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1 is associated with pathogenesis of familial adenomatous polyposis.
2 ng causes of death in patients with familial adenomatous polyposis.
3 t with Apc, are important models of familial adenomatous polyposis.
4 a development in an animal model of familial adenomatous polyposis.
5 n combination in an animal model of familial adenomatous polyposis.
6 mice provide a good model of human familial adenomatous polyposis.
7 n additional recessive subtype of colorectal adenomatous polyposis.
8 pathogenic variants associated with familial adenomatous polyposis.
9 m 102 unrelated individuals with unexplained adenomatous polyposis.
10 equently remains unresolved in patients with adenomatous polyposis.
11 sies from IPAA patients with UC and familial adenomatous polyposis.
12 ch are similar to those observed in familial adenomatous polyposis.
13 is (chronic ulcerative colitis 97%, familial adenomatous polyposis 3%) and previous operative history
14 es of hereditary syndromes, such as familial adenomatous polyposis, a cancer predisposition syndrome
16 rome and the phenotypic features of familial adenomatous polyposis aid significantly in syndrome diag
17 , germline mutation of which causes familial adenomatous polyposis, an autosomal intestinal cancer sy
20 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
23 e conditionally expressed a mutant allele of adenomatous polyposis coli (APC(cKO)) in murine uterine
24 n on chronic hypoxia-induced PH, we used the adenomatous polyposis coli (Apc(Min/+)) mouse, where red
28 contribution of the Wnt-regulating proteins adenomatous polyposis coli (APC) and APC2 in the pathoge
29 ested that specific GSK3 substrates, such as adenomatous polyposis coli (APC) and collapsin response
30 we show that two tumor suppressor proteins, adenomatous polyposis coli (APC) and Dlg1-SAP97, are req
31 wo microtubule plus end-associated proteins, adenomatous polyposis coli (APC) and EB1, providing a po
32 onal and transcriptional mechanisms and that adenomatous polyposis coli (APC) and GSK3beta, which are
33 expression of the gut tumor suppressor gene adenomatous polyposis coli (Apc) and its role in the oli
35 ed by the colorectal cancer tumor suppressor adenomatous polyposis coli (APC) and that KLF4 repressed
36 ther, we find that both the tumor suppressor adenomatous polyposis coli (APC) and the ADP-ribose poly
37 nce microscopy to image the tumor suppressor adenomatous polyposis coli (APC) and the formin mDia1 du
38 firmed an expected loss in the expression of adenomatous polyposis coli (APC) and the transcriptional
39 First, patients with germline mutations in adenomatous polyposis coli (APC) are susceptible to stom
40 polyposis (FAP) but further study identified adenomatous polyposis coli (APC) as responsible for FAP
42 C57BL/6J mice carrying the Min allele of Adenomatous polyposis coli (Apc) develop numerous adenom
44 rectal cancers consistently contained mutant adenomatous polyposis coli (APC) DNA molecules in their
46 mice bearing a heterozygote mutation in the adenomatous polyposis coli (APC) gene (Apc(Min/+) mice).
47 ted gene-targeted pigs with mutations in the adenomatous polyposis coli (APC) gene (APC) that are ort
49 of these models involve modification of the adenomatous polyposis coli (Apc) gene and are excellent
50 ased in human cells with deficiencies in the adenomatous polyposis coli (APC) gene and in cells stimu
57 l cancer cell lines bearing mutations on the adenomatous polyposis coli (APC) gene as a model of FAP-
64 ost colorectal cancers have mutations of the adenomatous polyposis coli (APC) gene or the beta-cateni
66 letion in mice with inactivating mutation of adenomatous polyposis coli (APC) gene reduces intestinal
68 ssf1a can cooperate with inactivation of the adenomatous polyposis coli (Apc) gene to accelerate inte
69 ization of beta-catenin or defective for the adenomatous polyposis coli (APC) gene to reinvestigated
70 n the bladder as conditional deletion of the adenomatous polyposis coli (Apc) gene within the adult b
71 intestinal carcinogenesis is mutation of the adenomatous polyposis coli (APC) gene, which leads to ac
72 requently bear inactivating mutations of the adenomatous polyposis coli (APC) gene, whose product is
79 e generated mice lacking the beta-catenin or adenomatous polyposis coli (Apc) genes in osteoblasts.
