ライフサイエンスコーパス: BCR

1 BCR diversity is induced by naturally occurring combinat

2 BCR is also activated by ligands presented at surfaces,

3 BCR might be explained by target miss.

4 BCR recruited a guanidine nucleotide exchange factor (GE

5 BCR sequences diversify through mutations introduced by

6 BCR signaling triggers a cascade of intracellular mediat

7 BCR signaling, involving phosphorylation of various down

8 BCR stimulation alone induced differentiation into CD5(h

9 BCR stimulation of B cells induced substantial apoptosis

10 BCR stimulation of BCALM-deficient B cells resulted in d

11 BCR-mediated tonic signaling is an indispensable require

12 Subset 2 expresses a BCR with the combination of IGHV3-21-derived heavy chain

13 p85:p110 heterodimeric PI3K, thereby abating BCR tonic signaling, resulting in their extremely short

14 kemia (CML), caused by constitutively active BCR-ABL1 fusion tyrosine kinase, has served as a paradig

15 radation may represent a strategy to address BCR-ABL1-dependent drug resistance, and warrant further

16 uitment of naive B cells with a low-affinity BCR into GCs to initiate the process of affinity maturat

17 re efficiently after acquiring high-affinity BCRs.

18 (HuGL18(HL)) or medium (HuGL17(HL)) affinity BCRs were primed, recruited to germinal centers, and the

19 with the former expressing even low-affinity BCRs efficiently capture and present sufficient antigen

20 mobilization and NF-kappaB activation after BCR stimulation.

21 r mechanisms and CD22 signaling events after BCR activation and revealed several new CD22-associated

22 lathrin-dependent CD22 internalization after BCR stimulation.

23 Results: In the consensus analysis, BCR localization rates were not higher using advanced re

24 ding of receptor crosstalk between IL-4R and BCR is summarized along with several possible mechanisms

25 geting of miR-185-mediated PAK6 activity and BCR-ABL1 may provide a valuable strategy for overcoming

26 ll subpopulations showed different basal and BCR stimulation-induced phosphorylation levels of downst

27 linical trials testing inhibitors of BTK and BCR signaling mediators in DLBCL.

28 g that CLEC16A controls both HLA-DR/CD74 and BCR/Ag processing in MIICs.

29 ion between isogenic untransformed cells and BCR-Abl-transformed cells and identified several compoun

30 composition or genetic diversity of HLA and BCR/TCR loci.

31 nowledge of the genetic diversity at HLA and BCR/TCR loci.

32 es had higher MTXPG levels (hyperdiploid and BCR-ABL like).

33 By comparing LMP2A and BCR signaling in primary human B cells using phosphoprot

34 The number, phenotype, and BCR clonotypes of GlcNAc-reactive B-1 B cells were modul

35 implications for B cell immune response and BCR-dependent cancers.

36 Both short-read RNA-seq-based HLA typing and BCR/TCR repertoire sequencing (AIRR-seq) currently rely

37 138 and $118 per additional YLL averted; and BCRs were 62, 29, and 9, respectively.

38 itor (CNI), while co-stimulation of TLRs and BCRs induced differentiation into CD5(dim) (B-1b) cells

39 binatorial targeting of JAK/STAT, PI3K, and "BCR-like" signaling with multiple TKIs and/or dexamethas

40 an expansion mixture containing IL-21, anti-BCR, CpG oligodeoxynucleotide, CD40L, and IL-2, we were

41 min D deficiency were studied in an Arf(-/-) BCR-ABL acute lymphoblastic leukemia murine model.

42 e demonstrate that this machinery attenuates BCR signaling intensity by mitigating the Kras/Erk and P

43 d by limiting BCR repertoires or attenuating BCR signaling strength.

44 ng been appreciated that highly autoreactive BCRs are actively removed from the developing B cell rep

45 s, supporting the incorporation of NGS-based BCR-ABL1 KD mutation screening results in the clinical d

46 ity, cost, and turnaround times of NGS-based BCR-ABL1 mutation screening in a routine setting.

