ライフサイエンスコーパス: myeloid and lymphoid

1 -alpha partially and transiently rescued the myeloid and lymphoid abnormalities found in NHD13(+) Tg

2 s are accumulated to the same degree in both myeloid and lymphoid acute leukemia cells, paralleling t

3 blood, demonstrating cross talk between the myeloid and lymphoid arms of disease.

4 each main hematopoietic cell lineage of both myeloid and lymphoid arms.

5 ermediates correlated with the levels of the myeloid- and lymphoid-associated transcription factors m

6 giving rise to progenitors that initiate the myeloid and lymphoid branches of hematopoiesis.

7 cells from healthy donors and patients with myeloid and lymphoid cancers, including cell types that

8 ies for therapeutic intervention in specific myeloid and lymphoid cancers.

9 igher in treated pups than in controls; both myeloid and lymphoid cell chimerism increased because of

10 Our findings revealed different myeloid and lymphoid cell clusters in the cohorts, each

11 emonstrate that BRGSF-HIS mice possess human myeloid and lymphoid cell compartments in the lung inter

12 e severe depression but differed in terms of myeloid and lymphoid cell counts.

13 Myeloid and lymphoid cell cytokine secretion was measure

14 lamprey cytokine networks that may regulate myeloid and lymphoid cell differentiation, including pot

15 evere pulmonary inflammation, with increased myeloid and lymphoid cell infiltration.

16 These results show that FL can affect both myeloid and lymphoid cell lineages in vivo and further d

17 et undefined role in immunity impacting both myeloid and lymphoid cell lineages spurring interest in

18 in long-term allogeneic repopulation of both myeloid and lymphoid cell lineages were observed in reci

19 Tissue-resident immune cells span both myeloid and lymphoid cell lineages, have been found in m

20 -sensitive and -resistant p210/p190(BCR/ABL) myeloid and lymphoid cell lines and CML-BC(CD34+) and Ph

21 ly activated in both transiently transfected myeloid and lymphoid cell lines by the 80-bp gene fragme

22 expression in multiple chronically infected myeloid and lymphoid cell lines using an anti-ASP monocl

23 the Pim kinases, kills a wide range of both myeloid and lymphoid cell lines with precursor T-cell ly

24 ctin ligands on granulocytes, monocytes, and myeloid and lymphoid cell lines, and not on peripheral b

25 levels of adenosine-metabolizing enzymes in myeloid and lymphoid cell lines.

26 HFV productively infects a variety of human myeloid and lymphoid cell lines.

27 Circulating myeloid and lymphoid cell populations were increased two

28 ematopoietic progenitor cell and nonexpanded myeloid and lymphoid cell product derived from a single

29 acquisition of immune-effector functions by myeloid and lymphoid cell subsets and the maturation of

30 tect clonal cytogenetic markers in different myeloid and lymphoid cell types of the peripheral blood

31 autophagy contributes to differentiation of myeloid and lymphoid cell types, coordinates multicellul

32 tile adults with a full immune complement of myeloid and lymphoid cell types.

33 ilure, and to patients with aplastic anemia, myeloid, and lymphoid cell malignancies.

34 ession, thereby providing protection to both myeloid and lymphoid cells against L. monocytogenes-indu

35 gen-conjugated scaffolds are invaded by host myeloid and lymphoid cells and exhibit a dose-dependent

36 es with Imatinib against BCR/ABL-transformed myeloid and lymphoid cells and increases survival in a m

37 ude that CD45 is regulated differentially in myeloid and lymphoid cells and that sequences critical t

38 Mature myeloid and lymphoid cells as well as immunoglobulins be

39 Myeloid and lymphoid cells as well as intestinal epithel

40 etected constitutively in both primary human myeloid and lymphoid cells by Northern blot hybridizatio

41 ctional data, EMSA demonstrated that in both myeloid and lymphoid cells C/EBPbeta binds specifically

42 monstrated significantly higher infiltrating myeloid and lymphoid cells compared with GBM, MED, or NT

43 lity to shape the transcriptome of activated myeloid and lymphoid cells controlling diverse biologica

44 Expression signatures in myeloid and lymphoid cells demonstrated that HOXA9 funct

45 to the same cellular chromosomal DNA site in myeloid and lymphoid cells descended from a common HSC p

46 tat5 in maintaining a normal balance between myeloid and lymphoid cells during hematopoiesis, and we

