ライフサイエンスコーパス: lymphocytic

1 SLAMF9 belongs to the conserved lymphocytic activation molecule family (SLAMF).

2 Signaling lymphocytic activation molecule-associated protein (SAP)

3 signatures of inflammation (IL-18 and IL-6), lymphocytic and myeloid chemotaxis and activation (CCL3,

4 detect and quantify cancer cells, along with lymphocytic and myeloid infiltration by flow cytometry.

5 mmune activation, and altered homeostasis of lymphocytic and myeloid lineages.

6 GNP-HCIm treatment significantly reduced lymphocytic and neutrophil infiltration and mast cells d

7 ts immunoregulatory functional activities on lymphocytic and nonlymphocytic cells during infection, a

8 malignancy uniquely comprising a mixture of lymphocytic and plasmacytic phenotypes.

9 vascular rejection [AR]) or peribronchiolar (lymphocytic bronchiolitis [LB]) distribution, is common

10 kers with respiratory symptoms found to have lymphocytic bronchiolitis and alveolar ductitis with B-c

11 ory specimens, acute cellular rejection, and lymphocytic bronchiolitis are associated with an increas

12 nas isolation, acute cellular rejection, and lymphocytic bronchiolitis remained independent risk fact

13 y events including acute cellular rejection, lymphocytic bronchiolitis, and Pseudomonas isolation aft

14 Lymphocytic bronchitis (LB) precedes CLAD and has a defi

15 ies analyzed viruses produced by transformed lymphocytic cell lines chronically infected with HTLV-1,

16 icant cytoprotection activity on three human lymphocytic cell lines exposed to an aggressive H(2)O(2)

17 ctivity of ADA and inhibits proliferation of lymphocytic cells.

18 atant, consistent with our pro-inflammatory, lymphocytic cellular landscape.

19 destructive, small bile duct, granulomatous lymphocytic cholangitis, with typical seroreactivity for

20 virus (ECTV) when chronically infected with lymphocytic choriomeningitis virus (LCMV) clone 13 (CL13

21 ly shown that mice chronically infected with lymphocytic choriomeningitis virus (LCMV) clone 13 (CL13

22 and hepatitis C virus or those of mice with lymphocytic choriomeningitis virus (LCMV) clone 13 (CL13

23 toire response against a massively exhausted lymphocytic choriomeningitis virus (LCMV) epitope.

24 Recent studies in chronic lymphocytic choriomeningitis virus (LCMV) infection have

25 ced in both CD4(+) and CD8(+) T cells during lymphocytic choriomeningitis virus (LCMV) infection in a

26 of virus-specific CD8 T cells during chronic lymphocytic choriomeningitis virus (LCMV) infection to e

27 In a mouse model of persistent lymphocytic choriomeningitis virus (LCMV) infection, it

28 nt mice exhibit reduced IFN-I responses upon lymphocytic choriomeningitis virus (LCMV) infection, whi

29 during the early stages of acute and chronic lymphocytic choriomeningitis virus (LCMV) infection.

30 dult mice with the clone 13 (CL13) strain of lymphocytic choriomeningitis virus (LCMV) is extensively

31 cine (HB-101) consisting of 2 nonreplicating lymphocytic choriomeningitis virus (LCMV) vectors expres

32 ion-experienced T(regs) generated upon acute Lymphocytic Choriomeningitis Virus (LCMV) WE and Vaccini

33 Lymphocytic choriomeningitis virus (LCMV) WE variant 2.2

34 -cell responses to chimeric vaccines against lymphocytic choriomeningitis virus (LCMV) were assessed

35 uced by chronic infections such as HIV, HPV, lymphocytic choriomeningitis virus (LCMV), and schistoso

36 We infected mice with chronic lymphocytic choriomeningitis virus (LCMV), performed RNA

37 eficient (Prf1 (-/-)) mice are infected with lymphocytic choriomeningitis virus (LCMV).

38 uring acute, but not chronic, infection with lymphocytic choriomeningitis virus (LCMV).