47 nment, we investigated the crosstalk between BCR and WNT/beta-catenin signaling and analyzed their im

48 As both BCR and beta-catenin are important mediators of cell sur

49 d anti-glycan Ab production by blocking both BCR and TLR-MyD88 signals.

50 lastic leukemia, with relapse driven by both BCR-ABL1 kinase-dependent and -independent mechanisms.

51 the ABO-blood group Ags, while blocking both BCRs and TLR-MyD88 by using Bruton's tyrosine kinase inh

52 New strategies to target cancers driven by BCR-Abl are therefore urgently needed.

53 most frequently in restaging M1, followed by BCR and initial staging.

54 ents markedly differed from those induced by BCR stimulation.

55 wever, whether BCR signaling is regulated by BCR mobility, and what factors mediate this regulation,

56 Biochemically recurrent prostate cancer (BCR) is the main indication to perform prostate-specific

57 relationship to authentic naive human B cell BCR sequences and affinities is unclear.

58 FcgammaR), and antigen receptors in B cells (BCR), promote an autoinflammatory loop in systemic lupus

59 rms of BCR subunits, reducing total cellular BCR levels.

60 ested each authentic naive human VRC01-class BCR mouse model under rare human physiological B cell pr

61 utilizing authentic naive human VRC01-class BCRs validate a central tenet of germline-targeting vacc

62 a novel machine learning method to classify BCR trajectories into distinct diffusive states.

63 ining the target selectivity of the clinical BCR-ABL inhibitor dasatinib in peripheral blood mononucl

64 gether, these findings suggest that combined BCR-ABL1 kinase inhibition and protein degradation may r

65 through the retinoid X receptor to decrease BCR-ABL leukemic cell viability.

66 d to reduced repertoire diversity, decreased BCR editing and developmental arrest of immature B cells

67 eating factors, Arp2/3 and formin, decreases BCR mobility.

68 NOD-PerIg mice are a previously developed BCR-transgenic model in which virtually all B lymphocyte

69 romotes negative feedback that downmodulates BCR-mediated Ca(+) signaling by promoting phosphorylatio

70 R-proximal kinase LYN, as well as downstream BCR signaling molecules in GCBCs.

71 Primary B cells undergo antigen-driven BCR affinity maturation through somatic hypermutation an

72 cell response showed converging IGHV3-driven BCR clusters closely associated with SARS-CoV-2 antibodi

73 PET/CT offers high detection rates in early BCR after radical prostatectomy, especially among patien

74 iciency permits BCR-induced CSR by elevating BCR-proximal signaling intensity.

75 l responses without the use of an engineered BCR.

76 re we use single molecule imaging to examine BCR movement during signaling activation and a novel mac

77 s limiting negative selection from excessive BCR engagement.

78 Upon Ag exposure, naive B cells expressing BCR able to bind Ag can undergo robust proliferation and

79 ed signal transduction in T cells expressing BCR or B cells expressing part of the TCR complex.

80 Mature naive B cells expressing BCRs of the IgM and IgD isotypes respond to Ag in second

81 els, liver-specific selection of the focused BCR IgH repertoire was found on hepatic B cells in Mdr2(

82 apy without meeting the Phoenix criteria for BCR, after other definitive local treatments, and with a

83 tes rapid searches in bulk immunome data for BCR or TCR sequences based on their CDR3 sequence or V3J

84 roach to Bayesian phylogenetic inference for BCR sequences that is based on a phylogenetic hidden Mar

85 patients with chronic myeloid leukaemia for BCR-ABL1 kinase domain mutation.

