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dict | cancer
dict | CGE
stringclasses 2
values | CCS
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stringclasses 3
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stringclasses 4
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dict | expression_change_keyword_2
dict |
|---|---|---|---|---|---|---|---|---|---|---|
14971644.s0 | Arsenite induces HIF-1alpha and VEGF through PI3K, Akt and reactive oxygen species in DU145 human prostate carcinoma cells. | prostate | {
"name": "Akt",
"pos": [
51,
53
]
} | {
"name": "prostate carcinoma",
"pos": [
98,
115
]
} | increased | unidentifiable | {
"name": "\nNone\n",
"pos": null,
"type": null
} | {
"name": "induces",
"pos": [
9,
15
],
"type": "Positive_regulation"
} |
||
14971644.s5 | Here we demonstrate that arsenite induces the expression of HIF-1alpha but not HIF-1beta subunit in DU145 human prostate carcinoma cells. | prostate | {
"name": "HIF-1alpha",
"pos": [
60,
69
]
} | {
"name": "prostate carcinoma",
"pos": [
112,
129
]
} | increased | unidentifiable | {
"name": "expression",
"pos": [
46,
55
],
"type": "Gene_expression"
} | {
"name": "induces",
"pos": [
34,
40
],
"type": "Positive_regulation"
} |
||
14971644.s5 | Here we demonstrate that arsenite induces the expression of HIF-1alpha but not HIF-1beta subunit in DU145 human prostate carcinoma cells. | prostate | {
"name": "HIF-1beta subunit",
"pos": [
79,
95
]
} | {
"name": "prostate carcinoma",
"pos": [
112,
129
]
} | increased | unidentifiable | {
"name": "expression",
"pos": [
46,
55
],
"type": "Gene_expression"
} | {
"name": "induces",
"pos": [
34,
40
],
"type": "Positive_regulation"
} |
||
10428464.s0 | The differentiation-related gene 1, Drg1, is markedly upregulated by androgens in LNCaP prostatic adenocarcinoma cells. | prostate | {
"name": "Drg1",
"pos": [
36,
39
]
} | {
"name": "prostatic adenocarcinoma",
"pos": [
88,
111
]
} | increased | normalTOcancer | observation | unidentifiable | {
"name": "\nNone\n",
"pos": null,
"type": null
} | {
"name": "upregulated",
"pos": [
54,
64
],
"type": "Positive_regulation"
} |
1978301.s1 | Basal levels and adrenocorticotropic hormone (ACTH)-induced increments (delta-values) of serum cortisol, dehydroepiandrosterone (DHA), dehydroepiandrosterone sulfate (DHAS), 4-androstene-3, 17-dione (A4), and 17-hydroxyprogesterone (170HP); basal testosterone (T), luteinizing hormone (LH), serum ASAT, gamma-GT, and albumin were measured in prostatic cancer patients before and after 6 months of treatment with LH-RH-agonist, with flutamide, and with LH-RH-agonist + flutamide, respectively. | prostate | {
"name": "luteinizing hormone",
"pos": [
265,
283
]
} | {
"name": "prostatic cancer",
"pos": [
342,
357
]
} | increased | unidentifiable | {
"name": "levels",
"pos": [
6,
11
],
"type": "Gene_expression"
} | {
"name": "increments",
"pos": [
60,
69
],
"type": "Positive_regulation"
} |
||
1978301.s1 | Basal levels and adrenocorticotropic hormone (ACTH)-induced increments (delta-values) of serum cortisol, dehydroepiandrosterone (DHA), dehydroepiandrosterone sulfate (DHAS), 4-androstene-3, 17-dione (A4), and 17-hydroxyprogesterone (170HP); basal testosterone (T), luteinizing hormone (LH), serum ASAT, gamma-GT, and albumin were measured in prostatic cancer patients before and after 6 months of treatment with LH-RH-agonist, with flutamide, and with LH-RH-agonist + flutamide, respectively. | prostate | {
"name": "ACTH",
"pos": [
46,
49
]
} | {
"name": "prostatic cancer",
"pos": [
342,
357
]
} | increased | unidentifiable | {
"name": "\nNone\n",
"pos": null,
"type": null
} | {
"name": "increments",
"pos": [
60,
69
],
"type": "Positive_regulation"
} |
||
1978301.s1 | Basal levels and adrenocorticotropic hormone (ACTH)-induced increments (delta-values) of serum cortisol, dehydroepiandrosterone (DHA), dehydroepiandrosterone sulfate (DHAS), 4-androstene-3, 17-dione (A4), and 17-hydroxyprogesterone (170HP); basal testosterone (T), luteinizing hormone (LH), serum ASAT, gamma-GT, and albumin were measured in prostatic cancer patients before and after 6 months of treatment with LH-RH-agonist, with flutamide, and with LH-RH-agonist + flutamide, respectively. | prostate | {
"name": "adrenocorticotropic hormone",
"pos": [
17,
43
]
} | {
"name": "prostatic cancer",
"pos": [
342,
357
]
} | increased | unidentifiable | {
"name": "\nNone\n",
"pos": null,
"type": null
} | {
"name": "increments",
"pos": [
60,
69
],
"type": "Positive_regulation"
} |
||
19706771.s3 | The most prominent of these progressive changes is the up-regulation of AR that occurs in >90% of prostate cancers. | prostate | {
"name": "AR",
"pos": [
72,
73
]
} | {
"name": "of prostate canc",
"pos": [
98,
113
]
} | increased | normalTOcancer | observation | unidentifiable | {
"name": "\nNone\n",
"pos": null,
"type": null
} | {
"name": "up-regulation",
"pos": [
55,
67
],
"type": "Positive_regulation"
} |
19706771.s8 | These events result in increased accumulation of AR and thus enhanced growth of prostate cancer cells at low levels of androgen. | prostate | {
"name": "AR",
"pos": [
49,
50
]
} | {
"name": "prostate cancer",
"pos": [
80,
94
]
} | increased | normalTOcancer | causality | unidentifiable | {
"name": "\nNone\n",
"pos": null,
"type": null
} | {
"name": "accumulation",
"pos": [
33,
44
],
"type": "Positive_regulation"
} |
21791629.s1 | About 50% of prostate cancers have TMPRSS2-ERG fusions with concurrent ERG overexpression. | prostate | {
"name": "ERG",
"pos": [
71,
73
]
} | {
"name": "prostate cancers",
"pos": [
13,
28
]
} | increased | normalTOcancer | observation | unchanged | {
"name": "overexpression",
"pos": [
75,
88
],
"type": "Gene_expression"
} | {
"name": "overexpression",
"pos": [
75,
88
],
"type": "Positive_regulation"
} |
12359757.s0 | Inhibition of ligand-mediated HER2 activation in androgen-independent prostate cancer. | prostate | {
"name": "HER2",
"pos": [
30,
33
]
} | {
"name": "androgen-independent prostate cancer",
"pos": [
49,
84
]
} | increased | unidentifiable | {
"name": "\nNone\n",
"pos": null,
"type": null
} | {
"name": "activation",
"pos": [
35,
44
],
"type": "Positive_regulation"
} |
||