47 Generation of myeloid and lymphoid cells from progenitors involves dyn

48 However, recent research shows that innate myeloid and lymphoid cells have the ability to retain me

49 Further, myeloid and lymphoid cells in ascites were predominantly

50 ass cytometry (CyTOF) to dissect circulating myeloid and lymphoid cells in children with severe (grad

51 gainst wild-type cells in the development of myeloid and lymphoid cells in in vivo reconstitution ass

52 er 21 to 413 days, percentages of donor type myeloid and lymphoid cells in recipient blood were measu

53 PI mice 28 wk posttransplant generated human myeloid and lymphoid cells in secondary recipients.

54 We demonstrate 3D imaging of live myeloid and lymphoid cells in suspension, including K562

55 ating CD4(+) T cells without affecting other myeloid and lymphoid cells in the HF mice.

56 reased L. monocytogenes-induced apoptosis of myeloid and lymphoid cells in the spleen that are requir

57 dicating that FcgammaRIIb expression on both myeloid and lymphoid cells is regulated by the naturally

58 Furthermore, myeloid and lymphoid cells likely synergize to promote o

59 s recently described as a diffuse network of myeloid and lymphoid cells located in the olfactory orga

60 y, PU.1(-/-) mice that are unable to develop myeloid and lymphoid cells received bone marrow transpla

61 tor-ligand cell surface interactions between myeloid and lymphoid cells regulate innate and adaptive

62 thro-myeloid cells and pre-B cells, and both myeloid and lymphoid cells seem to be derived from the C

63 Transient transfection experiments in both myeloid and lymphoid cells showed an increase in CCR5 pr

64 higher level of chimerism and generated both myeloid and lymphoid cells that contained molecular or c

65 microbes promote a crosstalk between innate myeloid and lymphoid cells that leads to immune homeosta

66 ilized CD34(+) cells with Neo(R) gene marked myeloid and lymphoid cells up to 32 months after transpl

67 rd distinct HLA type and donor and recipient myeloid and lymphoid cells were identified after 8 to 10

68 have a potential to differentiate in vivo to myeloid and lymphoid cells, and (4) have a high prolifer

69 d to tumor cells, tissue architecture, CD45+ myeloid and lymphoid cells, and immune activation.

70 CD300a is broadly expressed on myeloid and lymphoid cells, and its expression is differ

71 iated genetic alterations on the function of myeloid and lymphoid cells, and the clinical and therape

72 as been shown in a wide range of circulating myeloid and lymphoid cells, but their role in normal hem

73 the responses, with broad divergence between myeloid and lymphoid cells, but with very few cell-type-

74 pts the development and function of multiple myeloid and lymphoid cells, compromising innate and adap

75 sed by widespread alterations in circulating myeloid and lymphoid cells, consistent with dysfunction

76 a dual hematopoietic origin and, like other myeloid and lymphoid cells, develop in waves.

77 lement receptors (CRs), expressed notably on myeloid and lymphoid cells, play an essential function i

78 oduction of TNF-alpha and IFN-gamma by liver myeloid and lymphoid cells, respectively.

79 tion in which innate immune cells, including myeloid and lymphoid cells, retain a trained state follo

80 Nanomedicines can modulate the behaviour of myeloid and lymphoid cells, thereby empowering anticance

81 ool of NF-kappaB transcriptional activity in myeloid and lymphoid cells, which is believed to be seco

82 L6 and TNF secretion from mature miR-146a-/- myeloid and lymphoid cells.

83 macrophages, with partial deletion in other myeloid and lymphoid cells.

84 that control the production and function of myeloid and lymphoid cells.

85 ration, proliferation and differentiation of myeloid and lymphoid cells.

86 regulation of growth and differentiation of myeloid and lymphoid cells.

87 eptor-SFK-Syk signalling events in mammalian myeloid and lymphoid cells.

88 ion, MN1-TEL expression was detected in both myeloid and lymphoid cells.

89 an essential role in the development of both myeloid and lymphoid cells.

90 lity to chromosomal damage may exist between myeloid and lymphoid cells.

91 Cs that gave rise stably to skewed ratios of myeloid and lymphoid cells.

92 stem and progenitor cells, as well as mature myeloid and lymphoid cells.

93 s virtually identical in all types of mature myeloid and lymphoid cells.

94 n, lineage-committed progenitors, and mature myeloid and lymphoid cells.

95 or microenvironment (TME) highly enriched in myeloid and lymphoid cells.