39 tivity against three distinct ssRNA viruses: lymphocytic choriomeningitis virus (LCMV); influenza A v

40 infected Il18-transgenic (Il18tg) mice with lymphocytic choriomeningitis virus (LCMV; strain Armstro

41 cell-dependent antiviral immunity using the lymphocytic choriomeningitis virus Armstrong strain acut

42 e infection with the natural murine pathogen lymphocytic choriomeningitis virus become more resistant

43 Pathogenic HIV or lymphocytic choriomeningitis virus chronic infections di

44 ls without altering Slamf6(+) numbers during lymphocytic choriomeningitis virus clone 13 infection.

45 ssential for viral control during persistent lymphocytic choriomeningitis virus clone 13 infection.

46 ted phenotype during chronic infections with lymphocytic choriomeningitis virus in mice and hepatitis

47 (but not a slow-spreading acute) isolate of lymphocytic choriomeningitis virus induced large-scale m

48 ay) on early T cell attrition in response to lymphocytic choriomeningitis virus infection and during

49 sential for the control of acute and chronic lymphocytic choriomeningitis virus infection in the join

50 Here we demonstrate that chronic lymphocytic choriomeningitis virus infection rapidly tri

51 pDC development and serum IFN-I responses to lymphocytic choriomeningitis virus infection were augmen

52 , as dual TCR cells predominated response to lymphocytic choriomeningitis virus infection, comprising

53 Here we show that, following lymphocytic choriomeningitis virus infection, resident m

54 ed the early T cell attrition resulting from lymphocytic choriomeningitis virus infection.

55 el of perforin (Prf1)(KO) mice infected with lymphocytic choriomeningitis virus to genetically elimin

56 Using murine infection with lymphocytic choriomeningitis virus, we demonstrate that,

57 rs, compromised Ig switch and low avidity of lymphocytic choriomeningitis virus-specific Abs despite

58 8(+) T cell fate during acute infection with lymphocytic choriomeningitis virus.

59 opic colitis (MC) (collagenous colitis (CC), lymphocytic colitis (LC)), traditionally considered rela

60 Furthermore, mice completely lacking the lymphocytic compartment were not protected from epitheli

61 Lymphocytic concentrations and phenotypes were matched w

62 We report multifocal perivascular lymphocytic cuffs contain increased numbers of lymphocyt

63 orn error of human immunity characterized by lymphocytic defects with early-onset Epstein-Barr virus

64 Diagnostic biopsy revealed T-lymphocytic encephalitis in an anti-Drebrin-seropositive

65 the risk allele being associated with lower lymphocytic expression of CALHM6.

66 d populations, but with higher expression of lymphocytic immune suppressive genes.

67 d clinical features, such as amount of tumor lymphocytic infiltrate and proliferation index.

68 In melanoma, the lymphocytic infiltrate is a prognostic parameter classif

69 positivity, and a conspicuous CD8-positive T-lymphocytic infiltrate was present in most tumors.

70 LELC-B lacked features to explain the robust lymphocytic infiltrate, such as loss of mismatch repair

71 included hepatic steatosis, portal fibrosis, lymphocytic infiltrates and ductular proliferation, lobu

72 uctural patterns and spatial distribution of lymphocytic infiltrates and facilitate improved quantifi

73 d by CD90 expression, and dense perivascular lymphocytic infiltrates are uncommon.

74 The majority of the lymphocytic infiltrates were CD4 T-cells.

75 reduced CD3+ and CD68+ cell abundance within lymphocytic infiltrates, and significantly increased sti

76 eta-cells, specifically found in islets with lymphocytic infiltrates.

77 lular fibrosis (rho = 0.527, P < 0.001), and lymphocytic infiltration (rho = 0.435, P < 0.0002).

78 ients requires demonstration of perivascular lymphocytic infiltration in alveolar tissue samples from

79 , LG and spleen, significantly reduced total lymphocytic infiltration into LG, reduced CD3+ and CD68+

80 chronic autoimmune disease characterized by lymphocytic infiltration of exocrine glands, mainly sali

81 secretion, while not significantly impacting lymphocytic infiltration of the LG.

82 ses on chromosome 11, having also the lowest lymphocytic infiltration rate.

83 lacrimal glands showed significantly greater lymphocytic infiltration, higher levels of MHC II, IFN-g

84 w ERCC1 expression correlates with increased lymphocytic infiltration.

85 ft in all the recipients with no evidence of lymphocytic infiltration.

