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1                                              FAP expression is minimal or absent in most normal adult
2                                              FAP inhibition is investigated as a therapeutic option f
3                                              FAP is a hereditary disease predisposing to cancer in mu
4                                              FAP knockout A. thaliana plants show elevated alpha-lino
5                                              FAP(+) cells from three sites, skeletal muscle, adipose
6                                              FAP(+) cells of skeletal muscle are the major local sour
7                                              FAP-1 was demonstrated to be responsible for the reduced
8                                              FAP-mediated collagen processing leads to increased coll
9                                              FAPs expressed desmosome proteins, including desmoplakin
10                                              FAPs isolated from the Pdgfra-Cre:Eyfp:Dsp(W/F) mouse he
11 tor type 13 or FAS associated phosphatase 1 (FAP-1) and 2.3 fold increase in expression of cSrc.
12                        Formaldehyde probe-1 (FAP-1) is capable of detecting physiologically relevant
13                    Between 1993 and 2009, 10 FAP patients required MMVTx.
14 organic phase is an ionic liquid [P6,6,6,14][FAP]/toluene mixture.
15 ase was fluorapatite, (Ca(10)(PO(4))(6)F(2), FAP).
16 9.7%), indeterminate colitis (n = 63, 1.7%), FAP (n = 223, 6%), Crohn's disease (n = 150, 4%), cancer
17  a polymer conjugate (an iBody) containing a FAP-specific inhibitor as the targeting ligand.
18 acid, fatty acid, and mineral profiles (AAP, FAP, and MP, respectively), as well as protein degradati
19 scFvs) after three rounds of panning against FAP.
20 s goal, a sample corresponding to 33% of all FAP patients who undergone a liver transplantation in th
21         Fibroblast activation protein-alpha (FAP) identifies stromal cells of mesenchymal origin in h
22 ncoding fibroblast activation protein-alpha (FAP).
23 presses fibroblast activation protein-alpha (FAP).
24        The incidence of thyroid cancer among FAP patients is high.
25       Using an MSC cell line derived from an FAP-associated desmoid tumor, we confirmed an expected l
26       Furthermore, preliminary studies in an FAP in vivo model at early stages of disease development
27 than 50 years were more likely to receive an FAP liver [odds ratio (OR) 1.94, confidence interval (CI
28 ipocyte 3T3-L1 and 3T3-F422A, while DPP4 and FAP inhibitors have no effect.
29 ted with FDG uptake (LY6E, RNF149, MCM6, and FAP) were also associated with survival.
30 to identify subjects with desmoid tumors and FAP.
31 oromethyl)sulfonyl]imide (NTf(2)(-)) anions, FAP-based ILs are significantly more hydrophobic and hyd
32  macrophage antibody), or (111)In-28H1 (anti-FAP antibody), respectively, with nonspecific controls i
33 arthritis was imaged with (111)In-28H1 (anti-FAP), (111)In-anti-F4/80-A3-1, and (111)In-RGD2.
34              Radioimmunoimaging with an anti-FAP antibody might be used to monitor the response to th
35 cotinamide ((99m)Tc-S-HYNIC)-conjugated anti-FAP antibody 28H1 at 2, 5, and 9 d after treatment.
36      The application of both inhibitory anti-FAP scFvs significantly affected the formation of 3-dime
37 nd PET with (111)In- and (89)Zr-labeled anti-FAP antibody 28H1 was performed in mice with CIA.
38 dy was to assess whether a radiolabeled anti-FAP antibody could be used to monitor the efficacy of tr
39               SPECT/CT imaging with the anti-FAP antibody (111)In-28H1 specifically visualized arthri
40 noimaging of activated fibroblasts with anti-FAP antibodies might be an attractive noninvasive imagin
41     Identifying a specific inhibitor of APCE/FAP continues to be intensely pursued.
42                                           As FAP enzymatic activity is a potent therapeutic target, w
43 and thus activates MG to a similar extent as FAPs based on single-chain variable fragments.
