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|---|---|---|---|---|---|---|---|---|---|---|
8600090.s9 | This decrease in the UTP and CTP pools promoted a fivefold increase in the incorporation of [3H]BrdUrd into the DNA of BG-1 cells. | ovarian | {
"name": "UTP",
"pos": [
21,
23
]
} | {
"name": "BG-1",
"pos": [
119,
122
]
} | decreased | unidentifiable | {
"name": "\nNone\n",
"pos": null,
"type": null
} | {
"name": "decrease",
"pos": [
5,
12
],
"type": "Negative_regulation"
} |
||
8600090.s9 | This decrease in the UTP and CTP pools promoted a fivefold increase in the incorporation of [3H]BrdUrd into the DNA of BG-1 cells. | ovarian | {
"name": "CTP",
"pos": [
29,
31
]
} | {
"name": "BG-1",
"pos": [
119,
122
]
} | decreased | unidentifiable | {
"name": "\nNone\n",
"pos": null,
"type": null
} | {
"name": "decrease",
"pos": [
5,
12
],
"type": "Negative_regulation"
} |
||
16584837.s0 | Specific inhibition of AKT2 by RNA interference results in reduction of ovarian cancer cell proliferation: increased expression of AKT in advanced ovarian cancer. | ovarian | {
"name": "AKT2",
"pos": [
23,
26
]
} | {
"name": "ovarian cancer",
"pos": [
72,
85
]
} | decreased | cancerTOnormal | causality | unidentifiable | {
"name": "\nNone\n",
"pos": null,
"type": null
} | {
"name": "inhibition",
"pos": [
9,
18
],
"type": "Negative_regulation"
} |
16584837.s0 | Specific inhibition of AKT2 by RNA interference results in reduction of ovarian cancer cell proliferation: increased expression of AKT in advanced ovarian cancer. | ovarian | {
"name": "AKT",
"pos": [
131,
133
]
} | {
"name": "ovarian cancer",
"pos": [
72,
85
]
} | increased | normalTOcancer | observation | unidentifiable | {
"name": "expression",
"pos": [
117,
126
],
"type": "Gene_expression"
} | {
"name": "increased",
"pos": [
107,
115
],
"type": "Positive_regulation"
} |
2910450.s8 | Despite these differences, ovarian carcinoma cells show substantial accumulation of araCTP from extracellular araC. | ovarian | {
"name": "araCTP from extracellular araC",
"pos": [
84,
113
]
} | {
"name": "ovarian carcinoma",
"pos": [
27,
43
]
} | increased | normalTOcancer | observation | unidentifiable | {
"name": "\nNone\n",
"pos": null,
"type": null
} | {
"name": "accumulation",
"pos": [
68,
79
],
"type": "Positive_regulation"
} |
11776599.s7 | Increase in nitric oxide synthase activity might be related to the growth and malignant behavior of ovarian cancer. | ovarian | {
"name": "nitric oxide synthase",
"pos": [
12,
32
]
} | {
"name": "ovarian cancer",
"pos": [
100,
113
]
} | increased | normalTOcancer | causality | unidentifiable | {
"name": "\nNone\n",
"pos": null,
"type": null
} | {
"name": "Increase",
"pos": [
0,
7
],
"type": "Positive_regulation"
} |
9590136.s0 | Human chorionic gonadotropin (hCG) inhibits cisplatin-induced apoptosis in ovarian cancer cells: possible role of up-regulation of insulin-like growth factor-1 by hCG. | ovarian | {
"name": "insulin-like growth factor-1",
"pos": [
131,
158
]
} | {
"name": "ovarian cancer",
"pos": [
75,
88
]
} | increased | normalTOcancer | causality | unidentifiable | {
"name": "\nNone\n",
"pos": null,
"type": null
} | {
"name": "up-regulation",
"pos": [
114,
126
],
"type": "Positive_regulation"
} |
9590136.s9 | Our findings suggest that LH/hCG influences the chemosensitivity of ovarian cancer cells through an apoptosis-inhibitory signal possibly via up-regulation of IGF-1 expression. | ovarian | {
"name": "IGF-1",
"pos": [
158,
162
]
} | {
"name": "ovarian cancer",
"pos": [
68,
81
]
} | increased | normalTOcancer | causality | unidentifiable | {
"name": "\nNone\n",
"pos": null,
"type": null
} | {
"name": "up-regulation",
"pos": [
141,
153
],
"type": "Positive_regulation"
} |
18088084.s2 | Mesothelin is a glycosyl-phosphatidyl inositol (GPI)-linked membrane protein of 40 kDa over-expressed in all pancreatic adenocarcinoma and mesothelioma, in >70% of ovarian adenocarcinoma, and in non-small cell lung and colorectal cancers. | ovarian | {
"name": "Mesothelin",
"pos": [
0,
9
]
} | {
"name": "of ovarian adenocarcin",
"pos": [
161,
182
]
} | increased | normalTOcancer | observation | unchanged | {
"name": "over-expressed",
"pos": [
87,
100
],
"type": "Gene_expression"
} | {
"name": "over-expressed",
"pos": [
87,
100
],
"type": "Positive_regulation"
} |
11459464.s10 | An in vitro internalization study showed that Av-G6Gd accumulated and was internalized into SHIN3 cells (a human ovarian cancer) 50- and 3.5-fold greater than Gd-DTPA (Magnevist) and G6-(1B4M-Gd)(256) (G6Gd). | ovarian | {
"name": "Av-G6Gd",
"pos": [
46,
52
]
} | {
"name": "ovarian cancer",
"pos": [
113,
126
]
} | increased | normalTOcancer | observation | unidentifiable | {
"name": "\nNone\n",
"pos": null,
"type": null
} | {
"name": "accumulated",
"pos": [
54,
64
],
"type": "Positive_regulation"
} |
1464654.s0 | Estradiol stimulates cell growth and secretion of procathepsin D and a 120-kilodalton protein in the human ovarian cancer cell line BG-1. | ovarian | {
"name": "procathepsin D",
"pos": [
50,
63
]
} | {
"name": "ovarian cancer",
"pos": [
107,
120
]
} | increased | normalTOcancer | observation | unidentifiable | {
"name": "\nNone\n",
"pos": null,
"type": null
} | {
"name": "stimulates",
"pos": [
10,
19
],
"type": "Positive_regulation"
} |
15781636.s6 | LPA increased COX-2 protein expression in a time- and concentration-dependent manner in two of three immortalized borderline ovarian epithelial cells as well as in four of six ovarian cancer cell lines. | ovarian | {
"name": "COX-2 protein",
"pos": [
14,
26
]
} | {
"name": "ovarian cancer",
"pos": [
176,
189
]
} | increased | unidentifiable | {
"name": "expression",
"pos": [
28,
37
],
"type": "Gene_expression"
} | {
"name": "increased",
"pos": [
4,
12
],
"type": "Positive_regulation"
} |
||
15138597.s6 | In patients with ovarian cancer, the increased leptin levels were associated with higher circulating follicle-stimulating hormone (FSH). | ovarian | {
"name": "leptin",
"pos": [
47,
52
]
} | {
"name": "ovarian cancer",
"pos": [
17,
30
]
} | increased | unidentifiable | {
"name": "levels",
"pos": [
54,
59
],
"type": "Gene_expression"
} | {
