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1 portion of the receptor tyrosine kinase ALK (anaplastic lymphoma kinase).
2 es the fusion protein NPM-ALK (nucleophosmin-anaplastic lymphoma kinase).
3 molecular target for the kinase activity of anaplastic lymphoma kinase.
7 ide 1 was identified as a novel inhibitor of anaplastic lymphoma kinase (ALK enzyme assay IC(50) = 0.
13 belly (Jeb) and its receptor tyrosine kinase Anaplastic lymphoma kinase (Alk) are localized to develo
14 ncogenic fusion genes consisting of EML4 and anaplastic lymphoma kinase (ALK) are present in a subgro
17 recently identified nucleophosmin (NPM) and anaplastic lymphoma kinase (ALK) as the genes on chromos
18 t inhibitors of the receptor tyrosine kinase anaplastic lymphoma kinase (ALK) blocked D2R desensitiza
19 The phylogenetic proximity of the ROS1 and anaplastic lymphoma kinase (ALK) catalytic domains led t
20 Abnormal expression of constitutively active anaplastic lymphoma kinase (ALK) chimeric proteins in th
21 essed CD30, epithelial membrane antigen, and anaplastic lymphoma kinase (ALK) consistent with a null
23 epidermal growth factor receptor (EGFR) and anaplastic lymphoma kinase (ALK) define two unique subty
25 lymphoma (ALCL) is a T-cell lymphoma, whose anaplastic lymphoma kinase (ALK) expression varies accor
27 This review describes the identification of anaplastic lymphoma kinase (ALK) fusion genes in approxi
28 microtubule-associated protein-like 4 (EML4)-anaplastic lymphoma kinase (ALK) fusion oncogene represe
29 ag in this study and was used to degrade the anaplastic lymphoma kinase (ALK) fusion protein by linki
30 microtubule-associated protein-like 4 (EML4)-anaplastic lymphoma kinase (ALK) fusion protein, presume
34 d here to detection of rearrangements in the anaplastic lymphoma kinase (ALK) gene associated with AL
35 ssed nucleophosmin (NPM) gene at 5q35 to the anaplastic lymphoma kinase (ALK) gene at 2p23, which is
36 Here we show that germline mutations in the anaplastic lymphoma kinase (ALK) gene explain most hered
38 he discovery of rearrangements involving the anaplastic lymphoma kinase (ALK) gene in thyroid cancer.
41 as (ALCLs) carry translocations in which the anaplastic lymphoma kinase (ALK) gene is juxtaposed to v
46 dermal growth factor receptor (EGFR) gene or anaplastic lymphoma kinase (ALK) gene rearrangements.
48 (2;5)(p23;q35) translocation which fuses the Anaplastic Lymphoma Kinase (ALK) gene with the Nucleopho
54 2 gene, which, we show, encodes the nematode anaplastic lymphoma kinase (ALK) homolog, a proto-oncoge
55 usly shown both humoral and CTL responses to anaplastic lymphoma kinase (ALK) in patients with ALK-po
61 that may rationalize clinical evaluation of anaplastic lymphoma kinase (ALK) inhibitors in this sett
62 lending impetus to the development of novel anaplastic lymphoma kinase (ALK) inhibitors with differe
63 naene macrocycles were prepared as potential anaplastic lymphoma kinase (ALK) inhibitors, designed to
81 MYCN overexpression combined with activated anaplastic lymphoma kinase (ALK) is sufficient to induce
83 ely half of IMTs carry rearrangements of the anaplastic lymphoma kinase (ALK) locus on chromosome 2p2
86 malignant transformation of T cells that are anaplastic lymphoma kinase (ALK) negative and CD30 posit
88 microtubule-associated protein-like 4 (EML4)-anaplastic lymphoma kinase (ALK) oncogenic fusion protei
90 The metabolic shift is mediated through the anaplastic lymphoma kinase (ALK) phosphorylation of the
91 , we found that a selective inhibitor of the anaplastic lymphoma kinase (ALK) potently suppressed gro
92 developed a folate-caged pomalidomide-based anaplastic lymphoma kinase (ALK) PROTAC, FA-S2-MS4048, w
94 hromosomal translocations that juxtapose the anaplastic lymphoma kinase (ALK) proto-oncogene to a dim
95 growth factor receptor (EGFR) mutations and anaplastic lymphoma kinase (ALK) rearrangements have dem
97 l fusion gene that incorporates parts of the anaplastic lymphoma kinase (ALK) receptor tyrosine kinas
99 ent work identified ALKAL2, a ligand for the Anaplastic Lymphoma Kinase (ALK) receptor, as a key medi
100 the oncogenic, chimeric nucleophosmin (NPM)/anaplastic lymphoma kinase (ALK) remain only partially u
101 romoting phenotype through activation of the anaplastic lymphoma kinase (ALK) signaling pathway.