86 Rationale: Acute rejection, manifesting as lymphocytic inflammation in a perivascular (acute periva

87 Granulomatous and lymphocytic interstitial lung disease (GLILD) is a life-

88 nts) and PDGFRB fusion-positive B-cell acute lymphocytic leukaemia (43 [88%] of 49 patients).

89 ewly diagnosed ABL-class fusion B-cell acute lymphocytic leukaemia (77 from European study groups, 25

90 Chronic lymphocytic leukaemia (CLL) is a clonal disorder of matu

91 Chronic lymphocytic leukaemia (CLL) is a highly informative mode

92 used the indolent growth dynamics of chronic lymphocytic leukaemia (CLL) to analyse the growth rates

93 patients with relapsed or refractory chronic lymphocytic leukaemia (CLL) who are on targeted therapie

94 Chronic lymphocytic leukaemia (CLL), the most frequent type of l

95 Experimentally, we focused on chronic lymphocytic leukaemia (CLL), where MIM showed high overa

96 e different mutational precursors of chronic lymphocytic leukaemia (including trisomy 12, loss of chr

97 nces predicted the relative rates of chronic lymphocytic leukaemia (which is more common among Europe

98 ith encouraging activity in advanced chronic lymphocytic leukaemia and B-cell non-Hodgkin lymphoma.

99 GH and AID off-target sites in human chronic lymphocytic leukaemia and mantle cell lymphoma cell line

100 and active in relapsed or refractory chronic lymphocytic leukaemia and mantle cell lymphoma, with a r

101 ibrutinib, in relapsed or refractory chronic lymphocytic leukaemia and mantle cell lymphoma.

102 Eligible patients had untreated chronic lymphocytic leukaemia and were aged 65 years or older, o

103 it has been shown to be expressed on chronic lymphocytic leukaemia cells and on the surface of newly

104 II, which is a phenotypic feature of chronic lymphocytic leukaemia cells, can skew B cell development

105 udy in patients with treatment-naive chronic lymphocytic leukaemia done at 142 academic and community

106 ve, and PDGFRB fusion-positive) B-cell acute lymphocytic leukaemia enrolled in clinical trials of mul

107 t-naive patients with IGHV-unmutated chronic lymphocytic leukaemia enrolled on the CLL8 trial of the

108 Chronic Lymphocytic Leukaemia Global Research Foundation and the

109 Children with ABL-class fusion B-cell acute lymphocytic leukaemia have poor outcomes when treated wi

110 patients with ABL-class fusion B-cell acute lymphocytic leukaemia in the pre-tyrosine-kinase inhibit

111 brutinib is active for patients with chronic lymphocytic leukaemia irrespective of IGHV mutation stat

112 utinib orally once daily (420 mg for chronic lymphocytic leukaemia or 560 mg for mantle cell lymphoma

113 ith relapsed or refractory high-risk chronic lymphocytic leukaemia or mantle cell lymphoma often do n

114 nd older with relapsed or refractory chronic lymphocytic leukaemia or mantle cell lymphoma, with an E

115 years or older with histologically confirmed lymphocytic leukaemia or relapsed or refractory B-cell n

116 ts: relapsed or refractory high-risk chronic lymphocytic leukaemia or small lymphocytic lymphoma (del

117 ith relapsed or refractory high-risk chronic lymphocytic leukaemia or small lymphocytic lymphoma (del

118 n previously untreated patients with chronic lymphocytic leukaemia or small lymphocytic lymphoma inde

119 (61%) of 36 patients with high-risk chronic lymphocytic leukaemia or small lymphocytic lymphoma, 13

120 n patients with previously untreated chronic lymphocytic leukaemia or small lymphocytic lymphoma, eit

121 orted with single-agent ibrutinib in chronic lymphocytic leukaemia or small lymphocytic lymphoma, fol

122 ucil plus obinutuzumab in first-line chronic lymphocytic leukaemia or small lymphocytic lymphoma.

123 homa to 19 (53%) of 36 patients with chronic lymphocytic leukaemia or small lymphocytic lymphoma; inc

124 in the dose-escalation cohort (n=14 chronic lymphocytic leukaemia or small lymphocytic lymphoma; n=1

125 22 in the dose-expansion cohort (n=9 chronic lymphocytic leukaemia or small lymphocytic lymphoma; n=1

126 lled on the CLL8 trial of the German Chronic Lymphocytic Leukaemia Study Group who were treated betwe

127 analyse the outcomes of patients with acute lymphocytic leukaemia treated with anti-CD19 CAR T cells

128 ed combination regimen for frontline chronic lymphocytic leukaemia treatment in younger fit patients.