"name": "increased",
"pos": [
37,
45
],
"type": "Positive_regulation"
} |
||
16825507.s2 | We previously reported that LTBP-1L is overexpressed in some patients with ovarian cancer. | ovarian | {
"name": "LTBP-1L",
"pos": [
28,
34
]
} | {
"name": "ovarian cancer",
"pos": [
75,
88
]
} | increased | normalTOcancer | observation | unchanged | {
"name": "overexpressed",
"pos": [
39,
51
],
"type": "Gene_expression"
} | {
"name": "overexpressed",
"pos": [
39,
51
],
"type": "Positive_regulation"
} |
16825507.s7 | Interestingly, ovarian cancer patients (n = 42) with G-A/G-A homozygous genotype had increased expression of LTBP-1 and apparently poorer survival than those with other genotypes (P = 0.02). | ovarian | {
"name": "LTBP-1",
"pos": [
109,
114
]
} | {
"name": "ovarian cancer",
"pos": [
15,
28
]
} | increased | normalTOcancer | observation | unidentifiable | {
"name": "expression",
"pos": [
95,
104
],
"type": "Gene_expression"
} | {
"name": "increased",
"pos": [
85,
93
],
"type": "Positive_regulation"
} |
18632752.s4 | Intriguingly, the loss of MKP3 protein was associated with ubiquitination/proteosome degradation mediated by high intracellular reactive oxygen species (ROS) accumulation such as hydrogen peroxide in ovarian cancer cells. | ovarian | {
"name": "MKP3 protein",
"pos": [
26,
37
]
} | {
"name": "ovarian cancer",
"pos": [
200,
213
]
} | decreased | unidentifiable | {
"name": "\nNone\n",
"pos": null,
"type": null
} | {
"name": "loss",
"pos": [
18,
21
],
"type": "Negative_regulation"
} |
||
18632752.s5 | Functionally, short hairpin RNA knock down of endogenous MKP3 resulted in increased ERK1/2 activity, cell proliferation rate, anchorage-independent growth ability and resistance to cisplatin in ovarian cancer cells. | ovarian | {
"name": "ERK1/2",
"pos": [
84,
89
]
} | {
"name": "ovarian cancer",
"pos": [
194,
207
]
} | increased | normalTOcancer | observation | unidentifiable | {
"name": "\nNone\n",
"pos": null,
"type": null
} | {
"name": "increased",
"pos": [
74,
82
],
"type": "Positive_regulation"
} |
18632752.s6 | Conversely, enforced expression of MKP3 in MKP3-deficient ovarian cancer cells significantly reduced ERK1/2 activity and inhibited cell proliferation, anchorage-independent growth ability and tumor development in nude mice. | ovarian | {
"name": "MKP3",
"pos": [
35,
38
]
} | {
"name": "ovarian cancer",
"pos": [
58,
71
]
} | increased | cancerTOnormal | causality | unidentifiable | {
"name": "expression",
"pos": [
21,
30
],
"type": "Gene_expression"
} | {
"name": "enforced",
"pos": [
12,
19
],
"type": "Positive_regulation"
} |
18632752.s6 | Conversely, enforced expression of MKP3 in MKP3-deficient ovarian cancer cells significantly reduced ERK1/2 activity and inhibited cell proliferation, anchorage-independent growth ability and tumor development in nude mice. | ovarian | {
"name": "ERK1/2",
"pos": [
101,
106
]
} | {
"name": "ovarian cancer",
"pos": [
58,
71
]
} | decreased | cancerTOnormal | observation | unidentifiable | {
"name": "\nNone\n",
"pos": null,
"type": null
} | {
"name": "reduced",
"pos": [
93,
99
],
"type": "Negative_regulation"
} |
17092940.s0 | Hyaluronan-CD44 interaction with neural Wiskott-Aldrich syndrome protein (N-WASP) promotes actin polymerization and ErbB2 activation leading to beta-catenin nuclear translocation, transcriptional up-regulation, and cell migration in ovarian tumor cells. | ovarian | {
"name": "ErbB2",
"pos": [
116,
120
]
} | {
"name": "ovarian tumor",
"pos": [
233,
245
]
} | increased | normalTOcancer | causality | unidentifiable | {
"name": "\nNone\n",
"pos": null,
"type": null
} | {
"name": "activation",
"pos": [
122,
131
],
"type": "Positive_regulation"
} |
18070364.s0 | Coordinate up-regulation of TMEM97 and cholesterol biosynthesis genes in normal ovarian surface epithelial cells treated with progesterone: implications for pathogenesis of ovarian cancer. | ovarian | {
"name": "TMEM97",
"pos": [
28,
33
]
} | {
"name": "ovarian cancer",
"pos": [
173,
186
]
} | increased | normalTOcancer | observation | unchanged | {
"name": "\nNone\n",
"pos": null,
"type": null
} | {
"name": "up-regulation",
"pos": [
11,
23
],
"type": "Positive_regulation"
} |
18070364.s0 | Coordinate up-regulation of TMEM97 and cholesterol biosynthesis genes in normal ovarian surface epithelial cells treated with progesterone: implications for pathogenesis of ovarian cancer. | ovarian | {
"name": "cholesterol biosynthesis genes",
"pos": [
39,
68
]
} | {
"name": "ovarian cancer",
"pos": [
173,
186
]
} | increased | normalTOcancer | observation | unchanged | {
"name": "\nNone\n",
"pos": null,
"type": null
} | {
"name": "up-regulation",
"pos": [
11,
23
],
"type": "Positive_regulation"
} |
12174912.s9 | Our findings indicate that: (I) VDR expression is increased in ovarian carcinomas as compared to normal ovarian tissue. | ovarian | {
"name": "VDR",
"pos": [
32,
34
]
} | {
"name": "ovarian carcinomas",
"pos": [
63,
80
]
} | increased | normalTOcancer | observation | unchanged | {
"name": "expression",
"pos": [
36,
45
],
"type": "Gene_expression"
} | {
"name": "increased",
"pos": [
50,
58
],
"type": "Positive_regulation"
} |
12174912.s10 | (II) Up-regulation of VDR in ovarian carcinomas is not exclusively induced by an increase of proliferation, but by different unknown mechanisms. | ovarian | {
"name": "VDR",
"pos": [
22,
24
]
} | {
"name": "ovarian carcinomas",
"pos": [
29,
46
]
} | increased | normalTOcancer | observation | unidentifiable | {
"name": "\nNone\n",
"pos": null,
"type": null
} | {
"name": "Up-regulation",
"pos": [
5,
17
],
"type": "Positive_regulation"
} |
17415999.s8 | Transfection with GSK-3betaS9A to upregulate the GSK-3beta activity resulted in the increase of BrdU incorporation in SKOV3 cells compared with that in the control vector. | ovarian | {
"name": "BrdU",
"pos": [
96,
99
]
} | {
"name": "SKOV3",
"pos": [
118,
122
]
} | increased | unidentifiable | {
"name": "\nNone\n",
"pos": null,
"type": null
} | {
"name": "increase",
"pos": [
84,
91
],
"type": "Positive_regulation"
} |
||
17415999.s8 | Transfection with GSK-3betaS9A to upregulate the GSK-3beta activity resulted in the increase of BrdU incorporation in SKOV3 cells compared with that in the control vector. | ovarian | {