103 and rhabdomyosarcoma, harbour activation of anaplastic lymphoma kinase (ALK) through different mecha
104 aim of the present review is to describe the anaplastic lymphoma kinase (ALK) translocation as a prom
106 ormation mediated by the nucleophosmin (NPM)/anaplastic lymphoma kinase (ALK) tyrosine kinase are onl
108 a potent, brain-penetrant, third-generation anaplastic lymphoma kinase (ALK) tyrosine kinase inhibit
109 h epidermal growth factor receptor (EGFR) or anaplastic lymphoma kinase (ALK) tyrosine kinase inhibit
110 epidermal growth factor receptor (EGFR) and anaplastic lymphoma kinase (ALK) tyrosine kinase inhibit
111 epidermal growth factor receptor (EGFR) and anaplastic lymphoma kinase (ALK) tyrosine kinase inhibit
113 ell transformation mediated by the oncogenic anaplastic lymphoma kinase (ALK) tyrosine kinase remain
114 n protein containing the catalytic domain of anaplastic lymphoma kinase (ALK) under the control of th
116 protein (p80) derived from the fusion of the anaplastic lymphoma kinase (ALK) with nucleophosmin (NPM
117 ;5)(p23;q35) results in the juxtaposition of anaplastic lymphoma kinase (ALK) with nucleophosmin (NPM
118 t down-regulation of TIMP1 expression in two anaplastic lymphoma kinase (ALK)(+) ALCL cell lines, Kar
119 vered in many T-cell malignancies, including anaplastic lymphoma kinase (ALK)(-) anaplastic large cel
122 ntained chromosomal translocations involving anaplastic lymphoma kinase (ALK), a novel receptor tyros
123 Jeb receptor is the Drosophila homologue of anaplastic lymphoma kinase (Alk), a receptor tyrosine ki
125 a distinct role for one of the DMGs encoding anaplastic lymphoma kinase (ALK), an important regulator
126 se domain that is physiologically related to anaplastic lymphoma kinase (ALK), and is undergoing Phas
127 EGFR), rearranged during transfection (RET), anaplastic lymphoma kinase (ALK), and MAPK1/3 and other
128 ts in nonsmall cell lung cancer fuse EML4 to anaplastic lymphoma kinase (ALK), causing expression of
130 otubule-associated protein like 4 (EML4) and anaplastic lymphoma kinase (ALK), generated by an invers
132 ecently identified receptor tyrosine kinase, anaplastic lymphoma kinase (ALK), in embryonic chick by
133 of epidermal growth factor receptor (EGFR), anaplastic lymphoma kinase (ALK), KRAS, and BRAF, induce
134 by R1-R6 axons interacts with its receptor, anaplastic lymphoma kinase (Alk), on budding dendrites t
135 omosome 5q35 to a novel protein kinase gene, Anaplastic Lymphoma Kinase (ALK), on chromosome 2p23.
139 genes encoding the receptor tyrosine kinases anaplastic lymphoma kinase (ALK), ROS proto-oncogene 1 (
140 r (TKI) with specificity for gene rearranged anaplastic lymphoma kinase (ALK), such as the EML4-ALK,
142 lating evidence indicates that expression of anaplastic lymphoma kinase (ALK), typically due to t(2;5
143 ), human epidermal growth factor receptor 2, anaplastic lymphoma kinase (ALK), v-Raf murine sarcoma v
146 SCD-2, the C. elegans ortholog of mammalian anaplastic lymphoma kinase (ALK), which has been implica
147 YCN cooperates with mutational activation of anaplastic lymphoma kinase (ALK), which promotes progres
148 absence of translocations that activate the anaplastic lymphoma kinase (ALK), with nucleophosmin-ALK
150 ied, angioimmunoblastic T-cell lymphoma, and anaplastic lymphoma kinase (ALK)-negative anaplastic lar
152 d) and active (underphosphorylated), in four anaplastic lymphoma kinase (ALK)-positive ALCL cell line
154 e SHH/GLI1 signaling pathway is activated in anaplastic lymphoma kinase (ALK)-positive anaplastic lar
156 ssion was seen in only 1 of 15 patients with anaplastic lymphoma kinase (ALK)-positive anaplastic lar
157 orrelates with relapse risk in children with anaplastic lymphoma kinase (ALK)-positive anaplastic lar
158 a small subset of cells purified from human anaplastic lymphoma kinase (ALK)-positive and -negative,
159 ngioimmunoblastic T-cell lymphoma (AITL), 31 anaplastic lymphoma kinase (ALK)-positive and 48 ALK-neg
