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1 ers reported that recessive mutations in the embryonal acetylcholine receptor g subunit (CHRNG) can c
2 ified germline-inactivating mutations in the embryonal acetylcholine receptor gamma subunit (CHRNG) i
3 n of clinical cases revealed that human RMS (embryonal, alveolar, and pleomorphic) harbored human cyt
7 yosarcoma has two major histologic subtypes, embryonal and alveolar, each with distinct clinical, mol
8 Y-DOTATOC; diagnoses included neuroblastoma, embryonal and astrocytic brain tumors, paraganglioma, mu
9 -catenin transcriptional target and multiple embryonal and neural crest malignancies have oncogenic a
10 though well-developed mouse models exist for embryonal and pleomorphic rhabdomyosarcomas, neither a s
11 ferentiated fetal cells, less differentiated embryonal and undifferentiated small cells (SCU) progres
14 e of the resemblance of the spheroids to the embryonal blastocyst and their resistance to traditional
16 ne profile resemblance of these spheroids to embryonal blastocysts, we wondered whether they might ex
17 d, constitutively active Notch1 or Notch2 in embryonal brain tumor cell lines caused antagonistic eff
20 with deregulated E2F1 show the formation of embryonal brain tumors such as medulloblastoma, choroid
23 T gene amplification is relatively common in embryonal brain tumors, and that increased expression of
24 of Notch2, we analyzed its gene dosage in 40 embryonal brain tumors, detecting an increased copy numb
25 in both nonneoplastic neural stem cells and embryonal brain tumors, such as medulloblastoma, which a
27 atric patients previously operated on for an embryonal brain tumour (13 patients prospectively diagno
28 alamocortical tract involvement in childhood embryonal brain tumour patients who developed posterior
34 ncer-predisposition syndrome associated with embryonal cancers, macroglossia, macrosomia, ear pits or
35 (NSE), the latter including the pluripotent embryonal carcinoma (EC) and its differentiated derivati
37 used the well-characterized pluripotent P19 embryonal carcinoma (EC) cell culture model of neuro-ect
38 e to all-trans retinoic acid (RA), the human embryonal carcinoma (EC) cell line, NT2/D1, differentiat
41 et of neuroectodermal differentiation in P19 embryonal carcinoma (EC) cells three independent techniq
42 OCT4 levels and increases the resistance of embryonal carcinoma (EC) cells to cisplatin and bleomyci
43 therapy, and testicular cancer-derived human embryonal carcinoma (EC) cells undergo a p53-dominant tr
44 silenced genes in cancer cells; however, in embryonal carcinoma (EC) cells, CBX7 can initiate stable
45 bryonic stem (ES) cells and can give rise to embryonal carcinoma (EC) cells, the stem cells of testic
47 wn that p53 repression in TGCT-derived human embryonal carcinoma (EC) is relieved upon treatment with
50 us GCTs (NSGCTs) can be further divided into embryonal carcinoma (EC), teratoma (T), yolk sac tumor (
51 t there is a subgroup of NSGCT patients with embryonal carcinoma (with or without other histologies)
53 Presence of vascular invasion together with embryonal carcinoma and rete testis invasion in the test
56 ct4 gene locus in retinoic acid (RA)-treated embryonal carcinoma cell line P19, which involves recept
58 Both species are repressed when the human embryonal carcinoma cell line, NT2/D1, is induced to dif
61 significantly greater levels in human ES and embryonal carcinoma cell lines than in control samples.
62 ines showed many similarities with the human embryonal carcinoma cell samples and more distantly with
63 the Hoxa1, RARbeta2, and Cyp26A1 RAREs in F9 embryonal carcinoma cells (teratocarcinoma stem cells) d
64 predominant form in embryonic stem cells and embryonal carcinoma cells and can also be detected from
65 lated during neuronal differentiation in P19 embryonal carcinoma cells and epigenetic changes play an
66 ted knockdown of USP2a in NTERA-2 testicular embryonal carcinoma cells and MCF7 breast cancer cells c
67 rget of GATA-6 regulation in differentiating embryonal carcinoma cells and that, in vivo, the express
69 protein synthesis-independent manner in P19 embryonal carcinoma cells by inactivation of NF-kappa B.
