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1 tumors with frequent Rb deficiency, such as mammary carcinoma.
2 rus middle T Ag (MMTV-PyMT)) mouse models of mammary carcinoma.
3 rat/neu transgenic mouse model of metastatic mammary carcinoma.
4 he invasive behavior of cells derived from a mammary carcinoma.
5 uggests that intestinal bacteria can trigger mammary carcinoma.
6 2 expression in 2 transgenic mouse models of mammary carcinoma.
7 g domain into a mouse model of ErbB2-induced mammary carcinoma.
8 lso linked to development and progression of mammary carcinoma.
9 henotype in genetically engineered mice with mammary carcinoma.
10 e PyMT transgenic mouse model of spontaneous mammary carcinoma.
11 tion, and Rap1 was activated in a metastatic mammary carcinoma.
12 venting metastasis in poorly immunogenic 4T1 mammary carcinoma.
13 mors using an in vivo mouse model of the 4T1 mammary carcinoma.
14 gnaling in a rat model of chemically induced mammary carcinoma.
15 or use of statins in many cancers, including mammary carcinoma.
16 changes were not the same in the HER2-driven mammary carcinomas.
17 efficacious in the prevention of neu-induced mammary carcinomas.
18 transgenic mice, which spontaneously develop mammary carcinomas.
19 egrins in the development and progression of mammary carcinomas.
20 i (apc) mouse adenomas, and implanted MCa-IV mammary carcinomas.
21 n both normal mammary tissue and spontaneous mammary carcinomas.
22 notypes associated with ERBB2-overexpressing mammary carcinomas.
23 BRCA1 downregulation observed in aggressive mammary carcinomas.
24 ce led to formation of poorly differentiated mammary carcinomas.
25 essed in approximately 24% of analyzed human mammary carcinomas.
26 importance against the less aggressive male mammary carcinomas.
27 of both Lewis lung carcinoma and spontaneous mammary carcinomas.
28 metastatic microenvironment in p120-negative mammary carcinomas.
29 ysyl oxidase (LOX) compared with PyMT(fl/fl) mammary carcinomas.
30 (15 invasive ductal carcinoma, 1 high-grade mammary carcinoma, 3 lobular carcinoma, 1 invasive papil
31 ell lines MCF-7 and MDA-MB-231 and the mouse mammary carcinoma 4T1 express low to undetectable levels
32 sing the well-characterized mouse metastatic mammary carcinoma 4T1 in a postsurgery setting, IFN-gamm
35 -term therapeutic benefit in mouse models of mammary carcinoma, accompanied by strikingly reduced met
37 tal microscopy of chemotherapy-treated mouse mammary carcinomas allowed us to follow drug distributio
38 is initiation by two murine tumor lines (4T1 mammary carcinoma and B16 melanoma), which constitutivel
40 ficial effects against both the parental DA3 mammary carcinoma and DA3 tumors transfected with H60, a
41 ng photoswitchable proteins in an orthotopic mammary carcinoma and followed them for extended periods
43 xenograft and in syngeneic animal models of mammary carcinoma and glioblastoma, the combination of s
44 d its downstream activities in TA3/St murine mammary carcinoma and HCT 116 human colon carcinoma cell
45 be involved in the growth and progression of mammary carcinoma and highlighted this protein as a pote
46 We have tested this hypothesis using the 4T1 mammary carcinoma and IL-1 receptor (IL-1R)-deficient mi
48 DAMTS-1 promotes pulmonary metastasis of TA3 mammary carcinoma and Lewis lung carcinoma cells and tha
49 er extended to spontaneously arising primary mammary carcinoma and lung metastases in a mouse tumor m
50 Nrf2(-/-)BALB/c and C57BL/6 mice bearing 4T1 mammary carcinoma and MC38 colon carcinoma, respectively
52 d the expression of three CKIs in EMT6 mouse mammary carcinoma and MEL28 human melanoma spheroids, as
53 production could inhibit the development of mammary carcinoma and metastasis in a rat model of breas
54 e a novel mouse model of inflammation-driven mammary carcinoma and suggest that epithelial carcinogen
55 mmunologically reject spontaneous metastatic mammary carcinoma and survive indefinitely if their prim
56 bal gene expression profiling of Ccn6(fl/fl) mammary carcinomas and comparison of orthologous genes w
57 non-transforming rat neu develop spontaneous mammary carcinomas and demonstrate immunotolerance to th
59 decreased the incidence and multiplicity of mammary carcinomas and prolonged cancer latency (P < 0.0
60 Instead, the autochthonous nature of the mammary carcinomas and their possession of a high percen
61 M signatures of poorly and highly metastatic mammary carcinomas and these signatures reveal up-regula
62 role in leukocyte trafficking, metastasis of mammary carcinoma, and human immunodeficiency virus type
63 ude regulation of the metastatic behavior of mammary carcinoma, and utilization as a coreceptor for i
65 growth of s.c. B16 melanomas, orthotopic 4T1 mammary carcinomas, and reducing 4T1 lung metastases.
