ライフサイエンスコーパス: mammary tumor

1 using a mouse model of bone metastasis from mammary tumor.

2 breast cancer cells (BCCs) from the primary mammary tumor.

3 he mammary gland is not sufficient to induce mammary tumor.

4 r burden in a mouse xenograft model of human mammary tumor.

5 ral oncogene in mice, Int3, able to initiate mammary tumors.

6 d pro-proliferative role for loss of Par3 in mammary tumors.

7 ed, mice lacking Pttg1 developed spontaneous mammary tumors.

8 ls (1 x 10(5) cells per injection) to induce mammary tumors.

9 omarkers for 102 chemicals that cause rodent mammary tumors.

10 g the formation of preneoplastic lesions and mammary tumors.

11 (50 mg/kg body weight) to induce ER-positive mammary tumors.

12 ial stem cells (MESCs) that give rise to the mammary tumors.

13 ion and promotes malignant transformation of mammary tumors.

14 2/HER2 oncomice, which spontaneously develop mammary tumors.

15 pathway is crucial for Wnt-driven growth of mammary tumors.

16 n breast cancer tissues and Runx3(+/-) mouse mammary tumors.

17 ce for existence of TICs in Her2/neu-induced mammary tumors.

18 s with proliferation in ERalpha-positive rat mammary tumors.

19 nce disrupted, would facilitate the onset of mammary tumors.

20 64)Cu-DOTA-alendronate in mammary glands and mammary tumors.

21 minal progenitors originated in Her2-induced mammary tumors.

22 ict pathway activity in subtypes of MMTV-Myc mammary tumors.

23 e rapid development of metastatic multifocal mammary tumors.

24 leads to premalignant lesions and eventually mammary tumors.

25 antitumor effects against chemically induced mammary tumors.

26 , Wap-Int3/P50 knockout mice did not develop mammary tumors.

27 of the hsp70 gene delayed the initiation of mammary tumors.

28 and heterozygote mice spontaneously develop mammary tumors.

29 nces AMPK and suppresses YAP/TAZ activity in mammary tumors.

30 rix stiffness both in vitro and within mouse mammary tumors.

31 ed with muscle was observed in both the SSM3 mammary tumors (2.4 +/- 0.17 vs. 1.6 +/- 0.14 percentage

32 breast cancer, we used the metastatic mouse mammary tumor 4T1, which expresses and secretes substant

33 on on two separate transposon screens of 123 mammary tumors and 20 B-cell acute lymphoblastic leukemi

34 Genomic profiling of paired mammary tumors and distant metastases showed that our mo

35 ng the transcriptional profiles of ErbB2(KI) mammary tumors and human ERBB2-positive breast cancers,

36 Primary STAT1(-/-) mammary tumors and implanted SSM2 and SSM3 tumors showed

37 ostructures within murine mammary glands and mammary tumors and other organs without the use of immun

38 n mice bearing metastatic 4T1 or 4TO7 murine mammary tumors, and assessed the immune-suppressive mech

39 nriched mammary basal cell population and in mammary tumors, and is regulated by NF-kappaB signaling.

40 r cells derived from tissue culture, primary mammary tumors, and pulmonary metastases.

41 ese Her2(+) PIK3CA(H1047R)-initiated primary mammary tumors are refractory to HER2-targeted therapy,

42 howed that HER2(+)/PIK3CA(H1047R) transgenic mammary tumors are resistant to the HER2 antibodies tras

43 The multiple mammary tumors arose in the same R175HmWnt-1 mouse exhib

44 for the sensitive and specific detection of mammary tumors as well as the differentiation of maligna

45 ased normal mammary gland lymphangiogenesis, mammary tumor-associated lymphangiogenesis, tumor cell i

46 75HmWnt-1) and p53(-/-)mWnt-1 mice died from mammary tumor at the same kinetics, which was much earli

47 maceuticals to image ERalpha and PR in mouse mammary tumors at baseline and after hormonal therapy an

48 s-2 may explain their non-redundant roles in mammary tumor biology.

