ライフサイエンスコーパス: mammary cancer

1 susceptible to 17beta-estradiol (E2)-induced mammary cancer.

2 the mammary gland of transgenic mice induced mammary cancer.

3 proach in the prevention and/or treatment of mammary cancer.

4 genetically conferred propensity to develop mammary cancer.

5 Two C75-treated animals never developed mammary cancer.

6 ently to modify susceptibility to E2-induced mammary cancer.

7 onetheless, all ksr1-/- animals succumbed to mammary cancer.

8 anistic role for cyclin D1 in progression of mammary cancer.

9 develop mouse models of ER-alpha-responsive mammary cancer.

10 els of E can induce protection against frank mammary cancer.

11 ancy and were highly effective in preventing mammary cancer.

12 is associated with an increased incidence of mammary cancer.

13 progression in murine models of melanoma and mammary cancer.

14 that, in turn, suppresses the development of mammary cancer.

15 during the early and intermediate stages of mammary cancer.

16 hormones that likely induce protection from mammary cancer.

17 g and splicing factors in multiple stages of mammary cancer.

18 ferative gland that is not as susceptible to mammary cancer.

19 (RME) is known to prevent the development of mammary cancer.

20 mmune-competent mouse models of melanoma and mammary cancer.

21 cations that are crucial in preventing ER(-) mammary cancer.

22 These mice developed spontaneous, metastatic mammary cancer.

23 n a therapeutic response in a mouse model of mammary cancer.

24 are of no significance in the diagnostics of mammary cancer.

25 cate that it has a protective effect against mammary cancer.

26 accelerated tumor growth in murine model of mammary cancer.

27 but not the progression of ErbB2-associated mammary cancer.

28 dimethylbenz[a]anthracene (DMBA) to initiate mammary cancer.

29 in the initiation as well as progression of mammary cancer.

30 radiosensitive and susceptible to radiogenic mammary cancer.

31 e wild-type animals, spontaneously developed mammary cancer.

32 ated with multiple forms of cancer including mammary cancer.

33 ntify mechanisms involved in hormone-induced mammary cancer.

34 only H-ras activation is associated with rat mammary cancers.

35 cally conferred susceptibility to E2-induced mammary cancers.

36 ecting them from chemical carcinogen induced mammary cancers.

37 ve tumor immune environment in both lung and mammary cancers.

38 that evolve into basal-like and claudin-low mammary cancers.

39 f this locus, termed Emca1 (estrogen-induced mammary cancer 1), acts in an incompletely dominant mann

40 In preclinical models of mammary cancer, a low dose of the RNA biogenesis inhibit

41 as(Q61L) mutations, which only progressed to mammary cancer after inducible Wnt1 oncogene expression.

42 a retrospective study of 45 cases of canine mammary cancer analysing 836 biopsies regions including

43 g this TAM inhibitor markedly reduced murine mammary cancer and melanoma metastases dependent on NK c

44 luding Lewis lung carcinoma, triple-negative mammary cancer and melanoma.

45 as a therapeutic target for the treatment of mammary cancer and presumably other types of cancer.

46 ect established, disseminated 4T1 metastatic mammary cancer and survive indefinitely if their primary

47 ting multiple hyperplastic nodules, invasive mammary cancers and cancer multiplicity.

48 vitro model to dissect interactions between mammary cancers and the hematopoietic system.

49 s a tumor progression factor in PymT-induced mammary cancer, and support the hypothesis that hemostat

50 effect of ferumoxytol on the growth of early mammary cancers, and lung cancer metastases in liver and

51 of polyomavirus middle T antigen (MT)-driven mammary cancer appears independent of KSR1, KSR1 is obli

52 susceptibility of the ACI rat to E2-induced mammary cancer appears to segregate as an incompletely d

53 es in their sensitivity to radiation-induced mammary cancer (BALB/c and C57BL/6) for the purpose of i

54 agenesis primarily induces hematopoietic and mammary cancer, but little else, while the majority of c

55 and/or high-density arrays on twelve canine mammary cancer cases, including seven simple carcinomas

56 othelial cells (ECs) or the metastatic human mammary cancer cell line MDA-MB-231 adhering to the gold

57 CR4 in murine 4T1 cells, a highly metastatic mammary cancer cell line that is a model for stage IV hu

58 higher transfection efficiency in 4T1 murine mammary cancer cell line, which expresses LAT-1, than 25

59 ary epithelial cells and several established mammary cancer cell lines were studied for caspases-3 ex

60 the detectable expression of PELP1 in human mammary cancer cell lines, and the enhanced expression o

61 trogen agonist/antagonist activities in some mammary cancer cell lines, but in the presence of E2, re

62 was assessed with MCF-7, T47D, LY2, and S30 mammary cancer cell lines.

