ライフサイエンスコーパス: BCR

1 BCR knockdown occludes OGD-induced Rac1 activation in hi

2 BCR ligation by endogenous or exogenous ligands induced

3 BCR post definitive therapy is often associated with dis

4 BCR signaling was mildly affected, whereas cell migratio

5 BCR was defined as 2 consecutive prostate-specific antig

6 BCR(-) lymphoma variants that restore competitive fitnes

7 BCR-mediated canonical NF-kappaB signaling was impaired

8 BCR/TCR repertoire analysis did not show significant dif

9 We present 2 BCR-ABL1 fusion-positive BCP-ALL patients with CD19(-) m

10 , n = 20), molecular response(4.5) (MR(4.5), BCR-ABL1 </=0.0032%, n = 16), and sustained TFR (BCR-ABL

11 correlates with the expression of ZAP-70, a BCR-associated kinase.

12 f Fos and Dusp1 suppressed tumor growth in a BCR-ABL fusion protein kinase-induced mouse model of chr

13 ared with non-CML stem/progenitor cells in a BCR-ABL kinase-independent manner.

14 rventions targeting road traffic injuries, a BCR of 5.9 (95% CI 5.8-6.0) was achieved on investment o

15 We have shown previously that when a BCR engages its cognate Ag on a cell surface that also e

16 tory disease after previous treatment with a BCR signalling pathway inhibitor.

17 Myc overexpression is sufficient to activate BCR and PI3K/Akt signaling pathways and further enhances

18 tically increased in Rictor KO B cells after BCR stimulation through dysregulating the dephosphorylat

19 less a factor in determining potency against BCR signaling.

20 Furthermore, alpha-BCR-induced signaling strength was variable across patie

21 Exposure to BMP2/BMP4 does not alter BCR-ABL transcript expression but is accompanied by the

22 Three manipulations that altered BCR genes without affecting surface BCR levels showed th

23 ely 57% and approximately 84% in the ALR and BCR, respectively.

24 ng cancer, HER2-amplified breast cancer, and BCR-ABL leukemia.

25 althy volunteers were activated via CD40 and BCR, either alone or in combination.

26 rvival signals provided by stromal cells and BCR cross-linking and was effective against CLL cells ha

27 on, consequently reducing BCR clustering and BCR signaling.

28 armacological inhibition of c-FOS, DUSP1 and BCR-ABL eradicated MRD in multiple in vivo models, as we

29 PTEN protein expression and BCR surface density may influence clinical response to t

30 investigate the relationship between Myc and BCR signaling in pre-malignant B cells.

31 Amplification (RCA) techniques for c-MYC and BCR-ABL1 genes, allowing for the real-time quantificatio

32 ol for analyses and visualization of TCR and BCR sequencing data of 13 species.

33 r77-GFP transgenes serve as specific TCR and BCR signaling reporters in murine transgenic models.

34 xpression can serve as a reporter of TCR and BCR specific signaling in human PBMCs.

35 uch an NTF impairs endosomal trafficking and BCR signal transduction.

36 d IgM levels were elevated upon ex vivo anti-BCR/TLR9 stimulation.

37 rectly, by the presence of oncogenes such as BCR-ABL1.

38 oblastic leukemia (ALL), also referred to as BCR-ABL1-like ALL, is a high-risk subset with a gene exp

39 nvestigators to use scRNA-seq for assembling BCR sequences at single-cell resolution.

40 In anti-thymocyte/Thy-1 autoreactive BCR knock-in mice lacking self-Thy-1 ligand, immunoglobu

41 We used the genomic breakpoint between BCR and ABL1 genes for the DNA-based monitoring of minim

42 Replacing antigen-binding BCR regions had no effect on BCR signaling in GCB-DLBCL

43 treatment of hematologic malignancies, block BCR-mediated lytic induction at clinically relevant dose

44 Although Ph(+) ALL is defined by BCR-ABL1 fusion, Ph-like ALL cases contain a variety of

45 her cellular contact nor factors released by BCR(+) tumour cells.

