ライフサイエンスコーパス: BM

1 BM adipocytes are another source of CXCL12 that blunts m

2 BM complex thickness was significantly co/BM complex thi

3 BM complexity, however, has hindered an understanding of

4 BM FATP4 and FATP6 expression was increased in MNR at GD

5 BM toxicity was estimated with activity measurements fro

6 BM transplantation (BMT) frequently requires irradiation

7 rospectively identified 40 patients with 107 BMs secondary to melanoma (n = 29 with 75 BMs) or non-sm

8 inhibition of BAD phosphorylation in KMS-12-BM multiple myeloma tumors for 16 h postdose.

9 Using genome editing, we tagged 29 BM matrix components and receptors in C. elegans with mN

10 r non-small cell lung cancer (n = 11 with 32 BMs) treated with ICI or TT who had (18)F-FET PET (n = 6

11 es of general formula [p-RPh(2) P(C(6) H(4) )BMes(2) ](+) have been synthesized and evaluated.

12 In the case of the BNB-phenalenyl 7 (BMes, NMe), the radical-anion salt K[7(*)] was generated

13 A failure of ternary blends with PC(71) BM is likely due to the near-ideal miscibility of Y6 to

14 ovoltaic devices based on a PM6:CH1007:PC(71)BM ternary blend delivered an exceptionally high short-c

15 s, we performed whole-exome sequencing of 73 BM-LUAD cases.

16 07 BMs secondary to melanoma (n = 29 with 75 BMs) or non-small cell lung cancer (n = 11 with 32 BMs)

17 Between 2004 and 2019, 998 BM samples were taken from 436 patients with newly diagn

18 isk LCH, the driver mutation is present in a BM-resident myeloid progenitor that can be mobilized to

19 Brain metastases from lung adenocarcinoma (BM-LUAD) frequently cause patient mortality.

20 onstrate improved antitumor activity against BMs in patients with HER2-positive breast cancer in a ra

21 Cs in beta-thalassemia induced by an altered BM microenvironment and provide novel and relevant insig

22 n, caused by the interaction with an altered BM niche.

23 Furthermore, in human AML, BM plasma CXCL12 levels were lower in patients with lowe

24 In the current study, we analyzed BM aspirates of 7 patients during the acute attack and 4

25 pied the pax2a(-/-) vasculature, F-actin and BM degradation phenotypes.

26 al basal domain, regulating both F-actin and BM.

27 enotype, reduces stromal cell activation and BM fibrosis, and decreases the activation of profibrotic

28 RNA-seq analysis of isolated TR-APhi and BM-APhi from 4- and 32-weeks exposed mice revealed a uni

29 n lung and airways and distally in blood and BM, whereas IL-5 and IL-4 only increased eosinophils in

30 with a fibrin gel in which CD34(+) cells and BM-derived stromal cells are co-cultured, a parallel cha

31 Paired cornea- and BM-derived myofibroblast specimens from each rabbit were

32 ood and bone marrow (BM) flow cytometry, and BM immunohistochemistry.

33 Paired cornea-derived and BM-derived alpha-SMA+ myofibroblast primary cultures wer

34 FL and BM FDG uptake lower than the liver background after ther

35 IL-4 only increased eosinophils in lung and BM.

36 -kappaB signaling pathway in bone marrow and BM-MSC of DeltaNC16A mice.

37 Upon helminth infection, recruited and BM-derived cells generated the entire spectrum of ILC2s

38 ROS- and JNK-mediated Mmp2 upregulation and BM damage.

39 tic drugs and ionizing radiation, as well as BM recovery after drug-induced myelosuppression.

40 In summary, biocompatible Zn-based BMs with strength close to pure Ti are promising candida

41 However, the relationship between BM fibrils and stress fibers and their respective impact

42 ville scale (DS) was applied to describe BM (BM score [BMS]) and focal lesion (FL; FL score [FS]) upt

43 tural and nonstructural VZV proteins in both BM and blood (peripheral blood mononuclear cells [PBMCs]

44 ignaling, but sustained Cxcl12 expression by BM adipocytes could limit full recovery of HSPC mobiliza

45 Secretion of ECM protein fibronectin (FN) by BM stromal cells from PMF patients correlates with fibro

46 ction of the osteogenic Wnt ligand Wnt10b by BM CD8+ T cells, which activated Wnt-dependent bone form

47 provide further insights, we purified CD71+ BM cells and demonstrated dyserythropoiesis and ineffici

