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1  increased copy number of a genomic segment (gene amplification).
2  programs: the mitotic cycle, endocycle, and gene amplification.
3 3 lose G1/S checkpoint and are permissive to gene amplification.
4 DNA replication, endoreplication and chorion gene amplification.
5  and KRAS mutations, MET expression, and MET gene amplification.
6 nse observed in osteosarcoma cells with MDM2 gene amplification.
7 d to breast cancers that do not display HER2 gene amplification.
8 tion in a process that does not require HER2 gene amplification.
9 vIII expression even in the presence of high gene amplification.
10 nd treatment of cancers displaying miR-17-92 gene amplification.
11 ssion of GATA6 is found in EACs that contain gene amplification.
12 ll-cycle arrest and in this setting promotes gene amplification.
13 ses, elevated TRIB2 expression resulted from gene amplification.
14 ration of biological diversification without gene amplification.
15  have gone through ruminant lineage-specific gene amplification.
16 c assay occurs either by 'point' mutation or gene amplification.
17 e-stage metastatic cancers in the absence of gene amplification.
18 tein expression in the absence of true ERBB2 gene amplification.
19 ts, including chromosomal translocations and gene amplification.
20 I unless compensated by adaptive mutation or gene amplification.
21              There was also no delta-catenin gene amplification.
22        29% of triple-negative BC had PIP5K1A gene amplification.
23 xpression and for HER2/topoisomerase IIalpha gene amplification.
24  in human prostate and breast cancers due to gene amplification.
25  at least in part to aberrant methylation or gene amplification.
26 mcitabine-resistant tumor cells by reversing gene amplification.
27 through mutations, alternative splicing, and gene amplification.
28 r progesterone receptor expression and ERBB2 gene amplification.
29 tastases of prostate cancer independently of gene amplification.
30 25% of ovarian cancers characterized by PAK1 gene amplification.
31 mall percentage of breast cancers with PHGDH gene amplification.
32 to methodological challenges in detection of gene amplification.
33 e the process of antibiotic pressure-induced gene amplification.
34 ecurrences are frequently dependent upon Met 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 is much broader than that explored by single-gene amplifications.
39 2 gene mutations, ALK gene fusions, or FGFR1 gene amplifications.
40 plication has been implicated as a source of gene amplifications.
41 ranscripts, of which 69% are associated with gene amplifications.
42 e mechanism proposed to initiate palindromic gene amplification, a common feature of cancer cells.
43 ogene at 17q12 is susceptible to palindromic gene amplification, a mechanism characterized by the inv
44                                              Gene amplification, a process that increases the copy nu
45        c-MET activation can be caused by MET gene amplification, activating mutations, and auto- or p
46 investigated the occurrence and frequency of gene amplification affecting genes mapping to ch13q34 in
47 icle cells, which begin synchronized chorion gene amplification after three rounds of endocycle, prov
48 o the "mountain-and-hill" view of mutations, gene amplification also shows high- and low-frequency al
49                    Activation occurs through gene amplification and activating mutations.
50 ion by quantitative and qualitative 16S rRNA gene amplification and amplicon sequencing.
51 using a culture-independent method (16S rRNA gene amplification and clone library analyses).
52     This method can be applied to studies of gene amplification and copy number variation among speci
53 mation on somatic mutations in cancer genes, gene amplification and deletion, tissue type and transcr
54 ic detection methods require gene isolation, gene amplification and detection with a fluorescent-tagg
55                  New enzymes often evolve by gene amplification and divergence.
56                                    Moreover, gene amplification and EGFR mutations have been identifi
57                                         EGFR gene amplification and EGFRvIII are associated with GBM
58                        Here, we focus on the gene amplification and expression of cyclin E in these l
59  dataset had frequent (44%) instances of YAP gene amplification and genetic inactivation of Hippo pat
60  cycle is a mutational process that produces gene amplification and genome instability.
