ライフサイエンスコーパス: CTCL

1 CTCL is distinctive in that somatic copy number variants

2 CTCL peripheral blood mononuclear cells and cell lines a

3 dy the impact of DMF in vivo, we developed 2 CTCL xenograft mouse models with different cutaneous loc

4 f CTCL, we performed genomic analysis of 220 CTCLs.

5 combination, and comparisons were made to 4 CTCL cell lines (Hut78, Sez4, HH, MyLa).

6 rtantly, analysis of a historic cohort of 60 CTCL patients indicates that IL-17F expression is associ

7 n 5 of 6 large plaque parapsoriasis cases (a CTCL precursor).

8 ations: Six patients with a total of 8 acral CTCL lesions received low-dose HDR brachytherapy during

9 role of low-dose HDR brachytherapy for acral CTCL lesions.

10 ellent palliation for local control of acral CTCL lesions, offering homogeneous, controlled dosing fo

11 promising new treatment option for advanced CTCL that can be integrated in an allogeneic stem cell t

12 However, its involvement in advanced CTCL and its biological effects on CTCL pathogenesis hav

13 Thus, our data indicate that advanced CTCL cell growth is facilitated, at least in part, by mu

14 We describe 4 patients with advanced CTCL, 3 with MF and 1 with Sezary syndrome, who were tre

15 ells isolated from 11 patients with advanced CTCL, but not those from healthy controls or patients wi

16 t recommended ECP for patients with advanced CTCL, particularly after skin-directed treatment options

17 y in the treatment of patients with advanced CTCL.

18 t of IPH4102 to treat patients with advanced CTCL.

19 short telomeres were observed in aggressive CTCL subtypes such as SS and T-MF and were restricted to

20 erapeutic strategy, especially in aggressive CTCL.

21 systemic compounds have been studied in all CTCL stages as well as in treatment-refractory disease.

22 Although CTCL cells exhibit resistance to ROS-induced apoptosis,

23 Although CTCL is a highly radiosensitive tumor, the complex topog

24 ith relapsed or refractory PTCL (n = 16) and CTCL (n = 19), along with in vitro and in vivo models of

25 in primary patient-derived CD4(+) cells and CTCL cell lines, but hardly in T cells from healthy dono

26 all response rates in patients with PTCL and CTCL were 50.0% and 31.6%, respectively (P = .32).

27 hts into the genetics of Sezary syndrome and CTCL and support the development of personalized therapi

28 on, and cytokine signaling, in MF tumors and CTCL cell lines.

29 Interestingly, augmented CTCL cell adhesion obtained with retinoid exposure was p

30 combination regimens of currently available CTCL therapies as well as treatments approved for other

31 Peripheral blood CTCL malignant cells were isolated from 25 patients and

32 However, we also observed a CD4(+) CTCL-like phenotype when cells are transplanted in an MH

33 des and Sezary syndrome, the two most common CTCL types, have led to an expansion of new treatments a

34 Currently, CTCL is incurable, highlighting the need for new therape

35 A phase 2 trial was conducted in cutaneous (CTCL) and peripheral (PTCL) T-cell lymphoma.

36 atients with peripheral (PTCL) or cutaneous (CTCL) T-cell lymphoma.

37 TGF-beta1 suppression decreases CTCL cell viability and increases apoptosis, and adding

38 In IL-2-dependent CTCL cells, CD80 expression is induced by the cytokine i

39 tic analogs of vitamin A embody an effective CTCL therapy with over three decades of clinical use.

40 uclear localization of pro-IL-16 facilitates CTCL cell proliferation by causing a decrease in express

41 So far, few CTCL cell lines have been adapted for in vivo experiment

42 so characterized genomic alterations in five CTCL cell lines (HH, HUT78, PNO, SeAx, and Sez4), reveal

43 activation is a critical oncogenic event for CTCL.

44 ampering the use of a reproducible model for CTCL biological evaluation.

