ライフサイエンスコーパス: HCL

1 HCL responds well to purine analogs but relapses are fre

2 8 (40%) HCLv and 6 (10%) classic (P = .004) HCL patients.

3 real-time PCR assay and validated it in 117 HCL patients and 102 non-HCL/BRAFwt patients.

4 A total of 115 of 117 HCL (98.3%) demonstrated percentage BRAFV600E/BRAFwt abo

5 The remaining 2 of 117 HCL with lower percentage BRAFV600E/BRAFwt ratios were a

6 onding to "non-HCL." Follow-up studies in 19 HCL cases demonstrated a decrease of percentage BRAFV600

7 We analyzed the course of 21 HCL patients treated with vemurafenib outside of trials

8 ed after prior treatment with cladribine, 24 HCL pts (21 male, 3 female) with a median age of 53.5 ye

9 VH4-34(+) HCL is an important disorder that only partly overlaps w

10 Data on 350 HCL patients was obtained from the M.D. Anderson Cancer

11 Analysis of 51 HCL patients demonstrated that 18 were CD38-positive.

12 n-HCL chronic B-cell neoplasms, including 79 HCL-like disorders, were invariably negative for BRAF-V6

13 Forty-nine patients with active HCL were treated with 2-CdA by continuous intravenous in

14 The BRAF V600E mutation was detected in all HCL cases and in only 2 of the remaining 178 patients.

15 ies occurred in 11 (24%) of 46 patients (all HCL).

16 ecular assays for detecting BRAF V600E allow HCL (highly responsive to purine analogs) to be better d

17 pical gel containing baclofen, amitriptyline HCL, and ketamine, these agents may be offered on the ba

18 ons of circulating HCL cells (P = .002), and HCL spleen size (P < .001).

19 sitivity was significantly higher in CLL and HCL in terms of percentage (65.9% and 67.8%, respectivel

20 lastic clone in 20 adults with LCH, ECD, and HCL.

21 based differential diagnosis between HCL and HCL-like tumors, even noninvasively in routine blood sam

22 henotypically defined HCL variant (HCLv) and HCL expressing the IGHV4-34 immunoglobulin rearrangement

23 20% of patients with the diagnosis of HD and HCL; more than 50% of patients with NHL, CLL, and CML su

24 rs (e.g., splenic marginal zone lymphoma and HCL variant).

25 , 1430); a score of 0 excluded CLL, MCL, and HCL; and the CD23/CD5 ratio differentiated CLL from leuk

26 o additional mutants, altered in the NSP and HCL genes, which show root hair branching in response to

27 6 mmol/L, P < 0.001), whereas hepatic Pi and HCL were similar in patients when compared with CON.

28 enetics-based differential diagnosis between HCL and HCL-like tumors, even noninvasively in routine b

29 e kinase (MEK) reach their targets and cause HCL cell death

30 roportional to concentrations of circulating HCL cells (P = .002), and HCL spleen size (P < .001).

31 arly diverging (EDL) and higher core clades (HCL).

32 ht patients with purine analog-naive classic HCL were randomly assigned 1:1 to concurrent versus dela

33 variant HCL forms and in a subset of classic HCL (HCLc).

34 Fifty-three classic HCL (HCLc) and 16 HCLv cases were analyzed for BRAF, inc

35 Occasionally, patients with classic HCL respond poorly.

36 articularly for the 41 patients with classic HCL suggested any superiority of DCFR vs BR might apply

37 th HCLv and 63 from 62 patients with classic HCL.

38 ated with cladribine from the Scripps Clinic HCL Database, of whom 83 were evaluable for response.

39 FCRL1-positive malignancies, including CLL, HCL, FL, MCL, and other B-NHL.

40 oncentrations (hepatocellular lipid content [HCL]) were measured with multinuclei magnetic resonance

41 , including the immunophenotypically defined HCL variant (HCLv) and HCL expressing the IGHV4-34 immun

42 ave treated 13 patients with newly diagnosed HCL (n = 11) or after failure of one prior chemotherapy

43 f HCL that require different treatments (eg, HCL-variant and splenic marginal zone lymphoma).

44 tibody proved effective against pre-existing HCL tumors.

45 t single-agent activity in cladribine-failed HCL patients when compared with other agents active in t

46 did not fulfill the diagnostic criteria for HCL.

47 r without CGM) or the intervention group for HCL therapy.

48 .7 years) showed an excellent PFS and OS for HCL patients after 2-CdA treatment.

