouse lymphocytic leukemia cells during normal proliferation and polyploid

157 nts targeting CD22 or CD20 on B lymphoma and leukemia cells exhibit clinical efficacy for treating th

158 bservations in mice, patient-derived myeloid leukemia cells exhibit KRAS/RAC1/ROS/NLRP3/IL-1beta axis

159 We found that leukemia cells exhibited mechanical differences compared

160 ncluding chemotherapy, facilitated escape of leukemia cells from targeted third-generation ABCB1 inhi

161 Of note, SKIP re-expression in leukemia cells increased ceramide levels 2-fold, inactiv

162 micking T-cell receptor activation in Jurkat leukemia cells induced sequential activation of downstre

163 ive polyglutamylated metabolites (MTXPGs) in leukemia cells influence its antileukemic effects.METHOD

164 Hopx(-/-) MN1-overexpressed leukemia cells showed higher proliferation rate and down

165 We show that exposure of leukemia cells to daunorubicin activated an integrated s

166 t oxidase-derived ROS promotes the growth of leukemia cells via the glycolytic regulator PFKFB3.

167 the cell size of SNORD42A deletion carrying leukemia cells was decreased.

168 HL60 (leukemia cells) were also studied as a model circulatory

169 -RARalpha in transforming myeloid cells into leukemia cells, but further uncover a topological framew

170 t SKIP re-expression enhances SK activity in leukemia cells.

171 occupancy of USF2 at HOXA9 promoter in MLLr leukemia cells.

172 ion is highly sensitized in STAG2-mutant CMK leukemia cells.

173 ommon in clonal hematopoiesis, acute myeloid leukemia, chronic lymphocytic leukemia, and a variety of

174 but was not required for in vitro or in vivo leukemia clearance.

175 Chronic lymphocytic leukemia (CLL) cells cycle between lymph node (LN) and p

176 Targeted therapies for chronic lymphocytic leukemia (CLL) include venetoclax, the oral inhibitor of

177 and immune dysfunction, chronic lymphocytic leukemia (CLL) patients may be at particularly high risk

178 ed prognostic factors in chronic lymphocytic leukemia (CLL) treated with chemoimmunotherapy, but are

179 tion and is disturbed in chronic lymphocytic leukemia (CLL).

180 ine in older adults with chronic lymphocytic leukemia (CLL).

181 malignancies, including chronic lymphocytic leukemia (CLL).

182 h relapsed or refractory chronic lymphocytic leukemia (CLL).

183 herapeutic landscape for chronic lymphocytic leukemia (CLL).

184 tcomes for patients with chronic lymphocytic leukemia (CLL)/small lymphocytic lymphoma (SLL).

185 on-Hodgkin's lymphoma or chronic lymphocytic leukemia [CLL]).

186 Patients with chronic myeloid leukemia (CML) often have comorbidities, at an incidence

187 al findings in patients with chronic myeloid leukemia (CML) suggest that the risk of molecular recurr

188 ss of K3 in a mouse model of chronic myeloid leukemia (CML) triggers the release of LSCs from the BM

189 rmal and cancerous states in chronic myeloid leukemia (CML).

190 tence of T cells and significantly prolonged leukemia control in vivo, confirmed by a second in vivo

191 viously shown to associate with poor BCR-ABL leukemia control, were present at higher frequencies amo

192 GN1, a target of recurrent DNA copy gains in leukemia, controls myeloid differentiation.

193 e analysis, including disease-related (acute leukemia, curative intent chemotherapy), laboratory-rela

194 Using The Cancer Genome Atlas acute myeloid leukemia data set, we found an inverse correlation of mi

195 rging therapeutic potential in acute myeloid leukemia, debilitating fibroses, and obesity-related liv

196 In leukemia, depletion of BAHCC1, or disruption of the BAHC

197 data shed new light on the role of SNAI1 in leukemia development and identify a novel mechanism of L

198 treatment with anti-IL7R antibodies prevents leukemia development in xenotransplantation models using

199 ication of gene and pathway contributions to leukemia development.

200 a indicate that repurposing the FDA-approved leukemia drug, nilotinib, may be effective for prolongin

201 mportant therapeutic target in acute myeloid leukemia due to high incidence of mutations associated w

202 h chemoimmunotherapy for chronic lymphocytic leukemia experienced a 9-week course of COVID-19 with hi

203 Pre-B cell leukemia factor 1 (PBX1) is an essential developmental t

204 roteomics-based approach to identify myeloid leukemia factor 2 (MLF2) as a luminal component of the b

205 mong cases, but not to acquired mutations in leukemia genes.