63 f breast cancer skeletal metastasis of human mammary cancer cell MDA-MB-231, which expresses the muta

64 istein was related with the activity against mammary cancer cells but flavonols and group B saponins

65 nize estrogen in uterine tissue and in human mammary cancer cells compared to raloxifene, tamoxifen o

66 toxicity of SeChry and SePQue in MCF-7 human mammary cancer cells demonstrated their capacity to effi

67 Non-metastatic Met-1 and metastatic Mvt-1 mammary cancer cells derived from MMTV-PyVmT/FVB-N trans

68 We confirmed that other mammary cancer cells embedded in tissue-mimetic hydrogel

69 ix, MSC cultured with conditioned media from mammary cancer cells expressed increased levels of alpha

70 o the CMV promoter is transfected into human mammary cancer cells having no detectable endogenous cav

71 ffect the growth and survival of PRL-induced mammary cancer cells in culture and in vivo.

72 f apoptotic cells and retarded the growth of mammary cancer cells in mice.

73 in receptor antagonists (LPrA2) on 4T1 mouse mammary cancer cells in vitro and LPrA2 on 4T1-MT develo

74 o effects of RNAi-mediated downregulation in mammary cancer cells on the migration, blood and lymphat

75 Ectopic expression of FOXP3 in mouse mammary cancer cells repressed SKP2 expression with a co

76 trajectories of these dye-labeled glycans in mammary cancer cells revealed constrained diffusion of b

77 that TAp63 is crucial for the transition of mammary cancer cells to TICs.

78 nome-wide RNA interference screen with E0771 mammary cancer cells to uncover drivers of endothelial m

79 termine how PKCalpha regulates metastasis of mammary cancer cells using a syngeneic and orthotopic mo

80 the JAK1 tyrosine kinase in KRAS-transformed mammary cancer cells using the dual recombinase approach

81 Furthermore, decreased viability of mammary cancer cells was directly related to Egfr functi

82 fted mammary tumors in nude mice using Notch mammary cancer cells which also express ras oncogene.

83 ed cell types of nonmelanocyte origin (e.g., mammary cancer cells) and beads that lacked the melanotr

84 Our results indicate that in BT-20 human mammary cancer cells, expression of IRS-1 activates prom

85 of tumor necrosis factor (TNF) alpha in many mammary cancer cells, we have found that TNF stimulates

86 effective in inhibiting the proliferation of mammary cancer cells.

87 , was inserted into the chromosomes of MCF-7 mammary cancer cells.

88 ton reorganization and signaling pathways in mammary cancer cells.

89 bilization of COX-2 mRNA in MDA-MB-231 human mammary cancer cells.

90 ering enhanced proliferation and survival of mammary cancer cells.

91 F-10 mammary epithelial cells and MDA-MB-231 mammary cancer cells.

92 al in vitro and in vivo effect on breast and mammary cancer cells.

93 and stem cell characteristics of claudin-low mammary cancer cells.

94 reast tumors and promoted lung metastasis of mammary cancer cells.

95 ion of Msi1 reduced invadopodia formation in mammary cancer cells.

96 comparative analysis of mouse and human SAGE mammary cancer data validates this p53 null mouse tumor

97 atment in mice with BRCA1 deficiency altered mammary cancer development by promoting development of d

98 ncer cells in vitro and in vivo and prevents mammary cancer development in a transgenic mouse model.

99 carcinoma appears to be a critical event for mammary cancer development in C3(1)/T(AG) transgenic mic

100 argeting of COX-2 and PPAR gamma may inhibit mammary cancer development more effectively than targeti

101 ctive effects of tamoxifen administration on mammary cancer development were found.