49 ca15382stop mutations predisposed animals to mammary tumors, but Brca1185stop tumors responded marked

50 In the MMTV-Wnt1 mouse model, regression of mammary tumors by Fzd8CRD treatment coincides with an ac

51 olony-stimulating factor (G-CSF) produced by mammary tumors can synergize with FLT3L and granulocyte

52 The mammary tumors caused by overexpression of Separase, alo

53 a transplantation model of an Erbb2-positive mammary tumor cell line confirmed the effect of Bcl3 in

54 e miRNAs in the weakly metastatic mouse 4TO7 mammary tumor cell line had no effect on proliferation o

55 Mechanistic investigations in mammary tumor cell lines derived from wild-type or Trask

56 ted that overexpression of Zpo2 in MMTV-PyMT mammary tumor cell lines enhances lung metastasis.

57 Furthermore, talin is required for mammary tumor cell motility, intravasation, and spontane

58 ZDHHC3 ablation in human MDA-MB-231 mammary tumor cell xenografts reduced the sizes of both

59 deacetylated PKM2 mutant in Sirt2-deficient mammary tumor cells altered glucose metabolism and inhib

60 ificantly reduced invasion and metastasis by mammary tumor cells and implicated its product Hsp72 in

61 ic immunity to radioresistant populations of mammary tumor cells and, thus, can complement radiothera

62 We demonstrate here that mammary tumor cells arising from more epithelial carcino

63 1), A77636, inhibited proliferation of 4T1.2 mammary tumor cells as well as MDA-MB-231 breast cancer

64 Here, we show that MMTV-Her2/Neu mammary tumor cells cultured as nonadherent spheres or a

65 In the current study, exposure of mammary tumor cells derived from mice transgenic for the

66 LOXL2 ablation in mammary tumor cells dramatically decreased lung metastas

67 us expression of N-cadherin in PyMT or MCF-7 mammary tumor cells enhanced cell motility and caused a

68 Chaos3 mammary tumor cells exhibit RAS hyperactivation and incr

69 ormed mouse embryonic fibroblasts as well as mammary tumor cells following their transplantation and

70 h to the treatment of local and disseminated mammary tumor cells in a murine model using a recently d

71 free conditioned medium derived from hypoxic mammary tumor cells resulted in increased bone marrow-de

72 Here we report that mammary tumor cells undergoing epithelial-mesenchymal tr

73 Mammary tumor cells were orthotopically implanted into t

74 show that deletion of Tsc1 in mouse primary mammary tumor cells, either before or after their transp

75 In mouse lung and mammary tumor cells, hypoxia led to increases in cell ad

76 Using nematodes and mammary tumor cells, we show that Ral GTPases are involv

77 Data show that invading mammary tumor cells, when cultured in a stiffened three-

78 ppressing its activity and inhibiting EMT in mammary tumor cells.

79 2 positively regulates aerobic glycolysis in mammary tumor cells.

80 g its expression (up- or down-regulation) in mammary tumor cells.

81 rrantly overexpressed in Her2-overexpressing mammary tumor cells.

82 eal that Runx2 promotes metastatic spread of mammary tumor cells.

83 male mice orthotopically injected with Py230 mammary tumor cells.

84 a molecular characterization of 50 p53 null mammary tumors compared with other mouse models and huma

85 red in cultured bone marrow cells exposed to mammary tumor-conditioned cell culture media.

86 ulation of STAT1 activity in human and mouse mammary tumors correlates with increasing disease progre

87 XCL12 isoforms produced comparable growth of mammary tumors, CXCL12-gamma significantly increased met

88 Three mice bearing orthotopically implanted mammary tumors derived from transgenic MMTV-PyMT mice we

89 Instead of the luminal mammary tumors developed in p18 single-mutant mice, mamm

90 tumors developed in p18 single-mutant mice, mammary tumors developed in the p18;Brca1 mice, similar

91 Rgamma deletion in mice not only exacerbates mammary tumor development but also impairs the anti-tumo

92 riments revealed that Tgif1 ablation impeded mammary tumor development in MMTV-Wnt1 mice, further und

93 Thus, Notch-induced mammary tumor development is Rbpj-independent.

94 We compared mammary tumor development with p,p -DDE with development

95 indings establish that FABP5 is critical for mammary tumor development, rationalizing the development

96 y) for 10 weeks during the 'risk window' for mammary tumor development.