86 Most current methods for BCR sequence analysis focus on separately modeling the a

87 angement model with a phylogenetic model for BCR sequence evolution but also naturally accounts for u

88 e disease-relevant Ags, without the need for BCR transgenic mice, in settings where tolerance pathway

89 t work has revealed an alternate pathway for BCR signaling, in which signalosome elements are bypasse

90 R and CXCR4 serves as molecular platform for BCR-ABL1-induced transformation and development of Ph(+)

91 s (>=3 readers regarding a scan positive for BCR), as well as the individual scan interpretations of

92 Furthermore, NF-kappaB2 is required for BCR-induced CSR in TRAF3-deficient B cells but not for C

93 CD79B ubiquitination, which is required for BCR-mediated antigen endocytosis and postendocytic sorti

94 tive of FFP at 3 y in men undergoing sRT for BCR after RP.

95 of FFP at 3 years in men undergoing sRT for BCR following RP.

96 ing (SS) is considered the gold standard for BCR-ABL1 KD mutation screening, next-generation sequenci

97 have opposing effects on mouse survival from BCR-ABL ALL.

98 Here, BCR sequences from authentic naive human VRC01-class B c

99 IGLV3-21*01 facilitates effective homotypic BCR-BCR interaction that results in autonomous, oncogeni

100 KI mice expressing functional human BCRs promise to accelerate the development of vaccines f

101 choline lipids, a natural ligand for the IgM BCR expressed in the CH27 cells used.

102 theranostic PSMA-targeting agent for imaging BCR of prostate cancer.

103 t-associated surface receptors, and impaired BCR signalling and cellular adhesion.

104 Cbls ligase activity is sufficient to impede BCR-mediated antigen processing and GC development.

105 m-dependent clonotypes, directly implicating BCR selection.

106 struction methods holds potential to improve BCR localization.

107 eletion of PTN suppressed CML development in BCR/ABL+ mice, suggesting that cell-autonomous PTN signa

108 s establish the CDR structure differences in BCR repertoires and have applications for many fields in

109 ived in advanced phases of the disease or in BCR-ABL1-positive acute lymphoblastic leukemia, with rel

110 nomous PTN signaling for CML pathogenesis in BCR/ABL+ mice.

111 on: (18)F-rhPSMA-7 PET/CT offers high PPV in BCR after RP.

112 r (18)F-DCFPyL PET/CT scans did not increase BCR localization in patients with BCR and low PSA values

113 ous regression was associated with increased BCR signaling, CLL proliferation, and clonal evolution.

114 ents outside the 2 main classic indications (BCR and presurgical staging) across all examined clinica

115 l) excluding the 2 main classic indications: BCR and presurgical staging.

116 ied the mechanism of soluble antigen-induced BCR clustering and internalization in a cultured human B

117 Galectins have been implicated in inhibiting BCR signaling in mature B cells but promoting pre-BCR si

118 tly induce early B cell activation, which is BCR driven and mechanistically dependent on the nuclear

119 he acquisition of the fusion tyrosine kinase BCR-ABL1 in a haematopoietic stem cell drives its transf

120 Breakpoint Cluster Region-Abelson kinase (BCR-Abl) is a driver oncogene that causes chronic myeloi

121 estrict BCR signaling strength for licensing BCR-induced CSR and whether deficiency of such molecule(

122 mune phenotypes can be rectified by limiting BCR repertoires or attenuating BCR signaling strength.

123 However, localizing BCR with prostate-specific membrane antigen PET/CT remai

124 auses B cell-mediated diseases by modulating BCR signaling.

125 nditional knockout model of alpha6 in murine BCR-ABL1+ B-cell ALL cells and showed that alpha6-defici

126 Ag recognition of a germline-reverted murine BCR that was selected after OVA immunization of mice, wh

127 pectedly, that of numerous non-myristoylated BCR effectors including c-Myc, NFkappaB and P-ERK, leadi

128 First, by visualizing nanoscale BCR clusters, we provide direct evidence that BCR cluste

129 om 261 consecutive patients with noncastrate BCR after radical prostatectomy who underwent (18)F-rhPS

130 Src family kinases (SFK) blocks TCR but not BCR signaling.

131 negative feedback and enhanced activation of BCR-proximal kinase LYN, as well as downstream BCR signa

132 BCR), sequence repertoire, and the amount of BCR data in public repositories is growing.

133 ry generation, and "humanness" assessment of BCR repertoires from transgenic animals.