48 essed by bone marrow mesenchymal stem cells (BM-MSC), and its functional deficiency leads to myeloid

49 bone marrow-derived mesenchymal stem cells (BM-MSC), and Michigan Cancer Foundation-7 (MCF-7) breast

50 show that a vascularized human BM-on-a-chip (BM chip) supports the differentiation and maturation of

51 BM complex thickness was significantly co/BM complex thickness increased with age in a healthy Whi

52 finding prompted us to develop a competitive BM chimera model, which demonstrated that expression of

53 significantly increasing blood cell counts, BM hematopoietic cellularity and stem and progenitor cel

54 ) beta-1 or generated directly from cultured BM treated with TGF beta-1 was pursued for insights into

55 Similarly, cultured BM stimulated to form OC demonstrated multiple fluoresce

56 d suggest a paradigm shift that deconstructs BM into distinct levels of processing and specific spati

57 reduces the release of G-CSF from DeltaNC16A BM-MSC in vitro and the level of serum G-CSF in DeltaNC1

58 Deauville scale (DS) was applied to describe BM (BM score [BMS]) and focal lesion (FL; FL score [FS])

59 s, their physical association with described BM populations, and their tissue-wide combinations.

60 imuli are an important factor in determining BM processing anomalies in ASD.

61 ) produced by M1 macrophages in the diabetic BM signals through p66Shc to induce Cxcl12 in stromal ce

62 ults: A TBR threshold of 1.95 differentiated BM relapse from treatment-related changes with an accura

63 f cancer cells cultured in three-dimensional BM-like matrices.

64 ion and cell migration in three-dimensional, BM-like environments.

65 ted with a CXCR4 inhibitor to mobilize donor BM cells pre-transplant.

66 Foxp3+ Treg population resident within donor BM.

67 facilitates type IV collagen removal during BM expansion and tissue growth.

68 emonstrated improved efficacy in eliminating BM PCs and reducing anti-HLA Abs in chronically HLA-sens

69 Using mice lacking the major endothelial BM components, laminin 411 or 511, in murine experimenta

70 B. mojavensis EPS (BM-EPS) was recovered, fractionated by ethanol precipita

71 Conversely, if memories are erased, BM-LTM should be reduced to resemble untrained levels.

72 f the amnesia is due to a retrieval failure, BM-LTM should remain at levels comparable to trained, un

73 Although fetal BM PreProB-progenitors and ProB-progenitors both give ri

74 ues using Promoter 2.0 program is higher for BM- CTQ41297 promoter than strong promoters such as beta

75 primarily from stromal keratocytes and from BM-derived fibrocytes after epithelial-stromal and endot

76 CD34+c-Kit+Flt3+ cells from BM of MS-RO+ LCH patients produced Langerhans cell (LC)-

77 differentiate treatment-related changes from BM relapse after ICI or TT.

78 eostasis mature OC derive predominantly from BM-resident OCP, whereas during fracture repair, circula

79 meostasis, maturation, and regeneration from BM.

80 Furthermore, BM fibrils act as a persistent cue for the orientation o

81 s the most abundant component in the gonadal BM, where it facilitates type IV collagen removal during

82 All patients had BM diffuse uptake (35.5% with BMS >= 4).

83 Osm, p66Shc, and Cxcl12 in the hematopoietic BM, restored the effects of granulocyte-colony stimulati

84 V617F transgenic mice (JAK2V617F+) have high BM FN content associated with megakaryocytosis and fibro

85 ransplanted with MN1-overexpressed Hopx(-/-) BM cells developed AML with more aggressive phenotypes c

86 and dissect the cellular crosstalk in human BM, we established humanized ex vivo and in vivo niche m

87 Here, we show that a vascularized human BM-on-a-chip (BM chip) supports the differentiation and

88 reflecting the relative abundance of imaged BM populations rather than active enrichment.

89 y of the BM perivascular niche and improving BM niche recovery after irradiation-induced injury.

90 In BM-MNCs this was associated with increased glycolysis an

91 spondyloarthritis in mice increased IL-33 in BM plasma, and IL-33 was required for inflammation-depen

92 ith more frequent copy-number aberrations in BM-LUAD compared to 503 primary LUADs.

93 utations affect MK migration and adhesion in BM or NMIIA activity and assembly prior to proplatelet p

94 moderate deficit of individuals with ASD in BM processing, but also a high heterogeneity.

95 ls in the BM and VZV-specific CD4 T cells in BM and blood.