67 tion against E2f3(-/-) cells from developing mammary carcinomas, and that such selection pressure is
69 was found in 21% of the MMTV-D1 and D1T286A mammary carcinomas, and the Dmp1 heterozygous status sig
71 12) to inhibit the vasculature and growth of mammary carcinomas arising in situ in mouse mammary tumo
72 , hyperplastic foci, cellular dysplasia, and mammary carcinoma, associated with increased genomic ins
75 of the C75-treated transgenic mice developed mammary carcinoma by 220 days, compared to 50% in the ve
80 iRNA or shRNA were sufficient to reduce MCF7 mammary carcinoma cell growth and increase cell death un
87 both a human melanoma cell line and a mouse mammary carcinoma cell line, our results indicate that t
90 ers of the ErbB family have been compared in mammary carcinoma cell lines differing in their ErbB exp
94 required for MDA-MB-231 and MDA-MB-435 human mammary carcinoma cell spreading on vitronectin or S1-sp
95 man lung adenocarcinoma cells (A549), murine mammary carcinoma cells (4T1) as well as a human tumor x
96 However, only c-Myc-overexpressing mouse mammary carcinoma cells (but not normal mouse mammary ep
97 on carcinoma as well as MCF-7 and MDA-MB-231 mammary carcinoma cells (cisplatin: 5.75, 12.72, 5.81 mu
100 mediated rejection of the neu-overexpressing mammary carcinoma cells (MMC) in wild-type FVB mice.
102 al lung metastasis of E(2)-nonresponsive 4T1 mammary carcinoma cells also leads to increased tumor bu
103 0-345) alone induced cell-matrix adhesion of mammary carcinoma cells and corneal stromal cells and in
104 sgenic mouse mammary tumor virus-c-Myc mouse mammary carcinoma cells are both calcium/calmodulin-depe
105 2 in HCT116 colon carcinoma cells and TA3/St mammary carcinoma cells are dependent on endogenous hyal
108 -1/Tcf-1 stimulates OPN transcription in rat mammary carcinoma cells by binding to a specific promote
109 ndicates that TIMP-4 protein is increased in mammary carcinoma cells compared with normal mammary epi
110 mouse models to show that Rab27a blockade in mammary carcinoma cells decreased secretion of exosomes
112 her that overexpression of CRABP-II in MCF-7 mammary carcinoma cells dramatically enhances their sens
113 MDA-231 human breast cancer cells and mouse mammary carcinoma cells expressing the polyomavirus midd
114 estrant-resistant, HER2+, or triple-negative mammary carcinoma cells in a manner that was not apparen
115 ecorin on the growth of ErbB2-overexpressing mammary carcinoma cells in comparison with AG879, an est
117 in-2 (Ang-2) in Lewis lung carcinoma and TA3 mammary carcinoma cells inhibited their ability to form
118 vidence that endogenous maspin expression in mammary carcinoma cells MDA-MB-435 enhanced staurosporin
119 CR4 signaling via dysregulation of CXCL12 in mammary carcinoma cells modulated their metastatic poten
120 dc2) activity with olomoucine in FM3A murine mammary carcinoma cells or by reducing the level and act
121 fspKO) mammary fibroblasts transplanted with mammary carcinoma cells promote growth and invasion, whi
122 e TM40D and highly aggressive TM40D-MB mouse mammary carcinoma cells revealed significantly higher ST
123 e demonstrate that knockdown of Eya2 in MCF7 mammary carcinoma cells reverses the ability of Six1 to
124 ion of Twist expression in highly metastatic mammary carcinoma cells specifically inhibits their abil
128 ncated CXCR4 (CXCR4-DeltaCTD) in MCF-7 human mammary carcinoma cells to determine whether the CTD is
129 ession is required for the ability of murine mammary carcinoma cells to metastasize to the lung, and
130 may be one common adaptive mechanism used by mammary carcinoma cells to promote cell survival and ren
131 ibits the migration of endothelial cells and mammary carcinoma cells while continuing to promote cell
132 pin bound specifically to the surface of the mammary carcinoma cells with a kd of 367 +/- 67 nM and 3
133 16 human colon carcinoma cells and 4T1 mouse mammary carcinoma cells with constitutively expressed re
134 vious studies showed that treatment of MCF-7 mammary carcinoma cells with the potent protein kinase C
135 1 human breast cancer cells and Py8119 mouse mammary carcinoma cells, and this inhibitory effect was