46 In both mouse and human B cells, BCR ligands that deliver a TLR9 agonist induce an initia

47 differ by age, whereas effectors of chronic BCR-->NF-kappaB signaling were associated with adult-mBL

48 neates chronic myeloid leukemia from classic BCR-ABL1(-) MPNs, which are largely defined by mutations

49 ation microscopy, demonstrate that clustered BCR resides within ordered phase-like domains capable of

50 sufficient mice, suggesting that the cognate BCR efficiently internalizes the Id in an IC with nucleo

51 Notably, leukemias driven by combined BCR-ABL1 expression and Ikaros suppression rapidly regre

52 In keeping with this, combining BCR signalling with CD40 ligation did not reduce IL-10 s

53 We hypothesized that constitutive BCR activation precluded functional B-cell maturation in

54 us supporting that IL4I1 negatively controls BCR-dependent activation.

55 blishes a detailed kinetic model of the core BCR signaling network and provides the means to explore

56 splenic B cell differentiation by decreasing BCR signaling.

57 Small, dense BCR clusters likely formed via protein-protein interacti

58 The strongly disturbed BCR signaling of CD21(low) B cells is characteristic for

59 MRI between prostate cancer patients who do (BCR (+)) and do not (BCR (-)) have BCR following definit

60 th the fundamental process of antigen-driven BCR clustering and differences in the spatial organizati

61 g in 52 of 270 patients (19%) with PCa early BCR (PSA < 1.0 ng/mL).

62 c-overexpressing B cells maintained elevated BCR signaling despite treatment with ibrutinib, a Bruton

63 In addition, artificially enhancing BCR signal strength permitted IgE(+) memory B cells-whic

64 To address this, we examined BCR-NOTCH2 synergy because NOTCH has been shown to incre

65 tically, we show that B cells, which express BCRs specific to hen egg lysozyme (HEL) display diminish

66 ear in the presence of their BCR-expressing (BCR(+)) counterparts in vitro and in vivo.

67 R expression enhances lymphoma cell fitness, BCR-targeted therapies may profit from combinations with

68 ays and further enhances signaling following BCR ligation.

69 (68)Ga-PSMA-11 PET/CT at 4 institutions for BCR after prostatectomy without prior radiotherapy at a

70 Quantitative PCR for BCR-ABL1 yielded a value of 29.6% on the International S

71 cogene well known as part of the fusion gene BCR-ABL1 in the Philadelphia chromosome of leukemia canc

72 the feasibility of producing clinical-grade BCR-ABL-specific cytotoxic T lymphocytes (CTLs), endowed

73 er se, significantly affect lymphoma growth, BCR-negative (BCR(-)) tumour cells rapidly disappear in

74 s who do (BCR (+)) and do not (BCR (-)) have BCR following definitive therapy.

75 These patients have BCR-ABL1-positive clonal hematopoiesis resembling a chro

76 ified Ikaros target genes in mouse and human BCR-ABL1(+) pre-B ALL, revealing novel conserved gene pa

77 on of wild-type Ikaros in IKZF1 mutant human BCR-ABL1(+) pre-B ALL.

78 This work identifies BCR as a critical player in Rac1 regulation during OGD i

79 ing and PI3K/Akt and Erk signaling in an IgD-BCR-dependent manner.

80 The specific role of the IgD-BCR is still enigmatic, but it is colocalized with sever

81 These results show that the IgD-BCR, CD19, and CXCR4 are not only colocalized at nanomet

82 CXCR4 is also found in proximity to the IgD-BCR.

83 IgG BCRs are more clustered than IgM BCRs on resting cells a

84 ganization of immunoglobulin M (IgM) and IgG BCRs on the surfaces of resting and antigen--activated h

85 vide evidence that although both IgM and IgG BCRs reside in highly heterogeneous protein islands that

86 s in the spatial organization of IgM and IgG BCRs that may contribute to the characteristic differenc

87 et B cells expressing an Igkappa or Iglambda BCR possess differential specificities, and highlight th

88 IgG BCRs are more clustered than IgM BCRs on resting cells and form larger protein islands af

89 ence of FcmuR, the surface expression of IgM-BCR was increased, which resulted in enhanced tonic BCR

90 transport and cell-surface expression of IgM-BCR.