83 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
102 esis that initiation of colorectal cancer by adenomatous polyposis coli (APC) mutation is mediated by
106 nt/beta-catenin pathway activation caused by adenomatous polyposis coli (APC) mutations occurs in app
108 (CRCs), an initiating mutation occurs in the adenomatous polyposis coli (APC) or beta-catenin gene, a
109 n that have been associated with loss of the adenomatous polyposis coli (APC) or constitutive activat
113 nestin expressing NeuN positive neurons and adenomatous polyposis coli (APC) positive mature oligode
115 ibition of GSK-3beta and accumulation of the adenomatous polyposis coli (APC) protein at the plus end
116 ere, we report that the expression status of adenomatous polyposis coli (APC) protein determines the
122 inked to deficiencies in mismatch repair and adenomatous polyposis coli (APC) proteins, diet, inflamm
123 ing a knockout allele in the gatekeeper gene Adenomatous polyposis coli (Apc) recapitulates familial
126 is functionally important for cell migration.Adenomatous polyposis coli (APC) regulates the localizat
127 gene targeting in mice, we demonstrate that adenomatous polyposis coli (APC) serves an essential fun
128 ne such pathway the tumor-suppressor protein adenomatous polyposis coli (APC) targets RNAs to cell pr
129 Here, we have defined a repeat sequence in adenomatous polyposis coli (APC) that binds to EB1's COO
130 ting factor-responsive cells were defined by adenomatous polyposis coli (APC) time-of-flight mass cyt
132 In turn, KIF17 participates in localizing adenomatous polyposis coli (APC) to the plus ends of a s
139 found in patients harboring mutations in the adenomatous polyposis coli (APC) tumor suppressor gene.
143 ce with IEC-specific allelic deletion of the adenomatous polyposis coli (Apc) tumor suppressor locus,
144 atase 2A (PP2A) and must be protected by the adenomatous polyposis coli (APC) tumor suppressor protei
146 rcinomas contain truncating mutations in the adenomatous polyposis coli (APC) tumor suppressor, a neg
147 in signaling is negatively controlled by the adenomatous polyposis coli (APC) tumor suppressor, which
148 calculating the in vivo mutation rate of the adenomatous polyposis coli (APC) tumor-suppressor gene i
149 ollows a genetic pathway whereby loss of the adenomatous polyposis coli (APC) tumour suppressor and a
150 RNAs in the granules associate with the adenomatous polyposis coli (APC) tumour suppressor and t
154 In this study, the tumor suppressor protein adenomatous polyposis coli (APC) was found to be importa
157 ne the genetic relationship between MPC1 and Adenomatous polyposis coli (APC), a key tumor suppressor
159 approaches suggest that the tumor suppressor adenomatous polyposis coli (APC), a regulator of Wnt sig
165 atenin destruction complex components Axin1, adenomatous polyposis coli (APC), and GSK3beta were also
166 ein complex containing the proteins axin and adenomatous polyposis coli (APC), both of which bind dir
167 forms a complex with axin (axis inhibitor), adenomatous polyposis coli (APC), casein kinase 1alpha (
168 Rac1-specific exchange factor stimulated by adenomatous polyposis coli (APC), contributing to colore
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
178 o develop colitis-associated and spontaneous adenomatous polyposis coli (APC)-related tumors of the i
184 ation suppresses beta-catenin activity in an adenomatous polyposis coli (APC)/glycogen synthase kinas
187 Arm is targeted for proteolysis by the Axin/Adenomatous polyposis coli (Apc1 and Apc2)/Zeste-white 3
188 V integration site family (WNT)/beta-catenin/adenomatous polyposis coli (CTNNB1/APC) pathway has been
191 sly in germ cells for proper localization of Adenomatous polyposis coli 2 and E-cadherin at the hub-G
194 tive regulators of beta-catenin, such as the adenomatous polyposis coli and Axin tumor suppressor pro
195 G-protein signaling (RGS) domain that binds adenomatous polyposis coli and Galpha subunits, thereby
196 atenin and the destruction complex component adenomatous polyposis coli at a similar SLS motif to the
198 iation domain family 1 gene RASSF1A, and the adenomatous polyposis coli gene APC in tumors and in his
199 Mice carrying and non-sense mutation in Adenomatous polyposis coli gene at site R850, which desi
200 eta-catenin by inhibiting its binding to the adenomatous polyposis coli gene product and subsequent g
207 ling induced by loss of the tumor suppressor adenomatous polyposis coli or casein kinase 1alpha uncov
208 Most information about the roles of the adenomatous polyposis coli protein (APC) and its binding
209 at RNAi-mediated depletion of two kMAPs, the adenomatous polyposis coli protein (APC) and its binding
211 Here we report that the tumour suppressor adenomatous polyposis coli protein (APC) directs the loc
213 n from Mlp of a region similar to one in the adenomatous polyposis coli protein involved in EB1 bindi
214 ows that the actin-nucleating ability of the adenomatous polyposis coli protein is required for disas
215 versely, RNAi of the beta-catenin antagonist adenomatous polyposis coli results in the regeneration o
216 W480 cells stably transformed with wild-type adenomatous polyposis coli showed decreased beta-catenin
217 on, and beta-catenin, a component of the Wnt-adenomatous polyposis coli signaling pathway, contribute
219 he microtubule motor cytoplasmic dynein, the adenomatous polyposis coli tumor suppressor protein (APC
222 member 1, insulin-like growth factor 2, and adenomatous polyposis coli) and other solid tumors (e.g.