61 ad relatively mild effects on origins during gene amplification and genomic replication compared with
62 on in HER2-positive breast cancers with HER2 gene amplification and HER2-low or HER2-negative breast
63                     Here we show that NOTCH1 gene amplification and increased expression in CAFs are
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  the species Zaire Ebola virus using partial gene amplification and nanopore sequencing backed up the
74 nes, EBC-1 and H1993, showed significant Met gene amplification and overexpressed Met receptors which
75  Accumulating evidence has demonstrated that gene amplification and overexpression of Aurora A are li
76 somal alterations, with heterogeneous NOTCH1 gene amplification and overexpression that also occur, t
77 nhibition in ovarian cancer cells with Rsf-1 gene amplification and overexpression, but not in those
78                                       Notch3 gene amplification and pathway activation have been repo
79 t that mammary tumors that contain both HER2 gene amplification and PIK3CA mutations should be treate
80  and prognostic impact of heterogeneous HER2 gene amplification and polysomy 17 in patients with esop
81 eptor 2 (HER2)-positive breast cancer, GSDMB gene amplification and protein overexpression indicate a
82                                              Gene amplification and protein overexpression of cMET dr
83                             We used 16S rRNA gene amplification and pyrosequencing to characterize, f
84 h no impairment of cancer genes, but massive gene amplification and rearrangements.
85 der (R/F) variants were determined by single-gene amplification and sequencing of viral RNA or DNA fr
86 lts obtained by universal bacterial 16S rRNA gene amplification and sequencing.
87        ESBL and pAmpC genes were detected by gene amplification and sequencing.
88                                          Our gene amplification and somatic mutation analysis of brea
89 nomic sequencing has revealed recurrent ACK1 gene amplification and somatic mutations in a variety of
90 tains TRIM5 identified different patterns of gene amplification and the independent birth of CypA gen
91 ts of breast cancers with heterogeneous HER2 gene amplification and to define the repertoire of poten
92                             Analysis for AAK gene amplification and total AAK protein revealed no dif
93 n prostate cancers demonstrated that both AR gene amplification and TP53 mutation are among the most
94 NA replication within the context of chorion gene amplification and transcriptional regulation of a w
95 yc expression in cancers can result from MYC gene amplification and translocation but also from alter
96 on by exposure of cell lines harboring FGFR3 gene amplification and translocation to the selective FG
97                                 Although MYC gene amplification and translocations have been observed
98                                       Target gene amplification and unknown mechanisms also contribut
99 verexpression by immunohistochemistry (IHC), gene amplification and/or elevated serum Her-2/neu, no p
100  growth factor (EGF) receptor (EGFR) through gene amplification and/or mutation resulting in excessiv
101 ion frequencies and the occurrence of cancer gene amplifications and homozygous deletions.
102 ducting the first comprehensive screening of gene amplifications and polymorphisms associated with in
103 1, MIR17HG, TERT, MYC, and MYCN), generating gene amplifications and remodeling regulatory regions.
104 ancers via protein overexpression, mutation, gene amplification, and also paracrine or autocrine up-r
105 gy was associated with increased DNA damage, gene amplification, and aneuploidy, and this genomic ins
106 ounds exhibit weak mutagenic activity, cause gene amplification, and disrupt cellular epigenetic home
107                         DNA extraction, rpoB gene amplification, and DNA sequencing analysis were per
108 at gene duplications, segmental duplication, gene amplification, and point mutations coupled to gene
109 uroblastoma, MYCN is frequently activated by gene amplification, and reducing its expression by RNA i
110 stream applications, such as cDNA synthesis, gene amplification, and RT-qPCR.
111 tion of genetic alterations (gene mutations, gene amplification, and so on) and epigenetic alteration
112 itro and in mammary tumors in vivo, promoted gene amplification, and synergized with defective apopto
113 hat lineage-specific X-Y coevolution through gene amplification, and the selfish forces underlying th
114         Viral titer estimation, nucleocapsid gene amplification, and viral antinucleocapsid staining
115 enty-seven percent of NSCLCs exhibited SRC-3 gene amplification, and we found that lung cancer cell l
116               We detected PEL-specific miRNA gene amplifications, and concordant changes in pre-miRNA
117 y mutation, transcriptional up-regulation or gene amplification appears required for lymphoid transfo
118 enings indicate that tumors displaying c-MET gene amplification are "addicted" to MET signaling and t
119                      MDMX overexpression and gene amplification are implicated in p53 inactivation an
120                 These re-replication-induced gene amplifications are mediated by nonallelic homologou
121 c analyses that identified cyclin E1 (CCNE1) gene amplification as a candidate oncogenic driver in hi
122 cetylation, yielding important insights into gene amplification as a metazoan replication model.
123                           This occurrence of gene amplification as an herbicide resistance mechanism
124 action (PCR) and RT loop-mediated isothermal gene amplification assays.
125 st these cyclic peptides evolved by internal gene amplification associated with recruitment of AEP fo
126                   CNV analysis identified 41 gene amplifications associated with resistance, most aff
127             However, SOX2 overexpression and gene amplification associates with favorable outcome in
128 as cooperating oncogenes activated by way of gene amplification at chromosome 14q13 in lung cancer.