97 hat drive cell proliferation, and suppressed mammary tumor development.

98 ected contributor to Brca1, Brca2, and Palb2 mammary tumor development.

99 sed gene profiling approach, we identified a mammary tumor DOCK1-associated gene signature enriched f

100 ave identified a role for Notch signaling in mammary tumor dormancy and recurrence.

101 In this study, we compared FDG uptake in mammary tumors driven by the Akt1, c-MYC, HER2/neu, Wnt1

102 Mammary tumors driven by the PyMT oncogene and skin tumo

103 nimals, focal, nonmetastatic Stat3-deficient mammary tumors escaped immune surveillance after a long

104 Translocation can also occur in mice bearing mammary tumors, even in the absence of chemotherapy.

105 aracterization of the ErbB2DeltaEx16-derived mammary tumors exhibit several unique features that dist

106 st tumors, the lung metastasis (met)-derived mammary tumors exhibited a slower growth rate and a redu

107 PPARgamma-null mammary tumors exhibited increased angiogenesis, which w

108 Chemotherapy-treated PPARgamma-null mammary tumors exhibited luminal phenotype and expansion

109 t increase in the growth and angiogenesis of mammary tumors expressing ShcR175Q, which displayed incr

110 g, Brk expression augmented MET(Mut)-induced mammary tumor formation and metastasis.

111 PKM2 deletion accelerated mammary tumor formation in a Brca1-loss-driven model of

112 In addition, JARID1B is required for mammary tumor formation in syngeneic or xenograft mouse

113 and breast cancer subtype by analyzing mouse mammary tumor formation in which each pathway was activa

114 c deletion of Palb2 driven by K14-Cre led to mammary tumor formation with long latency.

115 1 in promoting macrophage recruitment during mammary tumor formation, suggesting that the CX3CL1/CX3C

116 K14cre;Cdh1(F/F);Trp53(F/F) model of de novo mammary tumor formation, we orthotopically transplanted

117 ng following the cessation of lactation, and mammary tumor formation.

118 lb2 and Tumor protein 53 (Trp53) accelerated mammary tumor formation.

119 ormal mammary development and predisposes to mammary tumor formation; however, the cooperation betwee

120 cyclin D1 expression are suppressed, primary mammary tumors from Muc4(ko)/NDL female mice exhibit sim

121 When mammary tumors from the F1 progeny were analyzed by miRN

122 y analysis was performed using her-2 induced mammary tumors from wild-type and GnT-V-null mice.

123 Further genomic analyses reveal mouse mammary tumors growing independent of myc have a higher

124 Mammary tumors grown in a Cav-1-deficient tumor microenv

125 Mammary tumors grown in a Cav-1-deficient tumor microenv

126 ing through its Pro-878/881 motif suppressed mammary tumor growth and metastasis in a well characteri

127 he ApoE(-/-) mice is a favorable setting for mammary tumor growth and metastasis.

128 YL719 in combination with lapatinib impaired mammary tumor growth and PI3K signaling more potently th

129 ion to tamoxifen, resulting in abrogation of mammary tumor growth and progression.

130 tination, is largely dispensable for primary mammary tumor growth but is required for metastatic spre

131 d that endogenous hyperinsulinemia increases mammary tumor growth by directly activating the IR rathe

132 Data analysis showed a delayed mammary tumor growth in Balb/c mice inoculated with sh-a

133 ompetent mice utilizing a syngeneic model of mammary tumor growth in FVB mice.