134 Calculation of BCR localization rates (scan positivity) was based on co

135 We show that this coalescence of BCR microclusters depends on the actin-related protein 2

136 subsequent analysis of a clinical cohort of BCR patients, (18)F-JK-PSMA-7 was useful in tumor locali

137 ich is known to be upregulated downstream of BCR signaling as a result of cross-reactivity with self-

138 K signaling mediated apoptosis downstream of BCR signaling.

139 ten used to model the mutational dynamics of BCR sequence data, but these techniques do not consider

140 domain stabilization is a general feature of BCR clustering.

141 ounds that selectively impair the fitness of BCR-Abl-transformed cells.

142 motes the turnover of immature glycoforms of BCR subunits, reducing total cellular BCR levels.

143 CR stimulation, CD22-dependent inhibition of BCR signaling results in a decreased calcium mobilizatio

144 vel mechanism of resistance to inhibition of BCR/BTK signaling in MCL.

145 tering the immunoglobulin M (IgM) isotype of BCR with an artificial soluble cross-linker stabilized a

146 ever, it is unclear whether the mechanism of BCR endocytosis changes in response to these factors.

147 524.1 (B cell-associated lncRNA modulator of BCR-mediated Ca(+) signaling [BCALM]) transcripts are lo

148 LM for B-Cell Associated LncRNA Modulator of BCR-mediated Ca(+) signaling.

149 D (1,25(OH)(2)VD(3)) increased the number of BCR-ABL ALL cells only when co-cultured with bone marrow

150 ncreased stromal migration and the number of BCR-ABL blasts.

151 anced signaling, increases the proportion of BCR trajectories with lower diffusivity.

152 ture, we found that LMP2A mimics a subset of BCR signaling events, including tyrosine phosphorylation

153 The natural development of BCRs must be understood in order to design vaccines for

154 ely as a result of a regulatory influence on BCR signaling.

155 advanced PET image reconstruction methods on BCR localization and interobserver agreement with (18)F-

156 he importance of TRAF3-mediated restraint on BCR signaling strength for controlling CSR, B cell homeo

157 action that results in autonomous, oncogenic BCR signaling after acquiring R110 as a single-point mut

158 TRAF3 deficiency permits BCR-induced CSR by elevating BCR-proximal signaling inte

159 utation profiles, we elucidate physiological BCR repertoires in mouse PP GCs.

160 lls, previously shown to associate with poor BCR-ABL leukemia control, were present at higher frequen

161 s model in which three receptors, IL-7R, pre-BCR, and CXCR4, work in concert to coordinate both the p

162 itive selection of B cells by augmenting pre-BCR/BCR signaling via CD19 surface retention, whereas li

163 In contrast, pre-BCR expression and escape from interleukin-7 have only m

164 stimulation but exacerbated by high-dose pre-BCR/BCR stimulation as well as antiapoptotic Bcl(xL) ove

165 Death was rescued by low-dose pre-BCR/BCR stimulation but exacerbated by high-dose pre-BCR

166 ignaling in mature B cells but promoting pre-BCR signaling during early development.

167 of two opposing receptors, IL-7R and the pre-BCR.

168 rkedly reduced surface expression of the pre-BCR/BCR coreceptor CD19 and promoted spontaneous death o

169 PP GCs from different mice expand public BCR clonotypes (clonotypes that are shared between many

170 ur results indicate that LMP2A is not a pure BCR mimic but rather rewires intracellular signaling in

171 the protocol is user friendly and quantifies BCR-mediated phosphorylation with high sensitivity at th

172 thod to evaluate bisulfite conversion ratio (BCR) is benefit for both quality control and data analys

173 eness ratios (ICER) and benefit-cost-ratios (BCR).

