ライフサイエンスコーパス: mammary carcinoma

1 gnaling in a rat model of chemically induced mammary carcinoma.

2 or use of statins in many cancers, including mammary carcinoma.

3 tumors with frequent Rb deficiency, such as mammary carcinoma.

4 rus middle T Ag (MMTV-PyMT)) mouse models of mammary carcinoma.

5 rat/neu transgenic mouse model of metastatic mammary carcinoma.

6 he invasive behavior of cells derived from a mammary carcinoma.

7 uggests that intestinal bacteria can trigger mammary carcinoma.

8 2 expression in 2 transgenic mouse models of mammary carcinoma.

9 g domain into a mouse model of ErbB2-induced mammary carcinoma.

10 response in an immunocompetent model using a mammary carcinoma.

11 venting metastasis in poorly immunogenic 4T1 mammary carcinoma.

12 lso linked to development and progression of mammary carcinoma.

13 henotype in genetically engineered mice with mammary carcinoma.

14 mors using an in vivo mouse model of the 4T1 mammary carcinoma.

15 e PyMT transgenic mouse model of spontaneous mammary carcinoma.

16 creased the latency of these very aggressive 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 changes were not the same in the HER2-driven mammary carcinomas.

21 i (apc) mouse adenomas, and implanted MCa-IV mammary carcinomas.

22 n both normal mammary tissue and spontaneous mammary carcinomas.

23 notypes associated with ERBB2-overexpressing mammary carcinomas.

24 BRCA1 downregulation observed in aggressive mammary carcinomas.

25 ce led to formation of poorly differentiated 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

33 Metastatic mouse mammary carcinoma 4T1-green fluorescent protein cells we

34 We have used the mouse 4T1 mammary carcinoma, a BALB/c-derived transplantable tumor

35 -term therapeutic benefit in mouse models of mammary carcinoma, accompanied by strikingly reduced met

36 Multiparous mice presented with mammary carcinomas after a latency of 12 months, and adm

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

39 Using syngeneic cancer cells (EO771 mammary carcinoma and B16-F10 melanoma cells) injected i

40 e agents selectively kill hypoxic EMT6 mouse mammary carcinoma and CHO cells.

41 ficial effects against both the parental DA3 mammary carcinoma and DA3 tumors transfected with H60, a

42 ng photoswitchable proteins in an orthotopic mammary carcinoma and followed them for extended periods

43 Cells, derived from a mammary carcinoma and from a glioblastoma, with reduced

44 xenograft and in syngeneic animal models of mammary carcinoma and glioblastoma, the combination of s

45 d its downstream activities in TA3/St murine mammary carcinoma and HCT 116 human colon carcinoma cell

46 be involved in the growth and progression of mammary carcinoma and highlighted this protein as a pote

47 We have tested this hypothesis using the 4T1 mammary carcinoma and IL-1 receptor (IL-1R)-deficient mi

48 middle-T (PyV-MT) transgenic mouse model of mammary carcinoma and Irs-1 null (Irs1(-/-)) mice.

49 DAMTS-1 promotes pulmonary metastasis of TA3 mammary carcinoma and Lewis lung carcinoma cells and tha

50 er extended to spontaneously arising primary mammary carcinoma and lung metastases in a mouse tumor m

51 Nrf2(-/-)BALB/c and C57BL/6 mice bearing 4T1 mammary carcinoma and MC38 colon carcinoma, respectively

52 SUM159PT mammary carcinoma and Mel 202 ocular melanoma cells tran

53 d the expression of three CKIs in EMT6 mouse mammary carcinoma and MEL28 human melanoma spheroids, as

54 production could inhibit the development of mammary carcinoma and metastasis in a rat model of breas

55 e a novel mouse model of inflammation-driven mammary carcinoma and suggest that epithelial carcinogen

56 mmunologically reject spontaneous metastatic mammary carcinoma and survive indefinitely if their prim

57 bal gene expression profiling of Ccn6(fl/fl) mammary carcinomas and comparison of orthologous genes w

58 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

64 ous RIP-Tag2 pancreatic islet tumors, MCa-IV mammary carcinomas, and Lewis lung carcinomas.