134 o-signal transduction in MSC, which promotes mammary tumor growth in part through secretion of the si

135 l agents NVP-BKM120 and NVP-BEZ235 decreased mammary tumor growth in the hyperinsulinemic MKR mouse.

136 Here we show that in mice, mammary tumor growth induces the accumulation of tumor-a

137 Here we show that mammary tumor growth is associated with defects in hemat

138 ssess the contribution of endogenous Muc4 to mammary tumor growth properties, we first created a gene

139 Mammary tumor growth was associated with histone methyla

140 enhanced, whereas overexpression, suppressed mammary tumor growth, consistent with a significant asso

141 esions with no significant effect on primary mammary tumor growth, cyclin D1 levels, or caspase-3 act

142 Loss of miR-31 compromises mammary tumor growth, reduces the number of cancer stem

143 s results in superior inhibition of PI3K and mammary tumor growth, suggesting a rational therapeutic

144 whether FABP5 is essential for EGFR-induced mammary tumor growth, we interbred FABP5-null mice with

145 To examine the effects of host aging on mammary tumor growth, we used caveolin (Cav)-1 knockout

146 of epidermal FABP (E-FABP) protects against mammary tumor growth.

147 s apoptosis, and blocks colony formation and mammary tumor growth.

148 mTOR pathway in association with accelerated mammary tumor growth.

149 breast cancer lesions and is a stimulator of mammary tumor growth.

150 ned whether deregulated NE activity enhances mammary tumor growth.

151 However, mammary tumors had no effect on hippocampal doublecortin

152 -exome analysis of the Pik3ca(H1047R)-driven mammary tumors identified multiple mutations, including

153 of Cdh1 does not predispose mice to develop mammary tumors, implying that mutations in additional ge

154 l was also estimated in-vivo in DMBA induced mammary tumor in female Sprague-Dawley rats.

155 and suppressed the growth and metastasis of mammary tumor in vivo.

156 Parous mice developed luminal mammary tumors in a cyclin D1-dependent manner.

157 n lung metastasis when compared with primary mammary tumors in a mouse model of metastatic breast can

158 hly effective at inhibiting the outgrowth of mammary tumors in a transgenic mouse model.

159 ation markers of EMT were present in primary mammary tumors in association with the epithelial or the

160 We induced orthotopic mammary tumors in control FVB/n and hyperinsulinemic MKR

161 Using both spontaneous and allografted mammary tumors in fully immune-competent mice, we discov

162 th and enhancing the lethality of late-stage mammary tumors in mice.

163 response to TGF-beta, and to form orthotopic mammary tumors in mice.

164 C59 blocked progression of mammary tumors in MMTV-WNT1 transgenic mice while downre

165 nol and reduce the growth and progression of mammary tumors in rats.

166 ion stimulates the growth of BRCA1-deficient mammary tumors in the fat pads of male mice.

167 gressed, thereby preventing the emergence of mammary tumors in the majority of animals.

168 ic expression of this mutant delays onset of mammary tumors in the MMTV-PyMT mouse model of breast ca

169 SCCA1 overexpression in neu(+) mammary tumors increased the unfolded protein response (

170 Metastatic mammary tumors induced the accumulation of distinct popu

171 , transgenic EZH2 overexpression accelerates mammary tumor initiation and increases NOTCH1 activation

172 mouse, the development of highly metastatic mammary tumors is associated with an accumulation of mye

173 Stromal collagen within and surrounding mammary tumors is frequently aligned and reoriented perp

174 2 transgenic mice dramatically shortened the mammary tumor latency and accelerated tumor growth due t

175 v mice bearing estrogen-dependent SSM3 mouse mammary tumors, male athymic nude mice bearing androgen-

176 ical Gpr132 inhibition significantly impedes mammary tumor malignancy.

177 n, and whether this difference affects later mammary tumor metabolism, we performed a nutrient tracer

178 h which endogenous hyperinsulinemia promotes mammary tumor metastases.