44                                      Because FAP was described as an independent risk factor for earl
45                                     Blocking FAP ciliation also enhanced myofiber regeneration after
46 , 1-butyl-1-methylpyrrolidinium FAP ([BMPL] [FAP]), and 1-(6-amino-hexyl)-1-methylpyrrolidinium FAP (
47 ing before sequencing (for types detected by FAP PCR).
48 xamine whether circulating CAF identified by FAP and alpha-SMA co-expression (cCAF) could be distingu
49 rved specificity in substrate recognition by FAP, but not by DPPIV or PREP.
50 d human multipotent BMSCs were recognized by FAP-reactive T cells.
51     We conclude that ciliary Hh signaling by FAPs orchestrates the regenerative response to skeletal
52 le structure of the ionic liquid [C18mim](+)[FAP](-) near its free surface was studied by complementa
53 al cells from patients with IBD, IBD-cancer, FAP-adenoma, and colorectal cancer, but not in patients
54                          A subset of cardiac FAPs, identified by the PDGFRA(pos):Lin(neg):THY1(neg):D
55 fluorescence intensity assay for circulating FAP activity based on a recently identified natural subs
56                                  Clinically, FAP expression serves as an independent negative prognos
57 ibition constants but does not inhibit close FAP homologues dipeptidyl peptidase IV, dipeptidyl pepti
58                                          CPP FAP-310, a randomized, double-blind, Phase III trial was
59                                  In cultured FAPs, IL-4 inhibited Dex-induced conversion of FAPs into
60                                    Depleting FAP-expressing cells in a subcutaneous model of pancreat
61                       In contrast, depleting FAP(+) FRCs during an ongoing influenza infection does n
62                       As expected, depleting FAP(+) FRCs causes the loss of naive T cells, B cells, a
63 ntly affected the formation of 3-dimensional FAP-positive cell matrix, as demonstrated by reducing th
64  family history, inflammatory bowel disease, FAP, HNPCC, and follow-up < 5 years.
65 nally, the assay was used to detect elevated FAP activity in human patients diagnosed with liver cirr
66 he c-myc protooncogene and the gene encoding FAP-1 phosphatase.
67  of yearly gastrointestinal follow-up, every FAP patient in our registry was offered thyroid ultrasou
68          Thirteen patients (11.4%) evidenced FAP disease but not before 6 years after DLT.
69  drugs was screened against cells expressing FAP-tagged beta(2)ARs, all 33 known beta(2)AR-active lig
70 atment arms: best (ie, longest time to first FAP-related event [rectal/pouch polyposis]), intermediat
71 he effectiveness of a chemical inhibitor for FAP in mice.
72   MMVTx is a valuable therapeutic option for FAP patients who are in need for visceral transplantatio
73       However, routine thyroid screening for FAP patients is not generally practiced in the United St
74 dentifying inhibitors that are selective for FAP over both the dipeptidyl peptidases (DPPs), with whi
75 unced stromal elements staining strongly for FAP, and hypothesized that targeting tumor stroma with F
76 ical challenges related to genetic tests for FAP have been newly examined.
77  results show the iBody is a useful tool for FAP targeting in vitro and potentially also for specific
78 yellow-white dots on funduscopy, typical for FAP or RPA.
79  a general hallmark of tubular adenomas from FAP patients.
80  administration stimulated adipogenesis from FAP-EGFP.
81 rozygous mutations in RDH5 and suffered from FAP with mild maculopathy.
82 his idea, we examined 16 desmoid tumors from FAP-associated and sporadic cases, finding that all 16 o
83              Genetically removing cilia from FAPs inhibited intramuscular adipogenesis, both after in
84 yfp:Dsp(W/F) mice, indicating an origin from FAPs.
85 the 1-hexyl-3-methylimidazolium FAP ([HMIM] [FAP]) IL.