136 of E- and N-cadherin to suppress movement of mammary carcinoma cells, as quantified from time-lapse v
138 hrough which RA inhibits the growth of MCF-7 mammary carcinoma cells, focusing on the involvement of
140 ouse tumour models such as HA-expressing 4T1 mammary carcinoma cells, OVA-expressing EG7 lymphoma cel
141 the metastatic potential of CXCR4-expressing mammary carcinoma cells, subsequent to epigenetic silenc
142 ing Sdc1 deletion mutants expressed in human mammary carcinoma cells, we identified the active site w
143 , we find Cbx7T118 phosphorylation in murine mammary carcinoma cells, which can be blocked by MEK inh
144 uses elevated ErbB2 phosphorylation in MCF-7 mammary carcinoma cells, which normally exhibit low leve
165 imilar inhibitory effect on the Py8119 mouse mammary carcinoma cells; however, adenosine had no effec
166 cycle of pregnancy and increased further in mammary carcinomas compared to mammary glands from wild-
167 distinct solid tumors (lung adenocarcinoma, mammary carcinoma, cutaneous melanoma, and uveal melanom
168 MGA1 expression in primary breast cancer and mammary carcinoma derived cell lines inversely correlate
169 ression of Cav-1 in a highly metastatic PyMT mammary carcinoma-derived cell line, namely Met-1 cells,
173 mal transition of estrogen receptor negative mammary carcinoma (ER-MC) cells associated with metastas
175 ghly aggressive, spontaneously metastasizing mammary carcinoma, followed by surgical removal of the p
176 also investigated allelic imbalance (AI) in mammary carcinomas from (WKy x WF)F1 rats and Mcs7 heter
180 tations in the endogenous Harvey ras gene in mammary carcinomas from the HrHr, HrKr transgenic rats a
182 show that Tgfbr2(FspKO) fibroblasts enhance mammary carcinoma growth and metastasis in mice while in
183 ndostatin gene efficiently suppresses murine mammary carcinoma growth and support the potential utili
184 el of breast cancer, most but not all of the mammary carcinomas had strongly increased Peg10 mRNA com
185 spontaneously metastatic BALB/c-derived 4T1 mammary carcinoma have delayed tumor growth and reduced
187 dings establish a model of luminal subtype B mammary carcinoma, identify critical role of cIAP1, cIAP
189 licobacter hepaticus, significantly promotes mammary carcinoma in females and enhances intestinal ade
190 und examinations are insufficient.Picture of mammary carcinoma in imaging studies is heterogeneous.
191 By high-resolution multiphoton microscopy of mammary carcinoma in mice, we detected two phenotypes of
193 mmary intraepithelial neoplasia and invasive mammary carcinomas in a significant proportion of aged f
194 polyoma middle T-antigen oncoprotein-induced mammary carcinomas in GnT-V null mice was significantly
196 expressing alphaB-crystallin formed invasive mammary carcinomas in nude mice that recapitulated aspec
200 The Wistar Kyoto (WKy) rat is resistant to mammary carcinomas induced with 7,12-dimethybenz[a]anthr
203 r nontoxic and low-dose coexposures of human mammary carcinoma MCF-7 cells against polycyclic aromati
207 moxic conditions in colorectal (HCT-116) and mammary carcinoma (MDA MB 231) cells but fails to induce
208 Furthermore, PyVmT-overexpressing mouse mammary carcinoma Met-1 cells are highly responsive to I
211 MMTV (mouse mammary tumor virus)-PyMT mouse mammary carcinoma model results in slower tumor growth a
212 outperformed (64)Cu-NOTA-RGD in a 4T1 murine mammary carcinoma model that expresses integrin on tumor
213 HA synthesis than oral MU in the 4T1 murine mammary carcinoma model using both a quantitative ELISA
214 ing neoadjuvant therapy in a triple-negative mammary carcinoma model, and suppressed cancer cell diss
225 n cell cycle regulation could be detected in mammary carcinomas occurring in 40% ER rats in compariso
226 The remarkable similarities between the mammary carcinomas of Bard1-, Brca1-, and Bard1/Brca1-mu
228 mice bearing poorly immunogenic 11A-1 murine mammary carcinomas or Meth A sarcomas and C57Bl/6 mice b
229 rs and leads to PVMT-induced hemangiomas and mammary carcinomas or SVER-induced disseminated sarcomas
231 d that increased expression of Tid1 in human mammary carcinomas overexpressing ErbB-2 suppresses the
233 ancy and suggest that its loss may influence mammary carcinoma pathogenesis in multiparous women.
