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 CTCL represents one of the disease indications for a cli

4 as detected in skin biopsies of 4/25 (16.0%) CTCL and 4/136 (2.9%) transplant patients but not in any

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

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

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

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

9 RAD23B knockdown in a CTCL cell line led to a reduction in FK228-induced apopt

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

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

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

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

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

15 el rationale for treatment of SA in advanced CTCL.

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

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

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

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

20 t of IPH4102 to treat patients with advanced CTCL.

21 y in the treatment of patients with advanced CTCL.

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

23 erapeutic strategy, especially in aggressive CTCL.

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

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

26 The CuV IgG seroprevalences were among CTCL patients 9.5% (4/42), transplant recipients 6.5% (8

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

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

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

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

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

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

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

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 DMF treatment in a xenograft mouse model for CTCL.

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

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 ific cell death in primary CD4(+) cells from CTCL patients as well as in the CTCL cell line SeAx, but

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

78 cl-2) has been shown to induce cell death in CTCL especially when combined with histone deacetylase i

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

80 ficiency that characteristically develops in CTCL patients.

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

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

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

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

85 RD4 cooperate to drive miR-214 expression in CTCL cell lines and in samples from patients with CTCL a

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

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

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

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

90 e molecular regulation of PLS3 expression in CTCL.

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

92 its NF-kappaB acting as a survival 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 V-DNA prevalence was significantly higher in CTCL patients than in the other subjects.

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

99 luding 17 genes not previously implicated in CTCL.

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

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

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 important, targetable, oncogenic pathway in CTCL.

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

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

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

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

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

115 y be as effective as traditional regimens in CTCL.

116 fier-dependent transcriptional regulation in CTCL is unknown.

117 1, which has not been previously reported in CTCL; and TP53 and DNMT3A, which were also identified co

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 aused synergistic cell death specifically in CTCL cells engaging 2 independent signaling pathways.

124 ng fast translation into clinical studies in CTCL.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

140 , revealing intact core features of leukemic CTCL.

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

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

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

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

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

146 eutic options for cutaneous T-cell lymphoma (CTCL) are limited and curative treatment regimens are no

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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 dministration for cutaneous T-cell lymphoma (CTCL), including the leukemic subtype Sezary syndrome.

179 25 assay-positive cutaneous T-cell lymphoma (CTCL), including the mycosis fungoides and Sezary syndro

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

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

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

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

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

185 utated in primary cutaneous T-cell lymphoma (CTCL).

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

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

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

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

190 f skin cancer and cutaneous T-cell lymphoma (CTCL).

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

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

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

194 n a proportion of cutaneous T-cell lymphoma (CTCL)/mycosis fungoides skin samples and in one melanoma

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

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

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

198 Cutaneous T-cell lymphomas (CTCLs) are a family of primary extranodal lymphomas of m

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

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

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

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

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

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

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

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

207 2A, and MAC2B) and indolent (FE-PD and MAC1) CTCL cell lines.

208 patient harbored CuV DNA in both malignant (CTCL, melanoma) and nonmalignant skin and sentinel lymph

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

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

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

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

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

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

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

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

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

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

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

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

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

222 The incidence of CTCL is no longer increasing.

223 verall survival via synergistic induction of CTCL cell death and suppression of tumor cell proliferat

224 reases apoptosis in malignant lymphocytes of CTCL.

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

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

227 se A inhibition as a therapeutic modality of CTCL.

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

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

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

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

232 g via JQ1 treatment, prevents progression of CTCL.

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

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

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

236 expressed in the clinically involved skin of CTCL patients.

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

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

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

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

241 988 as a medical device for the treatment of CTCL patients, one of many treatment options for such pa

242 tial therapeutic target for the treatment of CTCL.

243 shown promising results in the treatment of CTCL.

244 hibition in a novel combination treatment of CTCL.

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

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

247 in Sezary Syndrome, the leukemic variant of CTCL.

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

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

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

251 milieu that drives the phenotypic changes of CTCLs.

252 of major importance for the pathogenesis of CTCLs.

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

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

255 apies in cancers, with a special emphasis on CTCL.

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

257 One CTCL patient harbored CuV DNA in both malignant (CTCL, m

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

259 h Sezary syndrome and 17 patients with other CTCLs.

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

261 ice with spontaneous, miR-214-overexpressing CTCL leads to significant decrease in disease severity u

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

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

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

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

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

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

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

269 with a JAK3 inhibitor significantly reduced CTCL cell survival.

270 oxicity in patients with relapsed/refractory CTCL.

271 therapeutic option for treatment refractory CTCL.

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

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

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

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

276 e activity in 8 patients with advanced-stage CTCL.

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

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

279 The CTCL incidence and survival data were obtained from the

280 not in T cells of healthy donors nor in the CTCL cell line HH, which lacks Bcl-2.

281 ) cells from CTCL patients as well as in the CTCL cell line SeAx, but not in T cells of healthy donor

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

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

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

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

286 h scrambled control-treated IL-15 transgenic CTCL mice.

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

288 g Bcl-2 and NF-kappaB inhibitors in treating CTCL.

289 t dermal CuV DNA carriage is associated with CTCL.

290 cell lines and in samples from patients with CTCL and that treatment with BRD4 inhibitor JQ1 leads to

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

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

293 CD4(+) neoplastic T cells from patients with CTCL than from healthy donors.

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 In a significant fraction of patients with CTCL, the neoplastic CD4(+) lymphocytes acquire extracut

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

298 el target for the treatment of patients with CTCL.

299 min as a therapeutic agent for patients with CTCL.

300 Five-year CTCL survival rates increased until 2004.