86  0.7 and 0.1 to 1.2 microg L(-1) for [HMIM] [FAP], [PH(3)T] [FAP], 1-butyl-1-methylpyrrolidinium FAP
87            Consistent with this model, human FAP adenomas showed robust upregulation of CtBP1 in the
88  excellent option for patients with MUC, IC, FAP, and select patients with Crohn's disease.
89                         Our study identifies FAP as a novel endogenous regulator of fibrosis and is t
90        There were no differences (P>0.05) in FAP, AAP, and MP.
91 conclusion, daily sulindac administration in FAP patients significantly altered colorectal stem cell
92  cancer is the most common cause of death in FAP.
93  be effective in preventing cancer deaths in FAP.
94 logical evidence of sudomotor denervation in FAP.
95 ate that HuR activation is an early event in FAP-adenoma but is not present in IBD-dysplasia.
96 sed mortality and increased lung fibrosis in FAP-deficient mice compared with wild-type mice.
97  of intermediate-sized collagen fragments in FAP-deficient mouse lungs, consistent within vitrostudie
98 39 and rapamycin, decreased proliferation in FAP-COs, but also affected cell proliferation in wild-ty
99 ention of early hepatic artery thrombosis in FAP patients after liver transplantation.
100                                           In FAPs, IL-4/IL-13 signaling serves as a key switch to con
101 noid and straight-chain alkyl alcohols as in FAPs.
102  FAPs into adipocytes; this did not occur in FAPs expressing knockdown of the IL-4 receptor.
103 ype 2 cytokine signaling is also required in FAPs, but not in myeloid cells, for rapid clearance of n
104 ential to selectively and completely inhibit FAP in vivo.
105 he first scFv antibody capable of inhibiting FAP function.
106   We have identified the apoptosis inhibitor FAP-1 as a target for miR-200c.
107 ation with late onset (>50 years; LateMet30) FAP (p = 0.0005).
108 French Ile107Val, Ser77Tyr, and LateVal30Met FAP showed more rapid and severe disease progression; on
109 ecules using the 1-hexyl-3-methylimidazolium FAP ([HMIM] [FAP]) IL.
110 PH(3)T] [FAP], 1-butyl-1-methylpyrrolidinium FAP ([BMPL] [FAP]), and 1-(6-amino-hexyl)-1-methylpyrrol
111  and 1-(6-amino-hexyl)-1-methylpyrrolidinium FAP ([HNH(2)MPL] [FAP]), respectively.
112                                    Moreover, FAP-1 can visualize endogenous FA produced by lysine-spe
113      The iBody inhibits both human and mouse FAP with low nanomolar inhibition constants but does not
114 xyl)-1-methylpyrrolidinium FAP ([HNH(2)MPL] [FAP]), respectively.
115 mal proliferation specifically in APC-mutant FAP-COs.
116 erred to and followed at the French National FAP Reference Center from 1988 to 2010.
117  hepatic artery thrombosis compared with non-FAP transplanted patients.
118 body, named E3, which could attenuate 35% of FAP cleavage of the fluorescent substrate Ala-Pro-7-amid
119 tively distinguish endopeptidase activity of FAP from that of other related enzymes such as prolyl en
120 ovel single mutation (Phe33Ile) in a case of FAP with vitreous amyloidosis from India is reported.
121  Prior studies established that depletion of FAP(+) cells inhibits tumor growth by augmenting antitum
122                                 Depletion of FAP-expressing cells, which made up only 2% of all tumor
123  sensor allowed femtomolar (fM) detection of FAP, a detection limit well adapted and promising for qu
124 ogies and for the therapeutic development of FAP inhibitors.
125 d provide support for further development of FAP(+) stromal cell-targeted therapies for the treatment
126 here could thus be utilized for diagnosis of FAP-related pathologies and for the therapeutic developm
127 t of 1 pedigree, confirming the diagnosis of FAP.