91 cells, mitochondrial proteins accumulated in BCR-stimulated cells, leading to protein synthesis inhib

92 nd CSR pipeline to analyze SHM and/or CSR in BCR rearrangements.

93 These individual differences in BCR levels and signaling might relate to differences in

94 evidence for the role of membrane domains in BCR signaling and a plausible mechanism of BCR activatio

95 Using a mouse model whose knock-in BCR does not functionally engage with immunizing antigen

96 rgy because NOTCH has been shown to increase BCR responsiveness in normal mouse B cells.

97 nd tacrolimus but not rapamycin also inhibit BCR-mediated EBV activation.

98 ugs cyclosporine and tacrolimus also inhibit BCR-mediated lytic induction but find that rapamycin doe

99 ion but find that rapamycin does not inhibit BCR-mediated lytic induction.

100 Instead, BCR loss induces the rewiring of central carbon metaboli

101 degradation of endocytic cargo, have intact BCR signaling, and do not exhibit any relevant defects i

102 We propose that this mechanism integrating BCR, TLR9, and cytokine signals provides a peripheral ch

103 aintain a high -frequency of single isolated BCR localizations, which likely represent BCR monomers.

104 of the constitutively active tyrosine kinase BCR/Abl.

105 patients had received ibrutinib as the last BCR inhibitor therapy before enrolment, 43 of whom were

106 Atypical chronic myeloid leukemia, BCR-ABL1 negative (aCML) is a rare myelodysplastic syndr

107 n levels and signal capacity have all linked BCR on CLL cells to disease prognosis.

108 Patients (6 of 8) with major BCR-ABL1 transcript encoding P210(BCR-ABL1) mainly showe

109 [8/32] with minor and 12.5% [1/8] with major-BCR-ABL1 variants in the consecutive cohorts) had signif

110 analyzing two certified reference materials (BCR-482 Lichen and SPS-WW1 Batch 114) and spiked chickpe

111 each year from 2015 to 2030 generated a mean BCR of 11.8 (95% CI 11.6-12.0).

112 riage ($3.8 per capita each year) had a mean BCR of 5.7 (95% CI 5.3-6.1), with the effect high in low

113 sults indicate that IgH isotype-specific mIg/BCR dosage may play a larger role in B cell fate than pr

114 in most of the patients (9 of 12) with minor BCR-ABL1 transcript encoding P190(BCR-ABL1), only the CD

115 ponse (pre-MMR, BCR-ABL1 >0.1%, n = 8), MMR (BCR-ABL1 </=0.1%, n = 20), molecular response(4.5) (MR(4

116 cular recurrence was defined as loss of MMR (BCR-ABL1:ABL1 ratio >0.1%) on two consecutive samples.

117 ratio <0.01%; MR4 cohort) or in stable MMR (BCR-ABL1:ABL1 ratio consistently <0.1%) but not MR4 (MMR

118 achieving major molecular response (pre-MMR, BCR-ABL1 >0.1%, n = 8), MMR (BCR-ABL1 </=0.1%, n = 20),

119 een and analyzed their endosomal morphology, BCR expression, and signal transduction.

120 years or more and were either in stable MR4 (BCR-ABL1:ABL1 ratio <0.01%; MR4 cohort) or in stable MMR

121 We found that the key positive and negative BCR signaling molecules, phosphorylated Brutons tyrosine

122 cantly affect lymphoma growth, BCR-negative (BCR(-)) tumour cells rapidly disappear in the presence o

123 or CD40L in combination with IL-21, but not BCR stimulation, suggesting the importance of the immune

124 cancer patients who do (BCR (+)) and do not (BCR (-)) have BCR following definitive therapy.

125 the molecular underpinnings of this "NOTCH2-BCR axis" in cGVHD revealed imbalanced expression of the

126 in Lck expression associated with ability of BCR to induce signal upon engagement.

127 tely 92's role in constitutive activation of BCR signaling and sensitivity to ibrutinib.