7686495.s10 | In both PC-3 and PC-3U cells, TGF-beta 1 was found to stimulate the induction of fibronectin and plasminogen activator inhibitor-1 and the expression of junB mRNA, and PMA did not affect these responses. | prostate | {
"name": "junB mRNA",
"pos": [
153,
161
]
} | {
"name": "PC-3",
"pos": [
8,
11
]
} | increased | unidentifiable | {
"name": "expression",
"pos": [
139,
148
],
"type": "Gene_expression"
} | {
"name": "stimulate",
"pos": [
54,
62
],
"type": "Positive_regulation"
} |
||
7686495.s10 | In both PC-3 and PC-3U cells, TGF-beta 1 was found to stimulate the induction of fibronectin and plasminogen activator inhibitor-1 and the expression of junB mRNA, and PMA did not affect these responses. | prostate | {
"name": "plasminogen activator inhibitor-1",
"pos": [
97,
129
]
} | {
"name": "PC-3",
"pos": [
8,
11
]
} | increased | unidentifiable | {
"name": "\nNone\n",
"pos": null,
"type": null
} | {
"name": "induction",
"pos": [
68,
76
],
"type": "Positive_regulation"
} |
||
7686495.s10 | In both PC-3 and PC-3U cells, TGF-beta 1 was found to stimulate the induction of fibronectin and plasminogen activator inhibitor-1 and the expression of junB mRNA, and PMA did not affect these responses. | prostate | {
"name": "fibronectin",
"pos": [
81,
91
]
} | {
"name": "PC-3",
"pos": [
8,
11
]
} | increased | unidentifiable | {
"name": "\nNone\n",
"pos": null,
"type": null
} | {
"name": "induction",
"pos": [
68,
76
],
"type": "Positive_regulation"
} |
||
15947099.s12 | Similarly, activation of the AR by phosphorylated protein kinase B, Akt, has also been reported in prostate cancer. | prostate | {
"name": "AR",
"pos": [
29,
30
]
} | {
"name": "prostate cancer",
"pos": [
99,
113
]
} | increased | normalTOcancer | observation | unidentifiable | {
"name": "\nNone\n",
"pos": null,
"type": null
} | {
"name": "activation",
"pos": [
11,
20
],
"type": "Positive_regulation"
} |
15947099.s12 | Similarly, activation of the AR by phosphorylated protein kinase B, Akt, has also been reported in prostate cancer. | prostate | {
"name": "AR",
"pos": [
29,
30
]
} | {
"name": "prostate cancer",
"pos": [
99,
113
]
} | increased | normalTOcancer | observation | unidentifiable | {
"name": "\nNone\n",
"pos": null,
"type": null
} | {
"name": "activation",
"pos": [
11,
20
],
"type": "Positive_regulation"
} |
9582091.s0 | Overexpression of manganese superoxide dismutase in DU145 human prostate carcinoma cells has multiple effects on cell phenotype. | prostate | {
"name": "superoxide dismutase",
"pos": [
28,
47
]
} | {
"name": "prostate carcinoma",
"pos": [
64,
81
]
} | increased | unidentifiable | {
"name": "Overexpression",
"pos": [
0,
13
],
"type": "Gene_expression"
} | {
"name": "Overexpression",
"pos": [
0,
13
],
"type": "Positive_regulation"
} |
||
9582091.s3 | DU145 human prostate carcinoma cells were transfected with the cDNA for manganese superoxide dismutase (MnSOD), and two clones overexpressing MnSOD activity were subsequently characterized by comparison with parental and plasmid control-transfected cells. | prostate | {
"name": "MnSOD",
"pos": [
142,
146
]
} | {
"name": "prostate carcinoma",
"pos": [
12,
29
]
} | increased | unidentifiable | {
"name": "overexpressing",
"pos": [
127,
140
],
"type": "Gene_expression"
} | {
"name": "overexpressing",
"pos": [
127,
140
],
"type": "Positive_regulation"
} |
||
9582091.s9 | Our results suggest novel mechanisms by which MnSOD overexpression may modulate the malignant phenotype, with potential applications in developing new therapies for prostate cancer. | prostate | {
"name": "MnSOD",
"pos": [
46,
50
]
} | {
"name": "prostate cancer",
"pos": [
165,
179
]
} | increased | unidentifiable | {
"name": "overexpression",
"pos": [
52,
65
],
"type": "Gene_expression"
} | {
"name": "overexpression",
"pos": [
52,
65
],
"type": "Positive_regulation"
} |
||
18490922.s5 | Overexpression of p45-sErbB3 in the osteolytic prostate cancer cell line PC-3 converted its phenotype from bone lysing to bone forming upon injection into the femurs of immunodeficient mice. | prostate | {
"name": "p45-sErbB3",
"pos": [
18,
27
]
} | {
"name": "prostate cancer",
"pos": [
47,
61
]
} | increased | unidentifiable | {
"name": "Overexpression",
"pos": [
0,
13
],
"type": "Gene_expression"
} | {
"name": "Overexpression",
"pos": [
0,
13
],
"type": "Positive_regulation"
} |
||
7511267.s3 | Accumulation of p53 protein in the absence of detectable mutant p53 was recognized more often in prostate cancer than in any other tumor examined. | prostate | {
"name": "p53 protein",
"pos": [
16,
26
]
} | {
"name": "prostate cancer",
"pos": [
97,
111
]
} | increased | unidentifiable | {
"name": "\nNone\n",
"pos": null,
"type": null
} | {
"name": "Accumulation",
"pos": [
0,
11
],
"type": "Positive_regulation"
} |
||
22116304.s0 | L-mimosine blocks cell proliferation via upregulation of B-cell translocation gene 2 and N-myc downstream regulated gene 1 in prostate carcinoma cells. | prostate | {
"name": "N-myc downstream regulated gene 1",
"pos": [
89,
121
]
} | {
"name": "prostate carcinoma",
"pos": [
126,
143
]
} | increased | cancerTOnormal | causality | unidentifiable | {
"name": "\nNone\n",
"pos": null,
"type": null
} | {
"name": "upregulation",
"pos": [
41,
52
],
"type": "Positive_regulation"
} |
22116304.s0 | L-mimosine blocks cell proliferation via upregulation of B-cell translocation gene 2 and N-myc downstream regulated gene 1 in prostate carcinoma cells. | prostate | {
"name": "B-cell translocation gene 2",
"pos": [
57,
83
]
} | {
"name": "prostate carcinoma",
"pos": [
126,
143
]
} | increased | cancerTOnormal | causality | unidentifiable | {
"name": "\nNone\n",
"pos": null,
"type": null
} | {
"name": "upregulation",
"pos": [
41,
52
],
"type": "Positive_regulation"
} |
22116304.s7 | Immunoblot assays indicated that hypoxia and L-mimosine stabilized hypoxia-inducible factor-1 α (HIF-1α) and induced Btg2 and Ndrg1 protein expression, but downregulated protein levels of cyclin A in both PC-3 and LNCaP cells. | prostate | {
"name": "Ndrg1 protein",
"pos": [
126,
138
]
} | {
"name": "LNCaP",
"pos": [
214,
218
]
} | increased | unidentifiable | {
"name": "expression",
"pos": [
140,
149
],
"type": "Gene_expression"
} | {
"name": "induced",
"pos": [
109,
115
],
"type": "Positive_regulation"
} |
||