65 growth of s.c. B16 melanomas, orthotopic 4T1 mammary carcinomas, and reducing 4T1 lung metastases.

66 ng ovarian sex cord stromal tumors, lung and mammary carcinomas, and spindle cell tumors.

67 tion against E2f3(-/-) cells from developing mammary carcinomas, and that such selection pressure is

68 Female mice spontaneously develop mammary carcinomas, and the C3(1)/T-Ag-derived tumor cel

69 was found in 21% of the MMTV-D1 and D1T286A mammary carcinomas, and the Dmp1 heterozygous status sig

70 LRRK2-mutated mammary carcinomas are enriched with stop-gain, truncati

71 In ovariectomized animals, the mammary carcinomas are hormonally nonresponsive and cann

72 12) to inhibit the vasculature and growth of mammary carcinomas arising in situ in mouse mammary tumo

73 We demonstrate, using 4T1 murine mammary carcinoma as model cell line, that unseeded non-

74 , hyperplastic foci, cellular dysplasia, and mammary carcinoma, associated with increased genomic ins

75 ong-circulating liposomes in immunocompetent mammary carcinoma-bearing FVB/n and BALB/c mice.

76 MDSC expansion in 4T1 mammary carcinoma-bearing hosts is associated with induc

77 of the C75-treated transgenic mice developed mammary carcinoma by 220 days, compared to 50% in the ve

78 breast cancers, but loss of BMP signaling in mammary carcinomas can accelerate metastasis.

79 In intact rats, approximately 50% of mammary carcinomas can be prevented by tamoxifen treatme

80 Its overexpression in human and mouse mammary carcinoma cancer cells leads to enhanced metasta

81 in reduced ErbB4 protein amount and reduced mammary carcinoma cell differentiation.

82 iRNA or shRNA were sufficient to reduce MCF7 mammary carcinoma cell growth and increase cell death un

83 Here, we show that inhibition of mammary carcinoma cell growth by RXR ligands stems from

84 ficiency on tumor behavior, using the murine mammary carcinoma cell line 4T1.

85 umor model using the highly aggressive mouse mammary carcinoma cell line EMT-6.

86 ents (EREs), repressing transcription in the mammary carcinoma cell line MCF-7.

87 nduction of caspase 9 gene expression in the mammary carcinoma cell line MCF-7.

88 12A, and the ER-negative, highly tumorigenic mammary carcinoma cell line MDA-MB-231.

89 both a human melanoma cell line and a mouse mammary carcinoma cell line, our results indicate that t

90 g of ATP7A inhibited LOX activity in the 4T1 mammary carcinoma cell line, resulting in a loss of LOX-

91 ytic subunit of calpain 2 in the AC2M2 mouse mammary carcinoma cell line.

92 d BRCA1 mRNA and protein expression in human mammary carcinoma cell lines and tissues.

93 metastatic melanoma, prostate carcinoma, or mammary carcinoma cell lines.

94 in both the A431 squamous and the MDA-MB-231 mammary carcinoma cell lines.

95 and -575 is important for its expression in mammary carcinoma cell lines.

96 However, the effects of acidity on mammary carcinoma cell morphology and phenotype have not

97 Acidification also increased mammary carcinoma cell motility when cultured with fibro

98 required for MDA-MB-231 and MDA-MB-435 human mammary carcinoma cell spreading on vitronectin or S1-sp

99 Acidification decreased overall mammary carcinoma cell viability, while increasing their

100 man lung adenocarcinoma cells (A549), murine mammary carcinoma cells (4T1) as well as a human tumor x

101 However, only c-Myc-overexpressing mouse mammary carcinoma cells (but not normal mouse mammary ep

102 on carcinoma as well as MCF-7 and MDA-MB-231 mammary carcinoma cells (cisplatin: 5.75, 12.72, 5.81 mu

103 The virus infected mouse mammary carcinoma cells (D2F2/E2) expressing Her2/neu 23

104 We show that mammary carcinoma cells (MCF7), which do not express CEA

105 mediated rejection of the neu-overexpressing mammary carcinoma cells (MMC) in wild-type FVB mice.

106 uDox complex was efficiently internalized by mammary carcinoma cells after release from LTSLs.