45 Effective treatment options for CTCL are limited, and the genetic basis of these T cell

46 experience with new therapeutic options for CTCL, particularly for patients with advanced stage and

47 TCL supported the approval of romidepsin for CTCL.

48 hus providing a new therapeutic strategy for CTCL.

49 Available systemic therapies for CTCL may variably decrease tumor burden and improve qual

50 nents as a potentially effective therapy for CTCL patients.

51 re effective and personalized treatments for CTCL.

52 gnant T cells from patients with SS and from CTCL cell lines constitutively expressed SD-4 at high le

53 and enhancer regions in CD4(+) T cells from CTCL patients.

54 We found that T cells from CTCL skin lesions contained a population of large, high-

55 ples) data of peripheral blood isolates from CTCL patients across a spectrum of stages.

56 TAT3 (pSTAT3) in skin biopsies obtained from CTCL patients enrolled in the vorinostat phase IIb trial

57 ined strategies, FAS-low as well as FAS-high CTCL cells can be killed effectively.

58 Analysis of 111 human CTCL and control samples revealed extensive chromatin si

59 IPH4102 were documented in allogeneic human CTCL cells and a mouse model of KIR3DL2(+) disease.

60 al of athymic nude mice implanted with human CTCL cells.

61 in CTCL tumorigenesis, we xenografted human CTCL tumor cells in immunocompromised mice and compared

62 In CTCL cells with suboptimal FAS expression, FAS can be up

63 ptional regulation of TGF-beta1 and IL-10 in CTCL, and about their function in regulating the CTCL ce

64 proinflammatory cytokines IL-8 and IL-17 in CTCL cells, suggesting that TGF-beta1 also regulates the

65 d that all three were targeted by miR-223 in CTCL.

66 in similar or improved apoptotic activity in CTCL assays compared to 1.

67 s review will highlight selected advances in CTCL treatment over the past year (2007-2008).

68 , specific miRNA were shown to be altered in CTCL.

69 ase 3 (GSK3) causes synergistic apoptosis in CTCL cell lines and patient cells.

70 arrest in G2 phase, as well as apoptosis in CTCL cell lines.

71 of FASL, and extrinsic pathway apoptosis in CTCL cells expressing adequate FAS.

72 -FMK decreased avicin D-induced apoptosis in CTCL cells.

73 icate that MUC1-C maintains redox balance in CTCL cells and is thereby a novel target for the treatme

74 athway featuring IL-15, miR-29b, and BRD4 in CTCL and suggest targeting of these components as a pote

75 cert with these results, targeting MUC1-C in CTCL cells increased ROS and, in turn, induced ROS-media

76 Targeting MUC1-C in CTCL tumor xenograft models demonstrated significant dec

77 TF deactivations that alter host T cells in CTCL patients.

78 The integrin-dependent adhesion changes in CTCL cells occurred through synergistic activation of RA

79 We sought to measure changes in CTCL incidence trends and survival rates.

80 xpression of the chemokine receptor CXCR4 in CTCL cells, resulting in their decreased migration, and

81 a decade that TCR signaling is defective in CTCL; however, the underlying mechanism has not been app

82 ficiency that characteristically develops in CTCL patients.

83 link between SEs and immune dysregulation in CTCL, strengthening the rationale for antibiotic treatme

84 oids relates to therapeutic effectiveness in CTCL has not been addressed and merits investigation.

85 y led to a clinical trial for Enzastaurin in CTCL in which it was well tolerated and showed modest ac

86 dentify a new mechanism of immune evasion in CTCL and suggest that the CD80-CD152 axis may become a t

87 se in CTCL, we manipulated its expression in CTCL cell lines.

88 show that TGF-beta1 and IL-10 expression in CTCL cells is regulated by NF-kappaB and suppressed by b

89 CD80 expression in CTCL cells is strictly dependent on the expression of bo

90 -regulated TGF-beta1 and IL-10 expression in CTCL cells, and indicate that TGF-beta1 has a key role i

91 e molecular regulation of PLS3 expression in CTCL.

