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1 es the fusion protein NPM-ALK (nucleophosmin-anaplastic lymphoma kinase).
2 portion of the receptor tyrosine kinase ALK (anaplastic lymphoma kinase).
3 molecular target for the kinase activity of anaplastic lymphoma kinase.
6 ide 1 was identified as a novel inhibitor of anaplastic lymphoma kinase (ALK enzyme assay IC(50) = 0.
10 belly (Jeb) and its receptor tyrosine kinase Anaplastic lymphoma kinase (Alk) are localized to develo
11 ncogenic fusion genes consisting of EML4 and anaplastic lymphoma kinase (ALK) are present in a subgro
13 recently identified nucleophosmin (NPM) and anaplastic lymphoma kinase (ALK) as the genes on chromos
14 The phylogenetic proximity of the ROS1 and anaplastic lymphoma kinase (ALK) catalytic domains led t
15 Abnormal expression of constitutively active anaplastic lymphoma kinase (ALK) chimeric proteins in th
16 essed CD30, epithelial membrane antigen, and anaplastic lymphoma kinase (ALK) consistent with a null
18 epidermal growth factor receptor (EGFR) and anaplastic lymphoma kinase (ALK) define two unique subty
20 lymphoma (ALCL) is a T-cell lymphoma, whose anaplastic lymphoma kinase (ALK) expression varies accor
22 This review describes the identification of anaplastic lymphoma kinase (ALK) fusion genes in approxi
23 microtubule-associated protein-like 4 (EML4)-anaplastic lymphoma kinase (ALK) fusion oncogene represe
24 microtubule-associated protein-like 4 (EML4)-anaplastic lymphoma kinase (ALK) fusion protein, presume
27 d here to detection of rearrangements in the anaplastic lymphoma kinase (ALK) gene associated with AL
28 ssed nucleophosmin (NPM) gene at 5q35 to the anaplastic lymphoma kinase (ALK) gene at 2p23, which is
29 Here we show that germline mutations in the anaplastic lymphoma kinase (ALK) gene explain most hered
31 he discovery of rearrangements involving the anaplastic lymphoma kinase (ALK) gene in thyroid cancer.
33 as (ALCLs) carry translocations in which the anaplastic lymphoma kinase (ALK) gene is juxtaposed to v
38 dermal growth factor receptor (EGFR) gene or anaplastic lymphoma kinase (ALK) gene rearrangements.
43 2 gene, which, we show, encodes the nematode anaplastic lymphoma kinase (ALK) homolog, a proto-oncoge
44 usly shown both humoral and CTL responses to anaplastic lymphoma kinase (ALK) in patients with ALK-po
48 that may rationalize clinical evaluation of anaplastic lymphoma kinase (ALK) inhibitors in this sett
49 lending impetus to the development of novel anaplastic lymphoma kinase (ALK) inhibitors with differe
50 naene macrocycles were prepared as potential anaplastic lymphoma kinase (ALK) inhibitors, designed to
63 MYCN overexpression combined with activated anaplastic lymphoma kinase (ALK) is sufficient to induce
65 ely half of IMTs carry rearrangements of the anaplastic lymphoma kinase (ALK) locus on chromosome 2p2
67 malignant transformation of T cells that are anaplastic lymphoma kinase (ALK) negative and CD30 posit
69 The metabolic shift is mediated through the anaplastic lymphoma kinase (ALK) phosphorylation of the
70 , we found that a selective inhibitor of the anaplastic lymphoma kinase (ALK) potently suppressed gro
72 hromosomal translocations that juxtapose the anaplastic lymphoma kinase (ALK) proto-oncogene to a dim
73 l fusion gene that incorporates parts of the anaplastic lymphoma kinase (ALK) receptor tyrosine kinas
75 the oncogenic, chimeric nucleophosmin (NPM)/anaplastic lymphoma kinase (ALK) remain only partially u
77 aim of the present review is to describe the anaplastic lymphoma kinase (ALK) translocation as a prom
79 ormation mediated by the nucleophosmin (NPM)/anaplastic lymphoma kinase (ALK) tyrosine kinase are onl
80 h epidermal growth factor receptor (EGFR) or anaplastic lymphoma kinase (ALK) tyrosine kinase inhibit
81 epidermal growth factor receptor (EGFR) and anaplastic lymphoma kinase (ALK) tyrosine kinase inhibit
82 epidermal growth factor receptor (EGFR) and anaplastic lymphoma kinase (ALK) tyrosine kinase inhibit
84 ell transformation mediated by the oncogenic anaplastic lymphoma kinase (ALK) tyrosine kinase remain
85 n protein containing the catalytic domain of anaplastic lymphoma kinase (ALK) under the control of th
87 protein (p80) derived from the fusion of the anaplastic lymphoma kinase (ALK) with nucleophosmin (NPM
88 ;5)(p23;q35) results in the juxtaposition of anaplastic lymphoma kinase (ALK) with nucleophosmin (NPM
89 t down-regulation of TIMP1 expression in two anaplastic lymphoma kinase (ALK)(+) ALCL cell lines, Kar
90 vered in many T-cell malignancies, including anaplastic lymphoma kinase (ALK)(-) anaplastic large cel
92 ntained chromosomal translocations involving anaplastic lymphoma kinase (ALK), a novel receptor tyros
93 Jeb receptor is the Drosophila homologue of anaplastic lymphoma kinase (Alk), a receptor tyrosine ki
94 a distinct role for one of the DMGs encoding anaplastic lymphoma kinase (ALK), an important regulator
95 se domain that is physiologically related to anaplastic lymphoma kinase (ALK), and is undergoing Phas
96 EGFR), rearranged during transfection (RET), anaplastic lymphoma kinase (ALK), and MAPK1/3 and other
97 ts in nonsmall cell lung cancer fuse EML4 to anaplastic lymphoma kinase (ALK), causing expression of
99 otubule-associated protein like 4 (EML4) and anaplastic lymphoma kinase (ALK), generated by an invers
101 ecently identified receptor tyrosine kinase, anaplastic lymphoma kinase (ALK), in embryonic chick by
102 by R1-R6 axons interacts with its receptor, anaplastic lymphoma kinase (Alk), on budding dendrites t
103 omosome 5q35 to a novel protein kinase gene, Anaplastic Lymphoma Kinase (ALK), on chromosome 2p23.
