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

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

34 Occasionally, patients with classic HCL respond poorly.

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

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

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

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

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

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

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

42 tibody proved effective against pre-existing HCL tumors.

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

44 did not fulfill the diagnostic criteria for HCL.

45 .7 years) showed an excellent PFS and OS for HCL patients after 2-CdA treatment.

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

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

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

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

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

51 8 microg/mL) and tetracycline hydrochloride (HCL) (only 30.2% susceptible) against A. baumannii isola

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

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

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

55 ool for improving the diagnostic accuracy in HCL.

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

57 BL22 activity in HCL is confirmed.

58 assay to monitor minimal residual disease in HCL.

59 2 was well tolerated and highly effective in HCL, even after one cycle.

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

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

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

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

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

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

66 1B as the second most common mutated gene in HCL.

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

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

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

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

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

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

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

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

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

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

77 so represents an ideal therapeutic target in HCL.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

112 00E driving mutation in hairy cell leukemia (HCL),provide extensive laboratory studies showing that i

113 hematopoietic neoplasm hairy cell leukemia (HCL).

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

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

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

117 relapsed or refractory hairy cell leukemia (HCL).

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

147 e key event in the molecular pathogenesis of HCL.

148 e of CDKN1B mutations in the pathogenesis of HCL.

149 mutation plays a role in the pathogenesis of HCL.

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

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

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

153 ilgrastim and cladribine in the treatment of HCL.

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

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

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

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

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

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

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

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

162 tional landscape of purine analog refractory HCL.

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

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

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

166 e therapeutic option for relapsed/refractory HCL.

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

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

169 Sixteen HCL-variant patients showed percentage BRAFV600E/BRAFwt

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

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

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

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

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

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

176 The HCL population had lower mitochondrial respiration, than

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

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

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

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

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

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

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

184 h the histiocytic disorders were distinct to HCL.

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

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

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

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

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

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

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

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

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

194 00E mutation is present in all patients with HCL and that, in combination with clinical and morpholog

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

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

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

198 All four patients with HCL responded to treatment.

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

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

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

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

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

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

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

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

207 kDa processed form in serum of patients with HCL.

208 d remission duration of CdA in patients with HCL.

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

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