22116304.s7 | Immunoblot assays indicated that hypoxia and L-mimosine stabilized hypoxia-inducible factor-1 α (HIF-1α) and induced Btg2 and Ndrg1 protein expression, but downregulated protein levels of cyclin A in both PC-3 and LNCaP cells. | prostate | {
"name": "Btg2",
"pos": [
117,
120
]
} | {
"name": "LNCaP",
"pos": [
214,
218
]
} | increased | unidentifiable | {
"name": "expression",
"pos": [
140,
149
],
"type": "Gene_expression"
} | {
"name": "induced",
"pos": [
109,
115
],
"type": "Positive_regulation"
} |
||
22116304.s7 | Immunoblot assays indicated that hypoxia and L-mimosine stabilized hypoxia-inducible factor-1 α (HIF-1α) and induced Btg2 and Ndrg1 protein expression, but downregulated protein levels of cyclin A in both PC-3 and LNCaP cells. | prostate | {
"name": "Btg2",
"pos": [
117,
120
]
} | {
"name": "LNCaP",
"pos": [
214,
218
]
} | increased | unidentifiable | {
"name": "\nNone\n",
"pos": null,
"type": null
} | {
"name": "induced",
"pos": [
109,
115
],
"type": "Positive_regulation"
} |
||
22116304.s8 | L-mimosine treatment decreased cyclin D1 protein in PC-3 cells, but not in LNCaP cells. | prostate | {
"name": "cyclin D1",
"pos": [
31,
39
]
} | {
"name": "LNCaP",
"pos": [
75,
79
]
} | decreased | unidentifiable | {
"name": "\nNone\n",
"pos": null,
"type": null
} | {
"name": "decreased",
"pos": [
21,
29
],
"type": "Negative_regulation"
} |
||
22116304.s9 | Dimethyloxalylglycine, a pan-prolyl hydroxylase inhibitor, also induced Btg2 and Ndrg1 protein expression in LNCaP cells. | prostate | {
"name": "Btg2",
"pos": [
72,
75
]
} | {
"name": "LNCaP",
"pos": [
109,
113
]
} | increased | unidentifiable | {
"name": "expression",
"pos": [
95,
104
],
"type": "Gene_expression"
} | {
"name": "induced",
"pos": [
64,
70
],
"type": "Positive_regulation"
} |
||
22116304.s9 | Dimethyloxalylglycine, a pan-prolyl hydroxylase inhibitor, also induced Btg2 and Ndrg1 protein expression in LNCaP cells. | prostate | {
"name": "Ndrg1 protein",
"pos": [
81,
93
]
} | {
"name": "LNCaP",
"pos": [
109,
113
]
} | increased | unidentifiable | {
"name": "expression",
"pos": [
95,
104
],
"type": "Gene_expression"
} | {
"name": "induced",
"pos": [
64,
70
],
"type": "Positive_regulation"
} |
||
22116304.s9 | Dimethyloxalylglycine, a pan-prolyl hydroxylase inhibitor, also induced Btg2 and Ndrg1 protein expression in LNCaP cells. | prostate | {
"name": "Btg2",
"pos": [
72,
75
]
} | {
"name": "LNCaP",
"pos": [
109,
113
]
} | increased | unidentifiable | {
"name": "\nNone\n",
"pos": null,
"type": null
} | {
"name": "induced",
"pos": [
64,
70
],
"type": "Positive_regulation"
} |
||
22116304.s11 | Knockdown of HIF-1α attenuated the increasing protein levels of both Btg2 and Ndrg1 by hypoxia or L-mimosine in LNCaP cells. | prostate | {
"name": "HIF-1α",
"pos": [
13,
18
]
} | {
"name": "LNCaP",
"pos": [
112,
116
]
} | decreased | unidentifiable | {
"name": "\nNone\n",
"pos": null,
"type": null
} | {
"name": "Knockdown",
"pos": [
0,
8
],
"type": "Negative_regulation"
} |
||
22116304.s11 | Knockdown of HIF-1α attenuated the increasing protein levels of both Btg2 and Ndrg1 by hypoxia or L-mimosine in LNCaP cells. | prostate | {
"name": "Btg2",
"pos": [
69,
72
]
} | {
"name": "LNCaP",
"pos": [
112,
116
]
} | increased | unidentifiable | {
"name": "\nNone\n",
"pos": null,
"type": null
} | {
"name": "increasing",
"pos": [
35,
44
],
"type": "Positive_regulation"
} |
||
22116304.s11 | Knockdown of HIF-1α attenuated the increasing protein levels of both Btg2 and Ndrg1 by hypoxia or L-mimosine in LNCaP cells. | prostate | {
"name": "Ndrg1",
"pos": [
78,
82
]
} | {
"name": "LNCaP",
"pos": [
112,
116
]
} | increased | unidentifiable | {
"name": "\nNone\n",
"pos": null,
"type": null
} | {
"name": "increasing",
"pos": [
35,
44
],
"type": "Positive_regulation"
} |
||
22116304.s13 | L-mimosine enhanced expression of Btg2 and Ndrg1, which attenuated cell proliferation of the PC-3 and LNCaP prostate carcinoma cells. | prostate | {
"name": "Ndrg1",
"pos": [
43,
47
]
} | {
"name": "prostate carcinoma",
"pos": [
108,
125
]
} | increased | cancerTOnormal | causality | unidentifiable | {
"name": "expression",
"pos": [
20,
29
],
"type": "Gene_expression"
} | {
"name": "enhanced",
"pos": [
11,
18
],
"type": "Positive_regulation"
} |
22116304.s13 | L-mimosine enhanced expression of Btg2 and Ndrg1, which attenuated cell proliferation of the PC-3 and LNCaP prostate carcinoma cells. | prostate | {
"name": "Btg2",
"pos": [
34,
37
]
} | {
"name": "prostate carcinoma",
"pos": [
108,
125
]
} | increased | cancerTOnormal | causality | unidentifiable | {
"name": "expression",
"pos": [
20,
29
],
"type": "Gene_expression"
} | {
"name": "enhanced",
"pos": [
11,
18
],
"type": "Positive_regulation"
} |
19633975.s7 | Further, treating specific inhibitors for PI3K (Wortmannin) or JNK (SP600125) to PC-3 cells could reduce the protein expressions of MMP-2 and MMP-9. | prostate | {
"name": "MMP-9",
"pos": [
142,
146
]
} | {
"name": "PC-3",
"pos": [
81,
84
]
} | decreased | unidentifiable | {
"name": "expressions",
"pos": [
117,
127
],
"type": "Gene_expression"
} | {
"name": "reduce",
"pos": [
98,
103
],
"type": "Negative_regulation"
} |
||
19633975.s7 | Further, treating specific inhibitors for PI3K (Wortmannin) or JNK (SP600125) to PC-3 cells could reduce the protein expressions of MMP-2 and MMP-9. | prostate | {
"name": "MMP-2",
"pos": [
132,
136
]
} | {
"name": "PC-3",
"pos": [
81,
84
]
} | decreased | unidentifiable | {
"name": "expressions",
"pos": [
117,
127
],
"type": "Gene_expression"
} | {
"name": "reduce",
"pos": [
98,
103
],
"type": "Negative_regulation"
} |
||
19633975.s8 | These results showed fisetin could inhibit the metastatic ability of PC-3 by reducing MMP-2 and MMP-9 expressions through suppressing phosphoinositide 3-kinase/Akt (PI3K/Akt) and JNK signaling pathways. | prostate | {
"name": "MMP-9",
"pos": [
96,
100
]
} | {
"name": "PC-3",
"pos": [
69,
72
]
} | decreased | cancerTOnormal | causality | unidentifiable | {
"name": "expressions",
"pos": [
102,
112
],
"type": "Gene_expression"
} | {
"name": "reducing",
"pos": [
77,
84
],
"type": "Negative_regulation"
} |
19633975.s8 | These results showed fisetin could inhibit the metastatic ability of PC-3 by reducing MMP-2 and MMP-9 expressions through suppressing phosphoinositide 3-kinase/Akt (PI3K/Akt) and JNK signaling pathways. | prostate | {
"name": "MMP-2",