179 erin in the PyMT mouse model, which enhances mammary tumor metastasis, results in selective inhibitio

180 t the contribution of N-cadherin and HER2 in mammary tumor metastasis, we targeted N-cadherin express

181 covered that postpartum involution increases mammary tumor metastasis.

182 hange (MNX)-we showed that mtDNA could alter mammary tumor metastasis.

183 dipocytes represent a major cell type in the mammary tumor microenvironment and are important for tum

184 Fibroblasts within the mammary tumor microenvironment are active participants i

185 y tumor-associated macrophages in the intact mammary tumor microenvironment.

186 n the tumor epithelia of the inducible PyVmT mammary tumor model and found that Stat3-deficient mice

187 This novel Wnt-driven mammary tumor model highlights the importance of functio

188 ese findings in vivo in the Polyoma middle T mammary tumor model in which p21CIP1 was deleted.

189 C (TApDC), we developed an orthotopic murine mammary tumor model that closely mimics the human pathol

190 Here, we show in the Polyoma Middle T mammary tumor model that N-cadherin (Cdh2) expression ca

191 In this study, we used the MMTV-Neu-Tg mouse mammary tumor model to identify potential new strategies

192 c endothelial cells (TEC) from a spontaneous mammary tumor model undergo distinct forms of EndMT in r

193 purpose of our study was to engineer a mouse mammary tumor model with intratumoral heterogeneity by u

194 ylated are resistant to lung metastases in a mammary tumor model, and that cells isolated from these

195 tally alter disease course in the PyMT mouse mammary tumor model, suggesting that functional metaboli

196 In a mouse mammary tumor model, the stability and therapeutic activ

197 ases has been principally studied in the 4T1 mammary tumor model, where silencing of Twist in vitro h

198 on of Nedd9 in the MMTV-HER2/ERBB2/neu mouse mammary tumor model.

199 sis in comparison to a comparable Myc-driven mammary tumor model.

200 d in tumor tissues of three different murine mammary tumor models.

201 These animals mainly developed mammary tumors, most of which had transposon insertions

202 3CL1 expression in the tumor milieu enhanced mammary tumor numbers in a dose-dependent manner.

203 hanges as early as 12 weeks, and ER-positive mammary tumors occurred at a latency of 14 to 16 months.

204 al of cancer stem cells (CSCs) isolated from mammary tumors of a Brca1-mutant mouse model.

205 These mice developed multiple independent mammary tumors of which the majority resembled human ILC

206 p,p -DDE implants significantly accelerated mammary tumor onset compared with vehicle Elvax implants

207 Chronic loss of Pygo2 significantly delays mammary tumor onset in MMTV-Wnt1 females, whereas acute

208 one metastatic cancer cells, but not primary mammary tumors or visceral metastases.

209 t of the R175HmWnt-1 mice developed multiple mammary tumors per mouse, whereas p53(-/-)mWnt-1 and mWn

210 onstrate that ErbB2-initiated ER/PR-negative mammary tumors primarily originate from the subset of th

211 on of the BMP receptor 2 (BMPR2) would alter mammary tumor progression in mice that express the Polyo

212 mega-3 PUFAs, independent of GPR120, inhibit mammary tumor progression in obese mice.

213 Our results show that obesity promotes mammary tumor progression in this model of postmenopausa

214 lopment, it is dispensable for ErbB2-induced mammary tumor progression.

215 aling in both normal mammary development and mammary tumor progression.

216 tracellular milieu accelerating ErbB2-driven mammary tumor progression.

217 e MMTV-ErbB2 mouse model resulted in delayed mammary tumor progression.

218 Interestingly, the mammary tumor-promoting effects of a Cav-1-deficient mic

219 that ceramide kinase (Cerk) is required for mammary tumor recurrence following HER2/neu pathway inhi

220 (MMTV)-Her2/neu transgenic mice that develop mammary tumors resembling human HER2-subtype breast canc

221 thways in suppressing luminal and basal-like mammary tumors, respectively.