129                     Moreover, in fancg cells gene amplification at the CAD and dhfr loci is elevated,
130 eased, suggesting that resistance was due to gene amplification at the chr11 p15.5 locus.
131 s with high copy number due to polyploidy or gene amplification because frameshifts in all alleles ca
132 se in HER2 protein expression was not due to gene amplification but rather was mediated by receptor a
133 ficient for Chiffon have a defect in chorion gene amplification but still undergo endocycling.
134  activated by kinase domain mutations and/or gene amplification, but the interaction between the two
135 sion by immunohistochemistry (n = 478), MDM2 gene amplification by fluorescence in situ hybridization
136 ysis of EGFR, KRAS, and PIK3CA mutations and gene amplification by fluorescence in situ hybridization
137 lts indicate that the MRN complex suppresses gene amplification by stabilizing replication forks and
138                                        Thus, gene amplification can be acquired and expanded through
139 se cases, heterogeneous distribution of HER2 gene amplification can be found, which creates clinicall
140                      These data suggest that gene amplification can improve viral replication in a re
141 y evolve new and essential functions and how gene amplification can increase sex chromosome transmiss
142 ven driver genetic alterations, such as HER2 gene amplification, can be heterogeneously distributed w
143 r-tagged RARalpha-containing proteins to the gene-amplification chromosomal region by lac operator re
144  carcinogenesis, usually as a consequence of gene amplification, chromosomal translocations, or postt
145    This is the first report of tandem target gene amplification conferring field-evolved herbicide re
146 lified in breast tumors, the extent to which gene amplification contributes to ANO1 overexpression, a
147  in patient's plasma samples, acquired LMTK3 gene amplification (copy number variation) was associate
148 pression levels of FGFR-2 and FGFR-3 through gene amplification correlate with treatment response and
149 ectively, this study demonstrates that FGF19 gene amplification corresponds with an increased depende
150 erties determine rate and fitness effects of gene amplification, deletions, and mutations compromisin
151  adjacent nonmalignant mucosa due in part to gene amplification determined by Southern blotting.
152 y was to determine whether the level of HER2 gene amplification determined by the HER2/CEP17 ratio an
153               Here, we report a mechanism of gene amplification due to a translocatable unit (TU) exc
154 elicase in regulating SCR and SCR associated gene amplification/duplications and imply that these fun
155 lates the origins that mediate developmental gene amplification during Drosophila oogenesis.
156 replication stress and gained substrates for gene amplification during replication, as evidenced by t
157 n excellent model for study of the endocycle/gene amplification (E/A) switch.
158 tein overexpression occurs in the absence of gene amplification, e.g., T cell lymphoma (TCL).
159  to automated dual in situ hybridization for gene amplification evaluation.
160 ns unclear that how the cells with different gene amplification events contribute to disease propagat
161 e results raise a novel possibility that the gene amplification events near the IS1236 elements arise
162 tion of cell-cycle progression contribute to gene amplification events that can drive cancer.
163  reporter allowed the selection of low-order gene amplification events, going from one copy to two co
164   In some isolates, subsequent or coincident gene-amplification events augment resistance.
165 on (immunohistochemical analysis [IHC]), and gene amplification (fluorescent in situ hybridization or
166                                              Gene amplification followed by functional diversificatio
167 uct analysis and 16S ribosomal RNA bacterial gene amplification for bacterial taxa identification.
168         They include activating mutations or gene amplification for c-Met and constitutively active s
169 chanism, a complex rearrangement followed by gene amplification, for the simultaneous formation of an
170 cence reporter that allows us to distinguish gene amplifications from other up-mutations, we track in
171  that examined the fitness effects of single-gene amplifications genome-wide, we found that a small n
172                       The fleeting nature of gene amplifications gives rise to a generic population-l
173                            Cyclin E1 (CCNE1) gene amplification has been reported to occur independen
174                                       Notch3 gene amplification has recently been identified in ovari
175          MET overexpression, with or without gene amplification, has been reported in a variety of hu
176              Elevated YAP protein levels and gene amplification have been implicated in human cancer.
177 tial amplification of CCNE1 (cells with this gene amplification have been reported to be sensitive to
178                               The origins of gene amplifications have remained elusive; however, DNA
179  evidence of protein overexpression (IHC) or gene amplification (HER2 copy number or HER2/CEP17 ratio
180 defined according to consensus guidelines as gene amplification (HER2/CEP17 ratio >/= 2.0) in more th
181             In breast cancer cells with HER2 gene amplification, HER2 receptors exist on the cell sur
182 spite being clinically defined by a specific gene amplification, HER2-positive tumours melt into the
183 ated levels of AURKA protein, few have AURKA gene amplification, implying that posttranscriptional me
184 ks contributes to the generation of GCRs and gene amplification in cancer, and to non-recurrent CNVs
185 vides the first evidence of somatic STAT5A/B gene amplification in clinical PCas.