128 rs (TKIs) that target the kinase activity of BCR-ABL1 have transformed CML from a once-fatal disease

129 +)-permeable AMPAR-dependent deactivation of BCR in hippocampal but not cortical neurons.

130 in Rictor KO B cells rescues the defects of BCR signaling and B cell differentiation.

131 gulated Nod1, providing a positive effect of BCR engagement on development of most B cells.

132 e of GCB-DLBCL lines, shown by the effect of BCR KO, was highly variable; in contrast, pan-AKT KO was

133 tor positively regulates the early events of BCR signaling.

134 over, a situation in which the generation of BCR-bearing IgLkappa is delayed until after IgLlambda be

135 ast crisis." The biological heterogeneity of BCR-ABL1-positive ALL may impact the patient outcomes an

136 The reduction in the initiation of BCR signaling caused by actin alteration is associated w

137 had significantly (>1 log) higher levels of BCR-ABL1 fusion than Ig/TCR rearrangements and/or IKZF1

138 n BCR signaling and a plausible mechanism of BCR activation via receptor clustering that could be gen

139 amily kinase Lck is a targetable mediator of BCR signalling in CLL cells, and that variance in Lck ex

140 Here, we analyzed a mouse model of BCR-ABL1(+) pre-B ALL together with a new model of induc

141 tein islands that vary in size and number of BCR single-molecule localizations, both resting and acti

142 recurrence (MR) was defined as positivity of BCR-ABL transcript in a quantitative reverse transcripta

143 ditional analyses because of the presence of BCR-ABL1 (n = 46) or ETV6-RUNX1 (n = 11).

144 ogram was underestimating the probability of BCR-free status in the ePLND+SNB group, whereas the ePLN

145 ledge regarding activation and regulation of BCR signaling in individual patients is needed.

146 domains capable of sorting key regulators of BCR activation, and present a minimal, predictive model

147 eviously treated MZL, confirming the role of BCR signaling in this malignancy.

148 logical synapse, resulting in suppression of BCR signaling and B cell apoptosis.

149 novel responses and decreased fine-tuning of BCR specificities by somatic hypermutation.

150 nsity area restricts the lateral movement of BCRs upon stimulation, consequently reducing BCR cluster

151 characterized by exploitable dependencies on BCR, mTOR, or MEK signaling and associated with mutation

152 antigen-binding BCR regions had no effect on BCR signaling in GCB-DLBCL lines, reflecting this subtyp

153 revealed off-target effects of ibrutinib on BCR signaling.

154 selected region within the leukemic oncogene BCR-ABL1 Using bulk competitions with a deep-sequencing

155 y, we engineered the known fusion oncogenes, BCR-ABL1, EML4-ALK, and ETV6-NTRK3, as well as 20 previo

156 Targeting the fusion oncoprotein BCR-ABL with tyrosine kinase inhibitors has significantl

157 id leukemia defined by mutations in RUNX1 or BCR-ABL1 translocations as well as a constellation of so

158 L1-dependent resistance; however, overcoming BCR-ABL1-independent mechanisms of resistance remains ch

159 with minor BCR-ABL1 transcript encoding P190(BCR-ABL1), only the CD19(+) leukemia compartments were B

160 emergence of bone marrow (BM)-resident (p190)BCR-ABL-specific T lymphocytes has been correlated with

161 Our results show that (p190)BCR-ABL-specific CTLs are capable of controlling treatme

162 with major BCR-ABL1 transcript encoding P210(BCR-ABL1) mainly showed HSC involvement, whereas in most

163 ABL1, ABL2, CSF1R, and PDGFRB that phenocopy BCR-ABL1 and alterations of CRLF2, JAK2, and EPOR that a

164 Pre-BCR(+) ALL cells were exquisitely sensitive to ibrutinib

165 emonstrated synergistic activity against pre-BCR(+) ALL.

166 Precursor BCR (pre-BCR) signaling, which is critical during normal B lympho

167 iption factors and B cell receptor (BCR)/pre-BCR-signaling genes.