128 peptidase DPPIV, the extracellular domain of FAP can be released into circulation as a functional enz
129                  Moreover, the expression of FAP by multipotent BMSCs may point toward the cellular o
130            Because of the high expression of FAP in arthritic joints, radioimmunoimaging of activated
131       These data distinguish the function of FAP(+) CASCs from other CASC subsets and provide support
132                        The identification of FAP-1 as an miR-200c target provides a molecular mechani
133 ine permitting the bioluminescent imaging of FAP(+) cells, we find that they reside in most tissues o
134 tic deletion and pharmacologic inhibition of FAP inhibited tumor growth in both an endogenous mouse m
135 icability of this iBody for the isolation of FAP from cell lysates and blood serum as well as for its
136 biopsies were performed on the distal leg of FAP patients with a follow-up duration of 3.8 +/- 1.6 ye
137 tudies suggest that the circulating level of FAP correlates with the degree of tissue fibrosis.
138 nesis-related genes, and increased levels of FAP-alpha, a crucial suppressor of antitumor immunity.
139 estoration of FAP expression in the lungs of FAP-deficient mice decreases lung hydroxyproline content
140  for HuR inhibition as an effective means of FAP chemoprevention, with caution advised in the setting
141  HuR inhibition in APC(Min) mice, a model of FAP and colon cancer, diminished the number of small int
142          This large-animal, genetic model of FAP will be useful in the development of diagnostics and
143 potential strategy to control progression of FAP-related intestinal polyposis.
144                  The specific recognition of FAP is based on the interaction between folic acid recep
145                   Conversely, restoration of FAP expression in the lungs of FAP-deficient mice decrea
146 umors, we set out to investigate the role of FAP in mouse models of epithelial-derived solid tumors.
147 ody has the potential to disrupt the role of FAP in tumor invasion and metastasis.
148               The SGIIPGP 9.5 and SGIIVIP of FAP patients were significantly lower than those of age-
149                         Adoptive transfer of FAP-CAR T cells also decreased tumor vascular density an
150                         Adoptive transfer of FAP-CAR T cells also restrained autochthonous pancreatic
151                However, adoptive transfer of FAP-reactive T cells into mice bearing a variety of subc
152 tion of these cells, by adoptive transfer of FAP-targeted chimeric antigen receptor (CAR) T cells, re
153 l mimetic of TIMP3 blocked the conversion of FAPs into adipocytes, pointing to a strategy to combat f
154 Ps, IL-4 inhibited Dex-induced conversion of FAPs into adipocytes; this did not occur in FAPs express
155 -4/IL-13 signaling promotes proliferation of FAPs to support myogenesis while inhibiting their differ
156 y (4-fold) and enhanced inhibitory effect on FAP enzyme activity (3-fold) than E3.
157 y of substrates or inhibitors toward APCE or FAP.
158 ector cytokines upon stimulation with FAP or FAP-expressing cell lines.
159 , 260 children (aged 8-18 years) with IBS or FAP(S) were included in this study.
160  performed by therapists in pediatric IBS or FAP(S).
161 families with and without Cowden syndrome or FAP.
162 entafluoroethyl)trifluorophosphate ([P66614][FAP]) ILs.
163                                Pharmacologic FAP inhibition decreases collagen internalization as exp
164 ned with the trihexyl(tetradecyl)phosphonium FAP ([PH(3)T] [FAP]) IL for compounds with high molecula
165 -adapted, filamentous anoxygenic phototroph (FAP) that lacks chlorosomes, the dominant antenna found
166 he green filamentous anoxygenic phototrophs (FAPs).
167 omponent of familial amyloid polyneuropathy (FAP) due to mutated transthyretin, with sudomotor failur
168 tients with familial amyloid polyneuropathy (FAP) is described.