92 implicating IL-13 as an autocrine factor in CTCL.

93 indicating TGF-beta1 prosurvival function in CTCL cells.

94 L, telomerase exerts additional functions in CTCL.

95 e results implicate mutations in 17 genes in CTCL pathogenesis, including genes involved in T cell ac

96 GFP966, resulted in decreased cell growth in CTCL cell lines due to increased apoptosis that was asso

97 estern blotting, and immunohistochemistry in CTCL cell lines and primary patient samples.

98 luding 17 genes not previously implicated in CTCL.

99 IL-17 receptor is significantly increased in CTCL skin lesions compared with control subjects.

100 RNA expression is significantly increased in CTCL skin lesions compared with healthy donors and patie

101 he T regulatory cell features are induced in CTCL T cells by common gamma chain signaling cytokines s

102 ssed genes of the serine/threonine kinase in CTCL.

103 nhibition led to increased protein levels in CTCL.

104 sed proliferative and survival mechanisms in CTCL may partially depend on the acquisition of somatic

105 ssion and functional significance of MUC1 in CTCL have not been previously investigated.

106 epresents a remarkable therapeutic option in CTCL because it restores CTCL apoptosis in vitro and in

107 ubiquitin ligase, c-CBL, is overexpressed in CTCL and that its knockdown overcomes defective TCR sign

108 demonstrate that MUC1-C is overexpressed in CTCL cell lines and primary CTCL cells but is absent in

109 f STAT-3 and NF-kappaB signaling pathways in CTCL cells.

110 geting of PKC and GSK3 signaling pathways in CTCL to enhance the therapeutic outcome.

111 eature of the malignant T-cell population in CTCL is resistance toward cell death resulting from cons

112 us effectiveness to inhibit proliferation in CTCL cells relative to 1 suggest that these compounds po

113 DMF treatment is of particular promise in CTCL because DMF is already in successful clinical use i

114 y be as effective as traditional regimens in CTCL.

115 fier-dependent transcriptional regulation in CTCL is unknown.

116 1, which has not been previously reported in CTCL; and TP53 and DNMT3A, which were also identified co

117 markers predictive of vorinostat response in CTCL using preclinical model systems and to assess these

118 Major and durable responses in CTCL supported the approval of romidepsin for CTCL.

119 hat mast cells play a protumorigenic role in CTCL and CBCL.

120 o demonstrate that macrophages had a role in CTCL tumorigenesis, we xenografted human CTCL tumor cell

121 ssion of SC-associated lncRNAs and SeCATs in CTCL.

122 (GSK3) as important in survival signaling in CTCL.

123 ng fast translation into clinical studies in CTCL.

124 resents an interesting therapeutic target in CTCL because an NF-kappaB-directed therapy would leave b

125 To understand the role of telomerase in CTCL, we manipulated its expression in CTCL cell lines.

126 Stable knockdown of TOX in CTCL cells promoted apoptosis and reduced cell cycle pro

127 Abnormal cytokine expression in CTCLs may be responsible for enhanced proliferation of t

128 ds, including Bexarotene, selectively induce CTCL lineages to increase integrin beta7 expression and

129 IL-13 induces CTCL cell growth in vitro and signaling through the IL-1

130 hat IL-13 synergizes with IL-4 in inhibiting CTCL cell growth and that blocking the IL-4/IL-13 signal

131 Interestingly, CTCL and CBCL patients with a progressive course showed

132 y, our analysis provides novel insights into CTCL pathogenesis and elucidates the landscape of potent

133 s conducted in patients with stage IB to IVA CTCL who had received one or more prior systemic therapi

134 , we studied the phenotype of T cells from L-CTCL and MF.

