ライフサイエンスコーパス: lymphoma cell

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

2 ays that support malignant transformation of lymphoma cells.

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

4 A lumbar puncture sample did not contain lymphoma cells.

5 favor elimination of residual chemoresistant lymphoma cells.

6 chromosome copy number changes affecting all lymphoma cells.

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

8 iral replication in CD95 apoptosis-resistant lymphoma cells.

9 dative stress induction to inhibit growth of lymphoma cells.

10 es a metabolic crisis and selective death of lymphoma cells.

11 nt distribution, and migration properties of lymphoma cells.

12 fected survival rather than proliferation of lymphoma cells.

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

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

15 and glucose utilization in rapamycin-treated lymphoma cells.

16 ectively depleting malignant CD30+ cutaneous lymphoma cells.

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

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

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

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

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

22 h doxorubicin to selectively target and kill lymphoma cells.

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

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

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

26 1, a high-affinity HDL receptor expressed by lymphoma cells.

27 KSHV lytic reactivation in primary effusion lymphoma cells.

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

29 a BCL2 family inhibitor in primary effusion lymphoma cells.

30 s9 screen was performed in EBV and Burkitt's lymphoma cells.

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

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

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

34 activation in KSHV-positive primary effusion lymphoma cells.

35 l as different types of diffuse large B cell lymphoma cells.

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

37 ression of endogenous retroviral elements in lymphoma cells.

38 , on maintenance DNA methylation in Jurkat T lymphoma cells.

39 l lines, clinical samples, and mouse primary lymphoma cells.

40 ey metabolic enzymes and immune receptors in lymphoma cells.

41 little effect on GC formation or GC-derived lymphoma cells.

42 of its transcription network in leukemia and lymphoma cells.

43 a-induced lytic replication in KSHV-positive lymphoma cells.

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

45 se cells could mediate killing of autologous lymphoma cells.

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

47 -grade B cell lymphoma (diffuse large B cell lymphoma) cells.

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

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

50 with HDL NPs in cholesterol uptake-addicted lymphoma cells abolishes GPX4, resulting in cancer cell

51 We show that lymphoma cells abundantly express GSK3alpha and GSK3beta

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

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

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

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

56 EZH2 mutant human lymphoma cells also require multiple divisions before H3

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

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

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

60 4A1 has proapoptotic functions in aggressive lymphoma cells and define NR4A1 as a novel gene with tum

61 analysis during KSHV reactivation in B-cell lymphoma cells and determined RTA-binding sites on both

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

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

64 selectins promote both targeted killing of B lymphoma cells and improved trafficking to sites where t

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

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

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

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

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

70 nal silencing of tumor-suppressing miRNAs in lymphoma cells and reinforce PRMT5's relevance for promo

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

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

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

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

75 omponents of the electron transport chain in lymphoma cells, and many of these effects are independen

76 Although lymphoma cells are efficiently killed by primed T cells,

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

78 Lymphoma cells are subject to higher levels of oxidative

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

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

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

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

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

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

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

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

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

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

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

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

91 Here, we demonstrate that lymphoma cells can directly prime T cells, but in vivo i

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

93 esistance to CX-5461 in previously sensitive lymphoma cells confers collateral resistance to the topo

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

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

96 ve signaling and that its inhibition induces lymphoma cell death, which warrants further clinical eva

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

98 CYCLIN D1, c-MYC, and SURVIVIN, and enhanced lymphoma cell death.

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

100 The lymphoma cells demonstrated chromosome instability along

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

102 Recent data suggest that lymphoma cells dependent upon lipoprotein-mediated chole

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

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

105 Re-expression of individual miRNAs in B-cell lymphoma cells down-regulated expression of PRMT5, CYCLI

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

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

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

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

110 Treated lymphoma cells exhibited a reduced mitochondrial membran

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

112 ates yet was readily cleaved to DON in P493B lymphoma cells, exhibiting a 55-fold enhanced tumor cell

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

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

118 Lymphoma cells from diffuse large B-cell lymphoma patien

119 lignant B cells, 5A6 selectively kills human lymphoma cells from fresh biopsy specimens while sparing

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

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

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

123 Loss of FBXW7 inhibited diffuse large B-cell lymphoma cell growth and further sensitized cells to OxP

124 demonstrated to be functionally important to lymphoma cell growth and proliferation.

125 nd reinforce PRMT5's relevance for promoting lymphoma cell growth and survival.

