ライフサイエンスコーパス: lymphoma cell

1 yeloid cell leukemia 1 (MCL-1) and BCL-XL in lymphoma cells.

2 ty on IL-21R-expressing diffuse large B-cell lymphoma cells.

3 d-type (WT) and kin(-) (PKA-null) murine S49 lymphoma cells.

4 t of KSHV replication in latently infected B-lymphoma cells.

5 red for LPS-induced IgM production in CH12 B lymphoma cells.

6 h doxorubicin to selectively target and kill lymphoma cells.

7 C50 37-150 nM) vs MCT1-expressing human Raji lymphoma cells.

8 in normal tissue and in rat sarcoma-induced lymphoma cells.

9 d the activation of caspase-3 in Myc-induced lymphoma cells.

10 1, a high-affinity HDL receptor expressed by lymphoma cells.

11 KSHV lytic reactivation in primary effusion lymphoma cells.

12 olocalized with Fas on the surface of B-cell lymphoma cells.

13 a BCL2 family inhibitor in primary effusion lymphoma cells.

14 a new possible mechanism of immune escape by lymphoma cells.

15 ical for the survival of Jdp2-overexpressing lymphoma cells.

16 sp90 interactome in KSHV(+) primary effusion lymphoma cells.

17 activation in KSHV-positive primary effusion lymphoma cells.

18 dependent DNA repair in diffuse large B-cell lymphoma cells.

19 zed via hCD22 resulting in killing of B-cell lymphoma cells.

20 great potential to kill apoptosis-resistant lymphoma cells.

21 th a decrease in mutant p53 levels in B-cell lymphoma cells.

22 premalignant Tcf7(-/-) early thymocytes and lymphoma cells.

23 Eph-receptor and blocks oncogenic signals in lymphoma cells.

24 aling can be blocked by PRT060318 in primary lymphoma cells.

25 ]-DHA were observed in suspensions of murine lymphoma cells.

26 rmal epigenetic mechanisms and potently kill lymphoma cells.

27 y molecules decelerated the proliferation of lymphoma cells.

28 he proliferation, survival, and migration of lymphoma cells.

29 ays that support malignant transformation of lymphoma cells.

30 ent cytotoxicity, and induces apoptosis of B-lymphoma cells.

31 A lumbar puncture sample did not contain lymphoma cells.

32 favor elimination of residual chemoresistant lymphoma cells.

33 chromosome copy number changes affecting all lymphoma cells.

34 d DNA repair processes in ixazomib-sensitive lymphoma cells.

35 iral replication in CD95 apoptosis-resistant lymphoma cells.

36 dative stress induction to inhibit growth of lymphoma cells.

37 nt distribution, and migration properties of lymphoma cells.

38 fected survival rather than proliferation of lymphoma cells.

39 se cells could mediate killing of autologous lymphoma cells.

40 ance to EZH2 inhibitor EI1 with EZH2-mutated lymphoma cells.

41 e arrest and apoptosis in Myc-induced B-cell lymphoma cells.

42 and glucose utilization in rapamycin-treated lymphoma cells.

43 ectively depleting malignant CD30+ cutaneous lymphoma cells.

44 sting T cells from healthy donors and B-cell lymphoma cells.

45 In resistant Bcl2-expressing mouse lymphoma cells, 2 missense mutations within the Bcl2 BH3

46 In resistant human lymphoma cells, a missense mutation in the C-terminal tr

47 absence of significant HAI-1 expression, the lymphoma cells activate and shed active matriptase when

48 B7-H6:7D8 bound by CD20(+) lymphoma cells activated human NK cells and triggered de

49 ed that cells in multicellular aggregates of lymphoma cells actually respond to hypoxia.