"pos": [
86,
90
]
} | {
"name": "PC-3",
"pos": [
69,
72
]
} | decreased | cancerTOnormal | causality | unidentifiable | {
"name": "expressions",
"pos": [
102,
112
],
"type": "Gene_expression"
} | {
"name": "reducing",
"pos": [
77,
84
],
"type": "Negative_regulation"
} |
16316409.s1 | The expression of the p75 neurotrophin receptor (p75NTR) is diminished in epithelial cells during progression of prostate cancer in vivo and in vitro. | prostate | {
"name": "p75 neurotrophin receptor",
"pos": [
22,
46
]
} | {
"name": "prostate cancer",
"pos": [
113,
127
]
} | decreased | normalTOcancer | observation | unidentifiable | {
"name": "expression",
"pos": [
4,
13
],
"type": "Gene_expression"
} | {
"name": "diminished",
"pos": [
60,
69
],
"type": "Negative_regulation"
} |
16316409.s1 | The expression of the p75 neurotrophin receptor (p75NTR) is diminished in epithelial cells during progression of prostate cancer in vivo and in vitro. | prostate | {
"name": "p75NTR",
"pos": [
49,
54
]
} | {
"name": "prostate cancer",
"pos": [
113,
127
]
} | decreased | normalTOcancer | observation | unidentifiable | {
"name": "expression",
"pos": [
4,
13
],
"type": "Gene_expression"
} | {
"name": "diminished",
"pos": [
60,
69
],
"type": "Negative_regulation"
} |
16316409.s12 | Hence, re-expression of the p75NTR appears to partially reverse de-differentiation of prostate cancer cells by up-regulating the expression of CRABPI for localized sequestration of retinoids that are available to newly up-regulated RAR-beta, RXR-alpha, and RXR-beta. | prostate | {
"name": "RAR-beta",
"pos": [
232,
239
]
} | {
"name": "prostate cancer",
"pos": [
86,
100
]
} | increased | unidentifiable | {
"name": "\nNone\n",
"pos": null,
"type": null
} | {
"name": "up-regulated",
"pos": [
219,
230
],
"type": "Positive_regulation"
} |
||
16316409.s12 | Hence, re-expression of the p75NTR appears to partially reverse de-differentiation of prostate cancer cells by up-regulating the expression of CRABPI for localized sequestration of retinoids that are available to newly up-regulated RAR-beta, RXR-alpha, and RXR-beta. | prostate | {
"name": "CRABPI",
"pos": [
143,
148
]
} | {
"name": "prostate cancer",
"pos": [
86,
100
]
} | increased | cancerTOnormal | causality | unidentifiable | {
"name": "expression",
"pos": [
129,
138
],
"type": "Gene_expression"
} | {
"name": "up-regulating",
"pos": [
111,
123
],
"type": "Positive_regulation"
} |
19415690.s0 | Ubiquitous mitochondrial creatine kinase is overexpressed in the conditioned medium and the extract of LNCaP lineaged androgen independent cell lines and facilitates prostate cancer progression. | prostate | {
"name": "mitochondrial creatine kinase",
"pos": [
11,
39
]
} | {
"name": "prostate cancer",
"pos": [
166,
180
]
} | increased | normalTOcancer | causality | unchanged | {
"name": "overexpressed",
"pos": [
44,
56
],
"type": "Gene_expression"
} | {
"name": "overexpressed",
"pos": [
44,
56
],
"type": "Positive_regulation"
} |
19415690.s8 | uMtCK was up-regulated in AIPC cells and in human prostate cancer tissues at WHO grade III. | prostate | {
"name": "uMtCK",
"pos": [
0,
4
]
} | {
"name": "prostate cancer",
"pos": [
50,
64
]
} | increased | normalTOcancer | observation | unchanged | {
"name": "\nNone\n",
"pos": null,
"type": null
} | {
"name": "up-regulated",
"pos": [
10,
21
],
"type": "Positive_regulation"
} |
19415690.s12 | Exogenous uMtCK in LNCaP cells surprisingly contributed to overproduction of ROS, activation of Akt signaling pathway and more aggressive phenotypes including androgen independence development. | prostate | {
"name": "ROS",
"pos": [
77,
79
]
} | {
"name": "LNCaP",
"pos": [
19,
23
]
} | increased | normalTOcancer | observation | unidentifiable | {
"name": "overproduction",
"pos": [
59,
72
],
"type": "Gene_expression"
} | {
"name": "contributed",
"pos": [
44,
54
],
"type": "Positive_regulation"
} |
16049707.s0 | Quercetin-induced growth inhibition and cell death in prostatic carcinoma cells (PC-3) are associated with increase in p21 and hypophosphorylated retinoblastoma proteins expression. | prostate | {
"name": "p21",
"pos": [
119,
121
]
} | {
"name": "prostatic carcinoma",
"pos": [
54,
72
]
} | increased | cancerTOnormal | observation | unidentifiable | {
"name": "\nNone\n",
"pos": null,
"type": null
} | {
"name": "increase",
"pos": [
107,
114
],
"type": "Positive_regulation"
} |
16049707.s0 | Quercetin-induced growth inhibition and cell death in prostatic carcinoma cells (PC-3) are associated with increase in p21 and hypophosphorylated retinoblastoma proteins expression. | prostate | {
"name": "hypophosphorylated retinoblastoma proteins",
"pos": [
127,
168
]
} | {
"name": "prostatic carcinoma",
"pos": [
54,
72
]
} | increased | cancerTOnormal | observation | unidentifiable | {
"name": "expression",
"pos": [
170,
179
],
"type": "Gene_expression"
} | {
"name": "increase",
"pos": [
107,
114
],
"type": "Positive_regulation"
} |
16049707.s0 | Quercetin-induced growth inhibition and cell death in prostatic carcinoma cells (PC-3) are associated with increase in p21 and hypophosphorylated retinoblastoma proteins expression. | prostate | {
"name": "p21",
"pos": [
119,
121
]
} | {
"name": "prostatic carcinoma",
"pos": [
54,
72
]
} | increased | cancerTOnormal | observation | unidentifiable | {
"name": "expression",
"pos": [
170,
179
],
"type": "Gene_expression"
} | {
"name": "increase",
"pos": [
107,
114
],
"type": "Positive_regulation"
} |
16049707.s0 | Quercetin-induced growth inhibition and cell death in prostatic carcinoma cells (PC-3) are associated with increase in p21 and hypophosphorylated retinoblastoma proteins expression. | prostate | {
"name": "hypophosphorylated retinoblastoma proteins",
"pos": [
127,
168
]
} | {
"name": "prostatic carcinoma",
"pos": [
54,
72
]
} | increased | cancerTOnormal | observation | unidentifiable | {
"name": "\nNone\n",
"pos": null,
"type": null
} | {
"name": "increase",
"pos": [
107,
114
],
"type": "Positive_regulation"
} |
15790678.s5 | Androgen-sensitive LNCaP prostate cancer cells engineered to stably overexpress CDK6 display increased expression of the prostate-specific antigen and enhanced growth in the presence of dihydrotestosterone. | prostate | {
"name": "CDK6",
"pos": [
80,
83
]
} | {
"name": "prostate cancer",