129 hest ever published in patients with chronic lymphocytic leukaemia unrestricted by prognostic marker

130 and April 23, 2018, 85 patients with chronic lymphocytic leukaemia were enrolled.

131 t-naive patients with IGHV-unmutated chronic lymphocytic leukaemia who might substantially benefit fr

132 r (age <=65 years) fit patients with chronic lymphocytic leukaemia with mutated IGHV.

133 x has a high anti-tumour activity in chronic lymphocytic leukaemia, achieving deep remissions by pote

134 ged 18 years or older, had untreated chronic lymphocytic leukaemia, and coexisting conditions with a

135 ly 3% of children with newly diagnosed acute lymphocytic leukaemia, and studies suggest that leukaemi

136 ven at least one dose of study drug (chronic lymphocytic leukaemia, n=21; mantle cell lymphoma, n=21)

137 ells for relapsed or refractory B-cell acute lymphocytic leukaemia, reported between Jan 1, 2012, and

138 tients with acute myeloid leukaemia or acute lymphocytic leukaemia, who received a HSCT at any age fr

139 ne-kinase inhibitor with activity in chronic lymphocytic leukaemia.

140 the setting of relapsed or refractory acute lymphocytic leukaemia.

141 r patients with previously untreated chronic lymphocytic leukaemia.

142 n patients with relapsed or refractory acute lymphocytic leukaemia.

143 e development of clinically apparent chronic lymphocytic leukaemia.

144 mab in patients with treatment-naive chronic lymphocytic leukaemia.

145 re standard first-line treatments in chronic lymphocytic leukaemia.

146 n patients with refractory or relapsed acute lymphocytic leukaemia.

147 or younger with previously untreated chronic lymphocytic leukaemia.

148 with non-Hodgkin B-cell lymphoma and chronic lymphocytic leukaemia.

149 with non-Hodgkin B-cell lymphoma and chronic lymphocytic leukaemia.

150 sponses in younger fit patients with chronic lymphocytic leukaemia.

151 aive patients (aged >=18 years) with chronic lymphocytic leukaemia.

152 t-naive patients with IGHV-unmutated chronic lymphocytic leukaemia.

153 unotherapy regimen for patients with chronic lymphocytic leukaemia.

154 n patients with previously untreated chronic lymphocytic leukaemia.

155 treatment regimen for patients with chronic lymphocytic leukaemia.

156 nts with treatment-naive symptomatic chronic lymphocytic leukaemia.

157 patients with ABL-class fusion B-cell acute lymphocytic leukaemia.

158 ibrutinib (420 mg for patients with chronic lymphocytic leukaemia; 560 mg for patients with B-cell n

159 with non-Hodgkin B-cell lymphoma and chronic lymphocytic leukaemia; and evaluation of the anti-glycop

160 dgkin lymphoma (3.53 [.48-25.9]) and chronic lymphocytic leukemia (1.45 [.45-4.66]) were increased bu

161 at residue 1099 (E1099K) in childhood acute lymphocytic leukemia (ALL), and cells harboring this mut

162 role for infection in the etiology of acute lymphocytic leukemia (ALL), and the involvement of the i

163 Clonal expansion of B cell chronic lymphocytic leukemia (B-CLL) occurs within lymphoid tiss

164 f B cell neoplasms, including B cell chronic lymphocytic leukemia (B-CLL).

165 inhibitors (BTKi's) are effective in chronic lymphocytic leukemia (CLL) after previous progression on

166 sequencing of multiple myeloma (MM), chronic lymphocytic leukemia (CLL) and acute myeloid leukemia, w

167 ersely correlated with DNA damage in chronic lymphocytic leukemia (CLL) and lymphoma patient-derived

168 b has been approved for treatment of chronic lymphocytic leukemia (CLL) and non-Hodgkin lymphoma, but

169 rs, current treatment strategies for chronic lymphocytic leukemia (CLL) are not curative, and the sea

170 ole for tumor-expressed CTLA-4 using chronic lymphocytic leukemia (CLL) as a disease model.