169 most common familial amyloid polyneuropathy (FAP), transthyretin (TTR) displays this role primarily a
170         Familial amyloidotic polyneuropathy (FAP) has a high prevalence in Portugal, and the most com
171 rs from familial amyloidotic polyneuropathy (FAP) patients is a well-described technique and useful f
172 ed with familial amyloidotic polyneuropathy (FAP), a neurodegenerative disease characterized by senso
173 n (TTR) familial amyloidotic polyneuropathy (FAP; n = 20), (2) TTR mutation carriers without peripher
174  those with familial adenomatosis polyposis (FAP) or inflammatory bowel disease (IBD).
175 atients with familial adenomatous polyposis (FAP) and the technical feasibility of performing spleen-
176 atients with familial adenomatous polyposis (FAP) are at markedly increased risk for duodenal polyps
177 atients with familial adenomatous polyposis (FAP) coli who have germ line mutations in the APC gene.
178 37 patients, familial adenomatous polyposis (FAP) in 12 patients, and colonic ischemia in 1 patient.
179 atients with Familial adenomatous polyposis (FAP) in a prospective study of thyroid neck US screening
180              Familial Adenomatous Polyposis (FAP) is characterized by marked up-regulation of ODC in
181 ons known as familial adenomatous polyposis (FAP) or Gardner syndrome.
182 reatment for familial adenomatous polyposis (FAP) patients.
183 PC) underlie familial adenomatous polyposis (FAP), an inherited cancer syndrome characterized by the
184 ate colitis, familial adenomatous polyposis (FAP), and a select group of patients with Crohn's diseas
185  efficacy in familial adenomatous polyposis (FAP), signal of benefit from imaging-based early detecti
186 atients with Familial Adenomatous Polyposis (FAP).
187 yndrome, and familial adenomatous polyposis (FAP).
188 hildren with familial adenomatous polyposis (FAP).
189 le for human familial adenomatous polyposis (FAP).
190 amilies with familial adenomatous polyposis (FAP).
191 atients with familial adenomatous polyposis (FAP-iPSCs) harboring germline mutations in the WNT-signa
192             Here, we report the first potent FAP inhibitor with selectivity over both the DPPs and PR
193 oy to inhibit PDGF signalling and to prevent FAP over-activation.
194 rimers (MGP) and Forslund-Antonsson primers (FAP) and identified by Luminex (for types detected by MG
195 ise to fibroblast and adipocyte progenitors (FAPs) and to their differentiated progeny, fibroblasts a
196 muscle resident fibro/adipocyte progenitors (FAPs).
197 lite cells and fibro/adipogenic progenitors (FAPs) from muscle; satellite cells did not differentiate
198 uscle-resident fibro/adipogenic progenitors (FAPs) proliferated and gave rise to adipocytes.
199 uscle-resident fibro/adipogenic progenitors (FAPs) that play a supportive role in muscle regeneration
200 e referred to as fibroadipocyte progenitors (FAPs).
201 sor for the detection of folic acid protein (FAP) using graphene-based SPR chips.
202 onsisting of a fluorogen-activating protein (FAP) and a beta-fibrillizing peptide (betaFP).
203 form combining fluorogen-activating protein (FAP) technology with high-throughput flow cytometry to d
204 ically encoded fluorogen-activating protein (FAP) that binds a heavy atom-substituted fluorogenic dye
205 e we identify fibroblast activation protein (FAP) as the enzyme that cleaves and inactivates human FG
206               Fibroblast activation protein (FAP) is a candidate universal target antigen because it
207               Fibroblast activation protein (FAP) is a cell surface-associated serine protease up-reg
208               Fibroblast activation protein (FAP) is a marker of a major subset of CASCs in virtually
209               Fibroblast Activation Protein (FAP) is a membrane-bound serine protease whose expressio
210               Fibroblast activation protein (FAP) is a serine protease related to dipeptidyl peptidas
211               Fibroblast activation protein (FAP) is a serine protease selectively expressed on react
212               Fibroblast activation protein (FAP) is a serine protease selectively expressed on tumor
213               Fibroblast activation protein (FAP) is overexpressed by fibroblastlike synoviocytes in
214 rine protease fibroblast activation protein (FAP) is selectively expressed on tumor-associated fibrob
215 Expression of fibroblast activation protein (FAP) is upregulated in stromal fibroblasts in more than
216 rane-inserted fibroblast activation protein (FAP) that is transiently expressed during epithelial-der
217 membrane DPP, fibroblast activation protein (FAP), did not affect NPY actions.