96 populations of HIV-1 p24-producing cells in BM early after infection, and quantification of these po

97 principal subset of virus-producing cells in BM over time.

98 ic tool to detect low-abundance PC clones in BM and assign them to POEMS syndrome, with all the conse

99 ioglitazone failed to downregulate Cxcl12 in BM adipocytes.

100 o assays, we investigated MK distribution in BM, chemotaxis toward stromal-derived factor 1, NMIIA ac

101 IL-5 increased the number of eosinophils in BM and lung tissue but failed to affect structural chang

102 n-dependent suppression of erythropoiesis in BM.

103 y revealed to be a poor prognostic factor in BM and PB.

104 ficantly higher amplification frequencies in BM-LUAD, including MYC (12 versus 6%), YAP1 (7 versus 0.

105 an (Dg) and Dystrophin (Dys) are involved in BM fibril deposition.

106 able information for treatment monitoring in BM patients treated with ICI or TT.

107 on >= 3 and achievement of MRD negativity in BM and PB were significantly associated with a lower CIR

108 gh regulating NF-kappaB signaling pathway in BM-MSC.

109 rescued HSPC mobilization, but it increased BM adipocytes.

110 anced hepatic VEGF-sdf1 signaling, increased BM sproc recruitment, and reduced alanine aminotransfera

111 , we report a common template that initiates BM formation, which rapidly diversifies during tissue di

112 Confocal microscopy of intact BM confirmed that ICLs are delivered independently of th

113 earch, we found 30 studies that investigated BM perception in both ASD and typical developing peers b

114 In contrast, cycling juvenile BM HSCs preferentially located close to Cxcl12 stroma an

115 Long-lived BM resident plasma cells constitutively secrete antibodi

116 phenotypes, including macrothrombocytopenia, BM fibrosis, megakaryocyte emperipolesis of neutrophils,

117 ell responses are detectable in bone marrow (BM) and blood up to 20 years after vaccination.

118 tween multiple myeloma (MM) and bone marrow (BM) are well documented to support tumour growth, yet th

119 ment studies have been based on bone marrow (BM) aspirates, which often do not fully reflect the cell

120 stem cells (HSCs) reside in the bone marrow (BM) but can be mobilized into blood for use in transplan

121 ed in lineage-negative (Lin(-)) bone marrow (BM) cells from Gfi1(-/-) mice.

122 BALB/c-GFP(+) bone marrow (BM) cells were transplanted into immunodeficient NSG mic

123 The contribution of bone marrow (BM) endothelial progenitor cells to capillarization was

124 (MPN) that leads to progressive bone marrow (BM) fibrosis.

125 pha-granules, splenomegaly, and bone marrow (BM) fibrosis.

126 MRD tests included blood and bone marrow (BM) flow cytometry, and BM immunohistochemistry.

127 Bone marrow (BM) from the sick mice showed myeloid hyperplasia with p

128 The inaccessibility of living bone marrow (BM) hampers the study of its pathophysiology under myelo

129 nonhematopoietic stromal cells, bone marrow (BM) immune cells with unique functions support the survi

130 isease (MRD) status outside the bone marrow (BM) in patients with multiple myeloma (MM).

131 a crucial component in driving bone marrow (BM) inflammation and HSC dysfunction observed following

132 the hematopoietic niche of the bone marrow (BM) is a major reservoir for parasite replication and th

133 rogenitor cells (HSPC) from the bone marrow (BM) is impaired in diabetes.

134 malaria parasites in the human bone marrow (BM) is still controversial.

135 Bone marrow (BM) is the central immunological organ and the origin of

136 Bone marrow (BM) mesenchymal stem and progenitor cells (MSPCs) are a

137 ) is tightly regulated by their bone marrow (BM) microenvironment (ME).

138 ng of B cell progenitors in the bone marrow (BM) microenvironment and their progression through the p

139 em cells (HSCs) in their native bone marrow (BM) microenvironment remains controversial, because mult

140 r matrix (ECM) is a hallmark of bone marrow (BM) milieu in primary myelofibrosis (PMF).

141 e regulated by signals from the bone marrow (BM) niche that tune hematopoiesis at steady state and in

142 sis is tightly regulated by the bone marrow (BM) niche.