171 r were more effectively activated by chronic lymphocytic leukemia (CLL) B-cell targets opsonized with

172 ession is a recognized phenomenon in chronic lymphocytic leukemia (CLL) but its biological basis rema

173 re present in approximately 4-13% of chronic lymphocytic leukemia (CLL) cases, where they are associa

174 Chronic lymphocytic leukemia (CLL) cells cycle between lymph nod

175 nd ROR1 are expressed in circulating chronic lymphocytic leukemia (CLL) cells, and because in other c

176 The prognosis of chronic lymphocytic leukemia (CLL) depends on different markers,

177 ty and mortality among patients with chronic lymphocytic leukemia (CLL) due to immune dysfunction and

178 The treatment of chronic lymphocytic leukemia (CLL) has been revolutionized by ta

179 The management of chronic lymphocytic leukemia (CLL) has undergone dramatic change

180 n patients with previously untreated chronic lymphocytic leukemia (CLL) have been limited.

181 om 841 treatment-naive patients with chronic lymphocytic leukemia (CLL) identified 89 (11%) patients

182 up substantially since then, and the chronic lymphocytic leukemia (CLL) incidence has increased conti

183 Targeted therapies for chronic lymphocytic leukemia (CLL) include venetoclax, the oral

184 Chronic lymphocytic leukemia (CLL) is a heterogenous disease tha

185 Chronic lymphocytic leukemia (CLL) is a malignancy of mature B c

186 The treatment landscape for chronic lymphocytic leukemia (CLL) is rapidly evolving.

187 Chronic lymphocytic leukemia (CLL) is the most common adult leuk

188 Chronic lymphocytic leukemia (CLL) is the most common human leuk

189 aD910A/D910A) in the Emu-TCL1 murine chronic lymphocytic leukemia (CLL) model impaired B cell recepto

190 Chronic lymphocytic leukemia (CLL) occurs in 2 major forms: aggr

191 for previously treated patients with chronic lymphocytic leukemia (CLL) or small lymphocytic lymphoma

192 NOTCH1 is mutated in 10% of chronic lymphocytic leukemia (CLL) patients and is associated wi

193 morbidities, and immune dysfunction, chronic lymphocytic leukemia (CLL) patients may be at particular

194 nses in relapsed or refractory (R/R) chronic lymphocytic leukemia (CLL) patients treated with CD19-ta

195 k, untreated, and previously treated chronic lymphocytic leukemia (CLL) patients.

196 tinib resistance have suggested that chronic lymphocytic leukemia (CLL) progression on ibrutinib is l

197 B-cell chronic lymphocytic leukemia (CLL) results from accumulation of

198 Chronic lymphocytic leukemia (CLL) risk stratification studies t

199 Chronic lymphocytic leukemia (CLL) therapy has changed dramatica

200 re established prognostic factors in chronic lymphocytic leukemia (CLL) treated with chemoimmunothera

201 rituximab in patients with relapsed chronic lymphocytic leukemia (CLL) was terminated early because

202 Patients with chronic lymphocytic leukemia (CLL) who achieve blood or bone mar

203 Treatment of patients with chronic lymphocytic leukemia (CLL) with inhibitors of Bruton's t

204 In chronic lymphocytic leukemia (CLL), acquired T-cell dysfunction

205 In chronic lymphocytic leukemia (CLL), AID is overexpressed in the

206 has shown activity in patients with chronic lymphocytic leukemia (CLL), but its efficacy in combinat

207 SF3B1 is recurrently mutated in chronic lymphocytic leukemia (CLL), but its role in the pathogen

208 leukemia but are less effective for chronic lymphocytic leukemia (CLL), focusing attention on improv

209 re associated with increased risk of chronic lymphocytic leukemia (CLL), follicular lymphoma (FL), an

210 In chronic lymphocytic leukemia (CLL), intra-tumoral DNA methylatio

211 Within chronic lymphocytic leukemia (CLL), responses to 62% of drugs we

212 In chronic lymphocytic leukemia (CLL), signaling through several pr

213 gy in B-cell malignancies, including chronic lymphocytic leukemia (CLL).

214 a remarkable prognostic biomarker of chronic lymphocytic leukemia (CLL).

215 kemia (T-ALL) and RPS15 mutations in chronic lymphocytic leukemia (CLL).