186  and CTCs provided that acquisition of HER-2 gene amplification in CTCs was taken into account.
187 2 was also overexpressed and associated with gene amplification in distinct CCRCC samples.
188                   Here, we use developmental gene amplification in Drosophila ovarian follicle cells
189 ion of origins responsible for developmental gene amplification in Drosophila.
190         In addition to its high frequency of gene amplification in glioblastoma multiforme, SEC61gamm
191 e rearrangement profiles linked to localized gene amplification in human cancers with acquired drug r
192 ctivating mutations in c-Met, as well as MET gene amplification in human cancers, points to c-Met as
193 in brains and imaginal discs, as well as for gene amplification in ovarian follicle cells.
194 k factors (HSFs), have undergone large-scale gene amplification in plants.
195 viously developed system was used to analyze gene amplification in selected mutants.
196 c specimens revealed a mutual exclusivity of gene amplification in the majority of glioblastoma tumor
197 s describe a complex pattern of differential gene amplification in the Trim5 cluster of rodents and i
198 PfRh1, PfRh2a, and PfRh2b, and an absence of gene amplification in these isolates.
199                             A causal role of gene amplification in tumorigenesis is well known, where
200 e copies per cell in >/= 40% of the cells or gene amplification) in 59.2%.
201 es existed between tumors with or without AR gene amplification, including a common loss of AR repres
202 n be activated through overexpression due to gene amplification, increased transcription, or changes
203 siae can strongly induce the initial step of gene amplification, increasing gene copy number from one
204 ly acquired higher fitness via recurrent K3L gene amplifications, incurring up to 7%-10% increases in
205 mpromised intra-S phase checkpoints promoted gene amplification independently from mutant p53.
206 or PfKelch13 mutations and for Pfplasmepsin2 gene amplification (indicating piperaquine resistance).
207 stemic lupus erythematosus (SLE) and whether gene amplification influences the autoantibody profiles
208                                 Differential gene amplification, insertions/deletions and inversions
209 aring complex chromosomal translocations and gene amplifications involving Igh and c-myc/pvt1 loci.
210                  A critical event initiating gene amplification is a DNA double-strand break (DSB), w
211  utility in cancers where drug resistance by gene amplification is a major obstacle to successful the
212     A critical step of BFB cycles leading to gene amplification is a palindromic fusion of sister chr
213                                              Gene amplification is a phenotype-causing form of chromo
214                  Therefore, an early step of gene amplification is a regulated process that is facili
215                                              Gene amplification is a tumor-specific event during mali
216 or more of these species, and within-species gene amplification is also evident.
217                           Here, we show that gene amplification is an additional evasion mechanism us
218 ntly in human B lymphoid tumors, while N-myc gene amplification is frequent in human neuroblastomas.
219                 As a developmental strategy, gene amplification is not the predominant means of achie
220 ver, the mechanism of hyperproduction due to gene amplification is not well understood.
221      Epidermal growth factor receptor (EGFR) gene amplification is the most common genetic alteration
222 stance level provided by point mutations and gene amplification is very low and antibiotic-resistant
223 rge DNA palindromes as a very early event in gene amplification is widely recognized, it is not known
224  Amplification of large chromosomal regions (gene amplification) is a common somatic alteration in hu
225 ll cycle-controlled DNA replication and rDNA gene amplification, is the T. thermophila origin recogni
226 x chromosomal rearrangements with associated gene amplification, known as complicons, characterize ma
227                                        PvDBP gene amplification leads to increased mRNA levels and pr
228                                Subsequently, gene amplification may have resulted via several other m
229      This study supports our hypothesis that gene amplification may provide a "molecular foothold," b
230 panel of nine lung cancer cell lines for Met gene amplification, Met expression, Met pathway activati
231                       A multistep process of gene amplification, mutation, and reduction allows poxvi
232      Epidermal growth factor receptor (EGFR) gene amplification, mutations, and/or aberrant activatio
233 on in clinical trials for subjects with FGFR gene amplifications, mutations and translocations.