107 al lung metastasis of E(2)-nonresponsive 4T1 mammary carcinoma cells also leads to increased tumor bu

108 0-345) alone induced cell-matrix adhesion of mammary carcinoma cells and corneal stromal cells and in

109 sgenic mouse mammary tumor virus-c-Myc mouse mammary carcinoma cells are both calcium/calmodulin-depe

110 2 in HCT116 colon carcinoma cells and TA3/St mammary carcinoma cells are dependent on endogenous hyal

111 Disruption of Smad3 expression in mammary carcinoma cells blocked CCL2-induced cell surviv

112 that promoted proliferation and survival of mammary carcinoma cells but inhibited metastasis.

113 -1/Tcf-1 stimulates OPN transcription in rat mammary carcinoma cells by binding to a specific promote

114 mouse models to show that Rab27a blockade in mammary carcinoma cells decreased secretion of exosomes

115 hibition of cyclin A1 in Six1-overexpressing mammary carcinoma cells decreases proliferation.

116 MDA-231 human breast cancer cells and mouse mammary carcinoma cells expressing the polyomavirus midd

117 estrant-resistant, HER2+, or triple-negative mammary carcinoma cells in a manner that was not apparen

118 ecorin on the growth of ErbB2-overexpressing mammary carcinoma cells in comparison with AG879, an est

119 al effects of environmental acidification on mammary carcinoma cells in standard two-dimensional cult

120 own HIF-1alpha target genes, and survival of mammary carcinoma cells in vitro.

121 vidence that endogenous maspin expression in mammary carcinoma cells MDA-MB-435 enhanced staurosporin

122 CR4 signaling via dysregulation of CXCL12 in mammary carcinoma cells modulated their metastatic poten

123 fspKO) mammary fibroblasts transplanted with mammary carcinoma cells promote growth and invasion, whi

124 e TM40D and highly aggressive TM40D-MB mouse mammary carcinoma cells revealed significantly higher ST

125 e demonstrate that knockdown of Eya2 in MCF7 mammary carcinoma cells reverses the ability of Six1 to

126 ion of Twist expression in highly metastatic mammary carcinoma cells specifically inhibits their abil

127 In mammary carcinoma cells that do not express endogenous E

128 We show in mammary carcinoma cells that mutant Arp2 lacking phospho

129 Indeed, RANK signalling in mammary carcinoma cells that overexpress the proto-oncog

130 ance and extracellular vesicle production by mammary carcinoma cells that promote tumor expansion.

131 ncated CXCR4 (CXCR4-DeltaCTD) in MCF-7 human mammary carcinoma cells to determine whether the CTD is

132 ession is required for the ability of murine mammary carcinoma cells to metastasize to the lung, and

133 may be one common adaptive mechanism used by mammary carcinoma cells to promote cell survival and ren

134 agy genes increased the sensitivity of mouse mammary carcinoma cells to radiation therapy in vitro an

135 ibits the migration of endothelial cells and mammary carcinoma cells while continuing to promote cell

136 pin bound specifically to the surface of the mammary carcinoma cells with a kd of 367 +/- 67 nM and 3

137 16 human colon carcinoma cells and 4T1 mouse mammary carcinoma cells with constitutively expressed re

138 vious studies showed that treatment of MCF-7 mammary carcinoma cells with the potent protein kinase C

139 1 human breast cancer cells and Py8119 mouse mammary carcinoma cells, and this inhibitory effect was

140 of E- and N-cadherin to suppress movement of mammary carcinoma cells, as quantified from time-lapse v

141 We show here that in MCF-7 mammary carcinoma cells, EGFR signaling directly up-regu

142 hrough which RA inhibits the growth of MCF-7 mammary carcinoma cells, focusing on the involvement of

143 In MCF-7 mammary carcinoma cells, growth inhibition by RA entails

144 ouse tumour models such as HA-expressing 4T1 mammary carcinoma cells, OVA-expressing EG7 lymphoma cel

145 the metastatic potential of CXCR4-expressing mammary carcinoma cells, subsequent to epigenetic silenc

146 ing Sdc1 deletion mutants expressed in human mammary carcinoma cells, we identified the active site w

147 , we find Cbx7T118 phosphorylation in murine mammary carcinoma cells, which can be blocked by MEK inh

148 uses elevated ErbB2 phosphorylation in MCF-7 mammary carcinoma cells, which normally exhibit low leve

149 t compressive stress stimulates migration of mammary carcinoma cells.