"name": "GSK-3beta",
"pos": [
49,
57
]
} | {
"name": "SKOV3",
"pos": [
118,
122
]
} | increased | unidentifiable | {
"name": "\nNone\n",
"pos": null,
"type": null
} | {
"name": "upregulate",
"pos": [
34,
43
],
"type": "Positive_regulation"
} |
||
17415999.s8 | Transfection with GSK-3betaS9A to upregulate the GSK-3beta activity resulted in the increase of BrdU incorporation in SKOV3 cells compared with that in the control vector. | ovarian | {
"name": "GSK-3betaS9A",
"pos": [
18,
29
]
} | {
"name": "SKOV3",
"pos": [
118,
122
]
} | increased | unidentifiable | {
"name": "Transfection",
"pos": [
0,
11
],
"type": "Gene_expression"
} | {
"name": "Transfection",
"pos": [
0,
11
],
"type": "Positive_regulation"
} |
||
17415999.s9 | On the contrary, transfection with GID5-6 to downregulate GSK-3beta activity decreased the BrdU incorporation in SKOV3 cells, compared with that in GID5-6LP, which is a control vector of GID5-6. | ovarian | {
"name": "GID5-6",
"pos": [
35,
40
]
} | {
"name": "SKOV3",
"pos": [
113,
117
]
} | increased | unidentifiable | {
"name": "transfection",
"pos": [
17,
28
],
"type": "Gene_expression"
} | {
"name": "transfection",
"pos": [
17,
28
],
"type": "Positive_regulation"
} |
||
21323863.s1 | Targeting and down-regulation of ErbB2, a member of EGF receptor family, is regarded as one of the key aspect for cancer treatment because it is often overexpressed in breast and ovarian cancer cells. | ovarian | {
"name": "ErbB2",
"pos": [
33,
37
]
} | {
"name": "ovarian cancer",
"pos": [
179,
192
]
} | increased | normalTOcancer | observation | unchanged | {
"name": "overexpressed",
"pos": [
151,
163
],
"type": "Gene_expression"
} | {
"name": "overexpressed",
"pos": [
151,
163
],
"type": "Positive_regulation"
} |
16093247.s8 | Knockdown of TRAIL receptor 4 by RNA interference or ectopic expression of Fas relieved the suppressive effect of 1,25-dihydroxyvitamin D3, showing that molecular manipulation of death receptors is a viable approach to overcome the protective effect of 1,25-dihydroxyvitamin D3 on the apoptosis of ovarian cancer. | ovarian | {
"name": "TRAIL receptor 4",
"pos": [
13,
28
]
} | {
"name": "ovarian cancer",
"pos": [
298,
311
]
} | decreased | cancerTOnormal | causality | unidentifiable | {
"name": "\nNone\n",
"pos": null,
"type": null
} | {
"name": "Knockdown",
"pos": [
0,
8
],
"type": "Negative_regulation"
} |
16136053.s6 | Quantitative PCR revealed decreased Notch 1 mRNA in ovarian adenocarcinomas compared with adenomas. | ovarian | {
"name": "Notch 1",
"pos": [
36,
42
]
} | {
"name": "ovarian adenocarcinomas",
"pos": [
52,
74
]
} | decreased | normalTOcancer | observation | unidentifiable | {
"name": "\nNone\n",
"pos": null,
"type": null
} | {
"name": "decreased",
"pos": [
26,
34
],
"type": "Negative_regulation"
} |
18519708.s6 | Compared with primary prostate tumors, castration-resistant metastases displayed alterations in genes encoding steroidogenic enzymes, including up-regulated expression of FASN, CYP17A1, HSD3B1, HSD17B3, CYP19A1, and UGT2B17 and down-regulated expression of SRD5A2 (P < 0.001 for all). | prostate | {
"name": "UGT2B17",
"pos": [
216,
222
]
} | {
"name": "prostate tumors",
"pos": [
22,
36
]
} | increased | normalTOcancer | observation | unidentifiable | {
"name": "expression",
"pos": [
157,
166
],
"type": "Gene_expression"
} | {
"name": "up-regulated",
"pos": [
144,
155
],
"type": "Positive_regulation"
} |
18519708.s6 | Compared with primary prostate tumors, castration-resistant metastases displayed alterations in genes encoding steroidogenic enzymes, including up-regulated expression of FASN, CYP17A1, HSD3B1, HSD17B3, CYP19A1, and UGT2B17 and down-regulated expression of SRD5A2 (P < 0.001 for all). | prostate | {
"name": "SRD5A2",
"pos": [
257,
262
]
} | {
"name": "prostate tumors",
"pos": [
22,
36
]
} | decreased | normalTOcancer | observation | unidentifiable | {
"name": "expression",
"pos": [
243,
252
],
"type": "Gene_expression"
} | {
"name": "down-regulated",
"pos": [
228,
241
],
"type": "Negative_regulation"
} |
15735018.s3 | Progression of benign prostate cancer to malignant metastasis is linked to increased production of basic fibroblast growth factor (bFGF), a powerful mitogen. | prostate | {
"name": "bFGF",
"pos": [
131,
134
]
} | {
"name": "prostate cancer",
"pos": [
22,
36
]
} | increased | normalTOcancer | observation | unidentifiable | {
"name": "production",
"pos": [
85,
94
],
"type": "Gene_expression"
} | {
"name": "increased",
"pos": [
75,
83
],
"type": "Positive_regulation"
} |
15735018.s4 | In this study, using in vitro model system we show that DPPIV loss is associated with increased bFGF production in metastatic prostate cancer cells. | prostate | {
"name": "bFGF",
"pos": [
96,
99
]
} | {
"name": "metastatic prostate cancer",
"pos": [
115,
140
]
} | increased | unidentifiable | {
"name": "production",
"pos": [
101,
110
],
"type": "Gene_expression"
} | {
"name": "increased",
"pos": [
86,
94
],
"type": "Positive_regulation"
} |
||
15735018.s5 | DPPIV reexpression in prostate cancer cells blocks nuclear localization of bFGF, reduces bFGF levels, inhibits mitogen-activated protein kinase (MAPK)-extracellular signal-regulated kinase (ERK)1/2 activation, and decreases levels of urokinase-type plasminogen activator, known downstream effectors of bFGF signaling pathway. | prostate | {
"name": "bFGF",
"pos": [
89,
92
]
} | {
"name": "prostate cancer",
"pos": [
22,
36
]
} | decreased | unidentifiable | {
"name": "\nNone\n",
"pos": null,
"type": null
} | {
"name": "reduces",
"pos": [
81,
87
],
"type": "Negative_regulation"
} |
||
15735018.s8 | These results indicate that DPPIV inhibits the malignant phenotype of prostate cancer cells by blocking bFGF signaling pathway. | prostate | {
"name": "bFGF",
"pos": [
104,
107
]
} | {
"name": "prostate cancer",
"pos": [
70,
84
]
} | decreased | cancerTOnormal | causality | unidentifiable | {
"name": "\nNone\n",
"pos": null,
"type": null
} | {
"name": "blocking",
"pos": [
95,
102
],
"type": "Negative_regulation"
} |
