コーパス検索結果 (1語後でソート)
通し番号をクリックするとPubMedの該当ページを表示します
1 ch are similar to those observed in familial adenomatous polyposis.
2 is associated with pathogenesis of familial adenomatous polyposis.
3 ng causes of death in patients with familial adenomatous polyposis.
4 t with Apc, are important models of familial adenomatous polyposis.
5 a development in an animal model of familial adenomatous polyposis.
6 n combination in an animal model of familial adenomatous polyposis.
7 pathogenic variants associated with familial adenomatous polyposis.
8 n additional recessive subtype of colorectal adenomatous polyposis.
9 h either drug alone, in adults with familial adenomatous polyposis.
10 m 102 unrelated individuals with unexplained adenomatous polyposis.
11 equently remains unresolved in patients with adenomatous polyposis.
12 sies from IPAA patients with UC and familial adenomatous polyposis.
13 es of hereditary syndromes, such as familial adenomatous polyposis, a cancer predisposition syndrome
15 rome and the phenotypic features of familial adenomatous polyposis aid significantly in syndrome diag
16 , germline mutation of which causes familial adenomatous polyposis, an autosomal intestinal cancer sy
17 tions affecting NTHL1 predispose carriers to adenomatous polyposis and colorectal cancer, but the com
19 types in a murine model of colon cancer, the adenomatous polyposis (APC) mutant (Apc (716/+)) model.
21 in animals and in patients with the familial adenomatous polyposis by downregulating beta-catenin sig
22 and inherited conditions (Lynch and familial adenomatous polyposis), by changing only 2 tissue-specif
24 e conditionally expressed a mutant allele of adenomatous polyposis coli (APC(cKO)) in murine uterine
25 al crypt, augmenting CRC tumorigenesis in an adenomatous polyposis coli (APC(Delta14/+)) mouse model.
26 n on chronic hypoxia-induced PH, we used the adenomatous polyposis coli (Apc(Min/+)) mouse, where red
27 as a binding partner of the tumor suppressor adenomatous polyposis coli (APC) [1]; however, the signi
31 contribution of the Wnt-regulating proteins adenomatous polyposis coli (APC) and APC2 in the pathoge
32 ested that specific GSK3 substrates, such as adenomatous polyposis coli (APC) and collapsin response
33 wo microtubule plus end-associated proteins, adenomatous polyposis coli (APC) and EB1, providing a po
34 onal and transcriptional mechanisms and that adenomatous polyposis coli (APC) and GSK3beta, which are
35 expression of the gut tumor suppressor gene adenomatous polyposis coli (Apc) and its role in the oli
37 ed by the colorectal cancer tumor suppressor adenomatous polyposis coli (APC) and that KLF4 repressed
38 ther, we find that both the tumor suppressor adenomatous polyposis coli (APC) and the ADP-ribose poly
39 nce microscopy to image the tumor suppressor adenomatous polyposis coli (APC) and the formin mDia1 du
40 firmed an expected loss in the expression of adenomatous polyposis coli (APC) and the transcriptional
41 First, patients with germline mutations in adenomatous polyposis coli (APC) are susceptible to stom
42 polyposis (FAP) but further study identified adenomatous polyposis coli (APC) as responsible for FAP
45 C57BL/6J mice carrying the Min allele of Adenomatous polyposis coli (Apc) develop numerous adenom
48 mice bearing a heterozygote mutation in the adenomatous polyposis coli (APC) gene (Apc(Min/+) mice).