50 Downregulation of Jun dramatically reduces lymphoma cell adhesion to extracellular matrix proteins,

51 ad transcriptional effects in Myc-transgenic lymphoma cells affecting many transcription factor netwo

52 A dynamic interaction occurs between the lymphoma cell and its microenvironment, with each profou

53 ort the utility of combined FCM detection of lymphoma cells and assessment of sCD19 levels in CSF, fo

54 mammary carcinoma cells, OVA-expressing EG7 lymphoma cells and CMS5 MCA-induced fibrosarcoma cells n

55 4A1 has proapoptotic functions in aggressive lymphoma cells and define NR4A1 as a novel gene with tum

56 Using Burkitt lymphoma cells and EBV(+) cell lines from patients with

57 inistration, downregulated IDO expression in lymphoma cells and improved the antitumor activity of CD

58 or, ixazomib, in T-cell lymphoma and Hodgkin lymphoma cells and in vivo SCID mouse models.

59 utilization even in Myc-driven human Burkitt lymphoma cells and inhibit glutamine-dependent prolifera

60 Here, we use murine CD4(+)/CD8(+) S49 lymphoma cells and isolated thymocytes to assess this me

61 Due to its selectivity for lymphoma cells and its ability to induce tumor-specific

62 allogeneic model rapidly eliminated residual lymphoma cells and led to long-term survival of 100% in

63 A striking common phenotype of CDDO-treated lymphoma cells and Lon-knockdown cells is the accumulati

64 o displayed different potencies in depleting lymphoma cells and normal B cells from whole blood ex vi

65 ivo, thereby sensitizing rituximab-resistant lymphoma cells and primary chronic lymphocytic leukemia

66 resence of nucleolin-Fas complexes in B-cell lymphoma cells and primary tissues, and the absence of s

67 arrest and cell death of Myc-induced murine lymphoma cells and synergized with BETi.

68 rutinib can induce immunogenic cell death of lymphoma cells and that concomitant stimulation of antig

69 clinical samples as well as in mouse primary lymphoma cells and that it up-regulates PRC2 expression

70 rapeutic strategy, but the effects of 2DG on lymphoma cells and the mechanism of action are unknown.

71 conditions were optimized by using EL4 mouse lymphoma cells, and labeling efficiency was examined by

72 e rate limiting in 2DG-induced cell death in lymphoma cells, and this cell killing is regulated by th

73 Neuroblastoma and B-lymphoma cells are selectively targeted and killed by bi

74 Lymphoma cells are subject to higher levels of oxidative

75 ibits proliferation and induces apoptosis of lymphoma cells arising in Myc-transgenic mice in vitro a

76 d the abundance of the targeted molecules on lymphoma cells as well as their HLA class II expression

77 at adding rituximab could target mantle cell lymphoma cells associated with redistribution lymphocyto

78 latently KSHV-infected and uninfected BJAB B lymphoma cells at the chip operational conditions of 1V,

79 ut whether this spatial organization affects lymphoma cell biology is unknown.

80 t this is an effect intrinsic to the Emu-Myc lymphoma cells but, counterintuitively, c-rel-/- Emu-Myc

81 EC and MHC-II expression on primary effusion lymphoma cells, but its effects on EC MHC-II expression

82 ecognition and killing of primary autologous lymphoma cells by activated NK cells from FL patients wa

83 patibility complex (MHC) class I antigens on lymphoma cells by anti-KIR antibodies prevents a tolerog

84 some (Xi) in female v-abl transformed thymic lymphoma cells by localizing enhanced green fluorescent

85 Latexin caused growth inhibition of lymphoma cells by significantly increasing apoptosis thr

86 s, including multiple myeloma, leukaemia and lymphoma cells, by activating the BAX/BAK-dependent mito

87 Because AKT in lymphoma cells can be regulated by other signals than BC

88 ctionalized nanoparticles by Raji and Jurkat lymphoma cells (CD20-positive and TAG-72-positive cells,

89 vels are substantially elevated in malignant lymphoma cells, compared with resting or activated B cel

90 hroughput RNA sequencing data from 50 common lymphoma cell culture models from the Cancer Cell Line E

91 those observed in the human CD22(+) Burkitt lymphoma cells, Daudi.

92 on plays a contributory role in CDDO-induced lymphoma cell death, and support the concept that mitoch

93 m by which dual DDR/mTORC1 inhibition caused lymphoma cell death.

94 , we demonstrate that Lon knockdown leads to lymphoma cell death.

95 reactivated proapoptotic genes and enhanced lymphoma cell death.