168 In pre-BCR(+) ALL, ibrutinib thwarted autonomous and induced pr

169 LK) are relevant targets of ibrutinib in pre-BCR(+) ALL.

170 poiesis, also plays an important role in pre-BCR(+) B cell acute lymphoblastic leukemia (B-ALL).

171 brutinib thwarted autonomous and induced pre-BCR signaling, resulting in deactivation of PI3K/Akt sig

172 Ibrutinib modulated the expression of pre-BCR regulators (PTPN6, CD22, CD72, and PKCbeta) and subs

173 recursor to the B cell antigen receptor (pre-BCR), including defects in BLNK, BTK, PKCbeta, NF-kappaB

174 Precursor BCR (pre-BCR) signaling, which is critical during normal

175 expression, B-cell/T-cell receptor profiles (BCR/TCR), and potential viral infections.

176 ivation significantly increased the proximal BCR adapter protein BLNK.

177 emory function, suggesting that quantitative BCR signal weakness contributes to restraint of IgE B ce

178 ad an unweighted mean benefit to cost ratio (BCR) of more than 10.0, whereas, for interventions targe

179 ss both IgM and IgD B-cell antigen receptor (BCR) classes, which are organized on the cell surface in

180 nases downstream of B-cell antigen receptor (BCR) represent attractive targets for therapy in non-Hod

181 signaling from the B cell antigen receptor (BCR), and thus for antibody responses.

182 s expression of the B cell antigen receptor (BCR), it remains unclear whether engagement of self-anti

183 vity of the pivotal B-cell antigen receptor (BCR)-proximal effector spleen tyrosine kinase (SYK), whi

184 signaling events, including B cell receptor (BCR) activation, are hypothesized to be facilitated by d

185 tions in the interconnected B-cell receptor (BCR) and CXCR4 signaling pathways.

186 cells is up-regulated upon B-cell receptor (BCR) engagement and IL-4 treatment.

187 mouse strain, we found that B cell receptor (BCR) ligation of Ubqln1(-/-) B cells led to a defect in

188 gh inhibitors targeting the B-cell receptor (BCR) pathway have been successful in the treatment of th

189 e mutations, and linked the B cell receptor (BCR) pathway to trisomy 12, an important driver of CLL.

190 ate the effects of aging on B-cell receptor (BCR) repertoire evolution during an immunological challe

191 dasatinib, drugs that block B cell receptor (BCR) signaling and are used in the treatment of hematolo

192 proteins implicated in pre-B-cell receptor (BCR) signaling and migration/adhesion, which could contr

193 -/-) mice display increased B cell receptor (BCR) signaling as judged by increased levels of phosphor

194 ever, the role of Rictor on B cell receptor (BCR) signaling as well as the underlying cellular and mo

195 modification to investigate B-cell receptor (BCR) signaling in cell lines of diffuse large B-cell lym

196 udy, we used chronic active B-cell receptor (BCR) signaling in diffuse large B-cell lymphoma as a mod

197 revealed the importance of B-cell receptor (BCR) signaling in maintaining MCL survival.

198 Targeting B-cell receptor (BCR) signaling is a successful therapeutic strategy in m

199 ween MYC overexpression and B-cell receptor (BCR) signaling molecules in B-NHL, signaling pathways es

200 infection, which may induce B-cell receptor (BCR) signaling, resulting in aberrant B-cell survival an

201 We discuss targeting of B cell receptor (BCR) signaling, with emphasis on identifying patients wh

202 rs mutations that reinforce B cell receptor (BCR) signaling.

203 tivation of Akt kinase upon B-cell receptor (BCR) stimulation.

204 signaling downstream of the B-cell receptor (BCR), Fc receptors (FcRs), and toll-like receptors.

205 ed a relationship among the B cell receptor (BCR), TLR9, and cytokine signals that regulate B cell re

206 n genes promoting the tonic B-cell receptor (BCR)-->PI3K pathway (TCF3 and ID3) did not differ by age

207 e transcription factors and B cell receptor (BCR)/pre-BCR-signaling genes.

208 repertoires, expressed as B cell receptors (BCRs).