174 as lost on expression of a non-self-reactive BCR or loss of MyD88 in Ikaros-deficient B cells.

175 quisition of a B1 cell-typical self-reactive BCR through a phase of proliferative expansion.

176 B cell antigen receptor (BCR) signals induce Syk activation followed by rapid pho

177 In addition, B cell antigen receptor (BCR) stereotypes as defined by IGHV usage and complement

178 gen receptor (TCR), B cell antigen receptor (BCR), and Fc receptors uses the same schematic and simil

179 eration sequencing of B and T cell receptor (BCR and TCR) repertoires, we demonstrate complex intesti

180 currently >14 million B and T cell receptor (BCR and TCR) sequences from the blood of these patients.

181 At high levels of B-cell receptor (BCR) activation, which may occur in individual CLL patie

182 ing variable regions of the B cell receptor (BCR) and of antibodies are encoded by exons that are ass

183 B cell receptor (BCR) and T cell receptor (TCR) repertoires are generated

184 However, engagement of the B cell receptor (BCR) induced both expression of IFITM3 and phosphorylati

185 B-cell receptor (BCR) knock-in (KI) mouse models play an important role i

186 ich has been described as a B cell receptor (BCR) mimic promoting malignant transformation.

187 180 million human and mouse B-cell receptor (BCR) repertoire sequences.

188 Donor B cell receptor (BCR) repertoires identified two bNAb lineages, M4008_N1

189 Analysis of the B cell receptor (BCR) repertoires in six IMDs provides insights into the

190 xt generation sequencing of B cell receptor (BCR) repertoires offers an additional source of sequence

191 , and are hyporesponsive to B-cell receptor (BCR) restimulation in vitro.

192 )J rearrangement, but their B cell receptor (BCR) sequence may differ due to the accumulation of soma

193 These processes require B cell receptor (BCR) signaling and occur in bone marrow, an environment

194 proteins and inhibits early B-cell receptor (BCR) signaling events critical for survival.

195 ma (DLBCL), which relies on B cell receptor (BCR) signaling for survival.

196 PKCbetaII, functions in the B cell receptor (BCR) signaling pathway and contributes to B cell develop

197 B-cell receptor (BCR) signaling pathways and interactions with the tumor

198 lection have been linked to B cell receptor (BCR) signaling strength and environmental cues, but how

199 g consistent with activated B cell receptor (BCR) signaling, although they do not express cell surfac

200 We surmise that, unlike B cell receptor (BCR) signaling, MYD88/IRAK signaling is constitutively a

201 no restricted IGHV usage or B-cell receptor (BCR) stereotypy.

202 d to query the antibody, or B-cell receptor (BCR), sequence repertoire, and the amount of BCR data in

203 nventional B cells, through B cell receptor (BCR)-dependent positive selection of fetally derived pre

204 mode of presentation to the B-cell receptor (BCR).

205 tors as well as B cell and T cell receptors (BCR and TCR).

206 On antigen binding, B cell receptors (BCR) cluster on the plasma membrane and are internalized

207 als, such as in binding of B cell receptors (BCR) to antigen, which initiates signaling.

208 gen-presenting cell (APC), B cell receptors (BCRs) are gathered into microclusters that recruit signa

209 of human antigen-specific B cell receptors (BCRs) generally depend on "inferred germline" sequences,

210 -like receptors (TLRs) and B cell receptors (BCRs) in the TI B cell immunity, we here used MyD88-, TR

211 odies, the soluble form of B cell receptors (BCRs), that bind to and neutralize invading pathogens.

212 with the chemokine receptor CXCR4 to recruit BCR-ABL1 and JAK kinases in close proximity.

213 gly used in men with biochemical recurrence (BCR) after radical prostatectomy (RP), but its longer-te

214 (PCa) patients with biochemical recurrence (BCR) is well established.