143 nds on the integrity of complex bone marrow (BM) niches; however, what role the BM microenvironment p

144 LC monoclonal expansion in the bone marrow (BM) of 83% of patients with POEMS syndrome, including so

145 ls (PCs) and CD4 T cells in the bone marrow (BM) of healthy young adults (n = 15) following childhood

146 llular environments such as the bone marrow (BM) plasma likely have unique metabolite profiles that d

147 due to impaired recruitment of bone marrow (BM) progenitors of liver sinusoidal endothelial cells (L

148 r PTH to increase the number of bone marrow (BM) regulatory T cells (Tregs).

149 responses; however, long-lived bone marrow (BM) resident PCs (LLPCs) demonstrate therapeutic resista

150 in adhesion controls homing and bone marrow (BM) retention of normal hematopoietic cells.

151 A total of 3733 bone marrow (BM) samples and 3793 peripheral blood (PB) samples from

152 oietic stem cells (HSCs) in the bone marrow (BM) sense peripheral inflammation and contribute to tiss

153 stem cells (HSCs) reside in the bone marrow (BM) stem cell niche, which provides a vital source of HS

154 ntestine and recruitment to the bone marrow (BM) that causes bone loss.

155 APhi, and the contribution from bone marrow (BM) to this population.

156 from the endosteal niche of the bone marrow (BM) toward the vasculature, extending proplatelets into

157 epleted, and monocytes from the bone marrow (BM) traffic to the lungs along a CCL2/CCR2 axis and diff

158 ulthood, but are regenerated by bone marrow (BM) under stress conditions.

159 a-glucan reprograms HSCs in the bone marrow (BM) via a type II interferon (IFN-II) or interleukin-1 (

160 to ensure that the dose to the bone marrow (BM) was acceptable.

161 tory behavior of eosinophils in bone marrow (BM), blood, lung, and bronchoalveolar lavage as well as

162 ir and fibrosis, and arise from bone marrow (BM)-derived fibrocytes and a variety of local progenitor

163 geing and is not replenished by bone marrow (BM)-derived macrophages.

164 sults from driver mutation in a bone marrow (BM)-resident multipotent hematopoietic progenitor, while

165 asts (OC) originate from either bone marrow (BM)-resident or circulating myeloid OC progenitors (OCP)

166 igh levels of TP53 or MYC in FA bone marrow (BM).

167 l as distant alterations in the bone marrow (BM).

168 are impeded in AML-infiltrated bone marrow (BM).

169 progenitor cells (HSPCs) in the bone marrow (BM).

170 human dental pulp (DP-MSCs) and bone marrow (BM-MSCs).

171 l types beneath the retina and basal matrix (BM) are relatively limited in insects.

172 -actin in the OF prior to basement membrane (BM) degradation.

173 ll basal domain, oriented basement membrane (BM) fibrils and F-actin stress fibers constrain follicle

174 s (ROS) and damage of the basement membrane (BM) in all neoplastic, but not hyperplastic, models exam

175 The endothelial cell basement membrane (BM) is a barrier to migrating leukocytes and a rich sour

176 ctures such as hair cells, basilar membrane (BM), and modiolus with external surface structures such

177 a membrane (MVM) and basal plasma membranes (BM) were isolated.

178 Basement membranes (BMs) are supramolecular matrices built on laminin and ty

179 typically invade through basement membranes (BMs) at key points during metastasis, including primary

180 in the brain mechanisms of long-term memory (BM-LTM).

181 o affect both haematopoietic and mesenchymal BM cells and we specifically identify a dramatic loss of

182 Magnesium-based biodegradable metals (BMs) as bone implants have better mechanical properties

183 ositive breast cancer with brain metastases (BMs) showed statistically significant improvement in pro

184 iotherapy in patients with brain metastasis (BM) since contrast-enhanced MRI often remains inconclusi

185 Plus, brain metastasis (BMs) is a major mortality cause for NSCLC; there is no d

186 ularity, the construct of biological motion (BM) and its putative anomalies in autism spectrum disord

187 t interferon (IFN)-gamma expression in mouse BM, decreased reactive oxygen species (ROS) level in the

188 m and progenitor cell clonogenicity in mouse BM.

189 and 5 (homogenate) and FATP2, 4, and 6 (MVM, BM) was determined by Western blotting.

190 rusions to create channels in the nanoporous BM through which they can invade, either via proteolytic

191 NSG mice to generate an immunocompetent NSG/BM-GFP(+) (NSG-R) mouse model.

192 However, between 5 and 10% of BM cells were ICL-positive.

193 ke an appropriate balance between absence of BM toxicity and therapeutic efficacy.