209 pattern of PCa early biochemical recurrence (BCR) after radical prostatectomy with (68)Ga-PSMA-11 PET

210 RM2 in patients with biochemical recurrence (BCR) of PCa and negative findings on conventional imagin

211 patients at risk for biochemical recurrence (BCR) post-therapy will potentially complement definitive

212 cer in patients with biochemical recurrence (BCR).

213 cancer patients with biochemical recurrence (BCR).

214 inhibited MALT1 proteolytic activity reduced BCR and NF-kappaB signaling, inhibited nuclear transloca

215 BCRs upon stimulation, consequently reducing BCR clustering and BCR signaling.

216 that the Rac1 GAP breakpoint cluster region (BCR) associates with NMDA receptors (NMDARs) along with

217 KO) mice to investigate how Rictor regulates BCR signaling.

218 ed BCR localizations, which likely represent BCR monomers.

219 ctivation in these cells and partly restored BCR signaling.

220 ic link between NOTCH2 activation and robust BCR responses to otherwise suboptimal amounts of surroga

221 Imatinib, a selective BCR-ABL1 kinase inhibitor, improved the prognosis for pa

222 ly reported teratogenic effects of selective BCR-ABL inhibitors in humans and developmental defects i

223 accompanied by the overexpression of several BCR kinases including LYN, spleen tyrosine kinase, Bruto

224 relapse after blinatumomab therapy and show BCR-ABL1 positivity in their hematopoietic stem cell (HS

225 CD79A-GFP fusion showed BCR clustering or diffuse distribution, respectively, in

226 Characterization of Ag-specific BCR repertoires is essential for understanding disease m

227 We examined IgH isotype-specific BCR function by analyzing naturally switched B cells fro

228 us, during positive selection in the spleen, BCR signaling causes immature T1 B cells to become recep

229 altered BCR genes without affecting surface BCR levels showed that BCR signaling differs between the

230 rofit from combinations with drugs targeting BCR(-) tumour cells.

231 n's tyrosine kinase (BTK) inhibitor, targets BCR signaling and is particularly active in lymphomas wi

232 ABL1 </=0.0032%, n = 16), and sustained TFR (BCR-ABL1 undetectable following cessation of TKI therapy

233 We determined that BCR repertoires become increasingly specialized over a s

234 lecular link between pathways, we found that BCR-NOTCH activation significantly increased the proxima

235 Finally, we show that BCR signaling can activate EBV lytic induction in freshl

236 out affecting surface BCR levels showed that BCR signaling differs between the germinal center B-cell

237 The BCR attenuates glycogen synthase kinase 3 beta (GSK3beta

238 The BCR-ABL specific tyrosine kinase inhibitors (TKI) change

239 ive in lymphomas with mutations altering the BCR subunit CD79B and MYD88.

240 model whereby the risk variant augments the BCR and coreceptor programs throughout B cell developmen

241 Consequently, the BCR signalling machinery has become an established targe

242 bition of HSP90 with PU-H71 destabilized the BCR kinases and caused apoptosis of CLL cells through th

243 Similarly, a possible role for the BCR or circulating Ab in mediating CTL responses to B ce

244 n serum transfer, implicating a role for the BCR, but not circulating Ab, in DC-derived exosome respo

245 f eleven currently targetable kinases in the BCR signaling network.

246 drugs that inhibit important kinases in the BCR signaling pathway inhibit activation of lytic viral

247 bserved at the mRNA level, expression in the BCR was examined.

248 ed GCB-DLBCL lines from knockout (KO) of the BCR or 2 mediators of tonic BCR signaling, SYK and CD19.

249 uestion, we performed deep sequencing of the BCR repertoire of AChR-MG, MuSK-MG, and healthy subjects

250 SP90 contributes to the over-activity of the BCR signaling in CLL and inhibition of HSP90 has the pot

251 constructed a detailed kinetic model of the BCR signaling network, which captured the known complex

252 y member, is an inhibitory coreceptor of the BCR with established roles in health and disease.

253 For patients with MPNs, detection of the BCR-ABL1 fusion delineates chronic myeloid leukemia from

254 aemia (CML) is driven by the activity of the BCR-ABL1 fusion oncoprotein.