102 ay diametrically opposed susceptibilities to mammary cancer development when treated chronically with

103 significance of the Ki-ras proto-oncogene in mammary cancer development, in vivo studies were conduct

104 s from transgenic mice engineered to develop mammary cancer due to expression in mammary epithelia of

105 ly with E2, BN rats did not develop palpable mammary cancer during the 196-day course of E2 treatment

106 Here we show that rats with mammary cancer exhibit depression- and anxiety-like beha

107 PRL-induced mammary cancers exhibited an upregulation of ErbB2 and o

108 an impact on susceptibility or resistance to mammary cancer, female littermates from FVB/N x WAP-TGF-

109 estrogen-dependent and independent MXT mouse mammary cancers, following a single subcutaneous adminis

110 This is the first interspecies comparison of mammary cancer gene expression profiles.

111 ng tumor cells (CTCs) in two mouse models of mammary cancer: genetically modified MMTV-PyMT mice and

112 tumor-inhibitory effects of DHEA and DFMO on mammary cancer growth appear to occur after the developm

113 therapeutic possibilities for the control of mammary cancer growth.

114 otential, supporting the notion that dormant mammary cancers harbor transformed mammary progenitor ce

115 Expression of Brca1 in mouse mammary cancer has yet to be analysed.

116 dy, we evaluate susceptibility to E2-induced mammary cancer in a cross between the ACI strain and the

117 study demonstrating efficacy of BITC against mammary cancer in an animal model provides impetus to de

118 has been shown to inhibit the development of mammary cancer in animal models.

119 ly to determine susceptibility to E2-induced mammary cancer in crosses between the susceptible ACI ra

120 ng mammary remnants, a major risk factor for mammary cancer in male mice, and one that would appear t

121 rmine susceptibility to LD radiation induced mammary cancer in mice are similar to the tissue mechani

122 onset but did not prevent the occurrence of mammary cancer in mice overexpressing wild-type ErbB2.

123 dence for efficacy of BITC for prevention of mammary cancer in MMTV-neu mice.

124 moval of the primary tumor, cured metastatic mammary cancer in most animals without inducing GVHD.

125 titumor and chemopreventive activity against mammary cancer in preclinical studies.

126 AB30 (4-Me-UAB30)] showed that all inhibited mammary cancer in rodents and two (TRG and 4-Me-UAB30) s

127 a indicate that susceptibility to E2-induced mammary cancer in the BN x ACI cross behaves as a comple

128 en exposure can influence the development of mammary cancer in the C3(1)/T(AG) transgenic model, wher

129 Two-thirds of the induced mammary cancers in ACI rats exhibited aneuploidy.

130 he growth and differentiation of spontaneous mammary cancers in mice transgenic for a mouse mammary t

131 ose estrogen results in human-like aneuploid mammary cancers in ovary-intact ACI rats.

132 prevention of N-methyl-N-nitrosourea induced mammary cancers in rats without signs of toxicity.

133 t either 800 or 400 mg/kg diet, DHEA reduced mammary cancer incidence from >70% in dietary controls t

134 cidence from >70% in dietary controls to 0%; mammary cancer incidence from >70% in dietary controls t

135 cidence from >70% in dietary controls to 0%; mammary cancer incidence in all DHEA combination regimen

136 ve contribution of progesterone to increased mammary cancer incidence is due to RANKL-dependent proli

137 s of E and was not effective in reducing the mammary cancer incidence.

138 s present in domesticated mammals with a low mammary cancer incidence.

139 AR has been shown also to prevent mammary cancer induced by N-methyl-N-nitrosourea in rats

140 s a highly effective agent for prevention of mammary cancer induced in the rat by the carcinogen nitr

141 ary-intact females develop high incidence of mammary cancers induced solely by hormones upon prolonge

142 s development in a mouse model of aggressive mammary cancer-induced peritoneal carcinomatosis.

143 wed Hsp72 to be upregulated in a fraction of mammary cancer initiating cells (CIC) within the MMT tum

144 he importance of Jak2/Stat5 signaling during mammary cancer initiation and progression, we generated

145 This phenomenon of parity protection against mammary cancer is also observed in rodents.

146 ansgenic mouse model in which Wnt1-initiated mammary cancer is doxycycline dependent.

