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1  increased copy number of a genomic segment (gene amplification).
2 e-linked immunosorbent assay (ELISA; without gene amplification).
3 tion in a process that does not require HER2 gene amplification.
4 vIII expression even in the presence of high gene amplification.
5 nd treatment of cancers displaying miR-17-92 gene amplification.
6 ssion of GATA6 is found in EACs that contain gene amplification.
7 ll-cycle arrest and in this setting promotes gene amplification.
8 ses, elevated TRIB2 expression resulted from gene amplification.
9 ration of biological diversification without gene amplification.
10  have gone through ruminant lineage-specific gene amplification.
11 c assay occurs either by 'point' mutation or gene amplification.
12 e-stage metastatic cancers in the absence of gene amplification.
13 tein expression in the absence of true ERBB2 gene amplification.
14 ts, including chromosomal translocations and gene amplification.
15 I unless compensated by adaptive mutation or gene amplification.
16              There was also no delta-catenin gene amplification.
17 tastases of prostate cancer independently of gene amplification.
18 xpression and for HER2/topoisomerase IIalpha gene amplification.
19  in human prostate and breast cancers due to gene amplification.
20  at least in part to aberrant methylation or gene amplification.
21 mcitabine-resistant tumor cells by reversing gene amplification.
22 25% of ovarian cancers characterized by PAK1 gene amplification.
23 through mutations, alternative splicing, and gene amplification.
24 rther support for the role of palindromes in gene amplification.
25 ts into the role of palindromic sequences in gene amplification.
26  cycles, is thought to play an early role in gene amplification.
27  chromosomal regions that are predisposed to gene amplification.
28 LUM-artemether treatment failures and pfmdr1 gene amplification.
29      HER-2 overexpression is caused by HER-2 gene amplification.
30 in elusive and often cannot be attributed to gene amplification.
31 active N-Ras and B-Raf mutants as well as by gene amplification.
32 mall percentage of breast cancers with PHGDH gene amplification.
33 to methodological challenges in detection of gene amplification.
34 e the process of antibiotic pressure-induced gene amplification.
35 eplication in the new host without requiring gene amplification.
36 ipt may be a passenger aberration related to gene amplification.
37           None of the equivocal cases showed gene amplification.
38  programs: the mitotic cycle, endocycle, and gene amplification.
39 3 lose G1/S checkpoint and are permissive to gene amplification.
40 DNA replication, endoreplication and chorion gene amplification.
41  and KRAS mutations, MET expression, and MET gene amplification.
42 nse observed in osteosarcoma cells with MDM2 gene amplification.
43 d to breast cancers that do not display HER2 gene amplification.
44 ranscripts, of which 69% are associated with gene amplifications.
45 is much broader than that explored by single-gene amplifications.
46 2 gene mutations, ALK gene fusions, or FGFR1 gene amplifications.
47 e mechanism proposed to initiate palindromic gene amplification, a common feature of cancer cells.
48 ogene at 17q12 is susceptible to palindromic gene amplification, a mechanism characterized by the inv
49                                              Gene amplification, a process that increases the copy nu
50        c-MET activation can be caused by MET gene amplification, activating mutations, and auto- or p
51 investigated the occurrence and frequency of gene amplification affecting genes mapping to ch13q34 in
52 icle cells, which begin synchronized chorion gene amplification after three rounds of endocycle, prov
53 o the "mountain-and-hill" view of mutations, gene amplification also shows high- and low-frequency al
54                    Activation occurs through gene amplification and activating mutations.
55 f EphB4 in breast cancer cells was driven by gene amplification and by the erbB family of receptors v
56 using a culture-independent method (16S rRNA gene amplification and clone library analyses).
