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|---|---|---|---|---|---|---|---|---|---|---|
20711231.s5 | We found a correlation between ErbB2 expression and activation of Pak in estrogen receptor-positive human breast tumor samples and observed that in 3D cultures, activation of Rac-Pak1 pathway by ErbB2 homodimers induced growth factor-independent proliferation and promoted disruption of 3D mammary acinar-like structures through activation of the Erk and Akt pathways. | breast | {
"name": "Erk",
"pos": [
347,
349
]
} | {
"name": "breast tumor",
"pos": [
106,
117
]
} | increased | unidentifiable | {
"name": "\nNone\n",
"pos": null,
"type": null
} | {
"name": "activation",
"pos": [
329,
338
],
"type": "Positive_regulation"
} |
||
20711231.s5 | We found a correlation between ErbB2 expression and activation of Pak in estrogen receptor-positive human breast tumor samples and observed that in 3D cultures, activation of Rac-Pak1 pathway by ErbB2 homodimers induced growth factor-independent proliferation and promoted disruption of 3D mammary acinar-like structures through activation of the Erk and Akt pathways. | breast | {
"name": "Pak",
"pos": [
66,
68
]
} | {
"name": "breast tumor",
"pos": [
106,
117
]
} | increased | normalTOcancer | causality | unidentifiable | {
"name": "\nNone\n",
"pos": null,
"type": null
} | {
"name": "activation",
"pos": [
52,
61
],
"type": "Positive_regulation"
} |
20711231.s7 | Finally, ErbB2-amplified breast cancer cells expressing a specific Pak inhibitor showed delayed tumor formation and downregulation of Erk and Akt signaling in vivo. | breast | {
"name": "Erk",
"pos": [
134,
136
]
} | {
"name": "breast cancer",
"pos": [
25,
37
]
} | decreased | cancerTOnormal | observation | unidentifiable | {
"name": "\nNone\n",
"pos": null,
"type": null
} | {
"name": "downregulation",
"pos": [
116,
129
],
"type": "Negative_regulation"
} |
20711231.s7 | Finally, ErbB2-amplified breast cancer cells expressing a specific Pak inhibitor showed delayed tumor formation and downregulation of Erk and Akt signaling in vivo. | breast | {
"name": "Akt",
"pos": [
142,
144
]
} | {
"name": "breast cancer",
"pos": [
25,
37
]
} | decreased | cancerTOnormal | observation | unidentifiable | {
"name": "\nNone\n",
"pos": null,
"type": null
} | {
"name": "downregulation",
"pos": [
116,
129
],
"type": "Negative_regulation"
} |
21809344.s4 | Runx2 expression in C4-2B PCa cells synergized with AR to promote PIP expression, whereas its knockdown in T47D BCa cells abrogated basal as well as hormone stimulated PIP expression. | breast | {
"name": "PIP",
"pos": [
66,
68
]
} | {
"name": "T47D",
"pos": [
107,
110
]
} | increased | unidentifiable | {
"name": "expression",
"pos": [
70,
79
],
"type": "Gene_expression"
} | {
"name": "promote",
"pos": [
58,
64
],
"type": "Positive_regulation"
} |
||
12442345.s6 | Similarly, neoadjuvant studies demonstrate that letrozole substantially inhibits aromatase activity in both malignant and nonmalignant breast tissues, and markedly suppresses endogenous estrogens within the breast cancers. | breast | {
"name": "aromatase",
"pos": [
81,
89
]
} | {
"name": "breast cancers",
"pos": [
207,
220
]
} | decreased | unidentifiable | {
"name": "\nNone\n",
"pos": null,
"type": null
} | {
"name": "inhibits",
"pos": [
72,
79
],
"type": "Negative_regulation"
} |
||
9849446.s4 | After a median follow-up of 65 months, an increase in TGF-beta 1 over 1 year was the only significant, independent predictor of a shorter survival free from secondary primary breast cancer. | breast | {
"name": "TGF-beta 1",
"pos": [
54,
63
]
} | {
"name": "breast cancer",
"pos": [
175,
187
]
} | increased | unidentifiable | {
"name": "\nNone\n",
"pos": null,
"type": null
} | {
"name": "increase",
"pos": [
42,
49
],
"type": "Positive_regulation"
} |
||
20302909.s0 | Estrogen receptor alpha 46 is reduced in tamoxifen resistant breast cancer cells and re-expression inhibits cell proliferation and estrogen receptor alpha 66-regulated target gene transcription. | breast | {