96 ivo, and Kaposi sarcoma and primary effusion lymphoma cells demonstrate high levels of D6 expression.

97 The lymphoma cells demonstrated chromosome instability along

98 Our results show that latently infected B lymphoma cells demonstrated significantly different elec

99 ipid (2mug/mouse) was much less efficient in lymphoma cell depletion.

100 was absent from the HHV-8-unrelated-PEL-like lymphoma cells despite retention of both copies of chrom

101 flux of tumor cells by injecting EL-Arf(-/-) lymphoma cells directly into the spleen and observing a

102 Furthermore, this effect may contribute to lymphoma cell dissemination and aggressiveness, characte

103 Targeting TCR signaling pathway in lymphoma cells, either with cyclosporine A or anti-CD1d

104 ressing Emu-Myc/Arf(-/-) (Cdkn2a(-/-)) mouse lymphoma cells (EL-Arf(-/-)) into C57BL/6NCrl mice intra

105 nce to ABT-737 treatment in Emicro-myc/Bcl-2 lymphoma cells engineered to rely on endogenous Mcl-1 fo

106 Here, multiple vaccinations using lymphoma cells engineered to secrete heat shock protein

107 Further, endogenous EZH2(Y641) mutants in lymphoma cells exhibit increased EZH2 stability and H3K2

108 Treated lymphoma cells exhibited a reduced mitochondrial membran

109 Accordingly, miR-17~92-driven lymphoma cells exhibited constitutive activation of the

110 We also demonstrate that primary lymphoma cells express TAK1 and pTAK1 and were sensitive

111 avidity of Ag recognition varied because the lymphoma cells expressed high or low levels of OVA.

112 The lymphoma cells expressed ligands for a natural killer (N

113 Here we show that lymphoma cells expressing high APOBEC3G levels display e

114 defective Fas signaling, we screened primary lymphoma cell extracts for Fas-associated proteins that

115 Thus, while BCR expression enhances lymphoma cell fitness, BCR-targeted therapies may profit

116 he survival of collagen-treated DG75 Burkitt lymphoma cells, following etoposide treatment.

117 ly processed and presented on the surface of lymphoma cells for recognition by cytotoxic T cells and

118 function for collagen in protecting Hodgkin lymphoma cells from apoptosis and suggest an important c

119 Stromal-cell coculture protects lymphoma cells from apoptosis in response to treatment w

120 Lymphoma cells from diffuse large B-cell lymphoma patien

121 titute a new therapeutic strategy to prevent lymphoma cells from reaching supportive microenvironment

122 Indeed, Emu-Myc-induced B cell lymphoma cells from SIRT4 null mice exhibit increased gl

123 ctedly, we detected a reproducible efflux of lymphoma cells from spleen and bone marrow, concomitant

124 antibody alemtuzumab effectively eliminates lymphoma cells from the spleen, liver and peripheral blo

125 insights into cellular pathways required for lymphoma cell growth and support the rationale for consi

126 the first to identify a role for a GPR34 in lymphoma cell growth, provide insight into GPR34-mediate

127 t, tumor-bearing mice with low C5a-producing lymphoma cells had a significantly reduced tumor burden

128 aring mice with high C5a-producing syngeneic lymphoma cells had significantly accelerated tumor progr

129 nts with high TP53 expression (>50% positive lymphoma cells) had a shorter TTF and poor OS independen

130 for Dex-promoted apoptosis imply that these lymphoma cells have adapted to selective pressure that p

131 production, glycolysis and glutaminolysis in lymphoma cells have been described.

132 Our results also suggest that apoptotic lymphoma cells help drive this signature.

133 f tumor progression we found that few if any lymphoma cells homed initially to the inguinal lymph nod

134 We also show that malignant lymphoma cells, identified by the coexpression of CD4 an

135 antibodies prevented engraftment of JAM-Cpos lymphoma cells in bone marrow, spleen, and lymph nodes o

136 Furthermore, EBV infection of lymphoma cells in HIV-positive individuals was associate

137 (over 90%) depleted CD19+/CD20+/CD45+ human lymphoma cells in mantle cell lymphoma (MCL) JeKo-1 mode

138 binding assay, DAB4 bound EL4 murine thymic lymphoma cells in preference to the normal counterpart o

139 cells greatly facilitated the engraftment of lymphoma cells in serial transplantation models.