57     This method can be applied to studies of gene amplification and copy number variation among speci
58 mation on somatic mutations in cancer genes, gene amplification and deletion, tissue type and transcr
59                                    Moreover, gene amplification and EGFR mutations have been identifi
60                                         EGFR gene amplification and EGFRvIII are associated with GBM
61                        Here, we focus on the gene amplification and expression of cyclin E in these l
62 ad relatively mild effects on origins during gene amplification and genomic replication compared with
63 on in HER2-positive breast cancers with HER2 gene amplification and HER2-low or HER2-negative breast
64     SHH/GLI1 activation is the result of SHH gene amplification and is further mediated by NPM-ALK th
65 ases, increased AR expression occurs without gene amplification and may be due to altered transcripti
66 ost shift of M. persicae to tobacco and that gene amplification and microsatellite polymorphism are e
67 breast cancer cell lines to investigate HER2 gene amplification and modelled a range of different CNV
68                                         EGFR gene amplification and mutation are common in glioblasto
69 tic alterations, such as EGF receptor (EGFR) gene amplification and mutation, plays a major role in g
70      Epidermal growth factor receptor (EGFR) gene amplification and mutations are the most common onc
71 uently found in human cancers, mainly due to gene amplification and Myc-mediated transcriptional upre
72        IGF2BP1 was also associated with MYCN gene amplification and MYCN mRNA abundance.
73 nes, EBC-1 and H1993, showed significant Met gene amplification and overexpressed Met receptors which
74  Accumulating evidence has demonstrated that gene amplification and overexpression of Aurora A are li
75 nhibition in ovarian cancer cells with Rsf-1 gene amplification and overexpression, but not in those
76                                       Notch3 gene amplification and pathway activation have been repo
77 t that mammary tumors that contain both HER2 gene amplification and PIK3CA mutations should be treate
78  and prognostic impact of heterogeneous HER2 gene amplification and polysomy 17 in patients with esop
79 eptor 2 (HER2)-positive breast cancer, GSDMB gene amplification and protein overexpression indicate a
80                                              Gene amplification and protein overexpression of cMET dr
81                                              Gene amplification and protein overexpression of MDM2, w
82                             We used 16S rRNA gene amplification and pyrosequencing to characterize, f
83 h no impairment of cancer genes, but massive gene amplification and rearrangements.
84 der (R/F) variants were determined by single-gene amplification and sequencing of viral RNA or DNA fr
85 lts obtained by universal bacterial 16S rRNA gene amplification and sequencing.
86        ESBL and pAmpC genes were detected by gene amplification and sequencing.
87                                          Our gene amplification and somatic mutation analysis of brea
88 nomic sequencing has revealed recurrent ACK1 gene amplification and somatic mutations in a variety of
89 ts of breast cancers with heterogeneous HER2 gene amplification and to define the repertoire of poten
90                             Analysis for AAK gene amplification and total AAK protein revealed no dif
91 NA replication within the context of chorion gene amplification and transcriptional regulation of a w
92 yc expression in cancers can result from MYC gene amplification and translocation but also from alter
93 on by exposure of cell lines harboring FGFR3 gene amplification and translocation to the selective FG
94                                 Although MYC gene amplification and translocations have been observed
95                                       Target gene amplification and unknown mechanisms also contribut
96 verexpression by immunohistochemistry (IHC), gene amplification and/or elevated serum Her-2/neu, no p
97  growth factor (EGF) receptor (EGFR) through gene amplification and/or mutation resulting in excessiv
98 ion frequencies and the occurrence of cancer gene amplifications and homozygous deletions.
99 ducting the first comprehensive screening of gene amplifications and polymorphisms associated with in
100 ancers via protein overexpression, mutation, gene amplification, and also paracrine or autocrine up-r
101 gy was associated with increased DNA damage, gene amplification, and aneuploidy, and this genomic ins
102 ounds exhibit weak mutagenic activity, cause gene amplification, and disrupt cellular epigenetic home
103                         DNA extraction, rpoB gene amplification, and DNA sequencing analysis were per
104 uroblastoma, MYCN is frequently activated by gene amplification, and reducing its expression by RNA i
105 tion of genetic alterations (gene mutations, gene amplification, and so on) and epigenetic alteration
106 itro and in mammary tumors in vivo, promoted gene amplification, and synergized with defective apopto
107 enty-seven percent of NSCLCs exhibited SRC-3 gene amplification, and we found that lung cancer cell l
108 es in spontaneous or induced gene mutations, gene amplifications, and chromosomal instability in prim
109               We detected PEL-specific miRNA gene amplifications, and concordant changes in pre-miRNA
110 either EGFR kinase domain mutations nor EGFR gene amplification appear to be essential for response t
111 y mutation, transcriptional up-regulation or gene amplification appears required for lymphoid transfo
112 enings indicate that tumors displaying c-MET gene amplification are "addicted" to MET signaling and t
113                      MDMX overexpression and gene amplification are implicated in p53 inactivation an
114 ar mechanisms by which palindromes can cause gene amplification are largely unknown.