16818637.s8 | Our findings suggest that blockage of osteopontin and/or COX-2 is a promising therapeutic approach for the inhibition of prostate tumor progression and angiogenesis. | prostate | {
"name": "osteopontin",
"pos": [
38,
48
]
} | {
"name": "prostate tumor",
"pos": [
121,
134
]
} | decreased | cancerTOnormal | causality | unidentifiable | {
"name": "\nNone\n",
"pos": null,
"type": null
} | {
"name": "blockage",
"pos": [
26,
33
],
"type": "Negative_regulation"
} |
10590366.s2 | Elevated expression of Met has been shown in advanced cases of carcinoma of the prostate, stomach, pancreas, and thyroid. | prostate | {
"name": "Met",
"pos": [
23,
25
]
} | {
"name": "carcinoma of the prostate",
"pos": [
63,
87
]
} | increased | normalTOcancer | observation | unidentifiable | {
"name": "expression",
"pos": [
9,
18
],
"type": "Gene_expression"
} | {
"name": "Elevated",
"pos": [
0,
7
],
"type": "Positive_regulation"
} |
14676836.s0 | Androgens repress Bcl-2 expression via activation of the retinoblastoma (RB) protein in prostate cancer cells. | prostate | {
"name": "Bcl-2",
"pos": [
18,
22
]
} | {
"name": "prostate cancer",
"pos": [
88,
102
]
} | decreased | unidentifiable | {
"name": "expression",
"pos": [
24,
33
],
"type": "Gene_expression"
} | {
"name": "repress",
"pos": [
10,
16
],
"type": "Negative_regulation"
} |
||
14676836.s1 | The oncogene Bcl-2 is upregulated frequently in prostate tumors following androgen ablation therapy, and Bcl-2 overexpression may contribute to the androgen-refractory relapse of the disease. | prostate | {
"name": "Bcl-2",
"pos": [
105,
109
]
} | {
"name": "prostate tumors",
"pos": [
48,
62
]
} | increased | normalTOcancer | causality | unidentifiable | {
"name": "overexpression",
"pos": [
111,
124
],
"type": "Gene_expression"
} | {
"name": "overexpression",
"pos": [
111,
124
],
"type": "Positive_regulation"
} |
14676836.s1 | The oncogene Bcl-2 is upregulated frequently in prostate tumors following androgen ablation therapy, and Bcl-2 overexpression may contribute to the androgen-refractory relapse of the disease. | prostate | {
"name": "Bcl-2",
"pos": [
13,
17
]
} | {
"name": "prostate tumors",
"pos": [
48,
62
]
} | increased | normalTOcancer | causality | unidentifiable | {
"name": "\nNone\n",
"pos": null,
"type": null
} | {
"name": "upregulated",
"pos": [
22,
32
],
"type": "Positive_regulation"
} |
14676836.s9 | Finally, androgen treatment of LNCaP cells upregulated specifically levels of the cyclin-dependent kinase inhibitors (CDKIs) p15INK4B and p27KIP1. | prostate | {
"name": "p27KIP1",
"pos": [
138,
144
]
} | {
"name": "LNCaP",
"pos": [
31,
35
]
} | increased | unidentifiable | {
"name": "\nNone\n",
"pos": null,
"type": null
} | {
"name": "upregulated",
"pos": [
43,
53
],
"type": "Positive_regulation"
} |
||
22199300.s6 | Prostate cancer cells transfected with EP4-siRNA and treatments with EP4 antagonist suggest a link between EP4, and Snail activation, potentially via p-Akt. | prostate | {
"name": "EP4-siRNA",
"pos": [
39,
47
]
} | {
"name": "Prostate cancer",
"pos": [
0,
14
]
} | increased | unidentifiable | {
"name": "transfected",
"pos": [
22,
32
],
"type": "Gene_expression"
} | {
"name": "transfected",
"pos": [
22,
32
],
"type": "Positive_regulation"
} |
||
18929692.s11 | Combined blockade of RANK/RANKL axis and BMP pathway resulted in reduced tumor burden and decreased bone loss compared to inhibition of either individual pathway alone in osteolytic prostate cancer lesion in bone. | prostate | {
"name": "BMP",
"pos": [
41,
43
]
} | {
"name": "prostate cancer",
"pos": [
182,
196
]
} | decreased | unidentifiable | {
"name": "\nNone\n",
"pos": null,
"type": null
} | {
"name": "blockade",
"pos": [
9,
16
],
"type": "Negative_regulation"
} |
||
10067845.s0 | Induction of androgen receptor by 1alpha,25-dihydroxyvitamin D3 and 9-cis retinoic acid in LNCaP human prostate cancer cells. | prostate | {
"name": "androgen receptor",
"pos": [
13,
29
]
} | {
"name": "prostate cancer",
"pos": [
103,
117
]
} | increased | unidentifiable | {
"name": "\nNone\n",
"pos": null,
"type": null
} | {
"name": "Induction",
"pos": [
0,
8
],
"type": "Positive_regulation"
} |
||
10067845.s10 | This increased expression of AR was followed by 1,25-(OH)2D3-induced inhibition of growth in LNCaP cells. | prostate | {
"name": "AR",
"pos": [
29,
30
]
} | {
"name": "LNCaP",
"pos": [
93,
97
]
} | increased | cancerTOnormal | observation | unidentifiable | {
"name": "expression",
"pos": [
15,
24
],
"type": "Gene_expression"
} | {
"name": "increased",
"pos": [
5,
13
],
"type": "Positive_regulation"
} |
10067845.s14 | In conclusion, our results demonstrate that growth inhibition of LNCaP cells by 1,25-(OH)2D3 and 9-cis RA is mediated by an AR-dependent mechanism and preceded by the induction of AR gene expression. | prostate | {
"name": "AR gene",
"pos": [
180,
186
]
} | {
"name": "LNCaP",
"pos": [
65,
69
]
} | increased | cancerTOnormal | observation | unidentifiable | {
"name": "expression",
"pos": [
188,
197
],
"type": "Gene_expression"
} | {
"name": "induction",
"pos": [
167,
175
],
"type": "Positive_regulation"
} |
18336887.s6 | The decrease in survivin gene expression by transfection of siRNA was accompanied by the inhibition of cell proliferation of PCa cells (31% and 25% decreased in LNCaP and PC-3 cells, P <0.01). | prostate | {
"name": "survivin gene",
"pos": [
16,
28
]
} | {
"name": "LNCaP",
"pos": [
161,
165
]
} | decreased | cancerTOnormal | observation | unidentifiable | {
"name": "expression",
"pos": [
30,
39
],
"type": "Gene_expression"
} | {
"name": "decrease",
"pos": [
4,
11
],
"type": "Negative_regulation"
} |
11410510.s10 | Antisense oligodeoxynucleotides, designed to block production of epidermal-FABP (a marker for normal prostate cells), caused increased proliferation in DU 145 prostate cancer cells. | prostate | {
"name": "epidermal-FABP",
"pos": [
65,
78
]
} | {
"name": "prostate cancer",
"pos": [
159,
173
]
} | decreased | normalTOcancer | causality | unchanged | {
"name": "production",
"pos": [
51,
60
],
"type": "Gene_expression"
} | {
"name": "block",
"pos": [
45,
49
],
"type": "Negative_regulation"
} |