224 g in T cell lineages by deletion of the Apc (adenomatous polyposis coli) gene causes spontaneous T ce
225 mutation of the Wnt repressor APC (encoding adenomatous polyposis coli) leads to a state of aberrant
226 that contained mutations in either the APC (adenomatous polyposis coli) locus or in an allele of bet
229 ectly targets the tumor suppressor gene APC (adenomatous polyposis coli), thereby affecting Wnt (Wing
231 aditionally attributed to mutations in Axin, adenomatous polyposis coli, and beta-catenin that lead t
232 I, IGF2; tumor suppressor candidate 33, N33; adenomatous polyposis coli, APC; mut-L homolog 1, MLH1;
233 a-catenin pathway mutations, such as loss of adenomatous polyposis coli, are insensitive to this nove
235 -catenin pathway regulatory genes, including adenomatous polyposis coli, GSK3beta, axin 1, beta-caten
237 e glycogen synthase kinase 3beta (GSK3beta)- adenomatous polyposis coli-axin-mediated degradation pat
238 otubule organization and capture dynamics in adenomatous polyposis coli-deficient radial progenitors.
239 ted signaling and glycogen synthase kinase-3/adenomatous polyposis coli-mediated beta-catenin activat
242 intestinal tumors driven by mutations in the adenomatous polyposis coli/beta-catenin pathway and acti
245 erived WNT2 activated canonical signaling in adenomatous polyposis coli/beta-catenin wild-type colon
246 denomas taken from individuals with familial adenomatous polyposis contain high levels of CtBP1 prote
247 edisposing to colorectal cancer are familial adenomatous polyposis (FAP) and hereditary nonpolyposis
248 ications of MMVTx for patients with familial adenomatous polyposis (FAP) and the technical feasibilit
250 amatically altered for the worse in familial adenomatous polyposis (FAP) because these patients harbo
252 identified as a candidate gene for familial adenomatous polyposis (FAP) but further study identified
253 tumors often occur in patients with familial adenomatous polyposis (FAP) coli who have germ line muta
254 rative colitis (UC) in 37 patients, familial adenomatous polyposis (FAP) in 12 patients, and colonic
255 of thyroid cancer in patients with Familial adenomatous polyposis (FAP) in a prospective study of th
259 n colonic and duodenal tumours from familial adenomatous polyposis (FAP) patients has shown that the
260 rliest colonic tissue alteration in familial adenomatous polyposis (FAP) patients, we present the hyp
262 ine mutation of which characterizes familial adenomatous polyposis (FAP), an autosomal intestinal can
263 atous polyposis coli (APC) underlie familial adenomatous polyposis (FAP), an inherited cancer syndrom
264 ive colitis, indeterminate colitis, familial adenomatous polyposis (FAP), and a select group of patie
265 inherited predisposition, including familial adenomatous polyposis (FAP), hereditary nonpolyposis col
266 atorial chemoprevention efficacy in familial adenomatous polyposis (FAP), signal of benefit from imag
267 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
275 nonpolyposis colorectal cancer and familial adenomatous polyposis has provided insight into some of
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 sporadic colorectal carcinomas and familial adenomatous polyposis, in 18 sporadic HPs from patients
280 enomas recovered from patients with familial adenomatous polyposis, including adenomas as small as a
283 yndromes, including Lynch syndrome, familial adenomatous polyposis, MUTYH-associated polyposis, and c
284 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 A diagnosis of Lynch syndrome, familial adenomatous polyposis, or another genetic syndrome can i
289 families showed recessive inheritance of the adenomatous polyposis phenotype and progression to CRC i
290 opic expression of APC, but not its familial adenomatous polyposis-related truncation mutant, promine
293 enomas in animals and patients with familial adenomatous polyposis suggest that COX-2 inhibitors may
296 ajority of the 30% of patients with familial adenomatous polyposis that do not test positive for muta
297 diseases, three females (1.6 %) had familial adenomatous polyposis; three patients (1 male and two fe
298 on-negative Lynch syndrome, 16 with familial adenomatous polyposis, two with constitutional mismatch
299 polyposis coli (APC) gene reduces intestinal adenomatous polyposis via Axin/beta-catenin axis and the
300 rom a 16-year-old male patient with familial adenomatous polyposis was insufflated, submerged in a co
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