147 Estrogen receptor-negative [ER(-)] mammary cancer is the most aggressive type of breast can

148 However, the mechanism(s) of alcohol-induced mammary cancer is unknown.

149 Here, we initially fine map mammary cancer loci in a rat carcinogenesis model and th

150 neuroendocrine tumors (NET; n = 77, 15.3%), mammary cancer (MAM; n = 68, 13.5%), hepatocellular carc

151 nting, delaying progression of, and treating mammary cancers, many of which are estrogen receptor-pos

152 of mammals with a naturally low incidence of mammary cancer mediate the elimination of cancer cells.

153 l inhibition of PKCalpha effectively reduces mammary cancer metastasis by targeting intravasation and

154 DF11 in vitro and suppresses triple-negative mammary cancer metastasis to the lung of syngeneic hosts

155 of normal and tumor samples from this mouse mammary cancer model (>300,000 mouse mammary-specific ta

156 /polyoma virus middle T oncogene (MMTV-PyMT) mammary cancer model demonstrate dramatically reduced ra

157 ted using the 1-methyl-1-nitrosourea-induced mammary cancer model in which rats were 0%, 20%, or 40%

158 Mammary cancer model systems can be used to explore inte

159 and progression, we generated a PRL-induced mammary cancer model that allows the functional ablation

160 in tumorigenesis, we have developed a mouse mammary cancer model, the Wnt-1 TG/p53 model.

161 Using the 4T1.2 mammary cancer model, we assessed spatial memory and obj

162 Using a murine mammary cancer model, we demonstrated that doxorubicin s

163 immunogenic and highly metastatic 4T1 murine mammary cancer model.

164 rexpress ERBB2, and in a new KRAS-associated mammary cancer model.

165 Using mouse mammary cancer models and syngeneic transplantation assa

166 Genetically engineered mouse mammary cancer models have been used over the years as s

167 arrow chimeric mice and syngeneic orthotopic mammary cancer models to show that hypoxia in the primar

168 Here, we utilize mammary cancer models to temporally delete essential aut

169 Employing hormone-independent mammary cancer models, Go6976 and ATRA combined treatmen

170 o in murine transgenic and cell line-derived mammary cancer models, showed that neoplastic cells enga

171 t component for the validation of transgenic mammary cancer models.

172 ic changes unlike those seen in other murine mammary cancer models.

173 ed (PD-1-based) ICI therapy in ICI-resistant mammary cancer models; and (c) acted in concert with PD-

174 Using a triple-negative mammary cancer mouse model and chronic neural interface

175 mca6, Emca7, and Emca8, were identified when mammary cancer number was evaluated as the phenotype.

176 determinant of susceptibility to E2-induced mammary cancer on distal rat chromosome 5.

177 e selective PPARgamma agonist efatutazone on mammary cancer pathogenesis in a mouse model of BRCA1 mu

178 f Malat1 in regulating critical processes in mammary cancer pathogenesis.

179 revent dimethylbenzanthracene (DMBA)-induced mammary cancers, presumably by inhibiting DMBA activatio

180 eting this kinase is a relevant strategy for mammary cancer prevention.

181 ional requirement for NEDD9 in the growth of mammary cancer progenitor cells.

182 inase that is needed for the self-renewal of mammary cancer progenitors and for prostate cancer metas

183 Results suggest a model of mammary cancer progression in which loss of full-length

184 sion, the chemopreventive effects of DFMO on mammary cancer progression were mediated by changes in b

185 a potent inducer of angiogenic switch during mammary cancer progression.

186 udy the effects of chemopreventive agents on mammary cancer progression.

187 analyzed the role of MAP17 expression during mammary cancer progression.

188 tly identified a period of vulnerability for mammary cancer promotion, which emerges during weight ga

189 Using a transgenic mouse susceptible to mammary cancer, PyMT mice, we have characterized the dev

190 The E2-induced mammary cancers regressed when hormone treatment was dis

191 hus, p19 Arf/p53 pathway lesions may promote mammary cancer relapse even when inhibition of a targete

192 Spontaneously occurring canine mammary cancer represents an excellent model of human br

193 a and tumor angiogenesis in oncogene-induced mammary cancer, resulting in attenuated blood flow and t

194 ects of maternal EE2 exposure on offspring's mammary cancer risk are associated with changes in the D

195 when homozygous for the Wky allele, reduces mammary cancer risk by 50%.