215 g (n = 93/388, 24%), biochemical recurrence (BCR) localization (n = 225/388, 58%), or restaging metas

216 /CT in patients with biochemical recurrence (BCR) of prostate cancer (PC).

217 F-rhPSMA-7 PET/CT in biochemical recurrence (BCR) of prostate cancer (PCa) after radical prostatectom

218 SMA-11 for restaging biochemical recurrence (BCR) of prostate cancer.

219 umor localization of biochemical recurrence (BCR).

220 us, persistent gut antigens select recurrent BCR clonotypes to seed chronic PP GC responses.

221 on; however, how degradation events regulate BCR functions in GCs is unclear.

222 activates SHP-1, which negatively regulates BCR signaling.

223 r cells (PBMCs) results in the most reliable BCR repertoire data, comparable T-cell enrichment strate

224 ibitors (TKIs) may select for drug-resistant BCR-ABL1 kinase domain (KD) mutants.

225 it remains unknown what molecule(s) restrict BCR signaling strength for licensing BCR-induced CSR and

226 two important functions mediated by the same BCR, operate in independent and distinct manners.

227 ations of antigen, B cells internalize small BCR clusters by classical clathrin-mediated endocytosis.

228 imple but robust method to QC and speculates BCR for WGBS experiments to make sure it achieves accept

229 ined for all 3 indications: initial staging, BCR, and restaging M1.

230 HIF-1alpha activation lowered surface BCR, CD19 and B cell-activating factor receptor and incr

231 romotes assembly of the MYD88-TLR9-BCR (My-T-BCR) supercomplex, which initiates prosurvival NF-kappaB

232 findings reinforce the central role of My-T-BCR-dependent NF-kappaB signaling in MCD DLBCL and sugge

233 ression of an oncogenic fusion kinase termed BCR-ABL1.

234 le Ab counterparts, only a few of the tested BCRs were autoreactive, although the cell-based assay se

235 ABL-class fusion genes other than BCR-ABL1 have been identified in approximately 3% of chi

236 CR clusters, we provide direct evidence that BCR cluster size increases with F(ab')2 concentration.

237 Together, our data indicate that BCR cross-reactivity with self-antigen is a common featu

238 The BCR recognizes foreign Ags to initiate humoral immunity

239 The BCR repertoires of primary B cells are vast owing to mec

240 anti-BAFF mAb in Mdr2(-/-) mice altered the BCR repertoire on hepatic B lymphocytes and resulted in

241 learned from AIRR-seq data by analyzing the BCR sequence, with the most common methods focused on th

242 cells in response to engagement of both the BCR and CD40 or strong cross-linking of CD40 alone.

243 endent on survival signals propagated by the BCR and the BAFFR.

244 This stabilization was hampered by the BCR-pathway inhibitor Ibrutinib, supporting beta-catenin

245 TRAF2, whose deletion in B cells enables the BCR to induce CSR in the absence of costimulation.

246 thus, it remains elusive whether and how the BCR induces CSR mechanistically.

247 ations further suggested that changes in the BCR-ABL1 dynamics resulting from TKI dose reduction conv

248 -1b cells enhanced downstream factors in the BCR-calcineurin pathway, including a nuclear factor of a

249 demonstrate that CLEC16A participates in the BCR-dependent HLA-II pathway in human B cells and that t

250 d whether and how CLEC16A is involved in the BCR-dependent HLA-II pathway.

251 t most cell surface receptors, including the BCR, were freely diffusing and randomly distributed.

252 a spectral clustering framework to infer the BCR clonal relationships.

253 kappaB2 activation to specifically limit the BCR's ability to induce CSR.

254 It is an inhibitory coreceptor of the BCR and inhibits B cell activation.

255 oximal signaling molecules downstream of the BCR but impaired Ca(2+) mobilization and NF-kappaB activ

256 r shared SHMs in the V and J segments of the BCR can be leveraged along with the junction sequence to

257 f kinases and phosphatases downstream of the BCR is essential for B cell differentiation and function

258 upporting beta-catenin as an effector of the BCR signaling.