"pos": [
25,
39
]
} | increased | normalTOcancer | causality | unidentifiable | {
"name": "overexpress",
"pos": [
68,
78
],
"type": "Gene_expression"
} | {
"name": "overexpress",
"pos": [
68,
78
],
"type": "Positive_regulation"
} |
14971642.s0 | Arsenite induces p70S6K1 activation and HIF-1alpha expression in prostate cancer cells. | prostate | {
"name": "HIF-1alpha",
"pos": [
40,
49
]
} | {
"name": "prostate cancer",
"pos": [
65,
79
]
} | increased | unidentifiable | {
"name": "expression",
"pos": [
51,
60
],
"type": "Gene_expression"
} | {
"name": "induces",
"pos": [
9,
15
],
"type": "Positive_regulation"
} |
||
14971642.s0 | Arsenite induces p70S6K1 activation and HIF-1alpha expression in prostate cancer cells. | prostate | {
"name": "p70S6K1",
"pos": [
17,
23
]
} | {
"name": "prostate cancer",
"pos": [
65,
79
]
} | increased | unidentifiable | {
"name": "\nNone\n",
"pos": null,
"type": null
} | {
"name": "activation",
"pos": [
25,
34
],
"type": "Positive_regulation"
} |
||
14971642.s7 | We have also shown that arsenite specifically induces HIF-1alpha, but not HIF-1beta, protein levels in prostate cancer cells in a mTOR-dependent manner. | prostate | {
"name": "HIF-1alpha",
"pos": [
54,
63
]
} | {
"name": "prostate cancer",
"pos": [
103,
117
]
} | increased | unidentifiable | {
"name": "\nNone\n",
"pos": null,
"type": null
} | {
"name": "induces",
"pos": [
46,
52
],
"type": "Positive_regulation"
} |
||
12771931.s0 | Quinazoline-based alpha 1-adrenoceptor antagonists induce prostate cancer cell apoptosis via TGF-beta signalling and I kappa B alpha induction. | prostate | {
"name": "I kappa B alpha",
"pos": [
117,
131
]
} | {
"name": "prostate cancer",
"pos": [
58,
72
]
} | increased | cancerTOnormal | causality | unidentifiable | {
"name": "\nNone\n",
"pos": null,
"type": null
} | {
"name": "induction",
"pos": [
133,
141
],
"type": "Positive_regulation"
} |
12771931.s4 | Treatment of the androgen-independent human prostate cancer cells PC-3 with doxazosin resulted in a strong caspase-3 activation within 24 h, whereas tamsulosin, a sulphonamide-based alpha 1-adrenoceptor antagonist, had no significant apoptotic effect against prostate cancer cells. | prostate | {
"name": "caspase-3",
"pos": [
107,
115
]
} | {
"name": "prostate cancer",
"pos": [
44,
58
]
} | increased | cancerTOnormal | observation | unidentifiable | {
"name": "\nNone\n",
"pos": null,
"type": null
} | {
"name": "activation",
"pos": [
117,
126
],
"type": "Positive_regulation"
} |
12771931.s11 | These findings suggest that the quinazoline-based doxazosin mediates prostate cancer apoptosis by initially inducing the expression of TGF-beta1 signalling effectors and subsequently I kappa B alpha. | prostate | {
"name": "TGF-beta1",
"pos": [
135,
143
]
} | {
"name": "prostate cancer",
"pos": [
69,
83
]
} | increased | cancerTOnormal | causality | unidentifiable | {
"name": "expression",
"pos": [
121,
130
],
"type": "Gene_expression"
} | {
"name": "inducing",
"pos": [
108,
115
],
"type": "Positive_regulation"
} |
19024511.s0 | [Overexpression of human tumor metastasis-related gene TMSG-1 suppresses cell proliferation and invasion of a highly metastatic prostate cancer cell line PC-3M-1E8 in vitro]. | prostate | {
"name": "human tumor metastasis-related gene TMSG-1",
"pos": [
19,
60
]
} | {
"name": "metastatic prostate cancer",
"pos": [
117,
142
]
} | increased | cancerTOnormal | causality | unidentifiable | {
"name": "[Overexpression",
"pos": [
0,
14
],
"type": "Gene_expression"
} | {
"name": "[Overexpression",
"pos": [
0,
14
],
"type": "Positive_regulation"
} |
17022003.s3 | The compound investigated is present in a herbal preparation extracted from Boswellia serrata oleo-gum-resin, it inhibits the growth of chemotherapy-resistant human PC-3 prostate cancer cells in vitro and induces apoptosis as shown by activation of caspase 3 and the induction of DNA fragmentation. | prostate | {
"name": "caspase 3",
"pos": [
249,
257
]
} | {
"name": "prostate cancer",
"pos": [
170,
184
]
} | increased | cancerTOnormal | causality | unidentifiable | {
"name": "\nNone\n",
"pos": null,
"type": null
} | {
"name": "activation",
"pos": [
235,
244
],
"type": "Positive_regulation"
} |
14607217.s6 | OC expression is elevated in prostate tumor cells and in prostate and bone stromal cells interdigitating with both localized and metastatic prostate epithelium. | prostate | {
"name": "OC",
"pos": [
0,
1
]
} | {
"name": "prostate tumor",
"pos": [
29,
42
]
} | increased | normalTOcancer | observation | unchanged | {
"name": "expression",
"pos": [
3,
12
],
"type": "Gene_expression"
} | {
"name": "elevated",
"pos": [
17,
24
],
"type": "Positive_regulation"
} |
20499410.s1 | After glioma pathogenesis-related protein 1 (GLIPR1/Glipr1) was identified, the expression of GLIPR1 was shown to be down-regulated in human prostate cancer, owing in part to methylation in the regulatory region of this gene in prostate cancer cells. | prostate | {
"name": "GLIPR1",
"pos": [
94,
99
]
} | {
"name": "prostate cancer",
"pos": [
141,
155
]
} | decreased | normalTOcancer | observation | unchanged | {
"name": "expression",
"pos": [
80,
89
],
"type": "Gene_expression"
} | {
"name": "down-regulated",
"pos": [
117,
130
],
"type": "Negative_regulation"
} |
15643450.s3 | Angiogenic cytokines such as vascular endothelial growth factor (VEGF) have been identified in prostate cancer cells and tumours, and androgens appear to stimulate VEGF. | prostate | {
"name": "VEGF",
"pos": [
164,
167
]
} | {
"name": "prostate cancer",
"pos": [
95,
109
]
} | increased | unidentifiable | {
"name": "\nNone\n",
"pos": null,
"type": null
} | {
"name": "stimulate",
"pos": [
154,
162
],
"type": "Positive_regulation"
} |
||
15720809.s0 | Overexpression of 12/15-lipoxygenase, an ortholog of human 15-lipoxygenase-1, in the prostate tumors of TRAMP mice. | prostate | {
"name": "12/15-lipoxygenase",
"pos": [
18,
35
]
} | {
"name": "prostate tumors",
"pos": [
85,
99
]
} | increased | normalTOcancer | observation | unchanged | {
"name": "Overexpression",
"pos": [
0,
13
],
"type": "Gene_expression"
} | {
"name": "Overexpression",
"pos": [
0,
13
],
"type": "Positive_regulation"
} |