216 effective therapy for patients with chronic lymphocytic leukemia (CLL).

217 patients with relapsed or refractory chronic lymphocytic leukemia (CLL).

218 eviously untreated (first line [1L]) chronic lymphocytic leukemia (CLL).

219 improved outcomes for patients with chronic lymphocytic leukemia (CLL).

220 ant for treatment decision-making in chronic lymphocytic leukemia (CLL).

221 inherited genetic predisposition to chronic lymphocytic leukemia (CLL).

222 n in many types of cancer, including chronic lymphocytic leukemia (CLL).

223 formed the therapeutic landscape for chronic lymphocytic leukemia (CLL).

224 r patients with previously untreated chronic lymphocytic leukemia (CLL).

225 have been approved for patients with chronic lymphocytic leukemia (CLL).

226 nd bendamustine in older adults with chronic lymphocytic leukemia (CLL).

227 ion and function and is disturbed in chronic lymphocytic leukemia (CLL).

228 to analyze CSs and apply it to study chronic lymphocytic leukemia (CLL).

229 tive-site occupancy in patients with chronic lymphocytic leukemia (CLL)/small lymphocytic lymphoma (S

230 survival outcomes for patients with chronic lymphocytic leukemia (CLL)/small lymphocytic lymphoma (S

231 ow-grade B-cell lymphoma (n = 8), or chronic lymphocytic leukemia (CLL; n = 7).

232 ctors for basal cell carcinomas were chronic lymphocytic leukemia (P = 0.003), reduced-intensity cond

233 mas were increased age (P < 0.0001), chronic lymphocytic leukemia (P = 0.02), and chronic graft-versu

234 (DLBCL; n = 34), DLBCL arising from chronic lymphocytic leukemia (Richter transformation; n = 7), Wa

235 cording to International Workshop on Chronic Lymphocytic Leukemia 2008 criteria.

236 undred thirty-eight patients (307 with acute lymphocytic leukemia [ALL], 311 with non-Hodgkin's lymph

237 e cancers (non-Hodgkin's lymphoma or chronic lymphocytic leukemia [CLL]).

238 le immunocompromised individual with chronic lymphocytic leukemia and acquired hypogammaglobulinemia.

239 oader utility in analogous models of chronic lymphocytic leukemia and breast adenocarcinoma and perfo

240 plication of these new techniques to chronic lymphocytic leukemia and examine the insights already at

241 tter understand the heterogeneity of chronic lymphocytic leukemia and how mutations, activation state

242 nase inhibition by ibrutinib in both chronic lymphocytic leukemia and mantle cell lymphoma (MCL).

243 and for monocytes from patients with chronic lymphocytic leukemia being treated with ibrutinib.

244 r mitochondrial membrane potential of single lymphocytic leukemia cells and demonstrate that mitochon

245 red growth efficiency of pseudodiploid mouse lymphocytic leukemia cells during normal proliferation a

246 on of BTK in patient-derived primary chronic lymphocytic leukemia cells.

247 treated with chemoimmunotherapy for chronic lymphocytic leukemia experienced a 9-week course of COVI

248 e show that venetoclax resistance in chronic lymphocytic leukemia is associated with complex clonal s

249 highly effective targeted agents for chronic lymphocytic leukemia offers the potential for fixed-dura

250 tion for relapsed or refractory (RR) chronic lymphocytic leukemia or small lymphocytic lymphoma (SLL)

251 erogeneity within primary cells from chronic lymphocytic leukemia patients, but it can be adapted to

252 A expression was decreased in B cell chronic lymphocytic leukemia samples compared with healthy contr

253 od and Drug Administration-approved drug for lymphocytic leukemia treatment, was administered intrape

254 with B cell non-Hodgkin lymphoma or chronic lymphocytic leukemia were treated on a phase 1 dose esca

255 e, 43-83 years), and 14 patients had chronic lymphocytic leukemia, 2 had classic Hodgkin lymphoma, an

256 matopoiesis, acute myeloid leukemia, chronic lymphocytic leukemia, and a variety of solid tumors.

257 owth and proliferation in pancreatic cancer, lymphocytic leukemia, and multiple myeloma.