49 L patients and are therefore recommended for HCL patients regardless of age.

50 Therapy for HCL includes splenectomy, interferon alfa-2a and alfa-2b

51 ival from the advent of systemic therapy for HCL was better than before this time (P = .0009).

52 is sometimes difficult to differentiate from HCL-like disorders (e.g., splenic marginal zone lymphoma

53 ine analogs) to be better distinguished from HCL-like disorders, which are treated differently.

54 All the patients who had HCL that had been refractory to chemotherapy (10 patient

55 domly assigned to receive either hydralazine HCL (25 mg, thrice daily) or a placebo for 12 months.

56 8 microg/mL) and tetracycline hydrochloride (HCL) (only 30.2% susceptible) against A. baumannii isola

57 These data identify HCL as having the highest frequency of CDKN1B mutations

58 confirmed by the demonstration of VCAM-1 in HCL spleen and by the fact that, in frozen sections, HCs

59 ut as a useful marker in HCL, its absence in HCL variant, and developed an RT-PCR-based assay to moni

60 ool for improving the diagnostic accuracy in HCL.

61 BL22 was active in HCL, with 19 complete remissions (CRs; 61%) and six part

62 BL22 activity in HCL is confirmed.

63 Its activity in HCL was unknown, so we conducted a multisite phase 2 stu

64 assay to monitor minimal residual disease in HCL.

65 2 was well tolerated and highly effective in HCL, even after one cycle.

66 ion as the disease-defining genetic event in HCL.

67 r, our data indicate that CD38 expression in HCL drives poor prognosis by promoting survival and hete

68 ermine the cause of CD11c gene expression in HCL the CD11c gene promoter was characterized.

69 ors, somatic hypermutation (SHM) features in HCL were examined in a series of 130 immunoglobulin gene

70 Rituximab should be explored further in HCL with regard to eradication of minimal residual disea

71 Knockout of the CD38 gene in HCL cells increased apoptosis, inhibited adherence to en

72 1B as the second most common mutated gene in HCL.

73 eveal what role these therapies will have in HCL treatment.

74 e clinical use of BRAF and MEK inhibitors in HCL.

75 , we confirmed BRAFmut as a useful marker in HCL, its absence in HCL variant, and developed an RT-PCR

76 We conclude that eradication of MRD in HCL is possible.

77 BRAF-V600E is the key driver mutation in HCL and distinguishes it from other B-cell lymphomas, in

78 CYC2-like paralogs in HCL show differential expression with higher expression

79 lar signal-regulated kinase (ERK) pathway in HCL by exposing in vitro primary leukemic cells purified

80 ter therapy, pointing to its pivotal role in HCL pathogenesis and maintenance of the leukemic clone.

81 n regulation of cell cycle and senescence in HCL with CDKN1B mutations.

82 F and MEK inhibitors caused, specifically in HCL (but not HCL-like) cells, marked MEK/ERK dephosphory

83 so represents an ideal therapeutic target in HCL.

84 significant activity and minimal toxicity in HCL and warrants further study.

85 mab, but there are few reports of its use in HCL.

86 HCL and likely cooperate with BRAF-V600E in HCL pathogenesis.

87 es it from other B-cell lymphomas, including HCL-like leukemias/lymphomas (HCL-variant and splenic ma

88 opsies of patients with hairy cell leukemia (HCL) after treatment with 2-chlorodeoxyadenosine (2-CdA)

89 l lymphomas, 4 cases of hairy cell leukemia (HCL) and 3 plasmacytomas.

90 eported in all cases of hairy cell leukemia (HCL) but not in other peripheral B-cell neoplasms.

91 as recently detected in hairy cell leukemia (HCL) by whole exome sequencing.

92 ses, 100% (32 of 32) of hairy cell leukemia (HCL) cases, 15% (5 of 34) of mantle cell lymphoma (MCL)

93 Hairy cell leukemia (HCL) derives from a mature B cell and expresses markers

94 d first-line therapy of hairy cell leukemia (HCL) for 30 years.

95 f effective therapy for hairy cell leukemia (HCL) has increased the relevance of long-term outcome.