96 surveillance and crosstalk with epithelial, myeloid and lymphoid cells.

97 mouse displays recombinase activity in both myeloid and lymphoid cells.

98 ily of nuclear receptors and is expressed in myeloid and lymphoid cells.

99 mune cell homeostasis by shaping the fate of myeloid and lymphoid cells.

100 t retain the potential to differentiate into myeloid and lymphoid cells.

101 ntiate within teratomas to derive functional myeloid and lymphoid cells.

102 sion and correction of functional defects in myeloid and lymphoid cells.

103 The generation of erythroid, myeloid, and lymphoid cells from human fetal liver proge

104 rsors plus a complex mixture of mesenchymal, myeloid, and lymphoid cells in the marrow space.

105 highly proliferating and serially replatable myeloid and lymphoid colony-forming cultures could be es

106 These cells are believed to derive from both myeloid- and lymphoid-committed precursors.

107 tential hematopoietic stem cells into common myeloid- and lymphoid-committed progenitors establishes

108 IFN production develop efficiently from both myeloid- and lymphoid-committed progenitors.

109 exhibit reduced infiltration of cells of the myeloid and lymphoid compartments, an effect that should

110 F1R inhibition by PLX5622 indeed affects the myeloid and lymphoid compartments, causes long-term chan

111 nt leukocytes, which recapitulated the liver myeloid and lymphoid composition, and underwent partial

112 In addition, evidence for the existence of myeloid and lymphoid DC lineages and their different fun

113 (i) reduces the numbers of Langerhans cells, myeloid and lymphoid DC, and activated CD4(+) T cells in

114 g the yield of plasmacytoid and conventional myeloid and lymphoid DC.

115 ombinant Adv readily targets transduction of myeloid and lymphoid DCs in the draining popliteal lymph

116 ch resulted in depletion of 88-95% of mature myeloid and lymphoid DCs, with less depletion (75%) of p

117 ription factor binding sites associated with myeloid- and lymphoid-derived cell types.

118 ha transgenic reporter was activated in both myeloid- and lymphoid-derived PDCs at a level comparable

119 s well as RAG transcripts were found in both myeloid- and lymphoid-derived PDCs.

120 is known about the function of FOG-1 during myeloid and lymphoid development or how FOG-1 expression

121 rmal and malignant processes associated with myeloid and lymphoid development.

122 ion factor PU.1, is indispensable for normal myeloid and lymphoid development.

123 (Spi-1) is a well-characterized regulator of myeloid and lymphoid development.

124 iesis, and highlight a close relationship of myeloid and lymphoid development.

125 factors and signaling components involved in myeloid and lymphoid development.

126 ineage competency factors to facilitate both myeloid and lymphoid developmental programs.

127 controlling hematopoietic stem cell biology, myeloid and lymphoid differentiation and lymphocyte effe

128 However, long-term myeloid and lymphoid differentiation is compromised beca

129 CD14+ and CD7+ cells, consistent with early myeloid and lymphoid differentiation, respectively.

130 now know that Gfi1 is primarily important in myeloid and lymphoid differentiation, whereas Gfi1b is c

131 eukemia fusion protein CBFbeta-SMMHC impairs myeloid and lymphoid differentiation.

132 eficit of transcription factors critical for myeloid and lymphoid differentiation.

133 haematopoietic stem cells (HSCs) as well as myeloid and lymphoid differentiation.

134 protein CBFbeta-SMMHC (CM) known to disrupt myeloid and lymphoid differentiation.

135 Our data indicate that Cbfb is required for myeloid and lymphoid differentiation; but does not play

136 Myeloid and lymphoid diseases arise from transformed mur

137 et al provide evidence for the existence of myeloid- and lymphoid-dominant human hematopoietic stem

138 ndomized controlled trial data revealed that myeloid and lymphoid dysregulation are associated with d

139 Myeloid and lymphoid dysregulation were associated with

140 cells (HSCs) rapidly proliferate to produce myeloid and lymphoid effector cells, a response that is

141 d infiltrating hematopoietic cells including myeloid and lymphoid elements that impact tumor growth,

142 onal maturation of promyelocytes (erythroid, myeloid, and lymphoid [EML]-derived promyelocytes) deriv

143 tment because recipients displayed increased myeloid and lymphoid engraftment and because sunitinib-t

144 bust (>80% human chimerism) and reproducible myeloid and lymphoid engraftment, with T cells arising 1

145 s, and sunitinib enhanced marrow, peripheral myeloid, and lymphoid engraftment after BMT in Rag1(-/-)

146 well as hematopoietic genes; MPPs coexpress myeloid and lymphoid genes; CMPs coexpress myeloerythroi

147 n or eliminate malignant solid tumours, both myeloid and lymphoid haematopoietic cells must not only

148 essor that plays a critical role during both myeloid and lymphoid haematopoietic lineage commitment.