115                 These re-replication-induced gene amplifications are mediated by nonallelic homologou
116 c analyses that identified cyclin E1 (CCNE1) gene amplification as a candidate oncogenic driver in hi
117 cetylation, yielding important insights into gene amplification as a metazoan replication model.
118                           This occurrence of gene amplification as an herbicide resistance mechanism
119      Indeed, some OSCC cell lines had PPP1CA gene amplification, as analysed by fluorescence in situ
120 action (PCR) and RT loop-mediated isothermal gene amplification assays.
121 st these cyclic peptides evolved by internal gene amplification associated with recruitment of AEP fo
122                   CNV analysis identified 41 gene amplifications associated with resistance, most aff
123 ong-tract gene conversion and in suppressing gene amplifications associated with sister chromatid rec
124             However, SOX2 overexpression and gene amplification associates with favorable outcome in
125 as cooperating oncogenes activated by way of gene amplification at chromosome 14q13 in lung cancer.
126                     Moreover, in fancg cells gene amplification at the CAD and dhfr loci is elevated,
127 eased, suggesting that resistance was due to gene amplification at the chr11 p15.5 locus.
128  as well as 4- to 10-fold increased rates of gene amplification at the dhfr and CAD loci, respectivel
129 se in HER2 protein expression was not due to gene amplification but rather was mediated by receptor a
130 ficient for Chiffon have a defect in chorion gene amplification but still undergo endocycling.
131  activated by kinase domain mutations and/or gene amplification, but the interaction between the two
132 sion by immunohistochemistry (n = 478), MDM2 gene amplification by fluorescence in situ hybridization
133 ysis of EGFR, KRAS, and PIK3CA mutations and gene amplification by fluorescence in situ hybridization
134 lts indicate that the MRN complex suppresses gene amplification by stabilizing replication forks and
135                                        Thus, gene amplification can be acquired and expanded through
136 se cases, heterogeneous distribution of HER2 gene amplification can be found, which creates clinicall
137                      These data suggest that gene amplification can improve viral replication in a re
138 ven driver genetic alterations, such as HER2 gene amplification, can be heterogeneously distributed w
139 r-tagged RARalpha-containing proteins to the gene-amplification chromosomal region by lac operator re
140  carcinogenesis, usually as a consequence of gene amplification, chromosomal translocations, or postt
141    This is the first report of tandem target gene amplification conferring field-evolved herbicide re
142 lified in breast tumors, the extent to which gene amplification contributes to ANO1 overexpression, a
143  in patient's plasma samples, acquired LMTK3 gene amplification (copy number variation) was associate
144 ules for the palindrome-dependent pathway of gene amplification defined in yeast may operate during t
145 erties determine rate and fitness effects of gene amplification, deletions, and mutations compromisin
146 We demonstrate that the specific outcomes of gene amplification depend on the applied selection, the
147  adjacent nonmalignant mucosa due in part to gene amplification determined by Southern blotting.
148 y was to determine whether the level of HER2 gene amplification determined by the HER2/CEP17 ratio an
149 sm resembling retroposition controls 5S rRNA gene amplification, dispersal, and integration in the ge
150 elicase in regulating SCR and SCR associated gene amplification/duplications and imply that these fun
151 lates the origins that mediate developmental gene amplification during Drosophila oogenesis.
152 replication stress and gained substrates for gene amplification during replication, as evidenced by t
153 n excellent model for study of the endocycle/gene amplification (E/A) switch.
154 tein overexpression occurs in the absence of gene amplification, e.g., T cell lymphoma (TCL).