16734726.s1 | Overexpression of the enhancer of zeste homolog 2 (EZH2) protein, a known repressor of gene transcription, has been reported to be associated with biological malignancy of prostate cancer and several other cancers. | prostate | {
"name": "EZH2",
"pos": [
51,
54
]
} | {
"name": "prostate cancer",
"pos": [
172,
186
]
} | increased | normalTOcancer | observation | unchanged | {
"name": "Overexpression",
"pos": [
0,
13
],
"type": "Gene_expression"
} | {
"name": "Overexpression",
"pos": [
0,
13
],
"type": "Positive_regulation"
} |
15982318.s2 | We critically review the recent advances in prostate cancer immunohistochemistry, including the introduction of newer basal cell markers such as p63 and the discovery of the overexpression of alpha-methylacyl coenzyme A racemase (AMACR) in prostate cancer. | prostate | {
"name": "alpha-methylacyl coenzyme A racemase",
"pos": [
192,
227
]
} | {
"name": "prostate cancer",
"pos": [
44,
58
]
} | increased | normalTOcancer | observation | unchanged | {
"name": "overexpression",
"pos": [
174,
187
],
"type": "Gene_expression"
} | {
"name": "overexpression",
"pos": [
174,
187
],
"type": "Positive_regulation"
} |
12507965.s2 | The proportion of PSA-ACT is increased in prostate cancer (PCa), but immunologic determination of PSA-ACT is hampered by a background produced by nonspecific adsorption of ACT to the solid phase. | prostate | {
"name": "PSA-ACT",
"pos": [
18,
24
]
} | {
"name": "prostate cancer",
"pos": [
42,
56
]
} | increased | normalTOcancer | observation | unchanged | {
"name": "\nNone\n",
"pos": null,
"type": null
} | {
"name": "increased",
"pos": [
29,
37
],
"type": "Positive_regulation"
} |
21099103.s3 | However, in this issue of the JCI, Sharma et al. show that RB1 loss is a late event in human prostate cancer that is coincident with the emergence of castrate-resistant metastatic disease. | prostate | {
"name": "RB1",
"pos": [
59,
61
]
} | {
"name": "prostate cancer",
"pos": [
93,
107
]
} | decreased | normalTOcancer | observation | unidentifiable | {
"name": "\nNone\n",
"pos": null,
"type": null
} | {
"name": "loss",
"pos": [
63,
66
],
"type": "Negative_regulation"
} |
14517586.s0 | Elevated serum chromogranin A precedes prostate-specific antigen elevation and predicts failure of androgen deprivation therapy in patients with advanced prostate cancer. | prostate | {
"name": "chromogranin A",
"pos": [
15,
28
]
} | {
"name": "prostate cancer",
"pos": [
154,
168
]
} | increased | unidentifiable | {
"name": "\nNone\n",
"pos": null,
"type": null
} | {
"name": "Elevated",
"pos": [
0,
7
],
"type": "Positive_regulation"
} |
||
18076023.s6 | The gene array revealed decreased expression of ADAMTS1, ephrin-A5, fibronectin 1, and neuropilin 1 in LNCaP-19 compared to LNCaP, while expression of midkine and VEGF were increased. | prostate | {
"name": "ephrin-A5",
"pos": [
57,
65
]
} | {
"name": "LNCaP",
"pos": [
124,
128
]
} | decreased | cancerTOnormal | observation | unidentifiable | {
"name": "expression",
"pos": [
34,
43
],
"type": "Gene_expression"
} | {
"name": "decreased",
"pos": [
24,
32
],
"type": "Negative_regulation"
} |
18076023.s6 | The gene array revealed decreased expression of ADAMTS1, ephrin-A5, fibronectin 1, and neuropilin 1 in LNCaP-19 compared to LNCaP, while expression of midkine and VEGF were increased. | prostate | {
"name": "fibronectin 1",
"pos": [
68,
80
]
} | {
"name": "LNCaP",
"pos": [
124,
128
]
} | decreased | cancerTOnormal | observation | unidentifiable | {
"name": "expression",
"pos": [
34,
43
],
"type": "Gene_expression"
} | {
"name": "decreased",
"pos": [
24,
32
],
"type": "Negative_regulation"
} |
18076023.s6 | The gene array revealed decreased expression of ADAMTS1, ephrin-A5, fibronectin 1, and neuropilin 1 in LNCaP-19 compared to LNCaP, while expression of midkine and VEGF were increased. | prostate | {
"name": "ADAMTS1",
"pos": [
48,
54
]
} | {
"name": "LNCaP",
"pos": [
124,
128
]
} | decreased | cancerTOnormal | observation | unidentifiable | {
"name": "expression",
"pos": [
34,
43
],
"type": "Gene_expression"
} | {
"name": "decreased",
"pos": [
24,
32
],
"type": "Negative_regulation"
} |
18076023.s6 | The gene array revealed decreased expression of ADAMTS1, ephrin-A5, fibronectin 1, and neuropilin 1 in LNCaP-19 compared to LNCaP, while expression of midkine and VEGF were increased. | prostate | {
"name": "VEGF",
"pos": [
163,
166
]
} | {
"name": "LNCaP",
"pos": [
124,
128
]
} | increased | cancerTOnormal | observation | unidentifiable | {
"name": "expression",
"pos": [
137,
146
],
"type": "Gene_expression"
} | {
"name": "increased",
"pos": [
173,
181
],
"type": "Positive_regulation"
} |
18076023.s6 | The gene array revealed decreased expression of ADAMTS1, ephrin-A5, fibronectin 1, and neuropilin 1 in LNCaP-19 compared to LNCaP, while expression of midkine and VEGF were increased. | prostate | {
"name": "neuropilin 1",
"pos": [
87,
98
]
} | {
"name": "LNCaP",
"pos": [
124,
128
]
} | decreased | cancerTOnormal | observation | unidentifiable | {
"name": "expression",
"pos": [
34,
43
],
"type": "Gene_expression"
} | {
"name": "decreased",
"pos": [
24,
32
],
"type": "Negative_regulation"
} |
12539225.s0 | Increased expression of bone morphogenetic protein-7 in bone metastatic prostate cancer. | prostate | {
"name": "bone morphogenetic protein-7",
"pos": [
24,
51
]
} | {
"name": "metastatic prostate cancer",
"pos": [
61,
86
]
} | increased | normalTOcancer | observation | unchanged | {
"name": "expression",
"pos": [
10,
19
],
"type": "Gene_expression"
} | {
"name": "Increased",
"pos": [
0,
8
],
"type": "Positive_regulation"
} |
10325519.s7 | (3) Of the 2,272 men, 284 had elevated PSA levels and prostate carcinoma was detected in 62 men. | prostate | {
"name": "PSA",
"pos": [
39,
41
]
} | {
"name": "prostate carcinoma",
"pos": [
54,
71
]
} | increased | unidentifiable | {
"name": "\nNone\n",
"pos": null,
"type": null
} | {
"name": "elevated",
"pos": [
30,
37
],
"type": "Positive_regulation"
} |
||
10325519.s11 | In the first prospective study, 106 of 158 men with elevated PSA levels <10.0 ng/ml were further evaluated and 37 prostate carcinomas were detected. | prostate | {
"name": "PSA",
"pos": [
61,
63
]
} | {
"name": "prostate carcinomas",
"pos": [
117,
135
]
} | increased | unidentifiable | {
"name": "\nNone\n",
"pos": null,
"type": null
} | {
"name": "elevated",
"pos": [
52,
59
],