96 Hairy-cell leukemia (HCL) is a CD20+ indolent B-cell cancer in which a BRAF V

97 Hairy cell leukemia (HCL) is a chronic B-cell leukemia noted for an indolent

98 Hairy cell leukemia (HCL) is a chronic lymphoproliferative disease, the cause

99 Hairy cell leukemia (HCL) is a chronic mature B-cell neoplasm with unique cli

100 Hairy cell leukemia (HCL) is a distinct clinicopathologic entity that respond

101 Hairy cell leukemia (HCL) is a distinct clinicopathological entity whose unde

102 Hairy cell leukemia (HCL) is a rare B-cell malignancy, and there is a need fo

103 Hairy cell leukemia (HCL) is a rare, indolent B-cell disorder in which single

104 Hairy cell leukemia (HCL) is an indolent B-cell neoplasm, strongly expressing

105 Hairy cell leukemia (HCL) is an uncommon, indolent, chronic B-cell lymphoprol

106 Hairy cell leukemia (HCL) is characterized by underexpression of the intracel

107 Cladribine treatment of hairy cell leukemia (HCL) is complicated by neutropenic fever in 42% of patie

108 Hairy cell leukemia (HCL) is marked by near 100% mutational frequency of BRAF

109 One hairy cell leukemia (HCL) patient achieved a complete remission, which is ong

110 Hairy cell leukemia (HCL) responds very well to frontline chemotherapy with p

111 Hairy cell leukemia (HCL) shows unique clinicopathological and biological fea

112 B1 (BRAF) mutations in hairy cell leukemia (HCL) subsets, demonstrating that BRAF V600E mutations ar

113 To compare hairy cell leukemia (HCL) with chronic lymphocytic leukemia (CLL) and normal

114 rates in patients with hairy cell leukemia (HCL), a significant number of patients eventually relaps

115 lymphoma (FL), 13 of 17 hairy cell leukemia (HCL), and 2 of 3 mantle cell lymphoma (MCL).

116 ytic leukemia (CLL) and hairy cell leukemia (HCL), are associated with myelosuppression and profound

117 ignancies, particularly hairy cell leukemia (HCL), but its soluble extracellular domain, sCD22, has n

118 jority of patients with hairy cell leukemia (HCL), neither the actual relapse rate, the clinical fact

119 Hodgkin's disease (HD), hairy cell leukemia (HCL), non-Hodgkin's lymphoma (NHL), chronic lymphocytic

120 key driver mutation in hairy cell leukemia (HCL), suggesting opportunities for therapeutic targeting

121 However, in hairy cell leukemia (HCL), these processes are particularly prominent and res

122 00E driving mutation in hairy cell leukemia (HCL),provide extensive laboratory studies showing that i

123 s a molecular marker of hairy cell leukemia (HCL).

124 ssions in patients with hairy cell leukemia (HCL).

125 t of choice in treating hairy cell leukemia (HCL).

126 relapsed or refractory hairy cell leukemia (HCL).

127 hematopoietic neoplasm hairy cell leukemia (HCL).

128 enic driver mutation in hairy cell leukemia (HCL).

129 in 16% of patients with hairy cell leukemia (HCL).

130 st-line monotherapy for hairy cell leukemia (HCL); however, patients continue to relapse.

131 lymphoma (FL; n = 44), hairy cell leukemia (HCL; n = 15), and reactive lymphoid hyperplasia (n = 14)

132 oach detected BRAF-V600E in all 123 leukemic HCL samples investigated containing as few as 0.1% leuke

133 Reconstitution of RhoH expression limits HCL pathogenesis in a mouse model, indicating this could

134 ds were measured [Deltahepatocellular lipid (HCL)_healthy_baseline: -15.9 +/- 10.7 compared with +/-

135 Hybrid closed-loop (HCL) therapy has improved glycemic control in children a

136 ude that most cases of mantle cell lymphoma, HCL, and plasmacytoma show high levels of pRB in contras

137 mas, including HCL-like leukemias/lymphomas (HCL-variant and splenic marginal zone lymphoma).

138 analogs (p=0.021) and lower baseline marrow HCL/HCLv infiltration (p=0.013).

139 ent a new Homeostatic-Circadian-Light model (HCL) which is simpler, more transparent and more computa

140 fter growing under elevated CO2 (1000 muatm, HCL, pHT : 7.70) for 1860 generations, showed significan

141 validated it in 117 HCL patients and 102 non-HCL/BRAFwt patients.

142 Conversely, 115 non-HCL chronic B-cell neoplasms, including 79 HCL-like diso

143 RAFV600E/BRAFwt values corresponding to "non-HCL." Follow-up studies in 19 HCL cases demonstrated a d

144 ibitors caused, specifically in HCL (but not HCL-like) cells, marked MEK/ERK dephosphorylation, silen

145 ive (O/E, 6.17; P < .001), mainly because of HCL-related infections and secondary malignancy.