155  to automated dual in situ hybridization for gene amplification evaluation.
156 ns unclear that how the cells with different gene amplification events contribute to disease propagat
157 e results raise a novel possibility that the gene amplification events near the IS1236 elements arise
158 tion of cell-cycle progression contribute to gene amplification events that can drive cancer.
159  reporter allowed the selection of low-order gene amplification events, going from one copy to two co
160 sults demonstrated EGFR high polysomy and/or gene amplification (FISH positive).
161 on (immunohistochemical analysis [IHC]), and gene amplification (fluorescent in situ hybridization or
162                                              Gene amplification followed by functional diversificatio
163 uct analysis and 16S ribosomal RNA bacterial gene amplification for bacterial taxa identification.
164         They include activating mutations or gene amplification for c-Met and constitutively active s
165 chanism, a complex rearrangement followed by gene amplification, for the simultaneous formation of an
166 cence reporter that allows us to distinguish gene amplifications from other up-mutations, we track in
167  that examined the fitness effects of single-gene amplifications genome-wide, we found that a small n
168                                          myc gene amplification has been identified in many large cel
169                            Cyclin E1 (CCNE1) gene amplification has been reported to occur independen
170 ng drug selection, especially in cases where gene amplification has occurred, MDR-1 transcripts can b
171                                       Notch3 gene amplification has recently been identified in ovari
172          MET overexpression, with or without gene amplification, has been reported in a variety of hu
173              Elevated YAP protein levels and gene amplification have been implicated in human cancer.
174  evidence of protein overexpression (IHC) or gene amplification (HER2 copy number or HER2/CEP17 ratio
175 defined according to consensus guidelines as gene amplification (HER2/CEP17 ratio >/= 2.0) in more th
176             In breast cancer cells with HER2 gene amplification, HER2 receptors exist on the cell sur
177 spite being clinically defined by a specific gene amplification, HER2-positive tumours melt into the
178 ated levels of AURKA protein, few have AURKA gene amplification, implying that posttranscriptional me
179 ks contributes to the generation of GCRs and gene amplification in cancer, and to non-recurrent CNVs
180 vides the first evidence of somatic STAT5A/B gene amplification in clinical PCas.
181  and CTCs provided that acquisition of HER-2 gene amplification in CTCs was taken into account.
182 2 was also overexpressed and associated with gene amplification in distinct CCRCC samples.
183                   Here, we use developmental gene amplification in Drosophila ovarian follicle cells
184 ion of origins responsible for developmental gene amplification in Drosophila.
185         In addition to its high frequency of gene amplification in glioblastoma multiforme, SEC61gamm
186 ctivating mutations in c-Met, as well as MET gene amplification in human cancers, points to c-Met as
187 in brains and imaginal discs, as well as for gene amplification in ovarian follicle cells.
188 k factors (HSFs), have undergone large-scale gene amplification in plants.
189 viously developed system was used to analyze gene amplification in selected mutants.
190 c specimens revealed a mutual exclusivity of gene amplification in the majority of glioblastoma tumor
191 ther microbes, M.oryzae exhibits very little gene amplification in the subtelomere regions-out of 261
192 PfRh1, PfRh2a, and PfRh2b, and an absence of gene amplification in these isolates.
193                             A causal role of gene amplification in tumorigenesis is well known, where
194                               The origins of gene amplifications in mammalian cells have been difficu
195 e copies per cell in >/= 40% of the cells or gene amplification) in 59.2%.
196 es existed between tumors with or without AR gene amplification, including a common loss of AR repres
197 n be activated through overexpression due to gene amplification, increased transcription, or changes
198 siae can strongly induce the initial step of gene amplification, increasing gene copy number from one
199 ly acquired higher fitness via recurrent K3L gene amplifications, incurring up to 7%-10% increases in
200 mpromised intra-S phase checkpoints promoted gene amplification independently from mutant p53.
201 or PfKelch13 mutations and for Pfplasmepsin2 gene amplification (indicating piperaquine resistance).