49 ted gene-targeted pigs with mutations in the adenomatous polyposis coli (APC) gene (APC) that are ort
50 of these models involve modification of the adenomatous polyposis coli (Apc) gene and are excellent
51 ased in human cells with deficiencies in the adenomatous polyposis coli (APC) gene and in cells stimu
66 letion in mice with inactivating mutation of adenomatous polyposis coli (APC) gene reduces intestinal
67 ssf1a can cooperate with inactivation of the adenomatous polyposis coli (Apc) gene to accelerate inte
68 ization of beta-catenin or defective for the adenomatous polyposis coli (APC) gene to reinvestigated
69 n the bladder as conditional deletion of the adenomatous polyposis coli (Apc) gene within the adult b
70 intestinal carcinogenesis is mutation of the adenomatous polyposis coli (APC) gene, which leads to ac
71 requently bear inactivating mutations of the adenomatous polyposis coli (APC) gene, whose product is
78 criptional and epigenetic changes induced by adenomatous polyposis coli (Apc) inactivation in intesti
82 ncluding the brain, and the tumor suppressor adenomatous polyposis coli (APC) is a key negative regul
98 aling following loss of the tumor suppressor adenomatous polyposis coli (APC) is thought to initiate
99 ore, the loss of heterozygosity rates at the adenomatous polyposis coli (Apc) locus are unaffected by
101 te that intestinal epithelial suppression of adenomatous polyposis coli (Apc) mitigates RIGS lethalit
103 ects of daily oral administration of HFCS in adenomatous polyposis coli (APC) mutant mice, which are
104 esis that initiation of colorectal cancer by adenomatous polyposis coli (APC) mutation is mediated by
109 nt/beta-catenin pathway activation caused by adenomatous polyposis coli (APC) mutations occurs in app
112 (CRCs), an initiating mutation occurs in the adenomatous polyposis coli (APC) or beta-catenin gene, a
113 n that have been associated with loss of the adenomatous polyposis coli (APC) or constitutive activat
116 nestin expressing NeuN positive neurons and adenomatous polyposis coli (APC) positive mature oligode
118 ibition of GSK-3beta and accumulation of the adenomatous polyposis coli (APC) protein at the plus end
119 ere, we report that the expression status of adenomatous polyposis coli (APC) protein determines the
124 inked to deficiencies in mismatch repair and adenomatous polyposis coli (APC) proteins, diet, inflamm
125 ing a knockout allele in the gatekeeper gene Adenomatous polyposis coli (Apc) recapitulates familial
128 is functionally important for cell migration.Adenomatous polyposis coli (APC) regulates the localizat
129 gene targeting in mice, we demonstrate that adenomatous polyposis coli (APC) serves an essential fun
130 ne such pathway the tumor-suppressor protein adenomatous polyposis coli (APC) targets RNAs to cell pr
131 ting factor-responsive cells were defined by adenomatous polyposis coli (APC) time-of-flight mass cyt
133 In turn, KIF17 participates in localizing adenomatous polyposis coli (APC) to the plus ends of a s
139 cells lines with truncating mutations in the adenomatous polyposis coli (APC) tumor suppressor gene t
143 ce with IEC-specific allelic deletion of the adenomatous polyposis coli (Apc) tumor suppressor locus,
145 atase 2A (PP2A) and must be protected by the adenomatous polyposis coli (APC) tumor suppressor protei
147 rcinomas contain truncating mutations in the adenomatous polyposis coli (APC) tumor suppressor, a neg
148 in signaling is negatively controlled by the adenomatous polyposis coli (APC) tumor suppressor, which
149 calculating the in vivo mutation rate of the adenomatous polyposis coli (APC) tumor-suppressor gene i
150 ollows a genetic pathway whereby loss of the adenomatous polyposis coli (APC) tumour suppressor and a
151 RNAs in the granules associate with the adenomatous polyposis coli (APC) tumour suppressor and t
155 In this study, the tumor suppressor protein adenomatous polyposis coli (APC) was found to be importa
158 ne the genetic relationship between MPC1 and Adenomatous polyposis coli (APC), a key tumor suppressor
161 approaches suggest that the tumor suppressor adenomatous polyposis coli (APC), a regulator of Wnt sig
167 atenin destruction complex components Axin1, adenomatous polyposis coli (APC), and GSK3beta were also
168 forms a complex with axin (axis inhibitor), adenomatous polyposis coli (APC), casein kinase 1alpha (
169 Together with its direct binding partner adenomatous polyposis coli (APC), EB1 can stabilize micr
172 in acromegaly patients induced colon p53 and adenomatous polyposis coli (APC), reversing progrowth GH
173 e designed against beta-catenin (Ctnnb1) and adenomatous polyposis coli (Apc), two commonly mutated g
174 ical Wnt signaling by targeting the gene for Adenomatous Polyposis Coli (Apc), which controls Wnt sig
175 e, we show that the tumor suppressor protein adenomatous polyposis coli (APC), which is a known MT-as
177 ulation and epithelial over-proliferation in Adenomatous polyposis coli (APC)-mutated intestine.