196 supplemented diet affects carcinogen-induced mammary cancer risk in daughters, granddaughters and gre

197 escence in mammary transplants and decreases mammary cancer risk in mouse mammary tumor virus (MMTV)-

198 oss experiments suggest that the increase in mammary cancer risk is transmitted to HF granddaughters

199 ation of the mechanisms underlying increased mammary cancer risk, reported here, revealed that IGF-1

200 fe-span of mammary epithelial stem cells and mammary cancer risk.

201 Glut-1 and 3H-FDG uptake in a syngeneic rat mammary cancer (RMC), an animal tumor model that closely

202 oned as an androgen induced protein in mouse mammary cancer SC3 cells.

203 Susceptibility to E2-induced mammary cancer segregated as a dominant or incompletely

204 was validated in independent mouse and human mammary cancer sets.

205 loci, Emca4 and Emca5, were identified when mammary cancer status at sacrifice was evaluated as the

206 epithelial-mesenchymal transition (EMT) and mammary cancer stem cell (MaCSC) activities in tumors de

207 nished metastasis and fewer cells expressing mammary cancer stem cell markers.

208 lopment and maintenance and may give rise to mammary cancer stem cells (MaCSC).

209 Mammary cancer stem cells (MaCSCs) have been identified

210 Vitamin D signaling in mammary cancer stem cells (MCSCs), which are implicated

211 w a novel function of FAK in maintaining the mammary cancer stem/progenitor cell population and provi

212 ll breast cancers and is the most aggressive mammary cancer subtype.

213 d tumor progression in a transgenic model of mammary cancer, suggesting that this is a useful approac

214 cs), which had no significant main effect on mammary cancer susceptibility in this genetic analysis.

215 for the purpose of identifying mechanisms of mammary cancer susceptibility.

216 Using mouse models of mammary cancer that elicit robust MDSC responses, we dem

217 two loci, Emca1 and Emca2 (estrogen-induced mammary cancer), that act independently to determine sus

218 n-induced ductal dysplasia is a precursor to mammary cancer, the results indicate that AT heterozygos

219 yrosine kinase ERB2 (HER2), that define most mammary cancers, there are no targeted therapies for pat

220 ues, we employed a transgenic mouse model of mammary cancer to identify molecular changes in precance

221 us, we tested the hypothesis that peripheral mammary cancer tumors alter the transcriptome of immune

222 ention in estrogen receptor-negative [ER(-)] mammary cancer using transgenic mice.

223 the lowest effective E dosage for preventing mammary cancer was determined.

224 hich is an initial event in the formation of mammary cancer, was able to override the functional role

225 whether PPARgamma regulates MSC expansion in mammary cancer, we deleted PPARgamma expression in the m

226 Using a mouse model of HR(+) mammary cancer, we demonstrate that a preestablished dis

227 Given the role of cyclin D1 in breast and mammary cancer, we examined involvement of IKKalpha in m

228 Using a highly metastatic model of mammary cancer, we identified previously inbred mouse st

229 ts of this polymorphism on susceptibility to mammary cancer, we used a humanized p53 mouse model, hom

230 ion and the sporadic occurrence of bona fide mammary cancers, we conclude that the Tsg101 protein has

231 tilizing the neu-N transgenic mouse model of mammary cancer, weekly treatment of the neu-N mice with

232 methylornithine (DFMO) on the development of mammary cancer were investigated utilizing the whey acid

233 d a significant reduction in NMU-induced rat mammary cancer when compared to their non-transgenic lit

234 hereas nearly 100% of the ACI rats developed mammary cancer when treated continuously with E2, BN rat

235 be induced by c-Myc to mediate the onset of mammary cancer, whereas overexpression of cyclins D1 and

236 MTV-PAK4 overexpression promotes spontaneous mammary cancer, while PAK4 gene depletion delays MMTV-Py

237 N female mice carrying the transgene develop mammary cancer with about a 15% incidence of lung metast

238 we crossed a transgenic mouse susceptible to mammary cancer with mice containing a recessive null mut

239 ession could be induced in murine chest wall mammary cancers with a topical toll-like receptor (TLR)-

240 rcinoma comprises approximately 10% of human mammary cancers, yet little is known about the molecular