255 activation and that this is dependent on the BCR.

256 s through two distinct pathways, one via the BCR leading to activation of SYK, ERK, and AKT and the o

257 at the cell surface in association with the BCR H chain.

258 p between expression of molecules within the BCR signalling pathway and disease outcome.

259 s rapidly disappear in the presence of their BCR-expressing (BCR(+)) counterparts in vitro and in viv

260 immune-precipitation demonstrated that these BCR constituents are present in a multi-client chaperone

261 gmu > mIggamma1 > mIgepsilon, and that these BCR expression differences influence respective developm

262 This BCR editing with increased Nod1 resulted in preferential

263 t patients develop resistance to TKI through BCR-ABL1-dependent and -independent mechanisms.

264 rapamycin complex 2 (mTORC2) contributes to BCR-mediated lytic induction and that FK506-binding prot

265 isease, the underlying mechanisms leading to BCR over-activity in CLL are not fully understood.

266 their wild-type counterparts in response to BCR cross-linking.

267 elate to differences in therapy responses to BCR-pathway inhibitors.

268 Tonic BCR signaling acts principally to activate AKT, and forc

269 increased, which resulted in enhanced tonic BCR signaling.

270 response to therapeutic inhibition of tonic BCR signaling in DLBCL.

271 The magnitude and importance of tonic BCR signaling to proliferation and size of GCB-DLBCL lin

272 kout (KO) of the BCR or 2 mediators of tonic BCR signaling, SYK and CD19.

273 ecting this subtype's exclusive use of tonic BCR signaling.

274 s BL cell survival by interfering with tonic BCR signaling, thus providing a molecular rationale for

275 Although total BCR is similar in the two neuronal types, BCR is more ac

276 al BCR is similar in the two neuronal types, BCR is more active in hippocampal compared with cortical

277 tients who achieve and maintain undetectable BCR-ABL1 transcript levels for at least 2 years remain d

278 cular response 4.5 (MR4.5) with undetectable BCR-ABL1 transcripts for the 2 preceding years at least

279 bilization, and inhibits SHP-1 activity upon BCR engagement, thus supporting that IL4I1 negatively co

280 ay contribute to the hyporesponsiveness upon BCR stimulation.

281 ellular Akt/S6 kinase signaling pathway upon BCR and CD40 stimulation.

282 only the CD19(+) leukemia compartments were BCR-ABL1 positive (P = .02).

283 Whereas BCR ablation does not, per se, significantly affect lymp

284 Thus, while BCR expression enhances lymphoma cell fitness, BCR-targe

285 ntities, AML with mutated RUNX1 and AML with BCR- ABL1, have been included in the current update of t

286 f adoptive immunotherapeutic approaches with BCR-ABL CTLs in Ph(+) ALL.

287 expression in CLL cells also associates with BCR signalling capacity, but also different because ZAP7

288 eveloped TKI can target Ph(+) ALL cells with BCR-ABL1-dependent resistance; however, overcoming BCR-A

289 e across patient samples and correlated with BCR subunit CD79B expression, but was inversely correlat

290 We enrolled 32 men with BCR of PCa, who were 59-83 y old (mean +/- SD, 68.7 +/-

291 re than 50% of prostate cancer patients with BCR (54/101; 53%).

292 for localization of disease in patients with BCR of PCa and negative findings on conventional imaging

293 sessment of GRPr expression in patients with BCR of PCa.

294 fter (68)Ga-PSMA PET/CT in 100 patients with BCR were retrospectively reviewed, and changes in plans

295 T altered management in 39% of patients with BCR, and changes occurred more often in patients with ra

296 d to avoid CD19(-) relapses in patients with BCR-ABL1-positive ALL.

297 tional diagnostic samples from patients with BCR-ABL1-positive BCP-ALL, we identified HSC involvement

298 ukemia (Ph(+) ALL) is currently treated with BCR-ABL1 tyrosine kinase inhibitors (TKI) in combination

299 -up for at least 3 years in patients without BCR were the inclusion criteria to select 77 patients ou

300 The 5-y BCR-free survival rate was 80.5% and 69.9% in the ePLND+