234  132; 4%), as well as gene fusions (n = 51), gene amplifications (n = 35), genes with missense mutati
235                              The Palaearctic gene amplification occurred concurrently with the appear
236                                              Gene amplification occurs frequently in all organisms an
237 pothesis, we found evidence for selection of gene amplification of core regulators of proliferation i
238     Genotyping of resistant cells identified gene amplification of EGFR, KRAS, and mutant BRAF, as we
239 recq4(23), which specifically reduce chorion gene amplification of follicle cells by 4-5 fold, result
240                   We conclude that selective gene amplification of GATA6 during EAC development susta
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       We show via a phylogenetic analysis of gene amplification on the mouse sex chromosomes that mul
248 anisms including chromosomal translocations, gene amplification or deletion, point mutations and alte
249 factor receptor-alpha (PDGFRalpha) caused by gene amplification or ligand overexpression maintained p
250                           The extent of EGFR gene amplification or mutation of the EGFR tyrosine kina
251 ivated in bladder cancer, either directly by gene amplification or mutation, or indirectly by mutatio
252 ion of the MET pathway, for example, through gene amplification or mutations.
253           Hyperactive FOXA1 signaling due to gene amplification or overexpression has been reported i
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 rs that would otherwise not be identified by gene amplification or translocation alone.
257 < 40 min without the need of gene isolation, gene amplification, or expensive fluorescent tag but wit
258 ng: chromosome 7 copy gain, focal MET or HGF gene amplification, or MET kinase domain mutations.
259 adleri RLAT/KE/1957/SKINK-7 showed extensive gene amplifications, pervasive aneuploidy, and fission o
260 e switch from the endoreplication cycle to a gene-amplification phase, during which special genomic r
261  cells harboring either mutation (PIK3CA) or gene amplification (PIK3CB).
262                                       NOTCH3 gene amplification plays an important role in the progre
263 d patient-derived xenograft models with YES1 gene amplifications presented a high sensitivity to dasa
264  copy number amplification (fCNA) - enabling gene amplification, rapid tumor evolution, and the rewir
265 l substantial evolutionary changes including gene amplifications, rearrangements, loss and fusion.
266  of HER2-blocking agents to tumors with HER2 gene amplification, recent retrospective analyses sugges
267               Recent studies have identified gene amplification, sequence polymorphism, and variant e
268                            Thus, palindromic gene amplification shaped the amplified ERBB2 locus.
269 hat first separates the HER2+ tumors using a gene amplification signal for Her2/neu amplicon genes an
270                            The level of HER2 gene amplification significantly predicts sensitivity to
271  in the majority (90%) of SCCs regardless of gene amplification status.
272                          Renewed interest in gene amplification stems from its importance in evolutio
273                      Using a tissue-specific gene amplification strategy, we generated a transgenic m
274 tions occur primarily in the absence of HER2 gene amplification such that most HER2-mutant tumors are
275  populations-but they show elevated rates of gene amplification, suggesting that copy-number variatio
276 ed global transcriptional changes and led to gene amplification, suggesting that the role of RM syste
277 cle switch at stage 6/7 and the endocycle to gene amplification switch at stage10A/10B.
278 dometrial carcinomas manifest recurrent ESR1 gene amplifications that truncate the hormone-binding do
279      We identified a mutant in which, during gene amplification, the replication forks move twice as
280 ce arose from target site mutation or target gene amplification, the resistance mechanism in horsewee
281                                  Despite the gene amplification, there was comparatively little effec
282 a model in which dosage compensation buffers gene amplification through aneuploidy to provide a natur
283 vely blocks the switch from the endocycle to gene amplification through its regulation of ttk69.
284 MDM2 expression is found to be regulated via gene amplification, transcription, protein translation a
285 ast tumor samples with a focus on regions of gene amplification using mate-pair sequencing of long-in
286       The mechanisms of ERBB2 dosage changes-gene amplification versus chromosome gain and loss-proba
287 tive in situ analysis revealed that STAT5A/B gene amplification was associated with increased STAT5A/
288                                              Gene amplification was associated with reduced disease-f
289          We have previously shown that Rsf-1 gene amplification was associated with the most aggressi
290                                    The EPSPS gene amplification was heritable in common waterhemp and
291                                        EPSPS gene amplification was heritable, correlated with resist
292  present on every chromosome and, therefore, gene amplification was likely not caused by unequal chro
293                                     STAT5A/B gene amplification was more frequently found in PCas of
294                                              Gene amplification was performed together with immunohis
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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