11410510.s11 | In vivid contrast, antisense oligodeoxynucleotides to L-FABP (overexpressed in prostate cancer) decreased proliferation and caused apoptosis. | prostate | {
"name": "L-FABP",
"pos": [
54,
59
]
} | {
"name": "prostate cancer",
"pos": [
79,
93
]
} | increased | normalTOcancer | causality | unchanged | {
"name": "overexpressed",
"pos": [
62,
74
],
"type": "Gene_expression"
} | {
"name": "overexpressed",
"pos": [
62,
74
],
"type": "Positive_regulation"
} |
16982748.s7 | Furthermore, elevated [Ca2+]o triggered activation of the Akt signaling pathway and enhanced PC-3 cell attachment. | prostate | {
"name": "Akt",
"pos": [
58,
60
]
} | {
"name": "PC-3",
"pos": [
93,
96
]
} | increased | unidentifiable | {
"name": "\nNone\n",
"pos": null,
"type": null
} | {
"name": "activation",
"pos": [
40,
49
],
"type": "Positive_regulation"
} |
||
12507906.s0 | The transcriptional co-activator cAMP response element-binding protein-binding protein is expressed in prostate cancer and enhances androgen- and anti-androgen-induced androgen receptor function. | prostate | {
"name": "androgen receptor",
"pos": [
168,
184
]
} | {
"name": "prostate cancer",
"pos": [
103,
117
]
} | increased | unidentifiable | {
"name": "\nNone\n",
"pos": null,
"type": null
} | {
"name": "enhances",
"pos": [
123,
130
],
"type": "Positive_regulation"
} |
||
12507906.s5 | In prostate cancer DU-145 cells, which were transiently transfected with CBP cDNA, hydroxyflutamide enhanced AR activity to a greater extent than bicalutamide in the presence of either wild-type or the mutated AR 730 val-->met. | prostate | {
"name": "AR",
"pos": [
109,
110
]
} | {
"name": "prostate cancer",
"pos": [
3,
17
]
} | increased | unidentifiable | {
"name": "\nNone\n",
"pos": null,
"type": null
} | {
"name": "enhanced",
"pos": [
100,
107
],
"type": "Positive_regulation"
} |
||
14687488.s4 | NP manifested no immunoreactivity, whereas Pca and BPH showed significantly increased HIF-1alpha protein expression. | prostate | {
"name": "HIF-1alpha protein",
"pos": [
86,
103
]
} | {
"name": "BPH",
"pos": [
51,
53
]
} | increased | normalTOcancer | observation | unidentifiable | {
"name": "expression",
"pos": [
105,
114
],
"type": "Gene_expression"
} | {
"name": "increased",
"pos": [
76,
84
],
"type": "Positive_regulation"
} |
14687488.s7 | Our findings of increased HIF-1alpha protein expression in BPH and Pca specimens suggests the potential role of this protein in BPH and Pca. | prostate | {
"name": "HIF-1alpha protein",
"pos": [
26,
43
]
} | {
"name": "BPH",
"pos": [
59,
61
]
} | increased | normalTOcancer | observation | unidentifiable | {
"name": "expression",
"pos": [
45,
54
],
"type": "Gene_expression"
} | {
"name": "increased",
"pos": [
16,
24
],
"type": "Positive_regulation"
} |
8978405.s17 | The same concentration of R1881 resulted in a decrease in intracellular glutathione concentrations and an increase in gamma-glutamyl transpeptidase activity in LNCaP cells. | prostate | {
"name": "gamma-glutamyl transpeptidase",
"pos": [
118,
146
]
} | {
"name": "LNCaP",
"pos": [
160,
164
]
} | increased | unidentifiable | {
"name": "\nNone\n",
"pos": null,
"type": null
} | {
"name": "increase",
"pos": [
106,
113
],
"type": "Positive_regulation"
} |
||
8978405.s18 | Treatment with the oxidizing agents H2O2 and menadione produced an increase in gamma-glutamyl transpeptidase activity in LNCaP cells, whereas treatment with the antioxidant compound ascorbic acid (100 mM) reduced the oxidative stress produced in LNCaP cells by 1 nM R1881 and completely blocked the gamma-glutamyl transpeptidase activity. | prostate | {
"name": "gamma-glutamyl transpeptidase",
"pos": [
79,
107
]
} | {
"name": "LNCaP",
"pos": [
121,
125
]
} | increased | unidentifiable | {
"name": "\nNone\n",
"pos": null,
"type": null
} | {
"name": "increase",
"pos": [
67,
74
],
"type": "Positive_regulation"
} |
||
8978405.s18 | Treatment with the oxidizing agents H2O2 and menadione produced an increase in gamma-glutamyl transpeptidase activity in LNCaP cells, whereas treatment with the antioxidant compound ascorbic acid (100 mM) reduced the oxidative stress produced in LNCaP cells by 1 nM R1881 and completely blocked the gamma-glutamyl transpeptidase activity. | prostate | {
"name": "gamma-glutamyl transpeptidase",
"pos": [
299,
327
]
} | {
"name": "LNCaP",
"pos": [
121,
125
]
} | decreased | unidentifiable | {
"name": "\nNone\n",
"pos": null,
"type": null
} | {
"name": "blocked",
"pos": [
287,
293
],
"type": "Negative_regulation"
} |
||
9790546.s1 | For patients with metastatic prostate cancer, treatment is primarily palliative, relying mainly on the suppression of systemic androgen hormone levels. | prostate | {
"name": "androgen hormone",
"pos": [
127,
142
]
} | {
"name": "metastatic prostate cancer",
"pos": [
18,
43
]
} | decreased | unidentifiable | {
"name": "\nNone\n",
"pos": null,
"type": null
} | {
"name": "suppression",
"pos": [
103,
113
],
"type": "Negative_regulation"
} |
||
11571633.s0 | Phenylbutyrate attenuates the expression of Bcl-X(L), DNA-PK, caveolin-1, and VEGF in prostate cancer cells. | prostate | {
"name": "VEGF",
"pos": [
78,
81
]
} | {
"name": "prostate cancer",
"pos": [
86,
100
]
} | decreased | unidentifiable | {
"name": "expression",
"pos": [
30,
39
],
"type": "Gene_expression"
} | {
"name": "attenuates",
"pos": [
15,
24
],
"type": "Negative_regulation"
} |
||
15958562.s8 | These findings indicate that FoxM1 depletion causes cell death due to mitotic catastrophe and that inhibiting FoxM1 represents a therapeutic strategy to target breast cancer. | breast | {
"name": "FoxM1",
"pos": [
29,
33
]
} | {
"name": "breast cancer",
"pos": [
160,
172
]
} | decreased | cancerTOnormal | causality | unidentifiable | {
"name": "\nNone\n",
"pos": null,
"type": null
} | {
"name": "depletion",
"pos": [
35,
43
],
"type": "Negative_regulation"
} |
17616457.s3 | Long-term culture of MCF-7 cells in estrogen deprived medium (LTED) mimics aromatase inhibition in patients. | breast | {
"name": "aromatase",
"pos": [
75,
83
]
} | {
"name": "MCF-7",
"pos": [
21,
25
]
} | decreased | normalTOcancer | observation | unidentifiable | {
"name": "\nNone\n",
"pos": null,
"type": null
} | {