202 stemic lupus erythematosus (SLE) and whether gene amplification influences the autoantibody profiles
203                                              Gene amplification initiates from origins in the 5' non-
204                                 Differential gene amplification, insertions/deletions and inversions
205 aring complex chromosomal translocations and gene amplifications involving Igh and c-myc/pvt1 loci.
206                                              Gene amplification is a copy number increase of a restri
207                  A critical event initiating gene amplification is a DNA double-strand break (DSB), w
208  utility in cancers where drug resistance by gene amplification is a major obstacle to successful the
209     A critical step of BFB cycles leading to gene amplification is a palindromic fusion of sister chr
210                                              Gene amplification is a phenotype-causing form of chromo
211                  Therefore, an early step of gene amplification is a regulated process that is facili
212                                              Gene amplification is a tumor-specific event during mali
213 or more of these species, and within-species gene amplification is also evident.
214 ntly in human B lymphoid tumors, while N-myc gene amplification is frequent in human neuroblastomas.
215                 As a developmental strategy, gene amplification is not the predominant means of achie
216                                              Gene amplification is one of the common mechanisms that
217  values for both HER2 protein expression and gene amplification is recommended: a positive HER2 resul
218      Epidermal growth factor receptor (EGFR) gene amplification is the most common genetic alteration
219 rge DNA palindromes as a very early event in gene amplification is widely recognized, it is not known
220  Amplification of large chromosomal regions (gene amplification) is a common somatic alteration in hu
221 ll cycle-controlled DNA replication and rDNA gene amplification, is the T. thermophila origin recogni
222 x chromosomal rearrangements with associated gene amplification, known as complicons, characterize ma
223                                        Thus, gene amplification, loss of silencing sequence and posit
224                                Subsequently, gene amplification may have resulted via several other m
225      This study supports our hypothesis that gene amplification may provide a "molecular foothold," b
226 panel of nine lung cancer cell lines for Met gene amplification, Met expression, Met pathway activati
227  cells resulted in increased gene mutations, gene amplification, micronuclei formation, and chromosom
228                       A multistep process of gene amplification, mutation, and reduction allows poxvi
229      Epidermal growth factor receptor (EGFR) gene amplification, mutations, and/or aberrant activatio
230 on in clinical trials for subjects with FGFR gene amplifications, mutations and translocations.
231                              The Palaearctic gene amplification occurred concurrently with the appear
232 kinase plasminogen activator receptor (uPAR) gene amplification occurs and whether analysis of indivi
233                                              Gene amplification occurs frequently in all organisms an
234                        Overexpression and/or gene amplification of c-Src and members of the epidermal
235                                              Gene amplification of chromosomal band 11q13 is observed
236 pothesis, we found evidence for selection of gene amplification of core regulators of proliferation i
237     Genotyping of resistant cells identified gene amplification of EGFR, KRAS, and mutant BRAF, as we
238 recq4(23), which specifically reduce chorion gene amplification of follicle cells by 4-5 fold, result
239                   We conclude that selective gene amplification of GATA6 during EAC development susta
240                                Unexpectedly, gene amplification of HER-2 and uPAR occurred most frequ
241   NEPC is associated with overexpression and gene amplification of MYCN (encoding N-Myc).
242 o-assembled 3,780-bp contig was confirmed by gene amplification of overlapping regions over almost th
243 of secondary mutations in the kinase target, gene amplification of the primary oncogene, and upregula
244  exhibit sustained stimulation, mutation, or gene amplification of the receptor tyrosine kinase human
245                                     Frequent gene amplification of the receptor-activated calcium-dep
246                     Subsequent reductions in gene amplifications offset the costs associated with lar
247 RCC4/p53-deficient MBs have high-level N-myc gene amplification, often intrachromosomally in the cont
248       We show via a phylogenetic analysis of gene amplification on the mouse sex chromosomes that mul
249 ; (2) increased levels of the protein due to gene amplification or altered mRNA expression; (3) activ
250 factor receptor-alpha (PDGFRalpha) caused by gene amplification or ligand overexpression maintained p
251                           The extent of EGFR gene amplification or mutation of the EGFR tyrosine kina
252 ivated in bladder cancer, either directly by gene amplification or mutation, or indirectly by mutatio
253 ion of the MET pathway, for example, through gene amplification or mutations.