150 with the TGF-beta signaling pathway in human mammary carcinoma cells.

151 motility and the invasive potential of human mammary carcinoma cells.

152 ing ASAP3 expression also slowed invasion of mammary carcinoma cells.

153 XC2 enhances the metastatic ability of mouse mammary carcinoma cells.

154 ocess by complementation of Bard1-null mouse mammary carcinoma cells.

155 involved in CXCR4-modulated proliferation of mammary carcinoma cells.

156 geneic mice challenged with P1A-negative 4T1 mammary carcinoma cells.

157 nhibits lung metastasis of highly metastatic mammary carcinoma cells.

158 ly affect the three-dimensional migration of mammary carcinoma cells.

159 eased cytotoxicity and apoptosis in mouse BA mammary carcinoma cells.

160 ion causes increased growth in vivo of human mammary carcinoma cells.

161 se to epidermal growth factor (EGF) in human mammary carcinoma cells.

162 0ctn is not involved in suppression of these mammary carcinoma cells.

163 marker that is downregulated in transformed mammary carcinoma cells.

164 ncreased extracellular vesicle production by mammary carcinoma cells.

165 p2c target gene in murine, as well as human, mammary carcinoma cells.

166 stimulated ErbB4-induced differentiation of mammary carcinoma cells.

167 edge, motivated by data from EGF-stimulated mammary carcinoma cells.

168 the cancer stem cell (CSC)-like phenotype in mammary carcinoma cells.

169 imilar inhibitory effect on the Py8119 mouse mammary carcinoma cells; however, adenosine had no effec

170 cycle of pregnancy and increased further in mammary carcinomas compared to mammary glands from wild-

171 distinct solid tumors (lung adenocarcinoma, mammary carcinoma, cutaneous melanoma, and uveal melanom

172 MGA1 expression in primary breast cancer and mammary carcinoma derived cell lines inversely correlate

173 ression of Cav-1 in a highly metastatic PyMT mammary carcinoma-derived cell line, namely Met-1 cells,

174 In a mouse model of mammary carcinoma driven by the polyomavirus middle T (P

175 H1+ population in estrogen receptor-positive mammary carcinoma (ER+MC) cells.

176 mal transition of estrogen receptor negative mammary carcinoma (ER-MC) cells associated with metastas

177 either from mouse or human mammary glands or mammary carcinomas express EMT markers.

178 ghly aggressive, spontaneously metastasizing mammary carcinoma, followed by surgical removal of the p

179 also investigated allelic imbalance (AI) in mammary carcinomas from (WKy x WF)F1 rats and Mcs7 heter

180 phosphorylation (activation) was reduced in mammary carcinomas from ER rats.

181 Here, we show that mammary carcinomas from mice heterozygous for a Foxp3 mu

182 Here, we extend our observations to mammary carcinomas from mice of different genetic backgr

183 show that Tgfbr2(FspKO) fibroblasts enhance mammary carcinoma growth and metastasis in mice while in

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

186 Genome-wide analysis of mammary carcinomas identified a recurrent amplification

187 dings establish a model of luminal subtype B mammary carcinoma, identify critical role of cIAP1, cIAP

188 ells, a line established from a MMTV-induced mammary carcinoma in C3H mice.

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

192 90% reduction in tumor growth of murine 4T1 mammary carcinoma in vivo.

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

195 The resulting mammary carcinomas in intact Wistar-Furth rats exhibit a

196 expressing alphaB-crystallin formed invasive mammary carcinomas in nude mice that recapitulated aspec

197 cells, and prevented or delayed the onset of mammary carcinomas in the mice.

198 in cultured cells, and genomically unstable mammary carcinomas in transgenic mice.

199 The majority of the cancers were mammary carcinomas in which the wild-type Foxp3 allele w

200 The Wistar Kyoto (WKy) rat is resistant to mammary carcinomas induced with 7,12-dimethybenz[a]anthr

201 Polyoma middle T-induced mammary carcinomas lacking the type II TGF-beta receptor

202 In human mammary carcinoma MCF-7 and mouse hepatoma Hepa-1 cells,

203 r nontoxic and low-dose coexposures of human mammary carcinoma MCF-7 cells against polycyclic aromati

204 lasts or estrogen-dependent proliferation of mammary carcinoma MCF-7 cells.