70 wn of Cripto-1 expression in human and mouse embryonal carcinoma cells desensitized the ligand-induce
72 rmation of primitive endoderm from mouse P19 embryonal carcinoma cells in response to retinoic acid,
73 neural cells derived from embryonic stem and embryonal carcinoma cells in vitro and neural stem cells
75 Studies of miR-125b function in mouse P19 embryonal carcinoma cells induced to develop into neuron
76 of the expressing differentiated cells with embryonal carcinoma cells or by treatment of the differe
77 Removal of endogenous OAZ from pluripotent embryonal carcinoma cells prevents the induction of Smad
79 that overexpressing Hoxa2 in cultures of P19 embryonal carcinoma cells reduced the frequency of spont
80 ion of p53 and p53 pathway genes and renders embryonal carcinoma cells relatively resistant to cispla
82 rentiation, whereas studies with pluripotent embryonal carcinoma cells suggest that this pathway prom
83 ed large sets of genes in embryonic stem and embryonal carcinoma cells that are associated with the t
84 tutive levels of this BH3-only protein prime embryonal carcinoma cells to undergo rapid and massive a
85 o DNA methylation-associated inactivation in embryonal carcinoma cells were transfected into differen
87 cardiomyocyte differentiation in pluripotent embryonal carcinoma cells, and we show that this involve
88 d in mES cells and in Ntera-2 or NCCIT human embryonal carcinoma cells, as compared with cells growin
90 we show that in mouse embryoid bodies or F9 embryonal carcinoma cells, RARs occupy a large repertoir
91 We have studied the function of LINC in F9 embryonal carcinoma cells, which are distinguished by a
104 ribosomal frameshifting signal of the mouse embryonal carcinoma differentiation regulated (Edr) gene
107 ates 9 of 15 genes in this pathway in the F9 embryonal carcinoma model and 11 of 15 pathway genes in
109 of neural progenitor cells, using the mouse embryonal carcinoma P19 cell line as a model system.
110 id receptor (KOR) gene is expressed in mouse embryonal carcinoma P19 cells and induced by retinoic ac
112 X protein levels are also increased in mouse embryonal carcinoma P19 cells during retinoic acid (RA)-
114 knockdown Smn gene expression in the murine embryonal carcinoma stem cell line P19, which can be dif
116 Cs across species and between human ESCs and embryonal carcinoma stem cells suggest that while plurip
117 r the differentiation of cultured P19 murine embryonal carcinoma stem cells to beating cardiac myocyt
118 quired for the differentiation of murine P19 embryonal carcinoma stem cells to beating cardiac myocyt
119 ed for 95 previously untreated patients with embryonal carcinoma with or without other germ cell comp
121 -cm tumor that was 95% yolk sac tumor and 5% embryonal carcinoma, and retroperitoneal lymph node diss
122 erentiated human GCTs, such as seminomas and embryonal carcinoma, but not in normal testis or in diff
123 ion of several stem cell-associated genes in embryonal carcinoma, including several core "stemness" g
125 btypes included immature teratoma, seminoma, embryonal carcinoma, yolk sac tumor, and choriocarcinoma
130 the pluripotent cells (embryonic stem cells, embryonal carcinomas and induced pluripotent cells).
131 that exhibited coordinated overexpression in embryonal carcinomas and seminomas, which included the k
133 and nonseminomas, which include pluripotent embryonal carcinomas as well as other histologic subtype
134 d malignant tumors, with yolk sac tumors and embryonal carcinomas positive for alpha-fetoprotein, cyt
135 t has implications for both undifferentiated embryonal cells and for cancers in which pocket protein
136 ctors and homeobox proteins predominating in embryonal cells and glycoproteins and immunoglobulin-rel
137 some Suz12 target genes are bound by OCT4 in embryonal cells and suggest that OCT4 maintains stem cel
141 ally led to the proposal that tumors take on embryonal characteristics, the so called embryonal theor
142 In the present study, we show that human embryonal CNS tumor cell lines and surgical tumor specim
145 esis is unknown, their relationship to other embryonal CNS tumours is debated, and patients' response
146 Doxycycline (Dox) was administered from embryonal day 14 to postnatal day 7, and lungs were stud
147 sL) overexpression, treated with Dox between embryonal day 15 and postnatal day 3, served as a model
148 rise of embryonic transgene expression until embryonal day 18, with an abrupt postnatal decline.