"name": "Estrogen receptor alpha 46",
"pos": [
0,
25
]
} | {
"name": "breast cancer",
"pos": [
61,
73
]
} | decreased | normalTOcancer | observation | unchanged | {
"name": "\nNone\n",
"pos": null,
"type": null
} | {
"name": "reduced",
"pos": [
30,
36
],
"type": "Negative_regulation"
} |
20302909.s3 | We observed reduced protein expression of an N-terminally truncated ERalpha46 in endocrine-resistant LCC2, LCC9, and LY2 compared to MCF-7 breast cancer cells. | breast | {
"name": "ERalpha46",
"pos": [
68,
76
]
} | {
"name": "breast cancer",
"pos": [
139,
151
]
} | decreased | unidentifiable | {
"name": "expression",
"pos": [
28,
37
],
"type": "Gene_expression"
} | {
"name": "reduced",
"pos": [
12,
18
],
"type": "Negative_regulation"
} |
||
20302909.s4 | Transfection of LCC9 and LY2 cells with hERalpha46 partially restored growth inhibition by TAM. | breast | {
"name": "hERalpha46",
"pos": [
40,
49
]
} | {
"name": "LY2",
"pos": [
25,
27
]
} | increased | cancerTOnormal | causality | unidentifiable | {
"name": "Transfection",
"pos": [
0,
11
],
"type": "Gene_expression"
} | {
"name": "Transfection",
"pos": [
0,
11
],
"type": "Positive_regulation"
} |
20302909.s5 | Overexpression of hERalpha46 in MCF-7 cells reduced estradiol (E(2))-stimulated endogenous pS2, cyclin D1, nuclear respiratory factor-1 (NRF-1), and progesterone receptor transcription. | breast | {
"name": "hERalpha46",
"pos": [
18,
27
]
} | {
"name": "MCF-7",
"pos": [
32,
36
]
} | increased | unidentifiable | {
"name": "Overexpression",
"pos": [
0,
13
],
"type": "Gene_expression"
} | {
"name": "Overexpression",
"pos": [
0,
13
],
"type": "Positive_regulation"
} |
||
20302909.s8 | Established miR-21 targets PTEN and PDCD4 were reduced in ERalpha46-transfected, E(2)-treated MCF-7 cells. | breast | {
"name": "PDCD4",
"pos": [
36,
40
]
} | {
"name": "MCF-7",
"pos": [
94,
98
]
} | decreased | unidentifiable | {
"name": "\nNone\n",
"pos": null,
"type": null
} | {
"name": "reduced",
"pos": [
47,
53
],
"type": "Negative_regulation"
} |
||
18294401.s0 | Obesity and HER 2 overexpression: a common factor for poor prognosis of breast cancer. | breast | {
"name": "HER 2",
"pos": [
12,
16
]
} | {
"name": "breast cancer",
"pos": [
72,
84
]
} | increased | normalTOcancer | observation | unchanged | {
"name": "overexpression",
"pos": [
18,
31
],
"type": "Gene_expression"
} | {
"name": "overexpression",
"pos": [
18,
31
],
"type": "Positive_regulation"
} |
18294401.s1 | Both obesity and over-expression of HER II are associated with poor prognosis of breast cancer. | breast | {
"name": "HER II",
"pos": [
36,
41
]
} | {
"name": "breast cancer",
"pos": [
81,
93
]
} | increased | normalTOcancer | observation | unchanged | {
"name": "over-expression",
"pos": [
17,
31
],
"type": "Gene_expression"
} | {
"name": "over-expression",
"pos": [
17,
31
],
"type": "Positive_regulation"
} |
18294401.s3 | The overexpression of HER II is also positively correlated with other markers of prognosis of breast cancer such as cathepsin expression. | breast | {
"name": "HER II",
"pos": [
22,
27
]
} | {
"name": "breast cancer",
"pos": [
94,
106
]
} | increased | normalTOcancer | observation | unchanged | {
"name": "overexpression",
"pos": [
4,
17
],
"type": "Gene_expression"
} | {
"name": "overexpression",
"pos": [
4,
17
],
"type": "Positive_regulation"
} |
17317102.s4 | One of these kinases, Erk5, has been found to reside in the nucleus of breast cancer cells that overexpress the ErbB2 receptor. | breast | {
"name": "ErbB2 receptor",
"pos": [
112,
125
]
} | {
"name": "breast cancer",
"pos": [
71,
83
]
} | increased | normalTOcancer | observation | unidentifiable | {
"name": "overexpress",
"pos": [
96,
106
],
"type": "Gene_expression"
} | {
"name": "overexpress",
"pos": [
96,
106
],
"type": "Positive_regulation"
} |