254 This regulation was lost, however, after MET gene amplification or overexpression of a constitutively
255 ive PPAR signaling, either due to PPAR gamma gene amplification or RXRA hot-spot mutation (S427F/Y) d
256 ng: chromosome 7 copy gain, focal MET or HGF gene amplification, or MET kinase domain mutations.
257 role of a dominant oncogene as the target of gene amplification, overexpression, and the activation o
258 adleri RLAT/KE/1957/SKINK-7 showed extensive gene amplifications, pervasive aneuploidy, and fission o
259 e switch from the endoreplication cycle to a gene-amplification phase, during which special genomic r
260  cells harboring either mutation (PIK3CA) or gene amplification (PIK3CB).
261                                       NOTCH3 gene amplification plays an important role in the progre
262  of HER2-blocking agents to tumors with HER2 gene amplification, recent retrospective analyses sugges
263               Recent studies have identified gene amplification, sequence polymorphism, and variant e
264                            Thus, palindromic gene amplification shaped the amplified ERBB2 locus.
265 hat first separates the HER2+ tumors using a gene amplification signal for Her2/neu amplicon genes an
266                            The level of HER2 gene amplification significantly predicts sensitivity to
267  in the majority (90%) of SCCs regardless of gene amplification status.
268                          Renewed interest in gene amplification stems from its importance in evolutio
269                      Using a tissue-specific gene amplification strategy, we generated a transgenic m
270 tions occur primarily in the absence of HER2 gene amplification such that most HER2-mutant tumors are
271  populations-but they show elevated rates of gene amplification, suggesting that copy-number variatio
272 ed global transcriptional changes and led to gene amplification, suggesting that the role of RM syste
273 dometrial carcinomas manifest recurrent ESR1 gene amplifications that truncate the hormone-binding do
274      We identified a mutant in which, during gene amplification, the replication forks move twice as
275 ce arose from target site mutation or target gene amplification, the resistance mechanism in horsewee
276                                  Despite the gene amplification, there was comparatively little effec
277 a model in which dosage compensation buffers gene amplification through aneuploidy to provide a natur
278 vely blocks the switch from the endocycle to gene amplification through its regulation of ttk69.
279 t fragile site 1q31 was associated with mdr1 gene amplification through the BFB mechanism.
280        Here, we focused on narrow regions of gene amplification to facilitate identification of genet
281 MDM2 expression is found to be regulated via gene amplification, transcription, protein translation a
282       Thus, selection favors a succession of gene-amplification types that make sequence changes more
283 ast tumor samples with a focus on regions of gene amplification using mate-pair sequencing of long-in
284       The mechanisms of ERBB2 dosage changes-gene amplification versus chromosome gain and loss-proba
285 atients with lung adenocarcinoma showed that gene amplification was associated with high protein expr
286 tive in situ analysis revealed that STAT5A/B gene amplification was associated with increased STAT5A/
287                                              Gene amplification was associated with reduced disease-f
288          We have previously shown that Rsf-1 gene amplification was associated with the most aggressi
289                                    The EPSPS gene amplification was heritable in common waterhemp and
290                                        EPSPS gene amplification was heritable, correlated with resist
291  present on every chromosome and, therefore, gene amplification was likely not caused by unequal chro
292                                     STAT5A/B gene amplification was more frequently found in PCas of
293                                              Gene amplification was performed together with immunohis
294                       Cancer cells with mdm2 gene amplification were most sensitive to nutlin-3 in vi
295 l to adenocarcinoma though tumour-associated gene amplifications were absent.
296 lian cells become proficient for spontaneous gene amplification when the function of the DSB repair p
297  pro-B lymphomas routinely activate c-myc by gene amplification, whereas Xrcc4/p53-deficient peripher
298 A expression was associated with focal PFGRA gene amplification, which was similarly detected in a sm
299 23) are overexpressed only in the context of gene amplification while two genes (ERMP1 and IL33) are
300 atellite in the promoter region and a recent gene amplification, with some aphid clones carrying up t

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