150 n many important cellular processes, notably embryonal development and cellular differentiation.
152 n tumors, may be associated with the special embryonal development morphologic transition of this mal
159 ant role in mitotic defects of Lsh-/- murine embryonal fibroblasts, possibly by altering chromatin st
160 reased risk of developing hepatoblastoma, an embryonal form of liver cancer, suggesting that Wnt affe
161 levels of tropoelastin mRNA were low during embryonal growth and increased substantially in neonates
162 eta-catenin and differentiation status, with embryonal hepatoblastomas expressing full-length beta-ca
163 In rhabdomyosarcoma, genitourinary site and embryonal histology confer a relatively favorable progno
169 epitope tagging in stably transfected human embryonal kidney (HEK) 293 cells, immunoaffinity purific
171 uclear antigen (LANA) was expressed in human embryonal kidney 293 cells and a bone marrow stromal cel
172 A) negatively regulate the adhesion of human embryonal kidney 293 cells expressing alpha(IIb)beta(3)
173 Ib)beta(3) in resting platelets and in human embryonal kidney 293 cells expressing alpha(IIb)beta(3).
174 PAR-/-murine embryonic fibroblasts and human embryonal kidney 293 cells, SuPAR functions as a partial
175 moter methylation arrays, we show that human embryonal kidney cells over-expressing WT1 acquire DNA m
178 Childhood solid tumors often arise from embryonal-like cells, which are distinct from the epithe
179 Neuroblastoma is a neural crest-derived embryonal malignancy, which accounts for 13% of all pedi
180 gradually changes from a fine network in the embryonal mass cells to thick cables in the suspensor ce
181 The microtubule arrays appear normal in the embryonal mass cells, but the microtubule network is par
182 or cell types: the meristematic cells of the embryonal mass on one pole and the terminally differenti
183 es and F-actin changes successively from the embryonal mass towards the distal end of the embryo susp
184 Pa ESP was expressed in the proliferating embryonal mass, while it was absent in the suspensor cel
185 , Cripto-1 is enriched in a subpopulation of embryonal, melanoma, prostate, and pancreatic cancer cel
186 netic alterations associated with the unique embryonal morphology of nonseminomatous subtypes of test
187 formed rhabdomyosarcoma-like tumors with an embryonal morphology, capable of invasion and metastasis
190 asomotor nerve cells, which originate in the embryonal neural crest can lead to their formation.
192 in low-stage neuroblastoma tumors and normal embryonal neuroblasts, but reduced in late-stage neurobl
193 quiescently HCMV-infected human pluripotent embryonal NTera2 cells (NT2) to model HCMV reactivation,
194 ase using the terms neoplasms, germ cell, or embryonal or testicular neoplasms restricted to humans,
195 ges: pediatric solid tumors are typically of embryonal origin, whereas adult tumors are usually carci
196 growth of two different rhabdomyosarcoma (RD embryonal P = 0.00008; Rh30 alveolar P = 0.0002) cell li
199 ant flow in the aorta and extending into the embryonal-placental circulation, which was evident after
200 actor Hnf4alpha leads to derepression of the embryonal proto-oncogene Hmga2 in Nkx2-1-negative tumors
201 n of the invadopodia component Tks5long, the embryonal proto-oncogene Hmga2, and the epithelial-to-me
204 ll carcinoma (BCC), medulloblastoma (MB) and embryonal rhabdhomyosarcoma (eRMS), three principle tumo
207 y resected, or gross residual (orbital only) embryonal rhabdomyosarcoma (ERMS) had 5-year failure-fre
211 fusion protein PAX3-FOXO1 or PAX7-FOXO1, and embryonal rhabdomyosarcoma (ERMS), which is genetically
213 n (VA) for patients with subset-one low-risk embryonal rhabdomyosarcoma (ERMS; stage 1/2 group I/II E
214 he spontaneous development of muscle-derived embryonal rhabdomyosarcoma (RMS) after 1 year of age.