146 s BRAF status in well-characterized cases of HCL associated with poor prognosis, including the immuno

147 intrinsic cell activation characteristic of HCL and the HC's consequent ability to interact with mat

148 pression of the CD11c gene characteristic of HCL is dependent upon activation of the proto-oncogenes

149 p sequencing of CDKN1B in a larger cohort of HCL patients identify deleterious CDKN1B mutations in 16

150 athogenesis or affect the clinical course of HCL are currently not described.

151 Achieving MRD-free CR of HCL after first-line cladribine is greatly enhanced by c

152 less need for additional therapy or cure of HCL.

153 idual disease (MRD) and potentially cured of HCL.

154 These data provide proof of dependence of HCL on active BRAF signaling.

155 pensive test for genetics-based diagnosis of HCL in whole-blood samples that detects BRAF-V600E throu

156 Diagnostic of HCL is abnormal expression of the gene that encodes the

157 ew insights into the mechanism of disease of HCL have led to research in new potential treatment agen

158 th type 1 diabetes; however, the efficacy of HCL on glycemic and psychosocial outcomes has not yet be

159 ow recognized as the causal genetic event of HCL because it is somatic, present in the entire tumor c

160 nd 3 of 19 (16%) had morphologic evidence of HCL in hematoxylin and eosin-stained bone marrow section

161 Clinical and molecular features of HCL and HCLv has not been compared.

162 , BRAF-V600E shapes key biologic features of HCL, including its specific expression signature, hairy

163 F-V600E kinase (the pathogenetic hallmark of HCL) through orally available specific inhibitors (vemur

164 her B-cell neoplasms, including mimickers of HCL that require different treatments (eg, HCL-variant a

165 this randomized clinical trial, 6 months of HCL therapy significantly improved glycemic control and

166 The enigmatic pathogenesis of HCL was recently clarified by the discovery of its under

167 e key event in the molecular pathogenesis of HCL.

168 e of CDKN1B mutations in the pathogenesis of HCL.

169 mutation plays a role in the pathogenesis of HCL.

170 olecular mechanisms underlying resistance of HCL cells to BRAF inhibitors.

171 der to probe the isotype switching status of HCL, RNA transcripts of V(H)DJ(H)--constant region seque

172 lgrastim with cladribine in the treatment of HCL cannot be recommended.

173 ilgrastim and cladribine in the treatment of HCL.

174 one of the best agents for the treatment of HCL.

175 icle was to report the extended follow-up of HCL patients treated with cladribine.

176 is new marker for diagnosis and follow-up of HCL, we developed a BRAFV600Emut-specific quantitative r

177 All cases of (HCL) and plasmacytoma showed strong pRB staining.

178 safely administered to patients with CLL or HCL without a significantly increased risk of secondary

179 in cutaneous T-cell lymphoma (one patient), HCL (three patients), chronic lymphocytic leukemia (one

180 Our data also indicate that CD38-positive HCL patients might benefit from treatments based on CD38

181 d patients with BRAF V600E mutation-positive HCL refractory to first-line treatment with a purine ana

182 e patients with BRAF V600E mutation-positive HCL were enrolled.

183 psed/refractory BRAF V600E mutation-positive HCL.

184 psed/refractory BRAF V600E mutation-positive HCL.

185 In vitro preclinical studies on purified HCL cells proved that BRAF and MEK inhibitors can induce

186 In addition, combined exposure of aBL and Q-HCL did not result in any significant apoptosis when exp

187 biofilms) when aBL was illuminated during Q-HCL exposure.

188 ed the capacity for quinine hydrochloride (Q-HCL) to enhance the antimicrobial effects of antimicrobi

189 Furthermore, the addition of Q-HCL significantly potentiated the antimicrobial effects

190 In conclusion, aBL in combination with Q-HCL may offer a novel approach for the treatment of infe

191 tional landscape of purine analog refractory HCL.

192 uximab, patients with relapsed or refractory HCL.

193 patients with relapsed or primary refractory HCL after nucleoside analogs received rituximab 375 mg/m

194 R) from 2004 to 2010 for relapsed/refractory HCL after first-line cladribine (n = 3) or after multipl

195 g QOD x3 has activity in relapsed/refractory HCL and has a safety profile that supports further clini

196 e therapeutic option for relapsed/refractory HCL.