149 are involved in the pathogenesis of several myeloid and lymphoid hematological malignancies.

150 ry progenitors that can reinitiate long-term myeloid and lymphoid hematopoiesis in vitro.

151 econdary and tertiary recipients, as well as myeloid and lymphoid hematopoietic progenitor subsets an

152 proinflammatory cytokine that interconnects myeloid and lymphoid host defense.

153 ed to distinct constellations of circulating myeloid and lymphoid immune cell types.

154 ferons and other cytokines and activate both myeloid and lymphoid immune cells to provide protection

155 A network of tissue-resident myeloid and lymphoid immune cells was evident in both fe

156 d temporal and spatial relationships between myeloid and lymphoid immune responses in wild-type C57BL

157 d unresolved DNA damage and limits extrinsic myeloid and lymphoid immunosuppression.

158 ng via the G protein-coupled receptor G2A on myeloid and lymphoid inflammatory cells.

159 ticipants with mLOX had an increased risk of myeloid and lymphoid leukaemias.

160 umor antigen that is aberrantly expressed in myeloid and lymphoid leukemia and in this issue of Blood

161 granulate when challenged with primary acute myeloid and lymphoid leukemia blasts; and (5) Vdelta2 ce

162 ng the equivalent cytotoxicity found between myeloid and lymphoid leukemia cell lines.

163 hnique to compare the deformability of human myeloid and lymphoid leukemia cells and neutrophils at l

164 echanism by which adaphostin can damage both myeloid and lymphoid leukemia cells, but also indicate t

165 mosomal translocations associated with acute myeloid and lymphoid leukemia, has >50 known partner gen

166 mosomal translocations associated with acute myeloid and lymphoid leukemia.

167 himeras that drive the pathogenesis of acute myeloid and lymphoid leukemia.

168 contribute to a selective GVL effect against myeloid and lymphoid leukemias after F-->M HSCT.

169 paB to the pathogenesis of BCR-ABL1-positive myeloid and lymphoid leukemias are unknown.

170 plays distinct roles in the pathogenesis of myeloid and lymphoid leukemias induced by BCR-ABL1, vali

171 Acute myeloid and lymphoid leukemias often harbor chromosomal

172 er, in our study, TP53-mutated or -deficient myeloid and lymphoid leukemias outcompeted isogenic cont

173 rapid death of primary human LSCs from both myeloid and lymphoid leukemias, and is also highly cytot

174 r proliferation of malignant clones in acute myeloid and lymphoid leukemias.

175 ons in RBPs lead to dysregulated splicing in myeloid and lymphoid leukemias.

176 a rational combination for the treatment of myeloid and lymphoid leukemias.

177 epitope is presented on the surface of both myeloid and lymphoid leukemic cells from male HLA-B*2705

178 Expression of DDX3Y is detected in all myeloid and lymphoid leukemic cells that carry an intact

179 ALL, we show here that GAB2 is essential for myeloid and lymphoid leukemogenesis by BCR-ABL1.

180 mportance of the Bcr/Abl-Grb2 interaction to myeloid and lymphoid leukemogenesis in vivo is unclear.

181 opposing functions of CEBP dysregulation in myeloid and lymphoid leukemogenesis.

182 ich P2X(7)R signaling occurs differs between myeloid and lymphoid leukocytes.

183 the emergence of erythroid-, megakaryocyte-, myeloid- and lymphoid-like cells.

184 quent genetic changes in infant leukemias of myeloid and lymphoid lineage and in treatment-induced se

185 ith the capacity to produce normal levels of myeloid and lymphoid lineage cells.

186 PU.1 protein appears not to be essential for myeloid and lymphoid lineage commitment, it is absolutel

187 miR-17-92-overexpressing mice are capable of myeloid and lymphoid lineage differentiation, and recapi

188 with diverse potencies and can give rise to myeloid and lymphoid lineage progenitors.

