ライフサイエンスコーパス: mammary cancer

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

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

3 the mammary gland of transgenic mice induced mammary cancer.

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

5 genetically conferred propensity to develop mammary cancer.

6 Two C75-treated animals never developed mammary cancer.

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

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

9 These mice developed spontaneous, metastatic mammary cancer.

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

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

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

13 ancy and were highly effective in preventing mammary cancer.

14 is associated with an increased incidence of mammary cancer.

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

16 during the early and intermediate stages of mammary cancer.

17 hormones that likely induce protection from mammary cancer.

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

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

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

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

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

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

24 accelerated tumor growth in murine model of mammary cancer.

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

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

27 radiosensitive and susceptible to radiogenic mammary cancer.

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

29 progression in murine models of melanoma and mammary cancer.

30 ated with multiple forms of cancer including mammary cancer.

31 ntify mechanisms involved in hormone-induced mammary cancer.

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

33 cally conferred susceptibility to E2-induced mammary cancers.

34 ecting them from chemical carcinogen induced mammary cancers.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

76 ton reorganization and signaling pathways in mammary cancer cells.

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

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

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

80 ering enhanced proliferation and survival of mammary cancer cells.

81 effective in inhibiting the proliferation of mammary cancer cells.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

98 therapeutic possibilities for the control of mammary cancer growth.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

139 Mammary cancer model systems can be used to explore inte

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

182 Mammary cancer stem cells (MaCSCs) have been identified

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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