197 gation of the clinical record of 23 relapsed HCL patients demonstrated those that were CD38-positive

198 R were highly effective in multiply relapsed HCL/HCLv.

199 volving patients with refractory or relapsed HCL, the targeting of BRAF V600E with the oral BRAF inhi

200 volving patients with refractory or relapsed HCL, we assessed the safety and efficacy of vemurafenib

201 in most patients with refractory or relapsed HCL.

202 overall response rate of refractory/relapsed HCL patients to the BRAF inhibitor vemurafenib approache

203 Sixteen HCL-variant patients showed percentage BRAFV600E/BRAFwt

204 Patches prepared using PVP and TE-HCL displayed enhanced hydrophobicity.

205 r antibiotic (tetracycline hydrochloride, TE-HCL) patches using polycaprolactone (PCL), polyvinyl pyr

206 FTIR demonstrated successful TE-HCL encapsulation in aligned fibers.

207 ro susceptibility testing using tetracycline HCL as a surrogate for the susceptibility other tetracyc

208 phenotype to Mtnin, but we demonstrate that HCL is not required in this process.

209 These results indicate that HCL is potentially curable after cladribine treatment.

210 The HCL population had lower mitochondrial respiration, than

211 a second cancer at least 6 months after the HCL diagnosis (O/E ratio, 1.34; P = .08).

212 62.5% (12.0%) at the end of the study in the HCL group and from 54.6% (12.5%) to 56.1% (12.2%) in the

213 expression signature, downregulation of the HCL markers CD25, tartrate-resistant acid phosphatase, a

214 pathway transcriptional output, loss of the HCL-specific gene expression profile signature, change o

215 pathway transcriptional output, loss of the HCL-specific gene expression signature, downregulation o

216 sought to identify druggable proteins on the HCL surface that were dependent upon RhoH underexpressio

217 andomized to the control group and 67 to the HCL group.

218 vivo to BRAF inhibitors are spoiled of their HCL identity and then undergo apoptosis.

219 rating genetic events that may contribute to HCL pathogenesis or affect the clinical course of HCL ar

220 h the histiocytic disorders were distinct to HCL.

221 atients with previously untreated or treated HCL were treated with 2-CdA at a dose of 0.1 mg/kg/d by

222 in vivo in samples from vemurafenib-treated HCL patients within a phase 2 clinical trial.

223 ant region sequences from 5 cases of typical HCL, all expressing multiple surface immunoglobulin isot

224 t BRAF V600E mutations are absent in variant HCL forms and in a subset of classic HCL (HCLc).

225 ly-relapsed hairy cell leukemia and variant (HCL/HCLv) was to determine if pentostatin-rituximab (DCF

226 ion and studied 62 patients with HCL, 1 with HCL variant, 91 with splenic marginal zone lymphoma, 29

227 ous CDKN1B mutations in 16% of patients with HCL (n = 13 of 81).

228 ibitor are recurrent in 16% of patients with HCL and likely cooperate with BRAF-V600E in HCL pathogen

229 els may be useful to follow in patients with HCL and may be more specific than sCD25 in patients with

230 regularly increases the ANC in patients with HCL and shortens the duration of severe neutropenia afte

231 00E mutation is present in all patients with HCL and that, in combination with clinical and morpholog

232 NHL during cycle 1 and in four patients with HCL during cycle 2 or 3.

233 e marrow core biopsies from 39 patients with HCL in complete remission (CR) 3 months after a single c

234 of cladribine administered to patients with HCL induce high response rates, the majority of which ar

235 All four patients with HCL responded to treatment.

236 and June 2003, 86 consecutive patients with HCL were treated with a single 7-day course of 2-CdA by

237 reated with fludarabine and in patients with HCL who are treated with DCF and CdA.

238 In clinical trials of patients with HCL who have experienced multiple relapses after purine

239 Two hundred nine patients with HCL who were treated with cladribine had at least 7 year

240 can be safely administered to patients with HCL with objective responses and results in prolonged di

241 r this mutation and studied 62 patients with HCL, 1 with HCL variant, 91 with splenic marginal zone l

242 ngthy remissions in nearly all patients with HCL, most patients will experience relapse while a small

243 Among the 30 enrolled patients with HCL, the median number of previous therapies was 3.

244 Among 350 patients with HCL, there was an increase in the number of second cance

245 bent assay was 18 ng/mL for 93 patients with HCL.

246 kDa processed form in serum of patients with HCL.

247 d remission duration of CdA in patients with HCL.

248 We report on 88 young HCL patients (</=40 years of age at diagnosis) treated w

249 d durable responses in the majority of young HCL patients and are therefore recommended for HCL patie