140 he survival of collagen-treated L428 Hodgkin lymphoma cells in the absence of specific apoptotic stim

141 lymph node (ILN), despite clear evidence of lymphoma cells in the bone marrow and spleen.

142 rrest in primary cutaneous anaplastic T-cell lymphoma cells in vitro and a xenograft model in vivo.

143 l targeting specifies the infection of CD20+ lymphoma cells in vitro and in vivo, while significantly

144 cally inactive Dnmt3a in Dnmt3a(Delta/Delta) lymphoma cells in vitro inhibited Dnmt3b expression, ind

145 sion diminished proliferation in primary and lymphoma cells in vitro.

146 se, only IL-10 activated the JAK2 pathway in lymphoma cells in vitro.

147 Antigen-dependent eradication of lymphoma cells in wild-type animals was dependent on cro

148 We found that lymphoma cells infected by Epstein-Barr virus or Kaposi

149 mediated latexin overexpression in A20 mouse lymphoma cells inhibited their in vitro growth by 16 fol

150 ant with a massive and synchronous influx of lymphoma cells into the ILN, several days after injectio

151 gh glucose uptake and glycolytic activity in lymphoma cells is now beginning to be understood.

152 that CXCL13 and CXCL12 mediate chemotaxis of lymphoma cells isolated from CNS lymphoma lesions.

153 By using Emicro-Myc lymphoma cells lacking p53, we showed that CR mimetics s

154 In keeping with this, Emicro-Myc lymphoma cells lacking the BH3-only proapoptotic members

155 Here, we show that FGF4 produced by B cell lymphoma cells (LCs) through activating FGFR1 upregulate

156 ed for the uptake of exosomes by myeloma and lymphoma cells, leading to their increased proliferation

157 letion of endogenous mutp53 protein in human lymphoma cells leads to cell sensitivity to glutamine wi

158 odgkin lymphoma cell lines and mouse primary lymphoma cells leads to RBL2 derepression and RB1 reacti

159 rated, using a cellular assay in a Burkitt's lymphoma cell line (CA46-specific), that these effects w

160 bited growth of a MYC-dependent human B cell lymphoma cell line (P493) by blocking DNA replication, l

161 of exosomes derived from the DG75 Burkitt's lymphoma cell line and its sublines (LMP1 transfected an

162 stitutive CCL17 secretion of a human Hodgkin lymphoma cell line and prevent upregulation of costimula

163 spond to HA22, we isolated an HA22-resistant lymphoma cell line and showed that resistance was due to

164 omes of a latently infected pleural effusion lymphoma cell line BCBL1.

165 Mfn2-knockdown clones of a B-cell lymphoma cell line BJAB exhibited an increased rate of c

166 mmortalized cell line IB4, and the Burkitt's lymphoma cell line BJAB.

167 r describe a unique feature of the Burkitt's lymphoma cell line CA46 that allowed us to clearly demon

168 ivo, the stable lentiviral-transduced SuDHL4 lymphoma cell line harboring an inducible NR4A1 construc

169 cing of PTPN1 by RNA interference in Hodgkin lymphoma cell line KM-H2 resulted in hyperphosphorylatio

170 s when challenged with the established mouse lymphoma cell line RMA-S-RAE-1beta, which overexpresses

171 xpression of this tRNA-derived microRNA in a lymphoma cell line suppresses proliferation and modulate

172 A T-cell lymphoma cell line that is SHP-1 deficient (Karpas 299)

173 osensitivity assays, using the L5178 mouse T lymphoma cell line transfected with the human MDR1 gene.

174 ng of a conditionally BCL6-deficient Burkitt lymphoma cell line, DG75-AB7, with a library of small mo

175 BV vIL-10 locus exclusively in the Hodgkin's lymphoma cell line, Hs 611.T, the expression of which we

176 In a cutaneous T-cell lymphoma cell line, promoter hypermethylation was shown

177 Remarkably, a murine lymphoma cell line, several human B cell cancer lines, a

178 We further show, in the BL2 Burkitt's lymphoma cell line, that KLHL6 interacts with Cullin3, b

179 n siRNA-mediated IRF8 knockdown mouse B cell lymphoma cell line, we showed that IRF8 represses Bcor a

180 ith western blotting in the HDLM-2 Hodgkin's lymphoma cell line.

