ライフサイエンスコーパス: mammary tumor

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

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

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

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

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

6 e rapid development of metastatic multifocal mammary tumors.

7 antitumor effects against chemically induced mammary tumors.

8 death response evident in early and advanced mammary tumors.

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

10 and heterozygote mice spontaneously develop mammary tumors.

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

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

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

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

15 ed, mice lacking Pttg1 developed spontaneous mammary tumors.

16 omarkers for 102 chemicals that cause rodent mammary tumors.

17 g the formation of preneoplastic lesions and mammary tumors.

18 with hyperplasia and development of de novo mammary tumors.

19 pplied to the knee, on metastasized bone and mammary tumors.

20 (50 mg/kg body weight) to induce ER-positive mammary tumors.

21 oated control in mice bearing 4T1 orthotopic mammary tumors.

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

23 ably, it also reduced remotely the growth of mammary tumors.

24 s to the regression of spontaneous MMTV-PyMT mammary tumors.

25 ession altered the HER2 signaling pathway in mammary tumors.

26 leads to premalignant lesions and eventually mammary tumors.

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

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

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

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

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

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

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

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

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

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

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

38 Mammary tumors arising in E-R72 mice also had an increas

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

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

41 n BC studies (n = 294) or from within canine mammary tumor associated regions (n = 471).

42 Here we report on Mammary Tumor Associated RNA 25 (MaTAR25), a nuclear enr

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

44 75HmWnt-1) and p53(-/-)mWnt-1 mice died from mammary tumor at the same kinetics, which was much earli

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

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

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

48 The mammary tumors caused by overexpression of Separase, alo

49 We used a human mammary tumor cell line (4T1) treated by an antitumor co

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

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

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

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

54 AK is required for their activity to promote mammary tumor cell migration.

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

56 matin associated lncRNA that plays a role in mammary tumor cell proliferation, migration, and invasio

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

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

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

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

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

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

63 ry tumor progression in mice and showed that mammary tumor cells become highly susceptible to replica

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 eta(D849V) also promoted brain metastases of mammary tumor cells expressing high PDGFB when injected

69 extracellular vesicles released from hypoxic mammary tumor cells facilitate intercellular communicati

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

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

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

73 Mice were injected with Cl66 murine mammary tumor cells, Cl66 cells resistant to doxorubicin

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 human breast cancer cell lines and 4T1 mouse mammary tumor cells, PD-L1 expression was regulated by t

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

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

79 opic tumor growth and intracranial growth of mammary tumor cells, while mesenchymal-specific expressi

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

81 male mice orthotopically injected with Py230 mammary tumor cells.

82 exerted proproliferative signals on adjacent mammary tumor cells.

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

84 2 positively regulates aerobic glycolysis in mammary tumor cells.

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

86 significantly reduced intracranial growth of mammary tumor cells.

87 stem cells and validation in KB2P1.21 mouse mammary tumor cells.

88 nhibition blocks transformation in cells and mammary tumors characterized by PIK3CA C-terminal mutati

89 Here, we used RNA-profiling of canine mammary tumors (CMTs) coupled with a robust analysis fra

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

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

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

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

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

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

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

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

98 breast cancer mouse model exhibits enhanced mammary tumor development with deficient ERalpha express

99 E-cadherin alone does not predispose mice to mammary tumor development, indicating that additional pe

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

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

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

103 rating the direct impact of gut dysbiosis on mammary tumor dissemination.

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

105 We demonstrate that mammary tumors driven by medroxyprogesterone acetate (M)

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

107 In vivo, irradiated autophagy-incompetent mammary tumors elicited robust immunity, leading to impr

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

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

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

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

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

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

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

115 cell proliferation and migration, as well as mammary tumor formation and metastasis.

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

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

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

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

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

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

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

123 ected from oncogene-driven spontaneous mouse mammary tumor growth and associated lung metastasis.

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

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

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

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

128 ectively) significantly inhibited aggressive mammary tumor growth and spontaneous lung metastasis in

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

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

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

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

133 to inhibit macrophage accumulation and slow mammary tumor growth in mouse models while also reducing

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

135 le models of basal-like TNBC and reduces PDX mammary tumor growth in vivo.

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 ion of autophagy strongly attenuates primary mammary tumor growth, impaired autophagy promotes sponta

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

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

145 brain tumor growth while minimally impacting mammary tumor growth.

146 ned whether deregulated NE activity enhances mammary tumor growth.

