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1 anel in the diagnosis of various subtypes of pituitary tumors.
2 sible therapeutic target in the treatment of pituitary tumors.
3 Gal-3 in the development and progression of pituitary tumors.
4 us sinus fistulae, parasellar syndromes, and pituitary tumors.
5 posed as novel oral medications for managing pituitary tumors.
6 rmone receptor PPAR-gamma in all of 39 human pituitary tumors.
7 role for selective antiestrogens in treating pituitary tumors.
8 -378 RB-producing ES cells failed to develop pituitary tumors.
9 adenomas compared with that in nonsecreting pituitary tumors.
10 tiation and increases the susceptibility for pituitary tumors.
11 of human anterior pituitary cells and human pituitary tumors.
12 al cell proliferation, and susceptibility to pituitary tumors.
13 ce and increased penetrance of hGHRH-induced pituitary tumors.
14 pressed in malignant human cell lines and in pituitary tumors.
15 the recently proposed genetic treatments for pituitary tumors.
16 gnostic and potential therapeutic targets in pituitary tumors.
17 fects in the Rb gene are not common in human pituitary tumors.
18 44) rat induces growth of large, hemorrhagic pituitary tumors.
19 product occurs at a high frequency in human pituitary tumors.
20 tiple parathyroid, pancreatic, duodenal, and pituitary tumors.
21 nostic yield for localizing small functional pituitary tumors.
22 period, excluding all craniopharyngioma and pituitary tumors.
23 e utility of this tracer in the detection of pituitary tumors.
24 ous role for these cells in the induction of pituitary tumors.
25 tumorigenesis in Rb1-deficient prostate and pituitary tumors.
26 CTH) and adrenal steroid secretion caused by pituitary tumors.
27 potential to improve care for patients with pituitary tumors.
28 Gli function may contribute to these common pituitary tumors.
29 anding mechanisms underlying uniquely benign pituitary tumors.
30 was significantly reduced due to aggressive pituitary tumors.
31 itary adenomas (NFPAs) are the most frequent pituitary tumors.
32 expressed in a specific cell-type manner in pituitary tumors.
33 statin ligand design to treat ACTH-secreting pituitary tumors.
36 ter, white matter, gliomas, meningiomas, and pituitary tumors, allowing their ready discrimination by
38 l pituitaries; however, in a small number of pituitary tumors analysed, 11 beta-HSD2 was readily demo
39 dentified a miRNA signature for GH-producing pituitary tumors and found that miR-26b and miR-128 regu
40 of mRNA for 11 beta-HSD1 and 2 in 105 human pituitary tumors and have performed enzyme expression an
41 types of normal anterior pituitary cells and pituitary tumors and in other neuroendocrine cells and t
44 chanism of silencing of the p27 gene in some pituitary tumors and possibly in other types of neoplasm
46 review current research in the treatment of pituitary tumors and summarize emerging medical, surgica
47 including four classes: glioma, meningioma, pituitary tumor, and healthy, on a dataset containing 32
48 ads to an overall increase in animal growth, pituitary tumors, and hyperplasia of hematopoietic organ
50 total number of reproductive system tumors, pituitary tumors, and metastases was increased in the of
51 ent therapy can generate menin expression in pituitary tumors, and significantly reduce tumor cell pr
53 drenocorticotrophic hormone (ACTH)-secreting pituitary tumors are associated with high morbidity due
54 dels of these neoplasms simply do not exist: pituitary tumors are common in rodents, but their histol
63 ain diseases, namely glioma, meningioma, and pituitary tumor, are chosen as abnormal brains, and the
64 hown to significantly reduce the severity of pituitary tumors arising in Rb1(+/-) animals by enhancin
65 o investigate the expression of p16 in human pituitary tumors as an indirect mechanism of Rb inactiva
68 crucial role during development of p27(-/-) pituitary tumors because loss of one copy of Sox2 impair
70 beta-catenin in Sox2(+) cells gives rise to pituitary tumors, but, unexpectedly, the tumor mass is n
72 cate that the suppression of pars intermedia pituitary tumors by p27(Kip1) is cell-autonomous and doe
73 stioned the mechanism of Gal-3 expression in pituitary tumors, by using methylation-specific PCR and
77 identified that miR-26b and miR-128 affected pituitary tumor cell behavior through regulation of thei
78 genesis we treated primary rat pituitary and pituitary tumor cell cultures with recombinant FGF-4 and
84 hibits the growth and DNA synthesis of mouse pituitary tumor cells and human choriocarcinoma cells.