"name": "inhibition",
"pos": [
85,
94
],
"type": "Negative_regulation"
} |
20536410.s8 | The findings of the present study suggest that COX-2 overexpression in lobular and ductal breast cancers, which correlates with traditional clinico-pathological parameters, may be considered as a negative prognostic marker. | breast | {
"name": "COX-2",
"pos": [
47,
51
]
} | {
"name": "ductal breast cancers",
"pos": [
83,
103
]
} | increased | normalTOcancer | observation | unchanged | {
"name": "overexpression",
"pos": [
53,
66
],
"type": "Gene_expression"
} | {
"name": "overexpression",
"pos": [
53,
66
],
"type": "Positive_regulation"
} |
21400218.s2 | Its stimulation on breast cancer cell lines induces β1 integrin and promotes tumor invasiveness. | breast | {
"name": "β1 integrin",
"pos": [
52,
62
]
} | {
"name": "breast cancer",
"pos": [
19,
31
]
} | increased | normalTOcancer | observation | unidentifiable | {
"name": "\nNone\n",
"pos": null,
"type": null
} | {
"name": "induces",
"pos": [
44,
50
],
"type": "Positive_regulation"
} |
11544097.s0 | P1, a high mobility group-like protein is depressed in human breast adenocarcinoma. | breast | {
"name": "high mobility group-like protein",
"pos": [
6,
37
]
} | {
"name": "breast adenocarcinoma",
"pos": [
61,
81
]
} | decreased | normalTOcancer | observation | unchanged | {
"name": "\nNone\n",
"pos": null,
"type": null
} | {
"name": "depressed",
"pos": [
42,
50
],
"type": "Negative_regulation"
} |
18840527.s6 | We showed, for the first time, that knockdown of PDI in MCF-7 human breast cancer cells with RNA interference down-regulates ERalpha protein but up-regulates ERbeta protein, resulting in a drastic increase in ERbeta/ERalpha ratio, which is a crucial determinant of different cellular responses to estrogens. | breast | {
"name": "ERbeta protein",
"pos": [
158,
171
]
} | {
"name": "breast cancer",
"pos": [
68,
80
]
} | increased | unidentifiable | {
"name": "\nNone\n",
"pos": null,
"type": null
} | {
"name": "up-regulates",
"pos": [
145,
156
],
"type": "Positive_regulation"
} |
||
18655371.s4 | A higher increase of the expression and maximal pixel intensity of ICAM-1, VCAM-1 and P-selectin was observed in endothelial cells cocultured with c-erbB2-positive breast carcinoma cells as compared to endothelial cells cocultured with c-erbB2-negative cell line. | breast | {
"name": "ICAM-1",
"pos": [
67,
72
]
} | {
"name": "breast carcinoma",
"pos": [
164,
179
]
} | increased | unidentifiable | {
"name": "expression",
"pos": [
25,
34
],
"type": "Gene_expression"
} | {
"name": "increase",
"pos": [
9,
16
],
"type": "Positive_regulation"
} |
||
18713757.s7 | In addition, even a transient, siRNA-mediated p21 suppression in fibroblasts sufficiently stimulates MCF7 and MDA-MB-231 growth in vivo. | breast | {
"name": "p21",
"pos": [
46,
48
]
} | {
"name": "MDA-MB-231",
"pos": [
110,
119
]
} | decreased | normalTOcancer | causality | unidentifiable | {
"name": "\nNone\n",
"pos": null,
"type": null
} | {
"name": "suppression",
"pos": [
50,
60
],
"type": "Negative_regulation"
} |
8838861.s6 | The butyrate-induced apoptosis in MCF-7 cells was closely linked with the down-regulation of expression of Bcl-2 mRNA and Bcl-2 protein, a gene product known to be involved in the regulation of apoptosis in mammalian cells. | breast | {
"name": "Bcl-2 mRNA",
"pos": [
107,
116
]
} | {
"name": "MCF-7",
"pos": [
34,
38
]
} | decreased | cancerTOnormal | observation | unidentifiable | {
"name": "expression",
"pos": [
93,
102
],
"type": "Gene_expression"
} | {
"name": "down-regulation",
"pos": [
74,
88
],
"type": "Negative_regulation"
} |
8838861.s7 | The observed relationship between the down-regulation of Bcl-2 and induction of apoptosis was not causal because stable overexpression of Bcl-2 resulted in protection of MCF-7 cells from the cytotoxic morphological changes and growth-inhibitory effects of butyrate (15% growth inhibition compared to 60% growth inhibition in the parental cells). | breast | {
"name": "Bcl-2",
"pos": [
57,
61
]
} | {
"name": "MCF-7",
"pos": [
170,
174
]
} | decreased | cancerTOnormal | observation | unidentifiable | {
"name": "\nNone\n",
"pos": null,
"type": null
} | {
"name": "down-regulation",
"pos": [
38,
52
],
"type": "Negative_regulation"
} |
21923922.s3 | The non-receptor PTK termed breast tumor kinase (Brk/PTK6) is overexpressed in approximately 86% of human breast tumors. | breast | {
"name": "Brk/PTK6",
"pos": [
49,
56
]
} | {
"name": "breast tumors",
"pos": [
106,
118
]
} | increased | normalTOcancer | observation | unchanged | {
"name": "overexpressed",
"pos": [
62,
74
],
"type": "Gene_expression"
} | {
"name": "overexpressed",
"pos": [
62,
74
],
"type": "Positive_regulation"
} |
21923922.s11 | Brk-dependent signaling to p38 MAPK was recapitulated by Brk overexpression in the HC11 murine mammary epithelial cell (MEC) line and human MEC, while Brk knock-down in breast cancer cells blocked EGF-stimulated p38 signaling. | breast | {
"name": "Brk",
"pos": [
57,
59
]
} | {
"name": "breast cancer",
"pos": [
169,
181
]
} | increased | unidentifiable | {
"name": "overexpression",
"pos": [
61,
74
],
"type": "Gene_expression"
} | {
"name": "overexpression",
"pos": [
61,
74
],
"type": "Positive_regulation"
} |
||
19995430.s13 | We conclude that 13q34 amplification may be of relevance in tumor progression of basal-like breast cancers by inducing overexpression of CUL4A and TFDP1, which are both important in cell cycle regulation. | breast | {
"name": "CUL4A",
"pos": [
137,
141
]
} | {
"name": "breast cancers",
"pos": [
92,
105
]
} | increased | normalTOcancer | causality | unchanged | {
"name": "overexpression",
"pos": [
119,
132
],
"type": "Gene_expression"
} | {
"name": "inducing",
"pos": [
110,
117
],
"type": "Positive_regulation"
} |
20217214.s6 |
Intercellular adhesion molecule 1 (ICAM-1) was down-regulated in MCF10A cells using short hairpin RNA. | breast | {
"name": "Intercellular adhesion molecule 1 (ICAM-1)",
"pos": [
0,
41
]
} | {
"name": "MCF10A",
"pos": [
65,
70
]
} | decreased | unidentifiable | {
"name": "\nNone\n",
"pos": null,
"type": null
} | {
"name": "down-regulated",
"pos": [
47,
60