194 ysis investigating the putative anomalies of BM perception in ASD.

195 enance, and that it recapitulates aspects of BM injury, including myeloerythroid toxicity after clini

196 do not fully reflect the cellular content of BM tissue itself.

197 e investigated the relative contributions of BM-resident and circulating OCP to osteoclastogenesis du

198 cytometry confirmed low-level engraftment of BM cells between parabionts but significant engraftment

199 ings suggest a time-dependent entrainment of BM-derived monocytes into the APhi population of PM(2.5)

200 model, which demonstrated that expression of BM-derived IRAK-M was necessary for monocyte trafficking

201 5) exposure for 4-weeks induced an influx of BM-derived monocytes into the lungs with no contribution

202 oduces methods for holistic investigation of BM regulation and reveals that BMs are highly dynamic an

203 actor 1 (sdf1) signaling, leading to lack of BM sproc recruitment.

204 uctures can facilitate the mineralization of BM-MSC cells, demonstrated by the formation of clusters

205 the effect of the drugs on mineralization of BM-MSCs are investigated using a variety of characteriza

206 functionally necessary for degradation of OF BM.

207 deficit in ASD is evident when perception of BM is serving a secondary purpose (e.g., inferring inten

208 lite and targeted complex lipid profiling of BM plasma to identify significant differences in the rel

209 tial macrophages is driven by recruitment of BM monocytes, while EMP-derived macrophages proliferate

210 ances VEGF-sdf1 signaling and recruitment of BM sprocs, which markedly protects against I/R injury, e

211 ile associated with increased recruitment of BM-derived monocytes and their incorporation into the AP

212 ternative to animal testing for the study of BM pathophysiology.

213 ts question the traditional understanding of BM anomalies in ASD as a monolithic deficit and suggest

214 Here we review the use of BM-LTM in a number of studies that induced amnesia by ta

215 In the absence of OSM, BM adipocytes produced less CXCL12, being arguably devoi

216 enhanced green fluorescent protein-positive BM.

217 in fiber orientation relies on the preceding BM fibril deposition, indicating two distinct but interd

218 sidered the key event underlying progressive BM failure (BMF) in Fanconi anemia (FA), the most freque

219 and growth in the remodeled tumor-promoting BM is unclear.

220 e interpenetrating networks of reconstituted BM matrix and alginate, which presented a range of elast

221 s and whether restoring signaling to recruit BM sprocs reduces I/R injury.

222 Lack of signaling to recruit BM sprocs that repair injured LSECs renders steatotic li

223 In summary, pioglitazone reprogrammed BM macrophages and suppressed OSM signaling, but sustain

224 At PM, 98% of patients retained residual BM diffuse uptake, which was significantly lower than at

225 cally approved for the osimertinib-resistant BMs of NSCLC yet.

226 specifically treating osimertinib-resistant BMs.

227 KI resistance and treating the TKI-resistant BMs.

228 nt correlation was found between qAF and RPE/BM complex thickness (r = 0.27, P = 0.004).

229 djusting for age and iris color, qAF and RPE/BM complex thickness were still correlated in subjects a

230 e retinal layer identification to assess RPE/BM complex thickness in vivo.

231 The mean RPE/BM complex thickness significantly increased with age (r

232 tation, were averaged to obtain a single RPE/BM complex thickness value in each eye.

233 The RPE/BM complex thickness could reflect the lipofuscin/melano

234 The correlation among the RPE/BM complex thickness, the qAF value, and the age of the

235 d positively with the number of VZV-specific BM PCs.

236 r cells were used to visualize the spiraling BM in the intact cochlea without time intensive dissecti

237 indicated distinct changes in SP-stimulated BM stroma.

238 Our results suggest BM-derived myofibroblasts may be more prone to the forma

239 GF as a niche-derived factor that suppresses BM inflammation and enhances hematopoietic recovery foll

240 cells was significantly higher in PBMCs than BM.

241 We report that BM mesenchymal stromal cells (MSC) undergo massive damag

242 We also show that BM chips containing cells from patients with the rare ge

243 We show that BM-CTQ41297 promoter control the expression of two genes

244 estigation of BM regulation and reveals that BMs are highly dynamic and capable of rapid change to su

245 Through photobleaching studies, we show that BMs are not static-surprisingly, many matrix proteins mo

246 The BM composition was skewed towards myelopoiesis and trans

247 The BM-EPS was found to be composed of (beta2 -> 6)-Fruf res

248 cone cell projections are present above the BM in T. evanescens, the sub-retinal extensions of the l

249 n characteristic frequency regions along the BM.