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

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

149 However, mammary tumors had no effect on hippocampal doublecortin

150 f 173 and 225 unique ECM proteins from mouse mammary tumors have been identified using 1D and 2D RPLC

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

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

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

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

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

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

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

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

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

160 esidual disease of lapatinib-treated HER2(+) mammary tumors in MMTV-Neu mice, increased immunosuppres

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

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

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

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

165 further reduced local invasion of orthotopic mammary tumors in vivo, and joint up-regulation of Cx43

166 HF diet in utero, VPA/hydralazine increased mammary tumor incidence and burden, and elevated express

167 led that R72 mice had a significantly higher mammary tumor incidence and reduced latency in both DMBA

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

169 Metastatic mammary tumors induced the accumulation of distinct popu

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

171 vasion, and metastasis; however, its role in mammary tumor initiation remains unknown.

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 h which endogenous hyperinsulinemia promotes mammary tumor metastases.

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

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

180 covered that postpartum involution increases mammary tumor metastasis.

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

182 Fibroblasts within the mammary tumor microenvironment are active participants i

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

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

185 traceable MMTV-Wnt1-driven in vivo chimeric mammary tumor model comprising an admixture of low-Myc-

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

187 d lung metastases using a syngeneic p53-null mammary tumor model of basal-like breast cancer.

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

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

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

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

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

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

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

195 Using the MMTV-PyVmT/FVB mammary tumor model, we demonstrate a novel role for CCL

196 Here, using an MMTV-PyMT mouse mammary tumor model, we discovered that deletion of TGFb

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

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

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

200 s to the lungs in a 4T1 syngeneic orthotopic mammary tumor model.

201 n both DMBA-induced and MMTV-Erbb2/Neu mouse mammary tumor models compared to P72 mice.

202 lls; indeed, fresh EC isolates from lung and mammary tumor models had differential abilities to degra

203 By creating new mammary tumor models, we find that tumor mutation burden

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

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

206 VPA/hydralazine reduced mammary tumor multiplicity and lengthened tumor latency

207 3CL1 expression in the tumor milieu enhanced mammary tumor numbers in a dose-dependent manner.

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

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

210 n of the tumor suppressor gene Cdkn2a/p16 in mammary tumors of HF offspring.

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

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

213 ed in pulmonary micrometastases, compared to mammary tumors or brain micrometastases.

214 herefore, here we tested the extent to which mammary tumors or tumor resection ("survivors") in mice

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

216 block dissemination of both murine and human mammary tumor organoids.

217 ally realistic microvessel in coculture with mammary tumor organoids.

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

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

220 we established its functional importance in mammary tumor progression in mice and showed that mammar

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

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

223 Using a p53-null model of early stage mammary tumor progression, we found that Gas6 is highly

224 tracellular milieu accelerating ErbB2-driven mammary tumor progression.

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

226 ammary gland that was sustained during HR(+) mammary tumor progression.

227 ting genome maintenance program required for mammary tumor progression.

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

229 Therefore, we tested the extent to which mammary tumor resection attenuates tumor-induced neuroin

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

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

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

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

234 ral effusion and atypical ductal hyperplasia mammary tumor specimens (21MT-1 and 21PT) enhances the f

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

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

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

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

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

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

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

242 as well as a delayed formation of detectable mammary tumors, thus suggesting a causal relationship be

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

244 that macrophages contribute to resistance of mammary tumors to the JAK/STAT inhibitor ruxolitinib in

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

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

247 tics of the microcalcifications in different mammary tumor types.

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

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

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

251 lasma membrane targeting of the B-type mouse mammary tumor virus (MMTV) and C-type HIV-1, which assem

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

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

254 42% of the maximal effect of DEX in a mouse mammary tumor virus (MMTV) luciferase reporter transacti

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

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

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

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

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

260 In the mouse mammary tumor virus (MMTV)-driven polyoma middle-T oncog

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

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

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

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

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

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

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

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

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

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

271 ell protein 0 (ICP0) promoter, and the mouse mammary tumor virus long terminal repeat (MMTV-LTR).

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

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

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

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

276 Mouse mammary tumor virus superantigens (vSAGs) are notorious

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

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

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

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

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

282 endogenous retrovirus-K (HERV-K) human mouse mammary tumor virus-like 2 (HML-2) is the most recently

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

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

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

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

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

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

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

290 tate, and pancreas) and a mouse model of the mammary tumor were employed to evaluate the effect of ur

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

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

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

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

295 ion of Mad1 accelerates growth of orthotopic mammary tumors, which show decreased levels of p53 and i

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

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

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

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

300 tissues of mice and rats bearing orthotopic mammary tumors without observation of acute toxic side e