85 ETS-2 repressor factor (ERF) is expressed in pituitary tumor cells and that overexpression of recombi
86 (p27) protein in rat GH3 and mouse GHRH-CL1 pituitary tumor cells compared with normal pituitary (NP
87 aneuploid GH-secreting cells, and GH(3) rat pituitary tumor cells overexpressing PTTG also exhibited
90 enesis and/or proliferation, and 3) cultured pituitary tumor cells respond to TGF-beta1 and PKC inhib
91 ctin promoter to dopamine was examined using pituitary tumor cells stably expressing dopamine D2 rece
92 e cell cycle and apoptotic response of these pituitary tumor cells to the dopamine analog bromocripti
93 ta-HCH occurs in estrogen-responsive GH3 rat pituitary tumor cells transfected with a luciferase repo
94 nsforming gene (PTTG1) was isolated from rat pituitary tumor cells, and subsequently identified as a
95 rat somatolactotroph, and murine gonadotroph pituitary tumor cells, and suppressed in vitro hormone s
105 nally discovered in a subpopulation of human pituitary tumors characterized by their invasive phenoty
107 Antiestrogen treatment of primary human pituitary tumor cultures reduced PTTG expression approxi
108 fe-threatening disorder attributed to excess pituitary tumor-derived adrenocorticotrophic hormone (AC
109 e PAs and in the (nonfunctioning) HP75 human pituitary tumor-derived cell line treated with phorbol-1
115 oci reside on chromosome 6 [Estrogen-induced pituitary tumor (Ept)1], chromosome 3 (Ept2 and Ept6), c
116 cognized that most clinically nonfunctioning pituitary tumors express gonadotropin hormones or their
118 near-real-time detection and delineation of pituitary tumors for intraoperative surgical decision-ma
119 ulating the PTEN-AKT pathway in GH-producing pituitary tumor formation in the context of hyperplasia
120 We have identified a 17-miRNA signature of pituitary tumors formed in the background of hyperplasia
123 he role of p185(her2/neu)/ErbB3 signaling in pituitary tumor function, we examined these receptors in
125 on therapy and stereotactic radiosurgery for pituitary tumors gains more widespread use, long-term da
127 K+ (I(K)) and Ca++ currents in rat anterior pituitary tumor (GH3) cells were analyzed by using a who
128 and circulating sex steroid hormones promote pituitary tumor growth and expansion into large invasive
130 Aneuploid pituitary cell p21 may constrain pituitary tumor growth, thus accounting for the very low
133 land and induce development of PRL-producing pituitary tumors in certain inbred rat strains but not o
135 orm aggressive growth-hormone (GH)-producing pituitary tumors in the background of hyperplasia caused
137 i-estrogens reduced PTTG expression in human pituitary tumors in vitro and suppressed experimental tu
138 pression of sigma-1 receptors in spontaneous pituitary tumors is detected as an increase in uptake an
139 iagnosis of various histological subtypes of pituitary tumors is made using serum based hormone panel
140 MP-dependent protein kinase pathway in human pituitary tumors; it also reviews briefly other pathways
141 cretion and ablation or stabilization of the pituitary tumor mass lead to improved comorbidities and
142 ty of therapeutic radiation in patients with pituitary tumor, medulloblastoma, and arteriovenous malf
143 e drugs are introduced for the management of pituitary tumors, more patients with hormone-secreting a
146 corticotropin excess is produced by a benign pituitary tumor, occurs in approximately 60% to 70% of p
147 eclinical evaluation of MEN1 gene therapy in pituitary tumors of Men1(+/-) mice, using a recombinant
148 These symptoms were not associated with pituitary tumors or multiple endocrine neoplasia but wer
151 racrine growth factor-mediated mechanism for pituitary tumor pathogenesis and potentially other estro
152 pituitary carcinomas that may contribute to pituitary tumor pathogenesis and/or proliferation, and 3
153 f surgically resected tumors from forty five pituitary tumor patients [gonadotropic (LH/FSH-secreting
156 undetectable levels of p16 mRNA in 13 of 14 pituitary tumors relative to 5 normal pituitary specimen
165 E2F3 loss suppresses the development of the pituitary tumors that normally account for the death of
167 rbB receptor family members are expressed in pituitary tumors, the effects of EGF signaling on pituit
173 ly, we cloned and sequenced cDNA of a potent pituitary tumor transforming gene (PTTG) from human test
180 transgenic zebrafish with overexpression of pituitary tumor transforming gene (PTTG/securin) targete
186 n was also independently identified as PTTG (pituitary tumor transforming gene), a gene overexpressed
196 identical to the product of the gene called pituitary tumor-transforming gene (PTTG), which is overe
197 revealed that known tumor promoters such as pituitary tumor-transforming gene were activated and tum
198 It is also known as the product of the human pituitary tumor-transforming gene, pttg, a proto-oncogen
199 brain tumors-such as glioma, meningioma, and pituitary tumors-using the U-Net architecture applied to
200 y proliferation to study the pathogenesis of pituitary tumors, we crossed the glycoprotein hormone al
202 H4C1 cells, a clonal line derived from a rat pituitary tumor, were stably transfected with the gene e
203 16 gene product was undetectable in 25 human pituitary tumors, whereas high levels of p16 could be de
204 Prolactinomas are the most frequent type of pituitary tumors, which represent 10-20% of all intracra
206 ice heterozygous for the Rb mutation develop pituitary tumors, with about 20% arising from the AL.