178 o develop colitis-associated and spontaneous adenomatous polyposis coli (APC)-related tumors of the i
179 iously disclosed the discovery of truncating adenomatous polyposis coli (APC)-selective inhibitor 1 (
186 ation suppresses beta-catenin activity in an adenomatous polyposis coli (APC)/glycogen synthase kinas
189 py, FRAP, live cell imaging, and a mutant of Adenomatous polyposis coli (APC-m4) defective in actin n
190 Arm is targeted for proteolysis by the Axin/Adenomatous polyposis coli (Apc1 and Apc2)/Zeste-white 3
191 V integration site family (WNT)/beta-catenin/adenomatous polyposis coli (CTNNB1/APC) pathway has been
192 alignancies due to inactivating mutations of adenomatous polyposis coli (in colorectal cancer) or act
195 sly in germ cells for proper localization of Adenomatous polyposis coli 2 and E-cadherin at the hub-G
198 tive regulators of beta-catenin, such as the adenomatous polyposis coli and Axin tumor suppressor pro
199 G-protein signaling (RGS) domain that binds adenomatous polyposis coli and Galpha subunits, thereby
200 atenin and the destruction complex component adenomatous polyposis coli at a similar SLS motif to the
203 iation domain family 1 gene RASSF1A, and the adenomatous polyposis coli gene APC in tumors and in his
204 Mice carrying and non-sense mutation in Adenomatous polyposis coli gene at site R850, which desi
208 olocalizes with the tumor suppressor protein adenomatous polyposis coli in the TJs of epithelial cell
212 ling induced by loss of the tumor suppressor adenomatous polyposis coli or casein kinase 1alpha uncov
213 Most information about the roles of the adenomatous polyposis coli protein (APC) and its binding
215 Here we report that the tumour suppressor adenomatous polyposis coli protein (APC) directs the loc
218 ows that the actin-nucleating ability of the adenomatous polyposis coli protein is required for disas
219 versely, RNAi of the beta-catenin antagonist adenomatous polyposis coli results in the regeneration o
220 W480 cells stably transformed with wild-type adenomatous polyposis coli showed decreased beta-catenin
222 he microtubule motor cytoplasmic dynein, the adenomatous polyposis coli tumor suppressor protein (APC
225 member 1, insulin-like growth factor 2, and adenomatous polyposis coli) and other solid tumors (e.g.
227 g in T cell lineages by deletion of the Apc (adenomatous polyposis coli) gene causes spontaneous T ce
228 mutation of the Wnt repressor APC (encoding adenomatous polyposis coli) leads to a state of aberrant
229 that contained mutations in either the APC (adenomatous polyposis coli) locus or in an allele of bet
231 her beta-catenin activation or loss of APC - adenomatous polyposis coli) upon expression of CRE recom
233 ectly targets the tumor suppressor gene APC (adenomatous polyposis coli), thereby affecting Wnt (Wing
236 aditionally attributed to mutations in Axin, adenomatous polyposis coli, and beta-catenin that lead t
237 I, IGF2; tumor suppressor candidate 33, N33; adenomatous polyposis coli, APC; mut-L homolog 1, MLH1;
238 a-catenin pathway mutations, such as loss of adenomatous polyposis coli, are insensitive to this nove
240 -catenin pathway regulatory genes, including adenomatous polyposis coli, GSK3beta, axin 1, beta-caten
242 e glycogen synthase kinase 3beta (GSK3beta)- adenomatous polyposis coli-axin-mediated degradation pat
243 otubule organization and capture dynamics in adenomatous polyposis coli-deficient radial progenitors.