181 egative control IgG2 in a CD20(+) human Raji lymphoma cell line.

182 ssed in three different types of non-Hodgkin lymphoma cell lines and clinical samples as well as in m

183 onstrate that PRMT5 knockdown in non-Hodgkin lymphoma cell lines and mouse primary lymphoma cells lea

184 uce reactive oxygen species (ROS) in human B-lymphoma cell lines and primary B-cell chronic lymphocyt

185 hat trigger nonapoptotic PCD in a range of B-lymphoma cell lines and primary B-cell malignancies.

186 diated adhesion to fibronectin and VCAM-1 of lymphoma cell lines and primary CLL cells.

187 a with hypocalcemic drugs sensitized human B lymphoma cell lines and primary human lymphoma cells to

188 B-cell lymphoma cell lines and primary malignant B cells from p

189 ositive and -negative, anaplastic large cell lymphoma cell lines and primary patient tumours using th

190 tion of EZH2 A677 to a glycine (A677G) among lymphoma cell lines and primary tumor specimens.

191 usokine treatment led to direct apoptosis of lymphoma cell lines and primary tumors that otherwise we

192 phoma kinase-positive, anaplastic large cell lymphoma cell lines and that ectopically expressed JunB

193 n a subset of KSHV-infected primary effusion lymphoma cell lines as a consequence of altered processi

194 down-regulated in a variety of leukemia and lymphoma cell lines as well as in CD34+ cells from the b

195 nes, whereas it was expressed in non-Hodgkin lymphoma cell lines at levels comparable with normal B c

196 NA expression in a panel of primary effusion lymphoma cell lines by real-time RT-PCR recapitulated so

197 Here we show that incubation of lymphoma cell lines in acidic conditions (pH 6.5) blocks

198 mples with data from RCOR1 knockdowns in the lymphoma cell lines KM-H2 and Raji yielded an RCOR1 loss

199 o PEL in vitro and in vivo, but not to other lymphoma cell lines tested.

200 itors are far more cytotoxic for myeloma and lymphoma cell lines than for hepatocarcinoma or non-acti

201 Exposure of splenic marginal zone lymphoma cell lines to a demethylating agent caused part

202 of target genes in stable STAT6 transfected lymphoma cell lines, and elevated baseline expression le

203 ession of miR-34a was not toxic in several B lymphoma cell lines, and inhibition of miR-34a impaired

204 hronic lymphocytic leukaemia and mantle cell lymphoma cell lines, and patients treated with idelalisi

205 In lymphoma cell lines, IMGN529 induced G2/M cell cycle arr

206 f TAK1 is abundantly expressed in a panel of lymphoma cell lines, including mantle cell, anaplastic l

207 rmation of cytosolic Myddosome aggregates in lymphoma cell lines, mimicking the effect of dimerized T

208 ith ibrutinib induced synergistic killing of lymphoma cell lines, primary human lymphoma specimens ex

209 ed cell survival and lymphoma progression in lymphoma cell lines, primary MCL and other B cell lympho

210 cells, on various lymphoblastoid and Burkitt lymphoma cell lines, some of them being inducible or not

211 In RL and CA46, two B-cell lymphoma cell lines, TGF-beta1 treatment caused down-reg

212 , of the ICOS gene, whereas cutaneous T-cell lymphoma cell lines, which strongly express ICOS, show n

213 lymphomas, we overexpressed NR4A1 in several lymphoma cell lines.

214 hosphorylation in human diffuse large B-cell lymphoma cell lines.

215 n in wild type B cells and human mantle cell lymphoma cell lines.

216 translation in both non-Hodgkin and Hodgkin lymphoma cell lines.

217 tive activities against multiple myeloma and lymphoma cell lines.

218 platin and were up to 10-fold more active in lymphoma cell lines.

219 oma cell lines, primary MCL and other B cell lymphoma cell lines.