160 heterogeneous disease that includes systemic anaplastic lymphoma kinase (ALK)-positive and ALK-negati
162 h crizotinib demonstrates robust efficacy in anaplastic lymphoma kinase (ALK)-positive non-small-cell
163 positive T-cell lymphoma, comprises systemic anaplastic lymphoma kinase (ALK)-positive, and ALK-negat
164 ere, we perform a phosphoproteomic screen in anaplastic lymphoma kinase (ALK)-rearranged ("ALK+") pat
165 oma, small molecule inhibitor crizotinib for anaplastic lymphoma kinase (ALK)-rearranged inflammatory
167 cacy of ceritinib in patients with untreated anaplastic lymphoma kinase (ALK)-rearranged non-small-ce
180 lymphomas characterized by the expression of anaplastic lymphoma kinase (ALK+ TCL) fail to express th
181 leophosmin/B23 (NPM) gene (5q35) and a novel anaplastic lymphoma kinase (ALK; 2p23) are the fused gen
182 chimeric tyrosine kinase nucleophosmin (NPM)-anaplastic lymphoma kinase [ALK; ALK(+) T-cell lymphoma
183 h epidermal growth factor receptor [EGFR] or anaplastic lymphoma kinase [ALK] genetic alterations wer
184 or survivin expression in 62 ALCL tumors (30 anaplastic lymphoma kinase [ALK]-positive and 32 ALK-neg
185 r inhibitors, 2.46% (range, 1.75%-4.66%) for anaplastic lymphoma kinase and ROS1 inhibitors, and 3.06
186 to be independent of nuclear localization of anaplastic lymphoma kinase; and phospholipase C-gamma wa
187 2;5) were mapped; constitutive activation of anaplastic lymphoma kinase by a chromosomal inversion wa
189 PF-2341066 was selective for c-Met (and anaplastic lymphoma kinase) compared with a panel of >12
190 noderm microtubule-associated protein-like 4-anaplastic lymphoma kinase (EML4-ALK) fusion protein is
192 idermal growth factor receptor mutations and anaplastic lymphoma kinase fusions, but significantly re
194 p studies, chromosomal rearrangements of the anaplastic lymphoma kinase gene (ALK) have been associat
195 xenograft models of the novel and selective anaplastic lymphoma kinase inhibitor 15b (LDK378) are de
197 r inhibitors, 0.999 (range, 0.982-0.999) for anaplastic lymphoma kinase inhibitors, and 0.999 for BRA
198 epidermal growth factor receptor inhibitors, anaplastic lymphoma kinase inhibitors, ROS1 inhibitors,
199 , we determined that the Midkine-a receptor, anaplastic lymphoma kinase, is upstream of the HLH regul
200 cell lymphoma (BIA-ALCL) is a CD30-positive, anaplastic lymphoma kinase-negative T-cell lymphoma.
201 CD30(+) T cell lymphoproliferative disorder (anaplastic lymphoma kinase-negative) 3 years after recei
202 d the resulting fusion protein nucleophosmin-anaplastic lymphoma kinase (NPM-ALK) are detected in 50%
203 utively active tyrosine kinase nucleophosmin-anaplastic lymphoma kinase (NPM-ALK) expressing anaplast
204 Constitutive overexpression of nucleophosmin-anaplastic lymphoma kinase (NPM-ALK) is a key oncogenic
207 mation of the chimeric protein nucleophosmin-anaplastic lymphoma kinase (NPM-ALK), which possesses si
214 ted by the oncogenic, chimeric nucleophosmin/anaplastic lymphoma kinase (NPM/ALK) tyrosine kinase rem
215 plying these design principles, we developed anaplastic lymphoma kinase oncoprotein-targeting PROTACs
216 microtubule-associated protein-like 4 (EML4)-anaplastic lymphoma kinase positive (ALK+) non-small-cel
217 t this receptor is expressed on T cells from anaplastic lymphoma kinase-positive (ALK(+)) anaplastic
218 r angioimmunoblastic T-cell lymphoma (AITL), anaplastic lymphoma kinase-positive (ALK(+)) anaplastic
224 sociated T-cell lymphoma patients (excluding anaplastic lymphoma kinase-positive anaplastic large cel
226 d in a caspase-dependent manner in apoptotic anaplastic lymphoma kinase-positive, anaplastic large ce
229 accompanied by mutational activation of ALK (anaplastic lymphoma kinase), suggesting their pathogenic
230 clude the possibility of an EGFR mutation or anaplastic lymphoma kinase translocation or to identify
231 assively parallel sequencing instrument, and anaplastic lymphoma kinase translocation was evaluated b
232 vity to epidermal growth factor receptor and anaplastic lymphoma kinase tyrosine kinase inhibitors ha