222 iling of ephrin-A1-null, HER2-overexpressing mammary tumors revealed a significant increase in glutam

223 ta85 mice developed metastatic ErbB2-induced mammary tumors secondary to mammary epithelial expressio

224 Together, our results show that mammary tumor-secreted factors induce profound perturbat

225 using (111)In-anti-gammaH2AX-TAT identified mammary tumors significantly earlier than MR imaging.

226 g mutant Atg7, nuclear IRF1 was increased in mammary tumors, spleen, and kidney.

227 in vivo selection process to isolate murine mammary tumor sublines possessing an enhanced ability to

228 hese mice are known to be susceptible to non-mammary tumors such as fibrosarcoma.

229 The mechanisms underlying Palb2 mammary tumor suppression functions can now be explored

230 hown that Cripto-1 promotes the formation of mammary tumors that display properties of EMT, including

231 immunocompetent mice bearing D2F2/E2 murine mammary tumors that express human HER2/neu.

232 cross-species analysis, we discovered mouse mammary tumors that have similar gene expression charact

233 igh levels of genomic instability leading to mammary tumors that have tumor gene expression profiles

234 promotes development of Wnt1-mediated murine mammary tumors that offer a model of TNBC.

235 effects on molecular heterogeneity in mouse mammary tumors that parallel subtypes of human breast ca

236 ic lungs differed significantly from that in mammary tumors, the reduction in metastasis may result f

237 s detected in a higher percentage in primary mammary tumor tissues from double-transgenic MMTV-Hoxb7/

238 e of luminal cells to cause luminal-to-basal mammary tumor transformation.

239 In vivo, oncogenic PIK3CA-driven mouse mammary tumors treated daily with aspirin resulted in de

240 tics of the microcalcifications in different mammary tumor types.

241 ry gland involution suggests that Wnt-driven mammary tumors use the same growth mechanism as prolifer

242 ng C-Met signaling were confirmed in vivo in mammary tumors using the in vivo invasion assay and intr

243 e of nucleosome A of the 3'-LTR of the mouse mammary tumor virus (147 bp MMTV-A).

244 ing sites for two of these viruses-the mouse mammary tumor virus (a retrovirus) and Machupo virus (an

245 Mouse mammary tumor virus (MMTV) encodes a Rev-like protein, R

246 many oncogenic viruses, including the mouse mammary tumor virus (MMTV) envelope (Env).

247 The mouse mammary tumor virus (MMTV) Gag protein directs the assem

248 pathogens, including HIV in humans and mouse mammary tumor virus (MMTV) in mice.

249 T (PyMT) oncogene under control of the mouse mammary tumor virus (MMTV) long-terminal repeat (MMT mic

250 42% of the maximal effect of DEX in a mouse mammary tumor virus (MMTV) luciferase reporter transacti

251 e Gag protein of the murine retrovirus mouse mammary tumor virus (MMTV) orchestrates the assembly of

252 The orally transmitted retrovirus mouse mammary tumor virus (MMTV) requires the intestinal micro

253 s report shows for the first time that mouse mammary tumor virus (MMTV), a mammalian retrovirus that

254 Jaagsiekte sheep retrovirus (JSRV) and mouse mammary tumor virus (MMTV), as well as many endogenous r

255 or mammary-specific deletion inhibited mouse mammary tumor virus (MMTV)- PyMT- and MMTV- Wnt1-driven

256 Mouse mammary tumor virus (MMTV)-ErbB2 mice lacking PKCdelta (

257 the role of HER2/Neu in breast cancer, mouse mammary tumor virus (MMTV)-Her2/neu transgenic mice that

258 A2 inhibits the formation of tumors in mouse mammary tumor virus (MMTV)-Neu mice.

259 reast tumor formation in xenograft and mouse mammary tumor virus (MMTV)-neu mouse models in a manner

260 c acid (PA), inhibits lung metastases in the mammary tumor virus (MMTV)-Neu transgenic mouse breast c

261 Apc(Min/+) mice were crossed with the mouse mammary tumor virus (MMTV)-Polyoma virus middle T antige

262 vator E2F transcription factors in the mouse mammary tumor virus (MMTV)-polyomavirus middle T oncopro