189 tern in that it is expressed on cells of the myeloid and lymphoid lineage, suggesting that it plays a

190 n clonal expansion of mutant cells into both myeloid and lymphoid lineages and an elevated abundance

191 lineage short-term progenitors reconstituted myeloid and lymphoid lineages at 1 month but were suppla

192 he hematopoietic flow from stem cells toward myeloid and lymphoid lineages during development and adu

193 of cytokines to induce differentiation into myeloid and lymphoid lineages following AAV infection, t

194 ematopoietic development with segregation of myeloid and lymphoid lineages from multipotent progenito

195 ent), compared with negligible expression in myeloid and lymphoid lineages in blood, BM, spleen, and

196 lta/Delta) HSCs contributed normally to both myeloid and lymphoid lineages in both primary and second

197 ells and are able to differentiate into both myeloid and lymphoid lineages in vitro.

198 Multipotential clones contributing to myeloid and lymphoid lineages were identified.

199 pressed by a variety of immune cells of both myeloid and lymphoid lineages, including dendritic cells

200 tained these high transduction levels in all myeloid and lymphoid lineages, including early progenito

201 characterized by a maturation arrest in the myeloid and lymphoid lineages, leading to early onset, r

202 of mice incapable of developing cells of the myeloid and lymphoid lineages, transplanted adult bone m

203 ntiate into more specific progenitors of the myeloid and lymphoid lineages, ultimately leading to dif

204 ould have to arise before the bifurcation to myeloid and lymphoid lineages.

205 into the erythroid lineage but not into the myeloid and lymphoid lineages.

206 hils, and basophils, but separate from other myeloid and lymphoid lineages.

207 plasma cells), and that tumors arise in both myeloid and lymphoid lineages.

208 tion (CD) antigens are expressed on cells of myeloid and lymphoid lineages.

209 ewal as well as commitment and maturation of myeloid and lymphoid lineages.

210 enitor cells (HPCs) and fully differentiated myeloid and lymphoid lineages.

211 velopment of XSCID CD34(+) cells into mature myeloid and lymphoid lineages.

212 establishes an early separation between the myeloid and lymphoid lineages.

213 arranged in acute human leukemia of both the myeloid and lymphoid lineages.

214 has only been previously demonstrated in the myeloid and lymphoid lineages.

215 poietic stem cells (HSCs) towards erythroid, myeloid and lymphoid lineages.

216 changes are conserved and inherited in both myeloid and lymphoid lineages.

217 on of hematopoietic stem cells (HSCs) to the myeloid and lymphoid lineages.

218 ting primarily to myeloid, lymphoid, or both myeloid and lymphoid lineages.

219 inhibits activation signals on cells of both myeloid and lymphoid lineages.

220 itor cells (HSPCs) and mature cells from the myeloid and lymphoid lineages.

221 tment, self-renewal and differentiation into myeloid and lymphoid lineages; however, the proper diffe

222 gests that the segregation of the erythroid, myeloid, and lymphoid lineages may not always be an earl

223 s confer a graft-versus-malignancy effect in myeloid and lymphoid malignancies and in metastatic rena

224 Myeloid and lymphoid malignancies associated with chimer

225 elapse rates, whereas patients with advanced myeloid and lymphoid malignancies had high relapse rates

226 In contrast, patients with advanced myeloid and lymphoid malignancies had rates of more than

227 igning improved strategies for treating both myeloid and lymphoid malignancies in this high-risk popu

228 neral terms, we review specific use cases in myeloid and lymphoid malignancies to highlight the utili

229 , we review recent major genetic advances in myeloid and lymphoid malignancies, the impact of these f

230 This is in contrast to myeloid and lymphoid malignancies, which harbor frequent

231 synergy between DNMT3A and TET2 mutations in myeloid and lymphoid malignancies.

232 ked to plasma cell abnormalities, as well as myeloid and lymphoid malignancies.

233 parameters to stratify the risk of incident myeloid and lymphoid malignancies.

234 es inactivating mutations in a wide range of myeloid and lymphoid malignancies.

235 is a rare subtype of leukemia in which both myeloid and lymphoid markers are co-expressed on the sam

236 rtilization, as well as normal expression of myeloid and lymphoid markers.

237 k leukemias characterized by coexpression of myeloid and lymphoid markers.

238 These data suggest that Delta-1 can enhance myeloid and lymphoid marrow-repopulating ability and pro

239 lymphoid somatic gene mutations, as well as myeloid and lymphoid mCAs, and found both to be associat

240 ors induce differentiation and cell death in myeloid and lymphoid model systems.