135 Clonal malignant T cells from the blood of L-CTCL patients universally coexpressed the lymph node hom

136 homa (CTCL) encompasses leukemic variants (L-CTCL) such as Sezary syndrome (SS) and primarily cutaneo

137 A consensus analysis of 108 leukemic CTCL samples demonstrated global similarities among pati

138 he malignant T cells in both MF and leukemic CTCL can be conclusively identified by a unique scatter

139 , revealing intact core features of leukemic CTCL.

140 the most comprehensive view of the leukemic CTCL genome to date, with implications for pathogenesis,

141 esent in the blood of patients with leukemic CTCL, absent in patients without blood involvement, and

142 rom patients with cutaneous T-cell lymphoma (CTCL) and cutaneous B-cell lymphoma (CBCL).

143 ukemic variant of cutaneous T-cell lymphoma (CTCL) and represents an ideal model for study of T-cell

144 Patients with cutaneous T-cell lymphoma (CTCL) are frequently colonized with Staphylococcus aureu

145 regulatory DNA in cutaneous T cell lymphoma (CTCL) by ATAC-seq.

146 y (TA) in primary cutaneous T-cell lymphoma (CTCL) by using quantitative polymerase chain reaction an

147 y low in 30 of 31 cutaneous T-cell lymphoma (CTCL) cases (mycosis fungoides/Sezary syndrome, SS) as w

148 ct of curcumin on cutaneous T-cell lymphoma (CTCL) cell lines and peripheral blood mononuclear cells

149 e, we report that cutaneous T cell lymphoma (CTCL) cells and tissues ubiquitously express the immunos

150 we selected HuT78 cutaneous T-cell lymphoma (CTCL) cells with romidepsin in the presence of P-glycopr

151 wo major forms of cutaneous T-cell lymphoma (CTCL) characterized by resistance to apoptosis.

152 Cutaneous T-cell lymphoma (CTCL) encompasses leukemic variants (L-CTCL) such as Sez

153 ative therapy for cutaneous T-cell lymphoma (CTCL) has not yet been developed.

154 Cutaneous T-cell lymphoma (CTCL) incidence and survival have been increasing steadi

155 mic treatment for cutaneous T-cell lymphoma (CTCL) involves the use of less aggressive, well-tolerate

156 Cutaneous T-cell lymphoma (CTCL) is a heterogeneous group of malignancies character

157 Cutaneous T-cell lymphoma (CTCL) is a heterogeneous group of primary cutaneous T-ce

158 Cutaneous T-cell lymphoma (CTCL) is a heterogeneous non-Hodgkin's lymphoma that may

159 Cutaneous T cell lymphoma (CTCL) is a non-Hodgkin lymphoma of skin-homing T lymphoc

160 Cutaneous T-cell lymphoma (CTCL) is an aggressive neoplasm with limited treatments

161 Cutaneous T-cell lymphoma (CTCL) is an incurable non-Hodgkin lymphoma of the skin-h

162 Cutaneous T-cell lymphoma (CTCL) is characterized by proliferation of malignant T c

163 Cutaneous T-cell lymphoma (CTCL) is characterized by the accumulation of malignant

164 , MBL2, and human cutaneous T-cell lymphoma (CTCL) lines, HH and Hut78, were used in syngeneic or sta

165 Importance: Cutaneous T-cell lymphoma (CTCL) of the hands and feet can be challenging to treat

166 is an aggressive cutaneous T-cell lymphoma (CTCL) of unknown etiology in which malignant cells circu

167 in patients with cutaneous T-cell lymphoma (CTCL) portend a worse clinical outcome.

168 Advanced cutaneous T-cell lymphoma (CTCL) remains an unmet medical need, which lacks effecti

169 ggressive form of cutaneous T cell lymphoma (CTCL) resulting from the malignant transformation of ski

170 y control and six cutaneous T-cell lymphoma (CTCL) samples from previously published cohorts.

