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1 ALCL cells that were deficient in ARNT exhibited defects
2 ALCL is defined by the presence or absence of translocat
3 ALCL was described initially as a subtype of T-cell/null
4 95L/FASL was expressed in only 3 (12%) of 26 ALCL tumors, although it was strongly expressed by surro
5 study, we report that SUDHL-1 and KARPAS 299 ALCL-derived cell lines present different sensitivity to
7 emistry, pAkt was detected in 24 (57%) of 42 ALCL tumors, including 8 (44%) of 18 ALK-positive tumors
8 TIMP1 expression and STAT3 activation in 43 ALCL tumors (19 ALK(+) and 24 ALK(-)) using immunohistoc
10 We assessed for survivin expression in 62 ALCL tumors (30 anaplastic lymphoma kinase [ALK]-positiv
11 SR-786) by Western blot analysis, and in 67 ALCL tumors (30 ALK-positive, 37 ALK-negative) using imm
14 alogues were also highly expressed in ALK(+) ALCL and may represent important downstream effectors of
18 ssion of Th17-associated molecules in ALK(+) ALCL was noted and may represent aberrant activation of
19 the high level of TIMP1 expression in ALK(+) ALCL, and TIMP1 expression correlates with high level of
24 ly, inhibition of ALK activity in NPM-ALK(+) ALCL cells resulted in a concentration-dependent dephosp
29 ogical significance in ALCL using two ALK(+) ALCL cell lines (Karpas 299 and SU-DHL-1) and an adenovi
31 -positive (ALK(+)) lymphomas and human ALK(+)ALCL cell lines, in the present study, we show that high
33 nalyzed circulating cytokine levels in ALK(+)ALCL patients and detected elevated levels of IL-22, IL-
35 e relationship between the ALK(+) and ALK(-) ALCL subtypes, we performed a genome-wide DNA profiling
38 notypic or genetic features to define ALK(-) ALCL are missing, and their distinction from other T-cel
40 samples of primary NPM-ALK(+) and NPM-ALK(-) ALCL to investigate the role of miR-150 downstream of NP
42 TMOD1) able to successfully separate ALK(-) ALCL from peripheral T-cell lymphoma not otherwise speci
45 53 and/or PRDM1 were present in 52% of ALK(-)ALCL, and in 29% of all ALCL cases with a clinical impli
48 y) had no effect on cell viability of 2 ALK+ ALCL cell lines, Karpas 299 and SU-DHL1, each expressing
50 expression of IL-9Ralpha and IL-9 in 3 ALK+ ALCL-cell lines and 75% and 83% of primary tumors, respe
52 rs may have therapeutic application for ALK+ ALCL and possibly other solid and hematologic tumors in
53 erum-free culture medium harvested from ALK+ ALCL-cell lines, supporting autocrine release of IL-9.
55 sponsible for the higher AR observed in ALK+ ALCL and provides a possible biological explanation for
58 iptional effector GLI1, is amplified in ALK+ ALCL tumors and cell lines, and that SHH and GLI1 protei
65 large cell lymphoma (ALCL) morphology (ALK+ ALCL), the vast majority of which harbor the well-charac
66 significant role in the pathogenesis of ALK+ ALCL and that it represents a potential therapeutic targ
70 The unique molecular pathogenesis of ALK+ ALCL is likely to lead to novel therapeutic approaches d
71 of variant ALK fusions in up to 20% of ALK+ ALCL, of which only one, a TPM3-ALK fusion resulting fro
73 that overexpression of c-FLIP protects ALK+ ALCL cells from death-receptor-induced apoptosis and may
75 ition of NPM-ALK phosphorylation in the ALK+ ALCL-derived cell lines resulted in significant inhibiti
76 location and a survival rate similar to ALK+ ALCL or a less common P63 translocation, the latter asso
80 ctively expressed in neoplastic cells of ALK+ALCL tissue biopsies, and showed a significant correlati
81 Anaplastic lymphoma kinase-positive (ALK+) ALCL is associated with the NPM-ALK t(2;5) translocation
82 inical application of targeting JAK for ALK- ALCL, we treated ALK- cell lines of various histological
86 wever, emerging data now highlight that ALK- ALCL is genetically and clinically heterogeneous with a
88 ystemic ALCL, but in many patients with ALK- ALCL, it is ineffective, and thus it is often followed b
95 o clinical responses in patients with HL and ALCL, indicating that further assessment of this therapy
98 Most patients with breast implant-associated ALCL who had disease confined within the fibrous capsule
99 ging studies in immunodeficient mice bearing ALCL xenotransplants were carried out with the cell line
102 sociated anaplastic large cell lymphoma (BIA-ALCL), a rare peripheral T-cell lymphoma, is increasing
111 totic proteins BAX and BCL-XS in T/null-cell ALCL using immunohistochemical methods and correlated th
112 pharmacologic inhibition partially controls ALCL cell growth and disease progression in an ERBB4-pos
118 F2alpha, but not HIF1alpha, was required for ALCL growth in vivo whereas the growth and metastasis po
119 ures of this malignancy were not typical for ALCL because tumor cells expressed both myeloid (CD13, C
120 confirmed these findings derived from human ALCL cells in murine pro-B cells that were transformed t
121 ith this, clonal TCR rearrangements in human ALCL are predominantly in-frame, but often aberrant, wit
127 signaling pathway and STAT3 is activated in ALCL, survivin expression was also correlated with STAT3
129 onstrate that inhibition of pAkt activity in ALCL decreases p27 phosphorylation and degradation, resu
131 d VEGFA production and tumor angiogenesis in ALCL and NSCLC, and the treatment with the anti-VEGFA an
133 p27(Kip1) (p27) is usually not expressed in ALCL, we hypothesized that activated Akt (pAkt) phosphor
135 hat that PRDM1 is a tumor suppressor gene in ALCL models, likely acting as an antiapoptotic agent.