],
"type": "Negative_regulation"
} |
||
20217214.s11 | The down-regulation of ICAM-1 by short hairpin RNA in MCF10A cells led to the induction of psoriasin, calgranulin-A, calgranulin-B, and MUC1, and we demonstrated that these up-regulations were not ROS dependent. | breast | {
"name": "calgranulin-A",
"pos": [
102,
114
]
} | {
"name": "MCF10A",
"pos": [
54,
59
]
} | increased | unidentifiable | {
"name": "\nNone\n",
"pos": null,
"type": null
} | {
"name": "induction",
"pos": [
78,
86
],
"type": "Positive_regulation"
} |
||
20217214.s11 | The down-regulation of ICAM-1 by short hairpin RNA in MCF10A cells led to the induction of psoriasin, calgranulin-A, calgranulin-B, and MUC1, and we demonstrated that these up-regulations were not ROS dependent. | breast | {
"name": "ICAM-1",
"pos": [
23,
28
]
} | {
"name": "MCF10A",
"pos": [
54,
59
]
} | decreased | unidentifiable | {
"name": "\nNone\n",
"pos": null,
"type": null
} | {
"name": "down-regulation",
"pos": [
4,
18
],
"type": "Negative_regulation"
} |
||
20217214.s14 | Our findings suggest that the down-regulation of ICAM-1 in mammary epithelial cells may contribute both to the high expression of psoriasin seen in some high-grade DCIS tumors and to the induction of MUC1. | breast | {
"name": "MUC1",
"pos": [
200,
203
]
} | {
"name": "DCIS",
"pos": [
164,
167
]
} | increased | unidentifiable | {
"name": "\nNone\n",
"pos": null,
"type": null
} | {
"name": "induction",
"pos": [
187,
195
],
"type": "Positive_regulation"
} |
||
20217214.s14 | Our findings suggest that the down-regulation of ICAM-1 in mammary epithelial cells may contribute both to the high expression of psoriasin seen in some high-grade DCIS tumors and to the induction of MUC1. | breast | {
"name": "ICAM-1",
"pos": [
49,
54
]
} | {
"name": "DCIS",
"pos": [
164,
167
]
} | decreased | unidentifiable | {
"name": "\nNone\n",
"pos": null,
"type": null
} | {
"name": "down-regulation",
"pos": [
30,
44
],
"type": "Negative_regulation"
} |
||
22228571.s10 | RT-PCR and Western blot showed that the expressions of only c-Met and STAT3 decreased obviously in colon and breast cancer cells exposed to LS-7. | breast | {
"name": "STAT3",
"pos": [
70,
74
]
} | {
"name": "breast cancer",
"pos": [
109,
121
]
} | decreased | unidentifiable | {
"name": "expressions",
"pos": [
40,
50
],
"type": "Gene_expression"
} | {
"name": "decreased",
"pos": [
76,
84
],
"type": "Negative_regulation"
} |
||
17986353.s8 | These compounds decreased ERalpha in MCF-7 cells at both mRNA and protein levels, and suppressed estrogen-stimulated genes. | breast | {
"name": "ERalpha",
"pos": [
26,
32
]
} | {
"name": "MCF-7",
"pos": [
37,
41
]
} | decreased | unidentifiable | {
"name": "\nNone\n",
"pos": null,
"type": null
} | {
"name": "decreased",
"pos": [
16,
24
],
"type": "Negative_regulation"
} |
||
11689445.s3 | Oestradiol acutely increases PI3-kinase and Akt activities in MCF-7 cells. | breast | {
"name": "Akt",
"pos": [
44,
46
]
} | {
"name": "MCF-7",
"pos": [
62,
66
]
} | increased | unidentifiable | {
"name": "\nNone\n",
"pos": null,
"type": null
} | {
"name": "increases",
"pos": [
19,
27
],
"type": "Positive_regulation"
} |
||
11689445.s5 | The Src inhibitor, PP1, prevents hormone stimulation of Akt and PI3-kinase activities in MCF-7 cells. | breast | {
"name": "Akt",
"pos": [
56,
58
]
} | {
"name": "MCF-7",
"pos": [
89,
93
]
} | increased | unidentifiable | {
"name": "\nNone\n",
"pos": null,
"type": null
} | {
"name": "stimulation",
"pos": [
41,
51
],
"type": "Positive_regulation"
} |
||
11689445.s6 | In turn, stimulation of Src activity is abolished in ERalpha-expressing NIH 3T3 fibroblasts by co-transfection of the dominant-negative p85alpha and in MCF-7 cells by the PI3-kinase inhibitor, LY294002. | breast | {
"name": "dominant-negative p85alpha",
"pos": [
118,
143
]
} | {
"name": "MCF-7",
"pos": [
152,
156
]
} | increased | unidentifiable | {
"name": "co-transfection",
"pos": [
95,
109
],
"type": "Gene_expression"
} | {
"name": "co-transfection",
"pos": [
95,
109
],
"type": "Positive_regulation"
} |
||
10602481.s7 | Our findings suggest loss of E-cadherin expression in some breast cancers may be due to dominant repression of the trans-acting pathways that regulate E-cadherin transcription. | breast | {
"name": "E-cadherin",
"pos": [
29,
38
]
} | {
"name": "breast cancers",
"pos": [
59,
72
]
} | decreased | normalTOcancer | observation | unchanged | {
"name": "expression",
"pos": [
40,
49
],
"type": "Gene_expression"
} | {
"name": "loss",
"pos": [
21,
24
],
"type": "Negative_regulation"
} |
9815853.s0 | Heregulin and agonistic anti-p185(c-erbB2) antibodies inhibit proliferation but increase invasiveness of breast cancer cells that overexpress p185(c-erbB2): increased invasiveness may contribute to poor prognosis. | breast | {
"name": "p185",
"pos": [
142,
145
]
} | {
"name": "breast cancer",
"pos": [
105,
117
]
} | increased | normalTOcancer | observation | unchanged | {
"name": "overexpress",
"pos": [
130,
140
],
"type": "Gene_expression"
} | {
"name": "overexpress",
"pos": [
130,
140
],
"type": "Positive_regulation"
} |
12942541.s0 | PKC-zeta is required for angiotensin II-induced activation of ERK and synthesis of C-FOS in MCF-7 cells. | breast | {
"name": "ERK",
"pos": [
62,
64
]
} | {
"name": "MCF-7",
"pos": [
92,
96
]
} | increased | unidentifiable | {
"name": "\nNone\n",
"pos": null,
"type": null
} | {
"name": "activation",
"pos": [
48,
57
],
"type": "Positive_regulation"
} |
||
12942541.s6 | When the epidermal growth factor-receptor (EGFR) tyrosine kinase activity was inhibited by the use of its inhibitor AG1478, Ang II was still able to induce ERK1/2 phosphorylation and c-fos expression, therefore proving that the transactivation of EGFR was not required for these Ang II effects in MCF-7 cells. | breast | {
"name": "epidermal growth factor-receptor",
"pos": [
9,
40
]
} | {
"name": "MCF-7",
"pos": [
297,
301
]
} | decreased | unidentifiable | {
"name": "\nNone\n",
"pos": null,
"type": null
} | {
"name": "inhibited",
"pos": [
78,
86
],
"type": "Negative_regulation"
} |
||
