pmid stringlengths 8 12 | sentence stringlengths 59 1.08k | cancer_type stringclasses 3
values | gene dict | cancer dict | CGE stringclasses 2
values | CCS stringclasses 3
values | PT stringclasses 3
values | IGE stringclasses 4
values | expression_change_keyword_1 dict | expression_change_keyword_2 dict |
|---|---|---|---|---|---|---|---|---|---|---|
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 pat... | 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 transp... | 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 transp... | 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 inhibitio... | 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 inh... | 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"
} |
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