244 ted signaling and glycogen synthase kinase-3/adenomatous polyposis coli-mediated beta-catenin activat
246 intestinal tumors driven by mutations in the adenomatous polyposis coli/beta-catenin pathway and acti
249 erived WNT2 activated canonical signaling in adenomatous polyposis coli/beta-catenin wild-type colon
250 ications of MMVTx for patients with familial adenomatous polyposis (FAP) and the technical feasibilit
252 amatically altered for the worse in familial adenomatous polyposis (FAP) because these patients harbo
254 identified as a candidate gene for familial adenomatous polyposis (FAP) but further study identified
255 tumors often occur in patients with familial adenomatous polyposis (FAP) coli who have germ line muta
256 rative colitis (UC) in 37 patients, familial adenomatous polyposis (FAP) in 12 patients, and colonic
257 of thyroid cancer in patients with Familial adenomatous polyposis (FAP) in a prospective study of th
261 rliest colonic tissue alteration in familial adenomatous polyposis (FAP) patients, we present the hyp
263 ine mutation of which characterizes familial adenomatous polyposis (FAP), an autosomal intestinal can
264 atous polyposis coli (APC) underlie familial adenomatous polyposis (FAP), an inherited cancer syndrom
265 ive colitis, indeterminate colitis, familial adenomatous polyposis (FAP), and a select group of patie
266 inherited predisposition, including familial adenomatous polyposis (FAP), hereditary nonpolyposis col
267 atorial chemoprevention efficacy in familial adenomatous polyposis (FAP), signal of benefit from imag
268 hallmark of many cancers, including familial adenomatous polyposis (FAP)-related desmoid tumors.
274 to iPSCs derived from patients with familial adenomatous polyposis (FAP-iPSCs) harboring germline mut
276 rosis, Duchenne Muscular Dystrophy, Familial Adenomatous Polyposis, Hereditary Non-polyposis Colorect
277 h as multiple endocrine neoplasias, familial adenomatous polyposis, hereditary nonpolyposis colon can
279 enomas recovered from patients with familial adenomatous polyposis, including adenomas as small as a
282 yndromes, including Lynch syndrome, familial adenomatous polyposis, MUTYH-associated polyposis, and c
283 testinal tissues from patients with familial adenomatous polyposis (n = 18) or sessile serrated adeno
285 ately 30% of families affected by colorectal adenomatous polyposis, no germline mutations have been i
286 inically from cases with attenuated familial adenomatous polyposis or MUTYH-associated polyposis.
287 associated with thyroid cancer (eg, familial adenomatous polyposis), or one or more first-degree rela
288 A diagnosis of Lynch syndrome, familial adenomatous polyposis, or another genetic syndrome can i
290 families showed recessive inheritance of the adenomatous polyposis phenotype and progression to CRC i
291 opic expression of APC, but not its familial adenomatous polyposis-related truncation mutant, promine
296 ajority of the 30% of patients with familial adenomatous polyposis that do not test positive for muta
297 this trial involving patients with familial adenomatous polyposis, the incidence of disease progress
298 diseases, three females (1.6 %) had familial adenomatous polyposis; three patients (1 male and two fe
299 on-negative Lynch syndrome, 16 with familial adenomatous polyposis, two with constitutional mismatch
300 polyposis coli (APC) gene reduces intestinal adenomatous polyposis via Axin/beta-catenin axis and the