12942541.s6 | When the epidermal growth factor-receptor (EGFR) tyrosine kinase activity was inhibited by the use of its inhibitor AG1478, Ang II was still able to induce ERK1/2 phosphorylation and c-fos expression, therefore proving that the transactivation of EGFR was not required for these Ang II effects in MCF-7 cells. | breast | {
"name": "c-fos",
"pos": [
183,
187
]
} | {
"name": "MCF-7",
"pos": [
297,
301
]
} | increased | unidentifiable | {
"name": "\nNone\n",
"pos": null,
"type": null
} | {
"name": "induce",
"pos": [
149,
154
],
"type": "Positive_regulation"
} |
||
12942541.s8 | Our results suggest that in MCF-7 cells Ang II activates multiple signalling pathways involving PKC-zeta, PI3K and MAPK; of these pathways only PKC-zeta appears responsible for the induction of c-fos. | breast | {
"name": "c-fos",
"pos": [
194,
198
]
} | {
"name": "MCF-7",
"pos": [
28,
32
]
} | increased | unidentifiable | {
"name": "\nNone\n",
"pos": null,
"type": null
} | {
"name": "induction",
"pos": [
181,
189
],
"type": "Positive_regulation"
} |
||
15868442.s7 | In the former group, ErbB2 overexpression was strongly associated with increased risk of recurrence (RR = 4.7; 95% CI, 2.1-10.4) and breast cancer death (RR = 5.4; 95% CI, 2.3-12.6). | breast | {
"name": "ErbB2",
"pos": [
21,
25
]
} | {
"name": "breast cancer",
"pos": [
133,
145
]
} | increased | normalTOcancer | observation | unchanged | {
"name": "overexpression",
"pos": [
27,
40
],
"type": "Gene_expression"
} | {
"name": "overexpression",
"pos": [
27,
40
],
"type": "Positive_regulation"
} |
16136053.s9 | Transfecting A2780 cells with active Notch 1-IC resulted in a proliferative and colony formation advantage compared to mock transfected cells. | ovarian | {
"name": "Notch 1-IC",
"pos": [
37,
46
]
} | {
"name": "A2780",
"pos": [
13,
17
]
} | increased | normalTOcancer | causality | unidentifiable | {
"name": "Transfecting",
"pos": [
0,
11
],
"type": "Gene_expression"
} | {
"name": "Transfecting",
"pos": [
0,
11
],
"type": "Positive_regulation"
} |
12149147.s6 | Immunoblotting analysis demonstrated that PRB protein expression was markedly up-regulated in OVCAR-3, whereas the PRA and PRB isoforms both appeared to be increased in NOV-31. | ovarian | {
"name": "PRB protein",
"pos": [
42,
52
]
} | {
"name": "OVCAR-3",
"pos": [
94,
100
]
} | increased | normalTOcancer | observation | unchanged | {
"name": "expression",
"pos": [
54,
63
],
"type": "Gene_expression"
} | {
"name": "up-regulated",
"pos": [
78,
89
],
"type": "Positive_regulation"
} |
12149147.s7 | These results suggest that down-regulation of PRA is associated with the development of ovarian epithelial carcinoma. | ovarian | {
"name": "PRA",
"pos": [
46,
48
]
} | {
"name": "ovarian epithelial carcinoma",
"pos": [
88,
115
]
} | decreased | normalTOcancer | observation | unidentifiable | {
"name": "\nNone\n",
"pos": null,
"type": null
} | {
"name": "down-regulation",
"pos": [
27,
41
],
"type": "Negative_regulation"
} |
10728592.s8 | Up-regulation of AR by 1,25(OH)2D3 and of VDR by DHT provides evidence of cross-talk between 2 signaling pathways in OVCAR-3 cells. | ovarian | {
"name": "VDR",
"pos": [
42,
44
]
} | {
"name": "OVCAR-3",
"pos": [
117,
123
]
} | increased | unidentifiable | {
"name": "\nNone\n",
"pos": null,
"type": null
} | {
"name": "Up-regulation",
"pos": [
0,
12
],
"type": "Positive_regulation"
} |
||
9815853.s1 | Overexpression of p185(c-erbB2) (p185/NEU/HER2) by tumor cells is associated with a poor prognosis in many but not all studies of breast and ovarian cancer. | ovarian | {
"name": "p185/NEU/HER2",
"pos": [
33,
45
]
} | {
"name": "ovarian cancer",
"pos": [
141,
154
]
} | increased | normalTOcancer | observation | unchanged | {
"name": "Overexpression",
"pos": [
0,
13
],
"type": "Gene_expression"
} | {
"name": "Overexpression",
"pos": [
0,
13
],
"type": "Positive_regulation"
} |
9815853.s13 | Moreover, the poor prognosis of breast and ovarian cancers that overexpress p185(c-erbB2) could relate in part to enhanced invasiveness rather than to increased proliferative capacity. | ovarian | {
"name": "p185",
"pos": [
76,
79
]
} | {
"name": "ovarian cancers",
"pos": [
43,
57
]
} | increased | normalTOcancer | observation | unchanged | {
"name": "overexpress",
"pos": [
64,
74
],
"type": "Gene_expression"
} | {
"name": "overexpress",
"pos": [
64,
74
],
"type": "Positive_regulation"
} |
15528975.s8 | Evaluation of differential gene expression in drug-sensitive (A2780) and drug-resistant (A2780cp) ovarian carcinoma cell lines exposed to 0.1 microg/ml HMN-176 up to 48 h using cDNA microarrays with 1,154 known human genes revealed significant drug effects on tumor associated genes, including upregulation of tissue inhibitor matrix metalloproteinases gene (TIMP) in both cell lines, suggesting that HMN-176 could potentially overcome tumor drug resistance. | ovarian | {
"name": "TIMP",
"pos": [
359,
362
]
} | {
"name": "ovarian carcinoma",
"pos": [
98,
114
]
} | increased | unidentifiable | {
"name": "\nNone\n",
"pos": null,
"type": null
} | {
"name": "upregulation",
"pos": [
294,
305
],
"type": "Positive_regulation"
} |
||
15162825.s9 | This study showed that IL-18 serum levels were elevated in ovarian cancer patients and were correlated with overall survival, although they were shown not to be an independent prognostic factor. | ovarian | {
"name": "IL-18",
"pos": [
23,
27
]
} | {
"name": "ovarian cancer",
"pos": [
59,
72
]
} | increased | normalTOcancer | observation | unchanged | {
"name": "\nNone\n",
"pos": null,
"type": null
} | {
"name": "elevated",
"pos": [
47,
54
],
"type": "Positive_regulation"
} |
18497984.s3 | Overexpression of TUBB3 protein was observed in 56 (85%) of the 66 ovarian cancers, and was significantly associated with aggressive tumor behavior (advanced stage, presence of ascites, suboptimal cytoreduction at surgery and presence of lymph node metastasis) (P<0.05). | ovarian | {
"name": "TUBB3 protein",
"pos": [
18,
30
]
} | {
"name": "ovarian cancers",
"pos": [
67,
81
]
} | increased | normalTOcancer | observation | unchanged | {
"name": "Overexpression",
"pos": [
0,
13
],
"type": "Gene_expression"
} | {
"name": "Overexpression",
"pos": [
0,
13
],
"type": "Positive_regulation"
} |