206 Several acute myeloid leukemia genetic sub-types converge on high expression o

207 arget these enzymes with the aim of blocking leukemia growth and improving disease outcomes.

208 tion obstructs A3 T-cell lymphoblastic acute leukemia growth in vitro and in vivo, validating OGG1 as

209 lloreactive T cells mediate the graft-versus-leukemia (GVL) effect.

210 A20-luciferase B-cell lymphoma graft-versus-leukemia (GVL).

211 models of human and murine NPM1mut and MLL-r leukemias harboring an FLT3 mutation.

212 ranged leukemia, targeted therapies for this leukemia have remained elusive and clinical outcomes rem

213 he standard first-line therapy of hairy cell leukemia (HCL) for 30 years.

214 .27 (7.19-7.35); metastatic cancer and acute leukemia (Hierarchical Condition Category 8), 6.76 (6.71

215 Analysis of 13 T-lineage acute lymphoblastic leukemias identified a recurrent intronic variant predic

216 sylation of its CD19 partner, the target for leukemia immunotherapies.

217 induced complete remission or regression of leukemia in mouse models of MLL1-rearranged or NPM1-muta

218 opagation of murine and human MLL-rearranged leukemia in vitro and in vivo.

219 se models of MLL1-rearranged or NPM1-mutated leukemia, including patient-derived xenograft models, th

220 Drug Administration (FDA)-approved drug for leukemia, indicates improvement in Alzheimer's disease p

221 predictor of infection during acute myeloid leukemia induction chemotherapy (IC) among clinical and

222 Leukemia inhibitory factor (LIF) injections were given i

223 s marked early on by their downregulation of leukemia inhibitory factor receptor and was promoted by

224 eral sclerosis) and influences on longevity (leukemia inhibitory factor, ceramides).

225 , the abnormal myeloid progenitors (AMPs), a leukemia-initiating cell population induced by Cbfb-MYH1

226 o block the colony-forming ability of murine leukemia-initiating cells.

227 proliferation, differentiation blockage, and leukemia initiation were differentially expressed betwee

228 The Friend leukemia integration 1 (Fli-1) signaling network has bee

229 Acute myeloid leukemia is characterized by the accumulation of clonal

230 ed acquired resistance to etoposide in human leukemia K562 cells.

231 Individually, lamin B1 highlights acute leukemias, lamin A/C helps distinguish normal from neopl

232 cells co-expressing NOTCH1 and NRARP develop leukemia later than mice transplanted with T-NOTCH1 cell

233 ithout impairing GVL against 2 acute myeloid leukemia lines (MLL-AF9-eGFP and C1498-luciferase).

234 report that the transcription factor B-cell leukemia/lymphoma 11A (BCL11A) is highly expressed in tr

235 exception was greater splenic uptake in the leukemia/MDS group than in the lymphoma or multiple myel

236 n AML by using the MN1 overexpression murine leukemia model.

237 (smoldering myeloma, n = 2; chronic lymphoid leukemia, n = 1; and refractory cytopenia with multiline

238 ing follow-up (non-Hodgkin lymphoma, n = 13; leukemia, n = 6; solid tumor, n = 25; unspecified malign

239 ssion is a hallmark of most aggressive acute leukemias, notably those with KMT2A (MLL) gene rearrange

240 that depends on ALT-associated promyelocytic leukemia nuclear bodies (APBs), whose function is unclea

241 tive targeted agents for chronic lymphocytic leukemia offers the potential for fixed-duration combina

242 ic test, especially in cancers such as acute leukemia or diffuse large B-cell lymphoma that require r

243 is unclear how CTCF binding is perturbed in leukemia or in cancer in general.

244 sors in the evolution of CH to acute myeloid leukemia or myelodysplastic syndrome.

245 nly altered in pediatric acute lymphoblastic leukemia (PALL).

246 teria were also found to be more abundant in leukemia patients undergoing radiotherapy, who also disp

247 All registered non-acute promyelocytic leukemia patients with intensive induction treatment and

248 a chromosome-like B cell acute lymphoblastic leukemia (Ph-like B-ALL) experience high relapse rates d

249 L and the cell(s) that sustain the bilineage leukemia phenotype remain unknown.

250 main containing 1 (SMCHD1), or promyelocytic leukemia (PML) protein increased basal level of cccDNA t

251 suppresses the accumulation of promyelocytic leukemia (PML) protein, BRCA1 and the SMC5/6 complex at

252 trinsic immunity driven by the promyelocytic leukemia (PML) protein, which limits ZIKV replication.