235 ed an average of 3.4 +/- 2.0 and 5.5 +/- 3.6 mammary carcinomas per rat +/- SD when females were Mcs1
236 tible genotype littermates (7.8 +/- 3.1 mean mammary carcinomas per rat +/- SD, P = 0.0001 and P = 0.
242 in a conditional mouse model of noninvasive mammary carcinoma results in formation of stromal-dense
243 -control studies carried out in Germany: the Mammary Carcinoma Risk Factor Investigation (MARIE), a b
246 for linkage mapping to genetically identify mammary carcinoma susceptibility (Mcs) loci underlying t
247 ic region of 2q, a region known to carry the mammary carcinoma susceptibility 1 (Mcs1) gene and sever
250 interaction that is synergistic to decrease mammary carcinoma susceptibility below the additive effe
253 y metastasis of Lewis lung carcinoma and TA3 mammary carcinoma (TA3) cells by inhibiting tumor angiog
255 l component of innate immunity to metastatic mammary carcinoma that probably mediates its effects via
256 nd correlation with lung metastases of human mammary carcinomas that are associated with myeloid cell
258 on of an adenovirus expressing CRABP-II into mammary carcinomas that spontaneously develop in TgN(MMT
259 able and compressed vessels (e.g., subset of mammary carcinomas), the two strategies need to be combi
260 ur results show that in usual types of human mammary carcinomas, the Id1 protein is expressed exclusi
264 kinase activity in mice bearing ErbB2-driven mammary carcinomas triggered tumor cell senescence, with
265 ignant growth of syngeneic lymphoma (A20) or mammary carcinoma (TSA) in BALB/c mice compared with rVS
267 erase activation and telomere maintenance in mammary carcinoma tumorigenesis, we generated mice expre
268 take of 2-(18)F-FEtOH in 4T1 and 67NR murine mammary carcinoma tumors grown in mice was measured usin
270 hus, it appears that ER induces apoptosis in mammary carcinomas via a cell survival factor-dependent
271 antitumor activity against MDA-MB-435 human mammary carcinoma was also determined for natural bengam
274 the BALB/NeuT model of spontaneously arising mammary carcinoma, we found that canonical MHC II(+)/CD1
276 tumor virus (MMTV)-Wnt-1 transgenic model of mammary carcinoma, we have identified an unvarying assoc
277 Using the spontaneously metastatic 4T1 mouse mammary carcinoma, we now demonstrate that cross-talk be
278 novel transgenic mouse model of spontaneous mammary carcinoma, we show here that the IL-12/pulse IL-
279 e reported that CtsB regulates metastasis of mammary carcinomas, we found that development of squamou
280 nsic to the mice that host the autochthonous mammary carcinomas were also not responsible for failure
284 al than the tumor surface of the R3230Ac rat mammary carcinoma when growing in a dorsal skin-fold win
285 al pulmonary metastases, and the other was a mammary carcinoma, where Fas expression was examined in
286 with established, spontaneous metastatic 4T1 mammary carcinoma, whose primary tumors are surgically e
287 echanisms, we have transfected the mouse 4T1 mammary carcinoma with the proinflammatory cytokine IL-1
288 activated protein kinase (AMPK) increased in mammary carcinomas with a concomitant increase in phosph
289 ;MMTV-Cre mice developed invasive high grade mammary carcinomas with bona fide EMT, histologically si
290 t in the majority of mouse and human primary mammary carcinomas with ErbB2/HER2 overexpression, E2f3a
291 ogen receptor-positive raloxifene-responsive mammary carcinomas with features of luminal subtype B.
292 HER2 antibodies, such as Herceptin, against mammary carcinomas with high levels of the HER2 proto-on
293 Upon aging, the development of Wnt activated mammary carcinomas with squamous differentiation was acc
294 mIL-15+Ad.mlL-15Ralpha)) were protected from mammary carcinomas, with 70% of animals tumor-free at 30
295 n validated against in-vivo data from murine mammary carcinomas, with particular focus placed on iden
296 1) and polyomavirus middle T (PyMT) develop mammary carcinomas within 15 weeks with 100% penetrance.
297 e proteomics to investigate the ECM of human mammary carcinoma xenografts and show that primary tumor
298 antitumor effects in nude mice bearing MX-1 mammary carcinoma xenografts without increasing toxicity
299 ed hormone-sensitive and hormone-insensitive mammary carcinoma xenografts, orthotopic prostate tumors
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