108 lating evidence indicates that expression of anaplastic lymphoma kinase (ALK), typically due to t(2;5
109 ), human epidermal growth factor receptor 2, anaplastic lymphoma kinase (ALK), v-Raf murine sarcoma v
111 YCN cooperates with mutational activation of anaplastic lymphoma kinase (ALK), which promotes progres
112 absence of translocations that activate the anaplastic lymphoma kinase (ALK), with nucleophosmin-ALK
113 ied, angioimmunoblastic T-cell lymphoma, and anaplastic lymphoma kinase (ALK)-negative anaplastic lar
115 d) and active (underphosphorylated), in four anaplastic lymphoma kinase (ALK)-positive ALCL cell line
117 e SHH/GLI1 signaling pathway is activated in anaplastic lymphoma kinase (ALK)-positive anaplastic lar
119 ssion was seen in only 1 of 15 patients with anaplastic lymphoma kinase (ALK)-positive anaplastic lar
120 orrelates with relapse risk in children with anaplastic lymphoma kinase (ALK)-positive anaplastic lar
121 a small subset of cells purified from human anaplastic lymphoma kinase (ALK)-positive and -negative,
122 ngioimmunoblastic T-cell lymphoma (AITL), 31 anaplastic lymphoma kinase (ALK)-positive and 48 ALK-neg
123 heterogeneous disease that includes systemic anaplastic lymphoma kinase (ALK)-positive and ALK-negati
125 h crizotinib demonstrates robust efficacy in anaplastic lymphoma kinase (ALK)-positive non-small-cell
126 oma, small molecule inhibitor crizotinib for anaplastic lymphoma kinase (ALK)-rearranged inflammatory
128 cacy of ceritinib in patients with untreated anaplastic lymphoma kinase (ALK)-rearranged non-small-ce
138 lymphomas characterized by the expression of anaplastic lymphoma kinase (ALK+ TCL) fail to express th
139 leophosmin/B23 (NPM) gene (5q35) and a novel anaplastic lymphoma kinase (ALK; 2p23) are the fused gen
140 or survivin expression in 62 ALCL tumors (30 anaplastic lymphoma kinase [ALK]-positive and 32 ALK-neg
141 to be independent of nuclear localization of anaplastic lymphoma kinase; and phospholipase C-gamma wa
142 2;5) were mapped; constitutive activation of anaplastic lymphoma kinase by a chromosomal inversion wa
144 PF-2341066 was selective for c-Met (and anaplastic lymphoma kinase) compared with a panel of >12
145 noderm microtubule-associated protein-like 4-anaplastic lymphoma kinase (EML4-ALK) fusion protein is
146 p studies, chromosomal rearrangements of the anaplastic lymphoma kinase gene (ALK) have been associat
147 xenograft models of the novel and selective anaplastic lymphoma kinase inhibitor 15b (LDK378) are de
148 d the resulting fusion protein nucleophosmin-anaplastic lymphoma kinase (NPM-ALK) are detected in 50%
149 utively active tyrosine kinase nucleophosmin-anaplastic lymphoma kinase (NPM-ALK) expressing anaplast
150 Constitutive overexpression of nucleophosmin-anaplastic lymphoma kinase (NPM-ALK) is a key oncogenic
153 mation of the chimeric protein nucleophosmin-anaplastic lymphoma kinase (NPM-ALK), which possesses si
160 ted by the oncogenic, chimeric nucleophosmin/anaplastic lymphoma kinase (NPM/ALK) tyrosine kinase rem
161 microtubule-associated protein-like 4 (EML4)-anaplastic lymphoma kinase positive (ALK+) non-small-cel
162 r angioimmunoblastic T-cell lymphoma (AITL), anaplastic lymphoma kinase-positive (ALK(+)) anaplastic
163 t this receptor is expressed on T cells from anaplastic lymphoma kinase-positive (ALK(+)) anaplastic
166 sociated T-cell lymphoma patients (excluding anaplastic lymphoma kinase-positive anaplastic large cel
168 d in a caspase-dependent manner in apoptotic anaplastic lymphoma kinase-positive, anaplastic large ce
169 accompanied by mutational activation of ALK (anaplastic lymphoma kinase), suggesting their pathogenic
170 clude the possibility of an EGFR mutation or anaplastic lymphoma kinase translocation or to identify
171 assively parallel sequencing instrument, and anaplastic lymphoma kinase translocation was evaluated b
172 vity to epidermal growth factor receptor and anaplastic lymphoma kinase tyrosine kinase inhibitors ha
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