136 activation is pathogenetically important in ALCL cells by deregulating the expression of multiple ta
141 ther examined its biological significance in ALCL using two ALK(+) ALCL cell lines (Karpas 299 and SU
142 possible role of JAK in activating STAT3 in ALCL using two ALK-positive ALCL cell lines, Karpas 299
143 he importance of JAK3 in activating STAT3 in ALCL, and that NPM-ALK-mediated activation of STAT3 is i
148 cers such as anaplastic large-cell lymphoma (ALCL) and inflammatory myofibroblastic tumor (IMT).
151 Most of the anaplastic large-cell lymphoma (ALCL) cases carry the t(2;5; p23;q35) that produces the
152 ALK-positive anaplastic large cell lymphoma (ALCL) cell lines to evaluate two inhibitors, the HSP90 i
154 LK)-positive anaplastic large cell lymphoma (ALCL) constitutes an ideal model disease to study tumor-
155 atients with anaplastic large cell lymphoma (ALCL) express CD30 and are usually positive for expressi
156 LK)-positive anaplastic large cell lymphoma (ALCL) frequently carries the t(2;5)(p23;q35) resulting i
158 vanced-stage anaplastic large-cell lymphoma (ALCL) harbor the balanced chromosomal rearrangement t(2;
160 hogenesis of anaplastic large-cell lymphoma (ALCL) have been well defined; nevertheless, the notion t
161 LK)-negative anaplastic large cell lymphoma (ALCL) is a CD30-positive T-cell non-Hodgkin lymphoma tha
167 t-associated anaplastic large-cell lymphoma (ALCL) is a recently described clinicopathologic entity t
168 Systemic anaplastic large-cell lymphoma (ALCL) is a T-cell lymphoma, whose anaplastic lymphoma ki
170 Systemic anaplastic large-cell lymphoma (ALCL) is an aggressive subtype of T-cell lymphoma charac
171 NHL) subtype anaplastic large-cell lymphoma (ALCL) is frequently associated with a t(2;5)(p23;q35) th
176 ell line, an Anaplastic Large Cell Lymphoma (ALCL) line, a DNA rearrangement was detected within the
177 mphomas with anaplastic large cell lymphoma (ALCL) morphology (ALK+ ALCL), the vast majority of which
185 K-rearranged anaplastic large cell lymphoma (ALCL), a specific subtype of T-cell lymphoma, the Rho fa
187 , three with anaplastic large-cell lymphoma (ALCL), and two with CD30+ T-cell lymphoma--were enrolled
188 and systemic anaplastic large cell lymphoma (ALCL), the single agent response rates were 75 and 86%,
189 oma (HL) and anaplastic large-cell lymphoma (ALCL), the study by Jacobsen and colleagues in this issu
190 0% to 70% of anaplastic large cell lymphoma (ALCL), which is a T/null cell non-Hodgkin's lymphoma sho
191 rotein in an anaplastic large cell lymphoma (ALCL)-derived cell line carrying the t(2;5)(p23;q35), an
208 [AITL], and anaplastic large-cell lymphoma [ALCL]) is difficult, with the morphologic and phenotypic
209 g pediatric anaplastic large cell lymphomas (ALCL) and inflammatory myofibroblastic tumors (IMTs).