215 ntreated patients with incompletely resected embryonal rhabdomyosarcoma (RMS), undifferentiated sarco
216 activity as single agents in both zebrafish embryonal rhabdomyosarcoma and a human cell line of rhab
219 e a cell of origin for Sonic Hedgehog-driven embryonal rhabdomyosarcoma in an adipocyte-restricted co
220 tiation block in the childhood muscle cancer embryonal rhabdomyosarcoma is often thought to hold prom
223 a secondary tumour (head and neck anaplastic embryonal rhabdomyosarcoma), all patients were alive at
224 nt of lineage (alveolar rhabdomyosarcoma and embryonal rhabdomyosarcoma), are particularly sensitive
225 partitioning of tumour-propagating cells in embryonal rhabdomyosarcoma, emergence of clonal dominanc
226 ic variegated aneuploidy, including two with embryonal rhabdomyosarcoma, we identified truncating and
227 Introduction of miR-1 and miR-133a into an embryonal rhabdomyosarcoma-derived cell line is cytostat
231 atous testicular germ-cell tumors, in 2 of 5 embryonal rhabdomyosarcomas, and in 1 of 266 epithelial
232 RMS (age 21 years or younger) or metastatic embryonal RMS (age 2 to 10 years) were enrolled between
233 ntly observed in alveolar RMS (ARMS) than in embryonal RMS (ERMS) (81% v 32%, respectively; P < .001)
234 urvival (FFS) rate was 90% for patients with embryonal RMS (ERMS) stage 1, group I or IIa; stage 2, g
236 arcoma, has two major histological subtypes: embryonal RMS (ERMS), which has a favorable prognosis, a
239 e environment for spontaneous development of embryonal RMS associated with mutation of p53 and mutati
243 MS cells express higher levels of c-MET than embryonal RMS cell lines and "home/seed" better into bon
245 ooperate to induce apoptosis in alveolar and embryonal RMS cells in a highly synergistic fashion (com
246 e embryonal RMS, stage 2/3, group III (33%); embryonal RMS, group IV, less than age 10 years (7%); al
247 MS), except those younger than 10 years with embryonal RMS, have an estimated long-term event-free su
252 actor critical for the pluripotency of human embryonal stem (ES) and induced pluipotency stem (IPS) c
256 isms, being required for the self-renewal of embryonal stem cells in response to leukemia inhibitory
259 type AML) and miR-1 and miR-133 (involved in embryonal stem-cell differentiation), respectively.
262 ion, i.e. the canonical pathway, in mouse F9 embryonal tetratocarcinoma cells expressing rat Frizzled
263 o oncogenic chromosome dynamics and that the embryonal theory for cancer cell growth/proliferation is
265 While there is a long history of targeting embryonal tissues toward cancer vaccines, recent identif
266 viously, we observed expression of Oct-4, an embryonal transcriptional regulator, in osteosarcoma cel
267 ule network is partially disorganised in the embryonal tube cells and the microtubules disrupted in t
269 ally invasive or metastatic tumors, in which embryonal tumor cells are EGFR-negative, while SCU cells
270 Conversely, at an older age, mice escaping embryonal tumor formation present with malignant gliomas
273 lopment and the medulloblastoma, a malignant embryonal tumor of the cerebellum, have proven especiall
277 ulloblastoma/primitive neuroectodermal tumor/embryonal tumor, 17 had malignant astrocytoma, nine had
280 or of unknown cause, is not associated with embryonal tumors and cells from these individuals show m
284 are highly aggressive, poorly differentiated embryonal tumors occurring predominantly in young childr
285 selective radioimmunoconjugates specific for embryonal tumors of childhood are currently being active
288 RIP13 or BUB1B mutations have a high risk of embryonal tumors, and here we show that their cells disp
289 c tumors representing sarcomas, extracranial embryonal tumors, brain tumors, hematologic malignancies
290 ne abdominal wall defects, macroglossia, and embryonal tumors, is a model for understanding the relat
298 gnificantly influenced by histology (47% for embryonal v 34% for all others, P =.026) and increasing
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