253 cells (LSCs) were highly differentiated, and leukemia progression was severely impaired in the absenc

254 However, in TAL1-expressing T-ALL cells, the leukemia-prone TAL1 promoter-IV specifically interacts w

255 se, we demonstrate that Kat2a contributes to leukemia propagation through preservation of leukemia st

256 usceptible to interaction with promyelocytic leukemia protein (PML) bodies, sites of many nuclear pro

257 e cells responsible for residual disease and leukemia re-growth is critical to better understanding h

258 However, leukemia relapse accounts for nearly half of deaths.

259 in each disease and their associations with leukemia risk are not well understood.

260 e them to outcompete other HSCs and increase leukemia risk.

261 German Study Alliance Leukemia-Acute Myeloid Leukemia (SAL-AML) registry.

262 3A loss after DNMT3A ablation in HSCs and in leukemia samples.

263 nt throughout the disease course, and highly leukemia specific, making them attractive neoantigen tar

264 ent substantially depends on an individual's leukemia-specific immune response.

265 AML), and ALKBH5 is required for maintaining leukemia stem cell (LSC) function but is dispensable for

266 g aberrant self-renewal in the heterogeneous leukemia stem cell (LSC) pool determine aggressiveness o

267 FGF2 induces leukemia stem cell expansion in MLL1-rearranged AML.

268 delineating the biological underpinnings of leukemia stem cell function, and highlight the Sdc1-Itgb

269 ly, it has been shown that CBFA2T3 maintains leukemia stem cell gene expression and promotes relapse

270 Relapse is caused by leukemia stem cells (LSC), the cells with self-renewal c

271 nd self-renewal of MLL-AF9 (MA9)-transformed leukemia stem cells (LSCs) in vivo.

272 )A demethylase ALKBH5 in maintaining myeloid leukemia stem cells.

273 leukemia propagation through preservation of leukemia stem-like cells.

274 termination of emergency granulopoiesis and leukemia suppressor function in MLL1-rearranged AML.

275 T-cell acute lymphoblastic leukemia (T-ALL) and T-cell acute lymphoblastic lymphoma

276 te cancer growth, T-cell acute lymphoblastic leukemia (T-ALL) cells require exogenous cells or signal

277 T-cell acute lymphoblastic leukemia (T-ALL) is an aggressive hematological malignan

278 cause myeloproliferative disorder and T cell leukemia (T-ALL) when induced in the bone marrow via Mx1

279 for patients with T cell acute lymphoblastic leukemia (T-ALL), and although resistance to GCs is a st

280 biologic features underlying MLL-rearranged leukemia, targeted therapies for this leukemia have rema

281 nd on neoplastic cell lines: acute monocytic leukemia THP-1 and lung adenocarcinoma A549.

282 te dehydrogenase level or stage IV) or acute leukemia to compare the addition of six doses of rituxim

283 ical points in the transition from health to leukemia to guide interpretation of changes in the trans

284 escents receiving treatment of acute myeloid leukemia, to those undergoing allogeneic HSCT pre-engraf

285 nd outcome but also plays a critical role in leukemia transformation and maintenance.

286 tional co-regulator, Mkl-1 (megakaryoblastic leukemia [translocation] 1).

287 en a new way toward drug dose adjustment for leukemia treatment.

288 osis of breast cancer, renal cell cancer, or leukemia underwent whole-body PET/CT imaging 90 min afte

289 ing viral spillover events.IMPORTANCE Feline leukemia virus (FeLV) can infect a variety of felid spec

290 While feline leukemia virus (FeLV) has been shown to infect felid spe

291 a close relative of KoRV and the gibbon ape leukemia virus (GALV), with virion morphology and Mn(2+)

292 It is not known if murine leukemia virus (MLV) encodes a Vif-like protein.

293 lycosylated Gag (glycoGag) protein of murine leukemia virus (MLV), the S2 protein of equine infectiou

294 ations present in a model retrovirus, murine leukemia virus (MLV), using mass spectrometry and sequen

295 Based on previous studies of murine leukemia virus and HIV-1, we hypothesized that unpaired

296 100 days after transplant, but donor-derived leukemia was not observed.

297 impaired the malignant glycophenotype of MDR leukemias, which typically overcomes drug resistance thr

298 Patients with B-cell acute lymphoblastic leukemia who experience relapse after or are resistant t

299 tologic malignancies, particularly pediatric leukemias with poor patient outcomes.

300 lastoma, breast cancer, and several forms of leukemia, with primary LSCs being particularly sensitive

301 nce and inhibition of tumor progression in a leukemia xenograft model.