210 slocated in Anaplastic Large Cell Lymphomas (ALCL) and the juxtaposition of the ALK gene to multiple
211 30-positive anaplastic large cell lymphomas (ALCL) with the NPM-ALK gene fusion arising from the t(2;
215 sion, Rb is absent or phosphorylated in most ALCL cell lines and tumors and absence of Rb expression
216 rrent translocation reported in ALK-negative ALCL and highlight the utility of massively parallel gen
217 we identified a new subclass of ALK-negative ALCL characterized by aberrant expression of ERBB4-trunc
219 it enhanced the distinction of ALK-negative ALCL from PTCL NOS, especially from some CD30+ PTCL NOS
221 77% for AITL and 98% to 93% for ALK-negative ALCL in test and validation sets of patient cases, respe
223 arkers and/or genes involved in ALK-negative ALCL pathogenesis, we applied the cancer outlier profile
226 patients with ALK-positive and ALK-negative ALCL, beta(2)-microglobulin was >/= 3 mg/L in 12% and 33
229 -free survival for patients with Rb-negative ALCL was 89.4% compared with 47.7% for patients with tot
231 supports the concept that a minority of null-ALCL may be derived from NK cells and expands the spectr
232 that t(2;5)(p23;q35) occurs in 40% to 60% of ALCL patients established a distinct clinicopathologic e
233 a comprehensive phosphoproteome analysis of ALCL cell lines was performed in the presence or absence
235 e useful in understanding the development of ALCL and in understanding the development of other close
236 tial overlap with pathologists' diagnosis of ALCL), to be defined and is invaluable in distinguishing
238 tor, NVP-TAE684, which blocked the growth of ALCL-derived and ALK-dependent cell lines with IC(50) va
239 rvivin is expressed in approximately half of ALCL tumors and independently predicts unfavorable clini
241 nd Rac1 control rather similar phenotypes of ALCL biology such as the proliferation, survival, and mi
243 Using this system, CD30 was stimulated on ALCL and HL cells, and the subsequent CD30 signaling pro
244 ch 9 patients with relapsed/refractory HL or ALCL were infused with autologous T cells that were gene
245 of uniformly treated ALK-positive pediatric ALCL patients to ascertain whether the titers of preexis
247 ur anaplastic lymphoma kinase (ALK)-positive ALCL cell lines (Karpas 299, JB-6, SU-DHL1, and SR-786)
248 tients with relapsed/refractory ALK-positive ALCL and 14 patients with metastatic or inoperable ALK-p
249 is in two independent models of ALK-positive ALCL and induced regression of established Karpas-299 ly
250 that morphologically resembles ALK-positive ALCL but lacks chromosomal rearrangements of the ALK gen
253 Early evaluation of MRD in NPM-ALK-positive ALCL identifies patients with a very high relapse risk a
255 ALK protein were present in all ALK-positive ALCL patients (11 out of 11 cases) studied while 10 pati
256 6), as being immunogenic in six ALK-positive ALCL patients but not in two ALK-negative ALCL patients
257 e immunotherapeutic options for ALK-positive ALCL patients who fail to respond well to conventional t
258 ave previously been detected in ALK-positive ALCL patients, their prognostic significance is unknown.
259 tumor cells in 15 of 15 (100%) ALK-positive ALCL samples, whereas no expression of either ALK or c-M
260 marrow of 180 patients with NPM-ALK-positive ALCL treated with Berlin-Frankfurt-Munster-type protocol
261 fficacy when dosed orally in an ALK-positive ALCL tumor xenograft model in SCID mice, warranting furt
264 was 34% for patients with survivin-positive ALCL compared with 100% for patients with survivin-negat
265 ically active in both cell lines and primary ALCL, whereas the nuclear portion was inactive because o
266 ere significantly enriched in ALK-rearranged ALCL and NSCLC, as compared with other types of T-cell l
269 2 or Rac1 in a mouse model of ALK-rearranged ALCL to show that either Cdc42 or Rac1 deletion impaired
270 nd durable remissions in relapsed/refractory ALCL and is under investigation in the first-line settin
271 crizotinib therapy in patients with relapsed ALCL and metastatic or unresectable IMT highlight the im
272 , in contrast to NSCLC cells, drug-resistant ALCL cells show no evidence of bypassing ALK by activati
277 efinement of the prognosis of adult systemic ALCL, with ALK prognostic value dependent on age, and co
278 tive clinical trials with confirmed systemic ALCL after immunohistopathologic review and defined ALK
279 ard first-line treatment choice for systemic ALCL, but in many patients with ALK- ALCL, it is ineffec
281 ma subtypes), including 36 cases of systemic ALCL, were surveyed for clusterin expression by immunohi
283 reatment for relapsed or refractory systemic ALCL and warrants further studies in front-line therapy.
284 atients with relapsed or refractory systemic ALCL, provide evidence that single-agent brentuximab ved
287 eks, significantly prolonged survival of the ALCL-bearing SCID/NOD wild-type and SCID/NOD FcRgamma(-/
289 own of IRF4 by RNA interference was toxic to ALCL cell lines in vitro and in ALCL xenograft mouse mod
291 tional 51 patients, 47 with HL and four with ALCL, were treated at doses of 1, 5, 10, and 15 mg/kg.
293 The overall response rates for patients with ALCL treated at doses of 165 (ALCL165) and 280 (ALCL280)
294 soluble CD30 (sCD30) levels in patients with ALCL treated with EPOCH (etoposide, prednisone, Oncovin,
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