259 lly-inactive BTK restored the ability of the BCR to mediate increases in [Ca(2+)] (i) Because catalyt

260 alling, which in part acts downstream of the BCR, is critical for the rapid expansion of B cells with

261 neither the presence nor the activity of the BCR-ABL1 protein for survival.

262 ell survival by exerting dual effects on the BCR signaling cascade.

263 ecombination (CSR); however, stimulating the BCR in the absence of costimulation (e.g., CD40) does no

264 udy, we employ mouse models to show that the BCR's capacity to induce CSR is restrained by B cell-int

265 ort that KLHL14 is in close proximity to the BCR in the endoplasmic reticulum of MCD cell line models

266 tubulin-targeting agent paclitaxel with the BCR-ABL inhibitor nilotinib in MDA-MB-468 breast cancer

267 The BCRs span the physiological range of affinities found in

268 chronic(4), and little is known about their BCR repertoires or patterns of somatic hypermutation.

269 aintain anergy via unresponsiveness of their BCRs to self-antigens.

270 echnology with the rapid generation of three BCR KI lines expressing native human precursors, instead

271 rs were selected for the generation of three BCR knockin mice.

272 yzing 4 independent clinical cohorts through BCR sequencing and by immunophenotyping with antibodies

273 inib and promotes assembly of the MYD88-TLR9-BCR (My-T-BCR) supercomplex, which initiates prosurvival

274 eated by B cell treatment with IL-4 prior to BCR triggering.

275 ermines the nature of the B cell response to BCR activation.

276 ntracellular Ca(2+) signaling in response to BCR activation.

277 m of internalization switches in response to BCR cluster size.

278 and thereby abrogated an anergic response to BCR stimulation in CLL cells.

279 y by elevating calcium influx in response to BCR stimulation, leading to lymphoid organ disorders and

280 Antigen-unexperienced BCR repertoires use the highest number and diversity of

281 turn, the repertoires of millions of unique BCR and TCR transcripts in each individual carry a vast

282 Upon BCR stimulation, beta-catenin translocated into the nucl

283 Upon BCR stimulation, CD22-dependent inhibition of BCR signal

284 Its expression increased further upon BCR stimulation to participate to the stabilization of b

285 s level of expression rapidly increased upon BCR stimulation.

286 formatics 27:1571-1572, 2011), a widely used BCR evaluator, suggests that our algorithm is much faste

287 ing and increased responsiveness to in vitro BCR stimulation compared with peritoneal B-2 cells and s

288 However, whether BCR signaling is regulated by BCR mobility, and what fac

289 is review, we discuss the many ways in which BCR repertoire data have been or could be exploited.

290 kely represents another player through which BCR signaling impacts on MCL cell survival.

291 applied it to 21 patients with CML for whom BCR-ABL1/ABL1 time courses had been quantified before an

292 52-91 y old; mean +/- SD, 71.5 +/- 7.2) with BCR after primary definitive treatment with prostatectom

293 y freedom from progression (FFP) in men with BCR after RP undergoing salvage radiotherapy (sRT).

294 In patients with BCR (after prostatectomy or radiotherapy), the capacity

295 Methods: Twenty-four patients with BCR and a PSA level of less than 2.0 ng/mL were included

296 Patients with BCR and candidates for curative surgery were excluded.

297 t increase BCR localization in patients with BCR and low PSA values (reader consensus).

298 h (18)F-DCFPyL PET/CT scans in patients with BCR and low PSA values.

299 (18)F-rhPSMA-7 PET/CT scans of patients with BCR between July 2017 and June 2018 were retrospectively

300 d lesions in oligometastasized patients with BCR.

301 Treatment with BCR-ABL1 kinase inhibitors results in elevated expressio