241 Myeloid and lymphoid neoplasm associated with FGFR1 is a

242 cation recognizes both molecularly defined ('myeloid and lymphoid neoplasms with eosinophilia and abn

243 sive molecular disease detection in selected myeloid and lymphoid neoplasms, with a focus on the curr

244 s, and mutation signatures in a broad set of myeloid and lymphoid neoplasms.

245 ddress the issue by the haematological group-myeloid and lymphoid-of diseases, with a special conside

246 y developed hematologic malignancies of both myeloid and lymphoid origin with myeloid malignancies di

247 uently rearranged in human leukemias of both myeloid and lymphoid origin, encodes a member of the Ets

248 mononuclear cells (PBMCs) and cell lines of myeloid and lymphoid origin.

249 rofile resembling that of tumor infiltrating myeloid and lymphoid populations, but with higher expres

250 1a regulates hematopoietic stem cells (HSC), myeloid and lymphoid populations, while its paralog, Gfi

251 a mitochondrial oxidative stress increase in myeloid and lymphoid populations.

252 volves marked changes in specific subsets of myeloid and lymphoid populations.

253 tentiality is conserved until segregation of myeloid and lymphoid potential has recently been challen

254 haematopoietic progenitor cells with erythro-myeloid and lymphoid potential, reflecting aspects of pr

255 bone marrow progenitor cells with a combined myeloid and lymphoid potential.

256 Myeloid and lymphoid potentials are present at the clona

257 ries from HSCs to erythrocyte/megakaryocyte, myeloid, and lymphoid primed progenitors.

258 gen expression leads to reduced apoptosis of myeloid and lymphoid progenitor cells, and a propensity

259 gand to primitive hematopoietic cells and to myeloid and lymphoid progenitor cells, in contrast to th

260 ar result was obtained with specified common myeloid and lymphoid progenitor cells.

261 h the MegE potential of downstream committed myeloid and lymphoid progenitors and with their ability

262 ndritic cells (DCs) can be derived from both myeloid and lymphoid progenitors in vivo.

263 asts alters the differentiation potential of myeloid and lymphoid progenitors leading to development

264 NA and protein levels in cultures of primary myeloid and lymphoid progenitors, and Bcl-X(L) and Bcl-2

265 differential capacity to generate committed myeloid and lymphoid progenitors, and diminished lymphoi

266 ved lineage-specific DNA methylation between myeloid and lymphoid progenitors, characterized immature

267 nt HSCs also failed to generate the earliest myeloid and lymphoid progenitors.

268 DC can develop from both myeloid and lymphoid progenitors.

269 required for the proper development of both myeloid and lymphoid progenitors.

270 ineage precursors were bipotential, yielding myeloid and lymphoid progeny, whereas most that were c-k

271 ings implicate MyD88 as the key initiator of myeloid and lymphoid proliferation in HLH, and suggest t

272 JL/J) and recipients (BALB/c) contributed to myeloid and lymphoid reconstitution.

273 To directly compare myeloid and lymphoid recovery using an animal model of b

274 f cord blood transplantation is the delay in myeloid and lymphoid recovery.

275 plasmacytoid DC was similar to that of liver myeloid and lymphoid-related DC.

276 s a heterogeneous population containing both myeloid- and lymphoid-related DC.

277 n of CD11b, which may represent the putative myeloid- and lymphoid-related subsets.

278 rn blood, liver, and spleen, were assayed as myeloid and lymphoid repopulating abilities relative to

279 We found that myeloid and lymphoid resident immune cells concentrate a

280 hallenge induced accelerated and coordinated myeloid and lymphoid responses without epithelial prolif

281 We distinguished myeloid and lymphoid somatic gene mutations, as well as

282 Blood myeloid and lymphoid subsets and interferon (IFN)-gamma-

283 (4) Mutual exclusiveness of myeloid and lymphoid support in that a given stromal cel

284 ler (NK)/T cell enhancers (MiTEs) harnessing myeloid and lymphoid synergy for immunotherapy.

285 s support a role for relative proportions of myeloid and lymphoid transcripts in tuberculosis outcome

286 fectors that propagate the signal to promote myeloid and lymphoid transformation.

287 ore can cooperate in the development of both myeloid and lymphoid tumors.

288 we focus on the role of such lesions in both myeloid and lymphoid tumors.