171 rom patients with cutaneous T-cell lymphoma (CTCL) spontaneously secrete IL-17F and that inhibitors o

172 nant cells of the cutaneous T-cell lymphoma (CTCL) subset, Sezary syndrome (SS), exhibit memory T-cel

173 st common form of cutaneous T-cell lymphoma (CTCL), a heterogeneous group of non-Hodgkin's lymphomas

174 s a treatment for cutaneous T-cell lymphoma (CTCL), although treatment with 1 can elicit side-effects

175 is a hallmark of cutaneous T-cell lymphoma (CTCL), an often-fatal malignancy of skin-homing CD4(+) T

176 st common type of cutaneous T-cell lymphoma (CTCL), as compared to normal skin or benign inflammatory

177 nosis of advanced cutaneous T-cell lymphoma (CTCL), including Sezary syndrome and mycosis fungoides (

178 25 assay-positive cutaneous T-cell lymphoma (CTCL), including the mycosis fungoides and Sezary syndro

179 , the most common cutaneous T-cell lymphoma (CTCL), is unknown.

180 In early-stage cutaneous T-cell lymphoma (CTCL), malignant T cells are confined to skin and are di

181 thogenesis of the cutaneous T-cell lymphoma (CTCL), mycosis fungoides (MF), is unclear.

182 to patients with cutaneous T-cell lymphoma (CTCL), or subtypes mycosis fungoides or Sezary syndrome,

183 dvanced stages of cutaneous T cell lymphoma (CTCL), where it has been associated with suppressed immu

184 umor formation in cutaneous T-cell lymphoma (CTCL).

185 ggressive form of cutaneous T-cell lymphoma (CTCL).

186 athogenic role in cutaneous T-cell lymphoma (CTCL).

187 ent of refractory cutaneous T cell lymphoma (CTCL).

188 atment refractory cutaneous T-cell lymphoma (CTCL).

189 in patients with cutaneous T-cell lymphoma (CTCL).

190 d Sezary syndrome cutaneous T-cell lymphoma (CTCL).

191 against advanced cutaneous T-cell lymphoma (CTCL).

192 derived from CD4+ cutaneous T-cell lymphoma (CTCL).

193 the treatment of cutaneous T-cell lymphoma (CTCL).

194 ng progression of cutaneous T-cell lymphoma (CTCL)/SS and that FCRL3 expression correlates with a hig

195 for treatment of cutaneous T-cell lymphoma (CTCL); however, 1 can provoke side effects by impacting

196 approval to treat cutaneous T-cell lymphoma (CTCL); however, its use can cause side effects such as h

197 Cutaneous T-cell lymphomas (CTCL) represent a spectrum of several distinct non-Hodgk

198 tes derived from cutaneous T cell lymphomas (CTCL) variably display some aspects of the T regulatory

199 for treatment of cutaneous T-cell lymphomas (CTCL).

200 Cutaneous T-cell lymphomas (CTCLs) accounted for 71% (age-adjusted incidence rate [I

201 Cutaneous T-cell lymphomas (CTCLs) are a heterogeneous group of diseases primarily i

202 Cutaneous T-cell lymphomas (CTCLs) are a heterogenous group of non-Hodgkin's lymphom

203 Cutaneous T-cell lymphomas (CTCLs) are non-Hodgkin's lymphomas derived from T cells

204 Cutaneous T-cell lymphomas (CTCLs) form a heterogeneous group of non-Hodgkin's lymph

205 Cutaneous T-cell lymphomas (CTCLs) primarily affect skin and are characterized by pr

206 Cutaneous T-cell lymphomas (CTCLs) represent a group of hematopoietic malignancies t

207 Cutaneous T cell lymphomas (CTCLs) represent a heterogeneous group of non-Hodgkin ly

208 the majority of cutaneous T cell lymphomas (CTCLs), disorders notable for their clinical heterogenei

209 gnant T cells of cutaneous T-cell lymphomas (CTCLs), such as Sezary syndrome, display aberrant cytoki

210 permethylated in cutaneous T-cell lymphomas (CTCLs), using standard bisulfite modification techniques

211 of CD8(+) human cutaneous T-cell lymphomas (CTCLs).