220 osphorylated TAK1, p38, and IkappaB-alpha in lymphoma cell lines.

221 rcoma-associated herpesvirus (KSHV)-infected lymphoma cell lines.

222 tle cell, anaplastic large cell, and Hodgkin lymphoma cell lines.

223 f NF-kappaB and p38 and induced apoptosis in lymphoma cell lines.

224 KSHV+ but not in Epstein-Barr virus (EBV)+ B-lymphoma cell lines.

225 nsive apoptosis in a variety of leukemia and lymphoma cell lines.

226 vels were observed in HL and part of Burkitt lymphoma cell lines.

227 n the growth of tumor xenografts produced by lymphoma cell lines.

228 s T cell lymphoma, epidermotropic CD4(+) TRM lymphoma cell localization depended on the presence of h

229 identify APOBEC3G as a prosurvival factor in lymphoma cells, marking APOBEC3G as a potential target f

230 tial observation that guinea pig serum kills lymphoma cells marks the serendipitous discovery of a ne

231 Interestingly, spontaneous myc-induced B lymphoma cells may selectively use NKR-P1B:Clr-b interac

232 ze ordered and disordered domains in mouse B lymphoma cell membranes using super-resolution fluoresce

233 ic Hodgkin lymphoma, inhibits lymphocyte and lymphoma cell motility by activating the RhoA signaling

234 ased spontaneous and chemoattractant-induced lymphoma cell motility.

235 or their activity against L5178 mouse T-cell lymphoma cells (non-MDR) and their subcell line transfec

236 monstrate that, upon induction of apoptosis, lymphoma cells not only activate expression of the tumor

237 ited translation of T-bet in EBV-infected YT lymphoma cells of NK-cell origin.

238 riants were characterized by the presence of lymphoma cells outside the B-cell nodules or B-cell depl

239 phomas overexpressing Mcl-1, but not Emu-myc lymphoma cells overexpressing Bcl-2.

240 ggest that BETi sensitize Myc-overexpressing lymphoma cells partly by inducing HDAC-silenced genes, a

241 manipulation of cellular cholesterol flux in lymphoma cells, promoting cellular cholesterol efflux an

242 MDA-MB-231 breast cancer cells or in DG75 B-lymphoma cells protects cells from apoptosis induced by

243 Acute inactivation of Dnmt1 in primary lymphoma cells rapidly induced apoptosis, indicating tha

244 en cells grew in multicellular aggregates of lymphoma cells rather than in suspension.

245 measured signaling nodes, whereas follicular lymphoma cells represented the opposite pattern with no

246 lymphomas, and down-regulation of E6AP in B-lymphoma cells restored PML expression with a concurrent

247 mal as Rpl22 reexpression in Rpl22-deficient lymphoma cells restores expression of KLF2 and S1P1R, wh

248 ed to modulation of the redox homeostasis in lymphoma cells resulting in oxidative stress.

249 In wild-type (WT) S49 T-lymphoma cells, signaling by cAMP and glucocorticoids co

250 sis-resistant, gammaherpesvirus-associated B lymphoma cells, suggesting a novel mechanism that indica

251 HDAC3 for the proliferation of leukemia and lymphoma cells, suggesting that HDAC3-selective inhibito

252 zed by these antibodies are not expressed in lymphoma cells, suggesting the tumor itself does not tri

253 /interleukin-1 receptor (TIR) domain sustain lymphoma cell survival due to constitutive nuclear facto

254 quitination, NF-kappaB activation, and human lymphoma cell survival.

255 proliferation of human diffuse large B cell lymphoma cells that depend upon aberrant CARD11 signalin

256 s miR-19:miR-92 antagonism is disrupted in B-lymphoma cells that favor a greater increase of miR-19 o

257 rs also reduce lytic reactivation in Burkitt lymphoma cells that have no p53, additional ATM substrat

258 eover, WASp KO mice controlled growth of A20 lymphoma cells that naturally produced IL-2.