263 ancer mutant knock-in (R175H) mice and mouse mammary tumor virus (MMTV)-Wnt-1 transgenic (mWnt-1) mic

264 an antagonist of the wingless-related mouse mammary tumor virus (WNT) signaling pathway, is one endo

265 an endogenous superantigen encoded by mouse mammary tumor virus 8 (Mtv-8) by either deletion or T-ce

266 they become inducible by wingless-type mouse mammary tumor virus integration site family member (WNT)

267 ance between mesenchymal Wingless-type Mouse Mammary Tumor Virus integration site family, member 10B

268 ll junctions, under the control of the mouse mammary tumor virus long terminal repeat promoter, devel

269 a neutralizing CSF-1R antibody in the mouse mammary tumor virus long-terminal region-driven polyoma

270 riven model of luminal breast cancer [murine mammary tumor virus promoter (MMTV-NIC)].

271 hibitors (KDACis) potently repress the mouse mammary tumor virus promoter through transcriptional mec

272 Mouse mammary tumor virus superantigens (vSAGs) are notorious

273 ed secretion of Wingless-related MMTV (mouse mammary tumor virus) integration site 3 (WNT3) by ingrow

274 e the morphogen Wingless-related MMTV (mouse mammary tumor virus) integration site 3 (WNT3).

275 s of the canonical wingless-type MMTV (mouse mammary tumor virus) integration site family (WNT) signa

276 e oligonucleotides (ASOs) in the MMTV (mouse mammary tumor virus)-PyMT mouse mammary carcinoma model

277 breast adenomas with lung metastases [mouse mammary tumor virus-driven polyoma virus middle T oncoge

278 rgets of tumorigenic transformation in mouse mammary tumor virus-erbB2 transgenic mice.

279 ion and increases NOTCH1 activation in mouse mammary tumor virus-neu mice.

280 In the mouse mammary tumor virus-Polyoma Middle T (MMTV-PyMT) model o

281 once tumors have developed, we use the mouse mammary tumor virus-Polyoma Middle T (MMTV-PyMT), which

282 tered breast cancer development in the mouse mammary tumor virus-polyoma middle T-antigen model.

283 ce were generated and crossed with the Mouse Mammary Tumor Virus-Polyoma Middle T-Antigen mouse.

284 t infections by viruses like HIV-1 and mouse mammary tumor virus.

285 Using mouse models with tagged mammary tumors, we demonstrate that CTC clusters arise f

286 To induce mammary tumors, we retrovirally introduced an oncogene,

287 the normal mammary tissue, but the resulting mammary tumors were all beta Gal-.

288 Overt mammary tumors were claudin-4-positive, and (111)In-cCPE

289 Rnf5-deficient MMTV-PyMT mammary tumors were less differentiated and showed eleva

290 The resulting mouse primary mammary tumors were reduced in size (65%, P<0.05) and th

291 DW images of MNU-induced mammary tumors were successfully obtained with minimal m

292 ansgenic mice (MMTV-HA-14-3-3zeta) developed mammary tumors, whereas control mice did not.

293 thers had higher rates of carcinogen-induced mammary tumors which were associated with delayed mammar

294 Remarkably, SP cleared DMBA-induced rat mammary tumors, which was clearly confirmed by morpholog

295 e found that MAP17 is expressed in 60% human mammary tumors while it is not expressed in normal or be

296 ammary gland development but still developed mammary tumors with a slightly longer latency than the W

297 Treatment of mice bearing EMT6 mammary tumors with ibrutinib resulted in reduced freque

298 , we show that, contrary to dogma, MMTV-Wnt1 mammary tumors with mutant p53 exhibited a superior clin

299 th-ligand 1 (PD-L1) in Her2 transgenic mouse mammary tumors, with high expression limited to tumor ce

300 cogene promotes metastasis of ErbB2-positive mammary tumors without affecting primary tumor growth or