212 2A, and MAC2B) and indolent (FE-PD and MAC1) CTCL cell lines.

213 ed knowledge of the molecular cues mediating CTCL migration may be used to interfere with their homin

214 r the development of new therapeutics for MF/CTCL.

215 Therefore, reduced levels of miR-223 in MF/CTCL lead to increased expression of E2F1, MEF2C, and TO

216 other inflammatory skin diseases and to non-CTCL cell lines that did not.

217 Mutational analyses of CTCL patient peripheral blood malignant cell samples sug

218 To clarify the genomic basis of CTCL, we performed genomic analysis of 220 CTCLs.

219 obility group box), in the skin and blood of CTCL patients produce IL-13 and express both receptors.

220 The total number of cases of CTCL from 1973 to 2009 was 6230.

221 Defining genomic characteristics of CTCL blood involvement included gains on 8q and 17q, and

222 Coculture of CTCL cells with normal T lymphocytes consisting of both

223 ical records of patients with a diagnosis of CTCL, including mycosis fungoides (MF), Sezary syndrome

224 ) and robust assay for in vivo evaluation of CTCL cell lines tumorigenicity and therapeutic response

225 DMF treatment delayed the growth of CTCL tumors and prevented formation of distant metastase

226 ize the compromised skin barrier and half of CTCL patients die of infection rather than from direct o

227 The incidence of CTCL is no longer increasing.

228 reases apoptosis in malignant lymphocytes of CTCL.

229 The majority of CTCL patient samples were sensitive to venetoclax, and B

230 its signaling mediators are novel markers of CTCL malignancy and potential therapeutic targets for in

231 s known about the dynamics and mechanisms of CTCL trafficking in vivo.

232 se A inhibition as a therapeutic modality of CTCL.

233 thway in our IL-15 transgenic mouse model of CTCL by showing that interference with BRD4-mediated pat

234 ings implicate IL-17F in the pathogenesis of CTCL and suggest that IL-17 cytokines and their receptor

235 The molecular pathogenesis of CTCL is largely unknown, although neoplastic cells show

236 tes to the development and/or progression of CTCL.

237 g via JQ1 treatment, prevents progression of CTCL.

238 ognostic value in predicting the response of CTCL patients to vorinostat.

239 ning assay for evaluating the sensitivity of CTCL cells to targeted molecular agents, and compared a

240 encing of MF samples and exome sequencing of CTCL cell lines were also performed.

241 nterotoxin A (SEA) from the affected skin of CTCL patients, as well as recombinant SEA, stimulate act

242 expressed in the clinically involved skin of CTCL patients.

243 and mast cell numbers in different stages of CTCL correlated positively with disease progression.

244 n for use in patients with earlier stages of CTCL.

245 ion of HDAC3 could be useful in treatment of CTCL by disrupting DNA replication of the rapidly cyclin

246 We show that treatment of CTCL cells with the MUC1-C inhibitor is associated with

247 988 as a medical device for the treatment of CTCL patients, one of many treatment options for such pa

248 tial therapeutic target for the treatment of CTCL.

249 shown promising results in the treatment of CTCL.

250 had MF, 15 had SS, and 9 had other types of CTCL.

251 with Sezary syndrome, a leukemic variant of CTCL, and that high TOX transcript levels correlate with

252 Sezary syndrome (SS), a leukemic variant of CTCL, in dermal microvessels in mouse ear skin.

253 ary syndrome (SS) is the leukemic variant of CTCL.

254 s fungoides (MF), the most common variant of CTCL.