259 ng in vitro studies and experiments with S49 lymphoma cells, that cis-autophosphorylation of Ser(338)

260 Lymphoma cells themselves neither expressed PDGFRbeta no

261 mature B cells and homologous CD20+ primary lymphoma cells through monocyte- and antibody-dependent

262 d BCL6 interact in germinal center-derived B lymphoma cells, through the POZ domain of PATZ.

263 decrease in Mcl-1 expression and sensitized lymphoma cells to ABT-737-induced death independently of

264 nd GM-CSF (IFN-DC) and loaded with apoptotic lymphoma cells to activate immune responses against FL c

265 re of EBV-transformed B cells and of Burkitt lymphoma cells to AgAbs led to antigen presentation, T-c

266 potent compounds, to sensitize EBV(+) human lymphoma cells to antiviral agents in vitro.

267 DAC inhibitors effectively sensitized EBV(+) lymphoma cells to ganciclovir.

268 tly, SIRT4 overexpression sensitizes Burkitt lymphoma cells to glucose depletion and synergizes with

269 ells in vitro as multicellular aggregates of lymphoma cells to investigate this question.

270 le cell lymphoma (MCL) and other non-Hodgkin lymphoma cells to lymphoma stromal cells confers drug re

271 increasing the sensitivity of receptor-less lymphoma cells to nutrient restriction.

272 uman B lymphoma cell lines and primary human lymphoma cells to rituximab-induced apoptosis in vitro,

273 ddition, loss of ATF2/7 desensitises Emu-Myc lymphoma cells to spontaneous as well as stress-induced

274 on of miR-34a using antisense RNA sensitized lymphoma cells to therapeutic apoptosis.

275 myc Arf-/- and drug-resistant Emu-myc p53-/- lymphoma cell tumors grown in live mice.

276 c lymphocytic leukemia and lymphoplasmacytic lymphoma cells, two other B cell malignancies that colon

277 is process appear to vary according to the B lymphoma cell type, suggesting that CRAC-channel targeti

278 ed peptides was not detected on B cells or B lymphoma cells under normal culture conditions.

279 ssion of NR4A1 led to a higher proportion of lymphoma cells undergoing apoptosis.

280 unctional testing of primary patient-derived lymphoma cells using a library of 106 US Food and Drug A

281 hibition of S1PR1 expression by shRNA in the lymphoma cells validates that blocking S1PR1 affects exp

282 tly into the spleen and observing a burst of lymphoma cells, validating that the burst originated in

283 hibitor that reduced HL but not other B-cell lymphoma cell viability.

284 ogous gammadelta T cells after exposition to lymphoma cells was dramatically reduced through BTLA-HVE

285 Apoptosis of lymphoma cells was equally induced following Cdc42 or Ra

286 Furthermore, in ixazomib-treated lymphoma cells, we identified that CHK1 was involved in

287 Using the SKW3 human T lymphoma cells, we show that integrin alphaLbeta2 engage

288 Using luciferase-labeled Raji lymphoma cells, we show that the heparanase-neutralizing

289 Finally, multicellular aggregates of lymphoma cells were also found to be less sensitive to p

290 all groups ( approximately 20 cells/well) of lymphoma cells were integrated into reconfigurable PDMS

291 ls but, counterintuitively, c-rel-/- Emu-Myc lymphoma cells were more sensitive to apoptotic stimuli.

292 deaminases family predominantly expressed in lymphoma cells, where it is involved in mutational DSB r

293 , promotes the growth of myeloma and Hodgkin lymphoma cells while inducing apoptosis in chronic lymph

294 the uptake of biotinylated nanoparticles by lymphoma cells with distinct surface antigens pretreated

295 atic activity turn out to be potent only for lymphoma cells with EZH2-activating mutation.

296 uman B cells, whereas treatment of Burkitt's lymphoma cells with inhibitors of the NF-kappaB/IkappaB

297 e expression of wild-type Galpha13 in B-cell lymphoma cells with mutant GNA13 has limited impact in v

298 d in the loss of EBV episomes from Burkitt's lymphoma cells with type I latency and reactivation from

299 rtantly, we identified human CD1d-restricted lymphoma cells within Vdelta1 TCR-expressing PTCL.

300 viral replication in the apoptosis-resistant lymphoma cells without influencing BCR signaling.