218 rgets, namely fibroblast activation protein (FAP), macrophages, and integrin alphavbeta3.
219 antly express fibroblast activation protein (FAP).
220 PP8, DPP9 and fibroblast activation protein (FAP).
221  that express fibroblast activation protein (FAP).
222 C97, LC7b, and flagellar-associated protein (FAP) 120--defining a new I1 subcomplex.
223 based probes, fluorogen-activating proteins (FAPs), has been reported.
224 se proteins are fatty-acid-binding proteins (FAPs).
225            In vivo, we transplanted purified FAPs from transgenic, EGFP mice into the injured muscles
226 ry promoter 1B point mutations but only rare FAP-affected families carry similar mutations, the colon
227                                  Recombinant FAP cleavage of peptide libraries of short amino acid se
228 nation) for preventing a clinically relevant FAP-related progression event in individuals with FAP.
229                              Of 192 screened FAP patients, 72 (38%) had thyroid nodules and 5 (2.6%)
230   In addition, administration of a selective FAP inhibitor acutely increased circulating intact FGF21
231 ossible entry to highly potent and selective FAP inhibitors.
232  basis of our findings, we propose selective FAP inhibition as a potential therapeutic approach to in
233 ciated with the most debilitating and severe FAP ever described, with rapid onset of tetraparesis and
234 gulator of fibrosis and is the first to show FAP's protective effects in the lung.
235 ancer have been previously described in some FAP-affected individuals with large deletions around pro
236  we concluded that glucocorticoids stimulate FAPs to differentiate into adipocytes in injured muscles
237                  In contrast, Dex stimulated FAP differentiation into adipocytes.
238  pain or functional abdominal pain syndrome (FAP[S]).
239 ihexyl(tetradecyl)phosphonium FAP ([PH(3)T] [FAP]) IL for compounds with high molecular weight and fu
240 1.2 microg L(-1) for [HMIM] [FAP], [PH(3)T] [FAP], 1-butyl-1-methylpyrrolidinium FAP ([BMPL] [FAP]),
241 ved after cell-based immunotherapy targeting FAP cautions against its use as a universal target.
242                  Herein, we demonstrate that FAP(+) CASCs are required for maintenance of the provisi
243                                We found that FAP was robustly expressed on PDGFR-alpha(+), Sca-1(+) m
244                    Our results indicate that FAP depletion inhibits tumor cell proliferation indirect
245                   Our findings indicate that FAP participates directly, in concert with MMPs, in coll
246                            We postulate that FAP is not only a marker of disease but influences the d
247  consistent within vitrostudies showing that FAP mediates ordered proteolytic processing of matrix me
248                                We found that FAPs produce multiple transcriptional variants of Pdgfra
249                                          The FAP domain generates fluorescence that reflects IgG bind
250 king on the graphene coated SPR chip and the FAP analyte in serum.
251 e coated with the chemokine, CXCL12, and the FAP(+) CAF was the principal source of CXCL12 in the tum
252 ined the overriding immunosuppression by the FAP(+) cell: T cells were absent from regions of the tum
253 for diverse applications and thus extend the FAP technology.
254                                 Notably, the FAP discovery defines the adaptive evolution of a stereo
255                         The depletion of the FAP(+) stromal cell also uncovered the antitumor effects
256                                    Thus, the FAP(+) stromal cell may have roles in two adverse conseq
257 he film was mediated by pAG(MG) bound to the FAP.