255 fect the proliferation rate and viability of CTCL cells, induced expression of the cell-inhibitory re

256 milieu that drives the phenotypic changes of CTCLs.

257 of major importance for the pathogenesis of CTCLs.

258 ed the effects of dimethyl fumarate (DMF) on CTCL cells in vitro and in vivo.

259 advanced CTCL and its biological effects on CTCL pathogenesis have not been explored.

260 ceptor KIR3DL2, which is widely expressed on CTCL cells but few normal immune cells.

261 dhesion molecules and chemokine receptors on CTCL cells has been studied extensively on ex vivo isola

262 sis fungoides (MF), Sezary syndrome (SS), or CTCL not otherwise specified seen at a multidisciplinary

263 h Sezary syndrome and 17 patients with other CTCLs.

264 Overall CTCL incidence has stabilized since 1998 (95% CI, 1994-2

265 us 1.0 somatic single-nucleotide variant per CTCL).

266 ) with biopsy-confirmed, CD25 assay-positive CTCL were randomly assigned to DD 9 microg/kg/d (n = 45)

267 overexpressed in CTCL cell lines and primary CTCL cells but is absent in resting T cells from healthy

268 DMF induced increased cell death in primary CTCL tumors and in liver metastases.

269 Incubating primary CTCL cells with mast cell supernatant, we observed enhan

270 Whereas all three cytokines protected CTCL cells from apoptosis, only IL-2 and IL-15 promoted

271 NA sequencing and RNA sequencing on purified CTCL and matched normal cells.

272 hibition of this pathway resulted in reduced CTCL cell proliferation and cell viability.

273 with a JAK3 inhibitor significantly reduced CTCL cell survival.

274 oxicity in patients with relapsed/refractory CTCL.

275 therapeutic option for treatment refractory CTCL.

276 that TGF-beta1 has a key role in regulating CTCL survival, inflammatory gene expression, and migrati

277 erapeutic option in CTCL because it restores CTCL apoptosis in vitro and in preclinical models in viv

278 retinoids that may be pivotal to sensitizing CTCL cells to growth arrest and apoptosis.

279 Six of the seven CTCL cell lines were grafted with a high rate of success

280 ofile in patients with early- and late-stage CTCL.

281 from 24 additional patients with tumor-stage CTCL confirmed the differential expression of SC-associa

282 The CTCL incidence and survival data were obtained from the

283 The CTCL IR was highest among blacks (10.0/1 000 000 person-

284 nd STAT5a/b-dependent manner, whereas in the CTCL cells with constitutive STAT5 activation, CD80 expr

285 dly diminished at the tumor stage and in the CTCL lymph node lesions with or without large cell trans

286 , and about their function in regulating the CTCL cell responses.

287 g in their decreased migration, and that the CTCL cell migration is mediated by TGF-beta1.

288 n a time- and dose-dependent manner in three CTCL cell lines (namely MJ, Hut78, and HH).

289 TGF-beta1 increases viability of BZ-treated CTCL cells, indicating TGF-beta1 prosurvival function in

290 a lesser degree, IL-10 was restricted to two CTCL cell lines that are dependent on exogenous IL-2.

291 There are conflicting reports as to whether CTCLs represent a malignancy of regulatory T cells (Treg

292 mononuclear cells (PBMCs) from patients with CTCL compared with healthy donors' controls.

293 lysis of samples obtained from patients with CTCL enrolled on the NCI1312 phase 2 study of romidepsin

294 mended pralatrexate dosing for patients with CTCL that demonstrated high activity, good rates of dise

295 DNAs from 11 patients with CTCL, both normal and tumoral, were target-enriched and

296 notyping in a new cohort of 42 patients with CTCL, where it was found in 19% of samples.

297 el target for the treatment of patients with CTCL.

298 min as a therapeutic agent for patients with CTCL.

299 icant and durable responses in patients with CTCL.

300 Five-year CTCL survival rates increased until 2004.