205 NMuMG, human normal bladder HCV29, and human mammary carcinoma MCF7 cells.

206 I collagen, fibronectin, and laminin and of mammary carcinoma MDA-MB-231 cells to fibronectin.

207 moxic conditions in colorectal (HCT-116) and mammary carcinoma (MDA MB 231) cells but fails to induce

208 ell (MCF-7, tamoxifen-resistant MCF-7, mouse mammary carcinoma, MDA-MB-231, and BT-549) viability, mi

209 Furthermore, PyVmT-overexpressing mouse mammary carcinoma Met-1 cells are highly responsive to I

210 vironment and that disruption can accelerate mammary carcinoma metastases.

211 vo HSPC-transduced mice with implanted mouse mammary carcinoma (MMC) tumors, after initial tumor grow

212 d hyperthermia in a neu deletion (NDL) mouse mammary carcinoma model (Her2(+), ER/PR negative).

213 The nonimmunogenic 4T1 murine mammary carcinoma model and a model surrogate tumor anti

214 MMTV (mouse mammary tumor virus)-PyMT mouse mammary carcinoma model results in slower tumor growth a

215 outperformed (64)Cu-NOTA-RGD in a 4T1 murine mammary carcinoma model that expresses integrin on tumor

216 HA synthesis than oral MU in the 4T1 murine mammary carcinoma model using both a quantitative ELISA

217 ing neoadjuvant therapy in a triple-negative mammary carcinoma model, and suppressed cancer cell diss

218 ered peritumorally in vivo in the EMT6 mouse mammary carcinoma model, OxLys-SNAs significantly increa

219 Using a mouse mammary carcinoma model, we found that VEGF-C was not su

220 ic breast cancer cell line and an orthotopic mammary carcinoma model.

221 umor growth and metastasis in the 4T1 murine mammary carcinoma model.

222 GRP94-elicited protective immunity in a 4T1 mammary carcinoma model.

223 2) had significantly improved survival in a mammary carcinoma model.

224 In two orthotopic mammary carcinoma models (human MDA-MB-231 and murine 4T

225 In orthotopic mammary carcinoma models, ADCC enhancement was crucial t

226 ficacy was demonstrated in vivo using murine mammary carcinoma models.

227 rapeutics and nanotherapeutics in orthotopic mammary carcinoma mouse models.

228 In a mammary carcinoma murine model, platelet depletion induc

229 n cell cycle regulation could be detected in mammary carcinomas occurring in 40% ER rats in compariso

230 The remarkable similarities between the mammary carcinomas of Bard1-, Brca1-, and Bard1/Brca1-mu

231 mice bearing poorly immunogenic 11A-1 murine mammary carcinomas or Meth A sarcomas and C57Bl/6 mice b

232 rs and leads to PVMT-induced hemangiomas and mammary carcinomas or SVER-induced disseminated sarcomas

233 pe (P = 0.9381), was associated with ectopic mammary carcinoma outcome.

234 d that increased expression of Tid1 in human mammary carcinomas overexpressing ErbB-2 suppresses the

235 t human erythropoietin (EPO) on R3230 rodent mammary carcinoma oxygenation.

236 ancy and suggest that its loss may influence mammary carcinoma pathogenesis in multiparous women.

237 ival, lymph node invasion, and metastasis of mammary carcinoma patients.

238 ed an average of 3.4 +/- 2.0 and 5.5 +/- 3.6 mammary carcinomas per rat +/- SD when females were Mcs1

239 tible genotype littermates (7.8 +/- 3.1 mean mammary carcinomas per rat +/- SD, P = 0.0001 and P = 0.

240 , 4.0 +/- 0.4, 11.6 +/- 0.6, and 3.5 +/- 0.4 mammary carcinomas per rat.

241 Like other cancers, mammary carcinoma progression involves acidification of

242 receptor tyrosine kinase ligands relevant to mammary carcinoma progression.