258 CXCL12, from a single stromal cell type, the FAP(+) CAF, may direct tumor immune evasion in a model o
259  extraction method at 20 degrees C using the FAP-based ILs was in the range of 1.5-9.4%.
260                                     When the FAP-dCMP analogue is located to the 3' side of the adduc
261                                   Therefore, FAP-expressing cells are a nonredundant, immune-suppress
262                                        These FAPs dynamically produced primary cilia, structures that
263 ear-infrared excitation and emission of this FAP-TAPs provides a new spectral range for photosensitiz
264                         Hh signaling through FAP cilia regulated the expression of TIMP3, a secreted
265 e expressed and characterized for binding to FAP by surface plasmon resonance and flow cytometry.
266 revealed that mutations in RLBP1 may lead to FAP with cone dystrophy.
267            Stage-specific, "delayed time to" FAP-related events are the primary endpoints.
268                        However, transplanted FAP patients have a significantly higher incidence of ea
269 s of exercise training in liver transplanted FAP patients have not been scrutinized yet.
270 the physical condition of liver transplanted FAP patients.
271 , and walking capacity of liver transplanted FAP patients.
272 odissected in placebo- and sulindac- treated FAP patient tissue after which the methylation patterns
273 he tris(pentafluoroethyl)trifluorophosphate (FAP) anion are paired with imidazolium, phosphonium, and
274 the French National Reference Center for TTR-FAP from June 1, 2013, to June 30, 2014.
275  biomarker to detect treatment effect in TTR-FAP drug trials.
276  PMNFD were all significantly reduced in TTR-FAP patients versus healthy controls, whereas TTR-noPN s
277 -type TTR staining was less prominent in TTR-FAP patients.
278 Cutaneous amyloid was detected in 70% of TTR-FAP and 20% of TTR-noPN subjects.
279 in Type Familial Amyloid Polyneuropathy (TTR-FAP) and demonstrated a slowing of disease progression i
280 hyretin familial amyloid polyneuropathy (TTR-FAP).
281                    Fifteen patients with TTR-FAP underwent a complete neurologic examination, includi
282                In these 15 patients with TTR-FAP, IVCM measurement permitted rapid, noninvasive evalu
283 lace of IVCM in monitoring patients with TTR-FAP.
284 ce group for APC mutations in the unselected FAP population, we used the UMD-APC database referenced
285       By comparison with Portuguese Val30Met FAP, French Ile107Val, Ser77Tyr, and LateVal30Met FAP sh
286       We created a transgenic mouse in which FAP-expressing cells can be ablated.
287                         Eligible adults with FAP will be randomized to: CPP-1X 750 mg and sulindac 15
288          T cells genetically engineered with FAP-reactive chimeric antigen receptors (CARs) specifica
289 s APC mutation data on 2040 individuals with FAP.
290 elated progression event in individuals with FAP.
291                            Participants with FAP were randomized to sulindac (150 mg) twice daily and
292 rolled trial, enrolling 92 participants with FAP, conducted from July 2010 through June 2014 at Hunts
293                      Among participants with FAP, the use of sulindac and erlotinib compared with pla
294 in 7 patients with RPA and in 1 patient with FAP and cone dystrophy.
295 at desmoid tumors may arise in patients with FAP after MSCs acquire somatic mutations during the prol
296                     Three of 5 patients with FAP and thyroid cancer were women.
297 tic mutations that put certain patients with FAP at high risk for desmoid tumors and could be future
298 cerous lesions that develop in patients with FAP.
299 id cancer screening program in patients with FAP.
300 ced effector cytokines upon stimulation with FAP or FAP-expressing cell lines.
301 ypothesized that targeting tumor stroma with FAP-reactive T cells would inhibit tumor growth in cance

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