"type": "Positive_regulation"
} |
||
15770517.s5 | Overexpression of clusterin in LNCaP cells confers resistance to both androgen ablation and chemotherapy. | prostate | {
"name": "clusterin",
"pos": [
18,
26
]
} | {
"name": "LNCaP",
"pos": [
31,
35
]
} | increased | normalTOcancer | causality | unidentifiable | {
"name": "Overexpression",
"pos": [
0,
13
],
"type": "Gene_expression"
} | {
"name": "Overexpression",
"pos": [
0,
13
],
"type": "Positive_regulation"
} |
15533896.s3 | In contrast to previous findings by others, PPAR-gamma ligands did not induce PPAR-gamma expression in EC or PC-3. | prostate | {
"name": "PPAR-gamma",
"pos": [
78,
87
]
} | {
"name": "PC-3",
"pos": [
109,
112
]
} | increased | unidentifiable | {
"name": "expression",
"pos": [
89,
98
],
"type": "Gene_expression"
} | {
"name": "induce",
"pos": [
71,
76
],
"type": "Positive_regulation"
} |
||
15533896.s7 | Low COX-2 expression in PC-3 was up-regulated by serum, and 15d-PGJ(2) blocked serum-induced COX-2 expression and activity in a dose-dependent manner. | prostate | {
"name": "COX-2",
"pos": [
93,
97
]
} | {
"name": "PC-3",
"pos": [
24,
27
]
} | decreased | unidentifiable | {
"name": "expression",
"pos": [
99,
108
],
"type": "Gene_expression"
} | {
"name": "blocked",
"pos": [
71,
77
],
"type": "Negative_regulation"
} |
||
15533896.s11 | The present study showed that PPAR-gamma activation can be an important regulator of COX-2 in prostate cells and may be an important target for prostate cancer chemoprevention. | prostate | {
"name": "PPAR-gamma",
"pos": [
30,
39
]
} | {
"name": "prostate cancer",
"pos": [
144,
158
]
} | increased | cancerTOnormal | causality | unidentifiable | {
"name": "\nNone\n",
"pos": null,
"type": null
} | {
"name": "activation",
"pos": [
41,
50
],
"type": "Positive_regulation"
} |
11774200.s3 | Overexpression of HER2 has independent prognostic significance in early breast cancer and may also predict response to hormonal and cytotoxic therapies, although this latter role is less well studied. | breast | {
"name": "HER2",
"pos": [
18,
21
]
} | {
"name": "breast cancer",
"pos": [
72,
84
]
} | increased | normalTOcancer | observation | unchanged | {
"name": "Overexpression",
"pos": [
0,
13
],
"type": "Gene_expression"
} | {
"name": "Overexpression",
"pos": [
0,
13
],
"type": "Positive_regulation"
} |
9042197.s2 | Loss of c-kit expression has been reported in 80-90% of breast cancer specimens, suggesting a possible role in the development of tumors. | breast | {
"name": "c-kit",
"pos": [
8,
12
]
} | {
"name": "breast cancer",
"pos": [
56,
68
]
} | decreased | normalTOcancer | observation | unchanged | {
"name": "expression",
"pos": [
14,
23
],
"type": "Gene_expression"
} | {
"name": "Loss",
"pos": [
0,
3
],
"type": "Negative_regulation"
} |
20853062.s1 | Triple-negative (TN) breast cancers lack estrogen receptor (ER), progesterone receptor (PR), and HER2/neu amplification (HER2). | breast | {
"name": "PR",
"pos": [
88,
89
]
} | {
"name": "breast cancers",
"pos": [
21,
34
]
} | decreased | normalTOcancer | observation | unidentifiable | {
"name": "\nNone\n",
"pos": null,
"type": null
} | {
"name": "lack",
"pos": [
36,
39
],
"type": "Negative_regulation"
} |
20853062.s1 | Triple-negative (TN) breast cancers lack estrogen receptor (ER), progesterone receptor (PR), and HER2/neu amplification (HER2). | breast | {
"name": "ER",
"pos": [
60,
61
]
} | {
"name": "breast cancers",
"pos": [
21,
34
]
} | decreased | normalTOcancer | observation | unidentifiable | {
"name": "\nNone\n",
"pos": null,
"type": null
} | {
"name": "lack",
"pos": [
36,
39
],
"type": "Negative_regulation"
} |
22364742.s6 | Importantly, this signaling circuit is manifest in human cancer cells and in a mouse model of ErbB2-driven breast cancer, where IL6 loss significantly impairs tumorigenesis. | breast | {
"name": "IL6",
"pos": [
128,
130
]
} | {
"name": "breast cancer",
"pos": [
107,
119
]
} | decreased | cancerTOnormal | causality | unidentifiable | {
"name": "\nNone\n",
"pos": null,
"type": null
} | {
"name": "loss",
"pos": [
132,
135
],
"type": "Negative_regulation"
} |
12615709.s1 | Treatment of MCF-7 cells with the peroxisome proliferator-activated receptor (PPAR) gamma agonists ciglitazone or 15-deoxy-Delta 12,14-prostaglandin J2 resulted in a concentration- and time-dependent decrease of cyclin D1 and estrogen receptor (ER) alpha proteins, and this was accompanied by decreased cell proliferation and G(1)-G(0)-->S-phase progression. | breast | {
"name": "estrogen receptor",
"pos": [
226,
242
]
} | {
"name": "MCF-7",
"pos": [
13,
17
]
} | decreased | cancerTOnormal | observation | unidentifiable | {
"name": "\nNone\n",
"pos": null,
"type": null
} | {
"name": "decrease",
"pos": [
200,
207
],
"type": "Negative_regulation"
} |
12615709.s1 | Treatment of MCF-7 cells with the peroxisome proliferator-activated receptor (PPAR) gamma agonists ciglitazone or 15-deoxy-Delta 12,14-prostaglandin J2 resulted in a concentration- and time-dependent decrease of cyclin D1 and estrogen receptor (ER) alpha proteins, and this was accompanied by decreased cell proliferation and G(1)-G(0)-->S-phase progression. | breast | {
"name": "cyclin D1",
"pos": [
212,
220
]
} | {
"name": "MCF-7",
"pos": [
13,
17
]
} | decreased | cancerTOnormal | observation | unidentifiable | {
"name": "\nNone\n",
"pos": null,
"type": null
} | {
"name": "decrease",
"pos": [
200,
207
],
"type": "Negative_regulation"
} |
11564899.s8 | In conclusion, three consecutive microarray (CGH, cDNA and tissue) experiments revealed high-level amplification and overexpression of the FGFR2 in a breast cancer cell line, but only a low frequency of involvement in primary breast tumors. | breast | {
"name": "FGFR2",
"pos": [
139,
143
]
} | {
"name": "breast tumors",
"pos": [
226,
238
]
} | increased | normalTOcancer | observation | unidentifiable | {
"name": "overexpression",
"pos": [
117,
130
],
"type": "Gene_expression"
} | {
"name": "overexpression",
"pos": [
117,
130
],
"type": "Positive_regulation"
} |
12761490.s4 | Transfection of HER2 in MCF7 breast cancer cells that express HER3 caused a phosphoinoside-3 kinase (PI-3K)-dependent activation of Akt, and was associated with an increased resistance of the cells to multiple chemotherapeutic agents (paclitaxel, doxorubicin, 5-fluorouracil, etoposide, and camptothecin). | breast | {