243 y role in the degradation of collagen during mammary carcinoma progression.

244 enetic silencing of CXCL12 in colorectal and mammary carcinomas promotes metastasis.

245 The development and spread of mammary carcinomas require synergetic interplay between

246 in a conditional mouse model of noninvasive mammary carcinoma results in formation of stromal-dense

247 -control studies carried out in Germany: the Mammary Carcinoma Risk Factor Investigation (MARIE), a b

248 Stable expression of CRABP-II in mammary carcinoma SC115 cells enabled activation of RAR,

249 Immunolabeling of human mammary carcinoma showed that WNT7B immunoreactivity was

250 ic region of 2q, a region known to carry the mammary carcinoma susceptibility 1 (Mcs1) gene and sever

251 One of these loci, mammary carcinoma susceptibility 1 (Mcs1), is located on

252 Rat mammary carcinoma susceptibility 1b (Mcs1b) is a quantit

253 interaction that is synergistic to decrease mammary carcinoma susceptibility below the additive effe

254 ments of the resistant Mcs5a allele modulate mammary carcinoma susceptibility.

255 y metastasis of Lewis lung carcinoma and TA3 mammary carcinoma (TA3) cells by inhibiting tumor angiog

256 By using TA3 murine mammary carcinoma (TA3) cells, which display CD44-depend

257 nd correlation with lung metastases of human mammary carcinomas that are associated with myeloid cell

258 In mouse models, prolactin promotes mammary carcinomas that resemble luminal breast cancers

259 on of an adenovirus expressing CRABP-II into mammary carcinomas that spontaneously develop in TgN(MMT

260 In mammary carcinoma the high Y(1)R density together with i

261 able and compressed vessels (e.g., subset of mammary carcinomas), the two strategies need to be combi

262 ur results show that in usual types of human mammary carcinomas, the Id1 protein is expressed exclusi

263 We have used animal models of mammary carcinoma to interrogate the contribution of PER

264 ophage infiltration and improves response of mammary carcinomas to chemotherapy.

265 kinase activity in mice bearing ErbB2-driven mammary carcinomas triggered tumor cell senescence, with

266 ignant growth of syngeneic lymphoma (A20) or mammary carcinoma (TSA) in BALB/c mice compared with rVS

267 ansferrin was visualized in the EMT-6 murine mammary carcinoma tumor with microPET.

268 erase activation and telomere maintenance in mammary carcinoma tumorigenesis, we generated mice expre

269 usly showed that mitochondrial SNPs regulate mammary carcinoma tumorigenicity and metastatic potentia

270 take of 2-(18)F-FEtOH in 4T1 and 67NR murine mammary carcinoma tumors grown in mice was measured usin

271 Like many cancers, mammary carcinomas use lymphatic vessels to disseminate,

272 hus, it appears that ER induces apoptosis in mammary carcinomas via a cell survival factor-dependent

273 rat/neu transgenic mouse model of metastatic mammary carcinoma was investigated.

274 In neu(+)/pfp(+) males, the incidence of mammary carcinomas was a sporadic and late event.

275 the BALB/NeuT model of spontaneously arising mammary carcinoma, we found that canonical MHC II(+)/CD1

276 In the MMTV-PymT mouse model of mammary carcinoma, we found tumor progression relied upo

277 tumor virus (MMTV)-Wnt-1 transgenic model of mammary carcinoma, we have identified an unvarying assoc

278 Using the spontaneously metastatic 4T1 mouse mammary carcinoma, we now demonstrate that cross-talk be

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

281 To do this, chemically induced mammary carcinomas were evaluated from rats that were ad

282 Female rats with chemically-induced mammary carcinomas were injected with either saline or l

283 MCa-4 and MCa-35 mammary carcinomas were treated with: (a) DC101; (b) 5 x

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 Upon aging, the development of Wnt activated mammary carcinomas with squamous differentiation was acc

293 mIL-15+Ad.mlL-15Ralpha)) were protected from mammary carcinomas, with 70% of animals tumor-free at 30

294 MMTV-PyMT mice, which spontaneously develop mammary carcinomas, with MC-deficient C57BL/6-Kit(W-sh/W

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

300 ered systemically to mice bearing orthotopic mammary carcinoma xenografts.