258 ecules (SFMBT1, CBX7, and EZH1) with chronic lymphocytic leukemia, and supported CDK6 as a disease-sp

259 rically derived treatment of pediatric acute lymphocytic leukemia, can consistently achieve curative

260 ria of the International Workshop on Chronic Lymphocytic Leukemia, had received at least three cycles

261 ility Genes, Genetic Epidemiology of Chronic Lymphocytic Leukemia, Impact of Remote Familial Colorect

262 In B-cell chronic lymphocytic leukemia, this is associated with poor progn

263 Crohn's disease, multiple sclerosis, chronic lymphocytic leukemia, veno-occlusive disease with immuno

264 l lymphoma, follicular lymphoma, and chronic lymphocytic leukemia, were enrolled.

265 We further determined that the chronic lymphocytic leukemia-associated H266L substitution signi

266 penetrance of cutaneous melanoma and chronic lymphocytic leukemia.

267 ine-rituximab in relapsed/refractory chronic lymphocytic leukemia.

268 as diffuse large B cell lymphoma and chronic lymphocytic leukemia.

269 -derived curative therapy in childhood acute lymphocytic leukemia.

270 s-of-function mutations recurrent in chronic lymphocytic leukemia.

271 d therapy over chemoimmunotherapy in chronic lymphocytic leukemia.

272 Chronic lymphocytic leukemia/small lymphocytic lymphoma (CLL/SLL

273 U2), was evaluated in patients with chronic lymphocytic lymphoma (CLL) or non-Hodgkin lymphoma (NHL)

274 Chronic lymphocytic leukemia/small lymphocytic lymphoma (CLL/SLL) and follicular lymphoma (

275 -risk chronic lymphocytic leukaemia or small lymphocytic lymphoma (del17p or del11q), follicular lymp

276 -risk chronic lymphocytic leukaemia or small lymphocytic lymphoma (del17p or del11q), follicular lymp

277 y (RR) chronic lymphocytic leukemia or small lymphocytic lymphoma (SLL) and RR follicular lymphoma (F

278 chronic lymphocytic leukemia (CLL) or small lymphocytic lymphoma (SLL) enrolled in 4 early-phase tri

279 ith chronic lymphocytic leukemia (CLL)/small lymphocytic lymphoma (SLL) that was maintained at 24 hou

280 ith chronic lymphocytic leukemia (CLL)/small lymphocytic lymphoma (SLL).

281 with chronic lymphocytic leukaemia or small lymphocytic lymphoma independent of high-risk features a

282 -risk chronic lymphocytic leukaemia or small lymphocytic lymphoma, 13 (33%) of 40 patients with folli

283 oved for B-cell malignancies like CLL, small lymphocytic lymphoma, and so forth.

284 eated chronic lymphocytic leukaemia or small lymphocytic lymphoma, either aged 65 years or older or y

285 ib in chronic lymphocytic leukaemia or small lymphocytic lymphoma, follicular lymphoma, and diffuse l

286 -line chronic lymphocytic leukaemia or small lymphocytic lymphoma.

287 with chronic lymphocytic leukaemia or small lymphocytic lymphoma; incidence of grade 3-4 anaemia ran

288 (n=14 chronic lymphocytic leukaemia or small lymphocytic lymphoma; n=10 B-cell non-Hodgkin lymphoma)

289 (n=9 chronic lymphocytic leukaemia or small lymphocytic lymphoma; n=13 B-cell non-Hodgkin lymphoma).

290 A prominent lymphocytic matrix metallopeptidase cell migration pathw

291 Lymphocytic myocarditis was observed in one patient with

292 od-onset antibody defects, cytopenias, and T lymphocytic pneumonitis and colitis, with reduced periph

293 Recently, it has been shown that lymphocytic populations can be very heterogeneous, and t

294 n more accurate classification of tumour and lymphocytic regions, is motivated by the biological defi

295 and microglia activation in the absence of a lymphocytic response.

296 Lymphocytic responses crucial for immune surveillance, i

297 The most common cause in adults is chronic lymphocytic thyroiditis (Hashimoto thyroiditis), but the

298 most indistinguishable, whereas Grade I with lymphocytic vasculitis was an easy and reproducible hist

299 Grade 0 Banff rejection and Grade I without lymphocytic vasculitis were almost indistinguishable, wh

300 lar components was performed with a focus on lymphocytic vasculitis, intravascular fibrin, vessel cal