"name": "HER2",
"pos": [
16,
19
]
} | {
"name": "breast cancer",
"pos": [
29,
41
]
} | increased | normalTOcancer | observation | unidentifiable | {
"name": "Transfection",
"pos": [
0,
11
],
"type": "Gene_expression"
} | {
"name": "Transfection",
"pos": [
0,
11
],
"type": "Positive_regulation"
} |
12761490.s4 | Transfection of HER2 in MCF7 breast cancer cells that express HER3 caused a phosphoinoside-3 kinase (PI-3K)-dependent activation of Akt, and was associated with an increased resistance of the cells to multiple chemotherapeutic agents (paclitaxel, doxorubicin, 5-fluorouracil, etoposide, and camptothecin). | breast | {
"name": "Akt",
"pos": [
132,
134
]
} | {
"name": "breast cancer",
"pos": [
29,
41
]
} | increased | normalTOcancer | observation | unidentifiable | {
"name": "\nNone\n",
"pos": null,
"type": null
} | {
"name": "activation",
"pos": [
118,
127
],
"type": "Positive_regulation"
} |
9010319.s1 | MCF-7 (estrogen receptor positive--ER+) and MDA-MB-231 (estrogen receptor negative--ER-) are human breast cancer cell lines which express functional thyroid hormone receptors (c-erb A alpha1 and c-erb beta1) as indicated by stimulation of mitochondrial alpha-glycerophosphate dehydrogenase. | breast | {
"name": "mitochondrial alpha-glycerophosphate dehydrogenase",
"pos": [
239,
288
]
} | {
"name": "breast cancer",
"pos": [
99,
111
]
} | increased | normalTOcancer | observation | unidentifiable | {
"name": "\nNone\n",
"pos": null,
"type": null
} | {
"name": "stimulation",
"pos": [
224,
234
],
"type": "Positive_regulation"
} |
9010319.s2 | In MCF-7, mimicking E2, T3 stimulated growth in a dose-dependent (10(10) M - 10(-8) M) manner, induced the expression of progesterone receptor and growth factor TGFalpha mRNAs and inhibited that of TGFbeta mRNA; T3 also increased progesterone binding and LDH5 isozyme activities. | breast | {
"name": "progesterone receptor",
"pos": [
121,
141
]
} | {
"name": "MCF-7",
"pos": [
3,
7
]
} | increased | normalTOcancer | observation | unidentifiable | {
"name": "expression",
"pos": [
107,
116
],
"type": "Gene_expression"
} | {
"name": "induced",
"pos": [
95,
101
],
"type": "Positive_regulation"
} |
9010319.s2 | In MCF-7, mimicking E2, T3 stimulated growth in a dose-dependent (10(10) M - 10(-8) M) manner, induced the expression of progesterone receptor and growth factor TGFalpha mRNAs and inhibited that of TGFbeta mRNA; T3 also increased progesterone binding and LDH5 isozyme activities. | breast | {
"name": "growth factor TGFalpha mRNAs",
"pos": [
147,
174
]
} | {
"name": "MCF-7",
"pos": [
3,
7
]
} | increased | normalTOcancer | observation | unidentifiable | {
"name": "expression",
"pos": [
107,
116
],
"type": "Gene_expression"
} | {
"name": "induced",
"pos": [
95,
101
],
"type": "Positive_regulation"
} |
9010319.s2 | In MCF-7, mimicking E2, T3 stimulated growth in a dose-dependent (10(10) M - 10(-8) M) manner, induced the expression of progesterone receptor and growth factor TGFalpha mRNAs and inhibited that of TGFbeta mRNA; T3 also increased progesterone binding and LDH5 isozyme activities. | breast | {
"name": "LDH5 isozyme",
"pos": [
255,
266
]
} | {
"name": "MCF-7",
"pos": [
3,
7
]
} | increased | normalTOcancer | observation | unidentifiable | {
"name": "\nNone\n",
"pos": null,
"type": null
} | {
"name": "increased",
"pos": [
220,
228
],
"type": "Positive_regulation"
} |
9010319.s4 | 10(-6) M tamoxifen (TAM) reverted growth stimulation, suppressed progesterone receptor and TGFalpha mRNA induction and restored TGFbeta mRNA to control levels in T3-treated MCF-7 cells. | breast | {
"name": "TGFbeta mRNA",
"pos": [
128,
139
]
} | {
"name": "MCF-7",
"pos": [
173,
177
]
} | increased | unidentifiable | {
"name": "\nNone\n",
"pos": null,
"type": null
} | {
"name": "restored",
"pos": [
119,
126
],
"type": "Positive_regulation"
} |
||
9010319.s4 | 10(-6) M tamoxifen (TAM) reverted growth stimulation, suppressed progesterone receptor and TGFalpha mRNA induction and restored TGFbeta mRNA to control levels in T3-treated MCF-7 cells. | breast | {
"name": "progesterone receptor",
"pos": [
65,
85
]
} | {
"name": "MCF-7",
"pos": [
173,
177
]
} | decreased | unidentifiable | {
"name": "\nNone\n",
"pos": null,
"type": null
} | {
"name": "suppressed",
"pos": [
54,
63
],
"type": "Negative_regulation"
} |
||
9010319.s4 | 10(-6) M tamoxifen (TAM) reverted growth stimulation, suppressed progesterone receptor and TGFalpha mRNA induction and restored TGFbeta mRNA to control levels in T3-treated MCF-7 cells. | breast | {
"name": "TGFalpha mRNA",
"pos": [
91,
103
]
} | {
"name": "MCF-7",
"pos": [
173,
177
]
} | increased | unidentifiable | {
"name": "\nNone\n",
"pos": null,
"type": null
} | {
"name": "induction",
"pos": [
105,
113
],
"type": "Positive_regulation"
} |
||
11118434.s4 | Expression of C2GnT1 is low or absent in around 50% of breast cancers, whereas expression of ST3Gal-I is consistently increased. | breast | {
"name": "ST3Gal-I",
"pos": [
93,
100
]
} | {
"name": "breast cancers",
"pos": [
55,
68
]
} | increased | normalTOcancer | observation | unchanged | {
"name": "expression",
"pos": [
79,
88
],
"type": "Gene_expression"
} | {
"name": "increased",
"pos": [
118,
126
],
"type": "Positive_regulation"
} |
11118434.s9 | Thus, even when C2GnT1 is expressed, the O-glycans added to MUC1 become core 1-dominated structures, provided expression of ST3Gal-I is increased as it is in breast cancer. | breast | {
"name": "ST3Gal-I",
"pos": [
124,
131
]
} | {
"name": "breast cancer",
"pos": [
158,
170
]
} | increased | normalTOcancer | observation | unchanged | {
"name": "expression",
"pos": [
110,
119
],
"type": "Gene_expression"
} | {
"name": "increased",
"pos": [
136,
144
],
"type": "Positive_regulation"
} |
12422056.s1 | HER2 overexpression/amplification, which is an early event in breast cancer development, is associated with a poor prognosis and may predict response to therapy. | breast | {
"name": "HER2",
"pos": [
0,
3
]
} | {
"name": "breast cancer",
"pos": [
62,
74
]
} | increased | normalTOcancer | observation | unchanged | {
"name": "overexpression",
"pos": [
5,
18
],
"type": "Gene_expression"
} | {
"name": "overexpression",
"pos": [
5,
18
],
"type": "Positive_regulation"
} |