126 These lymphoma cells had high Lef1 levels and were highly sens

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

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

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

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

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

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

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

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

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

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

137 Culture of the lymphoma cells in simulated microgravity (SMG), and not

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

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

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

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

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

143 sites were gained in the earliest identified lymphoma cells, indicating they are an early and stable

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

145 For example, in low-MYC conditions, lymphoma cells initiate translation of the CD19 mRNA fro

146 During constitutive Salpha CSR in CH12F3 B lymphoma cells, inversional CSR can be activated by inse

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

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

149 For effective lymphoma cell killing in vivo, we further functionalized

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

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

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

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

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

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

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

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

158 me-scale screens of the BCL-2-driven OCI-Ly1 lymphoma cell line after venetoclax exposure along with

159 ects of clofoctol on an EBV-positive Burkitt lymphoma cell line and confirmed the upregulation of all

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

176 ation screen in a CD20xCD3-sensitive human B lymphoma cell line.

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

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

179 loss-of-function screening in eight Burkitt lymphoma cell lines and integrated non-Burkitt lymphoma

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

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

182 Engineered lymphoma cell lines and primary FL B cells carrying muta

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

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

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

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

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

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

189 e myeloid leukemia and anaplastic large-cell lymphoma cell lines by inducing cell-cycle arrest and/or

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

191 pesvirus (KSHV)-transformed primary effusion lymphoma cell lines contain ~70 to 150 copies of episoma

192 EBV-negative Burkitt lymphoma cell lines infected with either wild-type or tw

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

194 or cholesterol depleting therapy, we treated lymphoma cell lines known to be sensitive to the reducti

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

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

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

198 Cultured lymphoma cell lines treated with 4.35 showed dephosphory

199 l growth inhibitory activity in leukemia and lymphoma cell lines with high levels of phosphorylated S

200 All compounds were further tested on six lymphoma cell lines, and eight showed potent growth inhi

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

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

203 C-to-U RNA editing in natural killer cells, lymphoma cell lines, and, to a lesser extent, CD8-positi

204 ng in three different types of non-Hodgkin's lymphoma cell lines, clinical samples, and mouse primary

205 We found that in mantle cell lymphoma cell lines, combined IKZF1/3 degradation with d

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

207 -497, miR-130a, miR24, and miR-155) in human lymphoma cell lines, mice engrafted with patient-derived

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

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

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

211 ulture system of primary human T cells and B lymphoma cell lines, we demonstrate a range of sensitivi

212 e arrest in Burkitt and diffuse large B-cell lymphoma cell lines, which are model cells for studying

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

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

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

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

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

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

219 tive activities against multiple myeloma and lymphoma cell lines.

220 ated to on-target cellular activity in model lymphoma cell lines.

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

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

223 nes that are targeted by PRMT5 in aggressive lymphoma cell lines.

224 raction was effective only in TP53wt Burkitt lymphoma cell lines.

225 nt antiproliferative activity in non-Hodgkin lymphoma cell lines.

226 ity in MM, mantle cell lymphoma, and Burkitt lymphoma cell lines.

227 g enzyme in primary natural killer cells and lymphoma cell lines.

228 were enriched in PDX DLBCL models and human lymphoma cell lines.

229 essential in TP53 wild-type (TP53wt) Burkitt lymphoma cell lines.

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

231 earing mice and human patients compared with lymphoma cell lysates, suggesting a concentration of the

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

233 We also discuss how oncogenic alterations in lymphoma cells may affect the cellular composition of th

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

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

236 ased spontaneous and chemoattractant-induced lymphoma cell motility.

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

238 ed in germinal centre B cells, the Burkitt's lymphoma cell of origin, providing a molecular link betw

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

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

241 Of note, these NPM-ALK+ lymphoma cells overexpress stem cell regulators (OCT4, S

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

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

244 We find that EBV episomes in Burkitt's lymphoma cells preferentially associate with cellular ge

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

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

247 eatment impacts the global myristoylation of lymphoma cell proteins and inhibits early B-cell recepto

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

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

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

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

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

253 ep sequencing from infected primary effusion lymphoma cells revealed that RBP-Jkappa binds nearly exc

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

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

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

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

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

259 edicted targets of these miRNAs, and reduced lymphoma cell survival.

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

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

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

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

264 Lymphoma cells themselves neither expressed PDGFRbeta no

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

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

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

268 phoblastic leukemia and diffuse large B-cell lymphoma cells to anti-CD19 CAR T cells.

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

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

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

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

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

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

275 a binds to centrosomes and microtubules, and lymphoma cells treated with 9-ING-41 become arrested in

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

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

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

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

280 g Zta and associated proteins from Burkitt's lymphoma cells undergoing EBV replication, followed by t

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

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

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

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

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

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

287 within transplanted fully malignant Emu-Myc lymphoma cells, we significantly extended transplant rec

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

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

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

291 A few lymphoma cells were sufficient to activate the angiogeni

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.