250 ns to form a separate population beneath the BM.

251 rix metalloproteinase 2 (Mmp2), damaging the BM, which recruits macrophages to the tissue.

252 tro model of haematopoietic dysfunction, the BM chip may serve as a human-specific alternative to ani

253 (CML) triggers the release of LSCs from the BM into the circulation and impairs their retention, pro

254 tedly dynamic nature of HSC residence in the BM and interaction with the SCF(+) stromal niche, which

255 ections, parasites are always present in the BM and that such infections induced dyserythropoiesis an

256 sured antibody-secreting plasma cells in the BM and VZV-specific CD4 T cells in BM and blood.

257 GMP accumulate in the BM in SpA and, unexpectedly, at extramedullary sites: in

258 munocompetent mice, few cells arrived in the BM intact.

259 Here, we show that Snai2 expression in the BM is restricted to the BM stromal compartment where it

260 survival of normal and malignant PCs in the BM niche, highlighting the diverse roles of immune cells

261 ies, and we detected VZV-specific PCs in the BM of all subjects.

262 to visualize genetically labeled HSCs in the BM of live mice for several hours.

263 idylinositols (PI) were also detected in the BM plasma samples from MM compared to MGUS patients.

264 ipated immune evasion strategy of Mtb in the BM that controls the magnitude and intrinsic anti-microb

265 -RD mutations suppressed MK migration in the BM without compromising bipolar filament formation but l

266 +) LSCs in vivo, which mobilized LSCs in the BM, induced disease remission, and prolonged survival of

267 rim pigment cells that penetrate gaps in the BM.

268 elease microparticles that accumulate in the BM.

269 C), that of maintaining the integrity of the BM perivascular niche and improving BM niche recovery af

270 ive (LepR+) cells led to a disruption of the BM perivascular niche.

271 etabolite and complex lipid profiling of the BM plasma identifies differences in levels of metabolite

272 F in order to facilitate availability of the BM remodeler mmp2.

273 ronment, thus proving the active role of the BM stroma.

274 patients, along with altered features of the BM stromal niche.

275 ped according to levels of complexity of the BM task employed (first-order, direct and instrumental),

276 and outer) as well as frequency maps of the BM were comparable to those obtained by other methods, b

277 l prepared for LSFM could be rehydrated, the BM dissected out and reimaged at higher resolution with

278 e marrow (BM) niches; however, what role the BM microenvironment plays in mediating the effects of in

279 Efficient and specific drug delivery to the BM is an unmet need.

280 ocyte cell line Jurkat delivered ICLs to the BM more efficiently than erythrocytes, and more selectiv

281 i2 expression in the BM is restricted to the BM stromal compartment where it regulates the HSC niche.

282 CXCR3-mediated TNF(+) T cell homing to the BM upregulated the Th17 chemoattractant CCL20, which rec

283 he mean estimated total absorbed dose to the BM was 0.992 Gy for all patients (range, 0.431-2.323 Gy)

284 owed that the delivery was restricted to the BM, lungs, liver and spleen, with no accumulation in the

285 ant CCL20, which recruited Th17 cells to the BM.

286 us, disrupting interactions of LSCs with the BM environment is a promising strategy to halt the disea

287 dent inflammatory stress response within the BM, leading to significant HSC dysfunction including los

288 al ECM-integrin receptor axis contributes to BM megakaryocytosis in JAK2V617F+ PMF.

289 atically increasing mitochondria transfer to BM MSC.

290 lization with up to 4 simultaneous (9 total) BM components in 152 full-bone sections from different b

291 the endothelial monolayer and the underlying BM for modulation of immune cell phenotype.

292 fects of SP and NK-A are mostly mediated via BM stroma.

293 with POEMS syndrome, including some in whom BM tests routinely performed to diagnose plasma cell dys

294 HSCs interact with BM niche cells that produce growth factor c-Kit ligand (

295 n an independent cohort of 105 patients with BM-LUAD.

296 tients with HER2-positive breast cancer with BMs, the addition of tucatinib to trastuzumab and capeci

297 l efficacy and survival in participants with BMs.

298 val (OS) were evaluated in all patients with BMs.

299 There were 291 patients with BMs: 198 (48%) in the tucatinib arm and 93 (46%) in the

300 brain magnetic resonance imaging; those with BMs were classified as active or stable.