17317102.s6 | In breast cancer cells overexpressing ErbB2, Erk5 dual phosphorylation required ErbB2 tyrosine kinase activity; however, Erk5 nuclear residency did not require ErbB2 activity. | breast | {
"name": "ErbB2",
"pos": [
38,
42
]
} | {
"name": "breast cancer",
"pos": [
3,
15
]
} | increased | normalTOcancer | observation | unidentifiable | {
"name": "overexpressing",
"pos": [
23,
36
],
"type": "Gene_expression"
} | {
"name": "overexpressing",
"pos": [
23,
36
],
"type": "Positive_regulation"
} |
15020607.s1 | In a pivotal phase III trial, the addition of trastuzumab to chemotherapy significantly improved response rate, time to disease progression, and overall survival in women with HER2 overexpressing metastatic breast cancer. | breast | {
"name": "HER2",
"pos": [
176,
179
]
} | {
"name": "metastatic breast cancer",
"pos": [
196,
219
]
} | increased | normalTOcancer | observation | unidentifiable | {
"name": "overexpressing",
"pos": [
181,
194
],
"type": "Gene_expression"
} | {
"name": "overexpressing",
"pos": [
181,
194
],
"type": "Positive_regulation"
} |
1985102.s0 | The growth inhibition of human breast cancer cells by a novel synthetic progestin involves the induction of transforming growth factor beta. | breast | {
"name": "transforming growth factor beta",
"pos": [
108,
138
]
} | {
"name": "breast cancer",
"pos": [
31,
43
]
} | increased | cancerTOnormal | causality | unidentifiable | {
"name": "\nNone\n",
"pos": null,
"type": null
} | {
"name": "induction",
"pos": [
95,
103
],
"type": "Positive_regulation"
} |
1985102.s5 | Furthermore, in four breast cancer cell lines, the extent of induction of TGF-beta correlated with intracellular levels of Gestodene binding site. | breast | {
"name": "TGF-beta",
"pos": [
74,
81
]
} | {
"name": "breast cancer",
"pos": [
21,
33
]
} | increased | unidentifiable | {
"name": "\nNone\n",
"pos": null,
"type": null
} | {
"name": "induction",
"pos": [
61,
69
],
"type": "Positive_regulation"
} |
||
16501249.s3 | Moreover, we examined the putative impact of p53 MspI 1798G>A, which is completely linked to p53PIN3, a 16 bp insertion/duplication that has been associated with reduced p53 expression, on familial breast cancer risk. | breast | {
"name": "p53",
"pos": [
170,
172
]
} | {
"name": "familial breast cancer",
"pos": [
189,
210
]
} | decreased | unidentifiable | {
"name": "\nNone\n",
"pos": null,
"type": null
} | {
"name": "reduced",
"pos": [
162,
168
],
"type": "Negative_regulation"
} |
||
16809439.s5 | From a clinical perspective, we suggest that if chemically stable FASN inhibitors or cell-selective systems able to deliver RNAi targeting FASN gene demonstrate systemic anticancer effects of FASN inhibition in vivo, additional preclinical studies to characterize their anti-breast cancer actions should be of great interest as the specific blockade of FASN activity may also provide a protective means against endometrial carcinoma associated with tamoxifen-based breast cancer therapy. | breast | {
"name": "FASN",
"pos": [
192,
195
]
} | {
"name": "breast cancer",
"pos": [
465,
477
]
} | decreased | cancerTOnormal | causality | unidentifiable | {
"name": "\nNone\n",
"pos": null,
"type": null
} | {
"name": "inhibition",
"pos": [
197,
206
],
"type": "Negative_regulation"
} |
16809439.s5 | From a clinical perspective, we suggest that if chemically stable FASN inhibitors or cell-selective systems able to deliver RNAi targeting FASN gene demonstrate systemic anticancer effects of FASN inhibition in vivo, additional preclinical studies to characterize their anti-breast cancer actions should be of great interest as the specific blockade of FASN activity may also provide a protective means against endometrial carcinoma associated with tamoxifen-based breast cancer therapy. | breast | {
"name": "FASN",
"pos": [
353,
356
]
} | {
"name": "breast cancer",
"pos": [
465,
477
]
} | decreased | cancerTOnormal | causality | unidentifiable | {
"name": "\nNone\n",
"pos": null,
"type": null
} | {
"name": "blockade",
"pos": [
341,
348
],
"type": "Negative_regulation"
} |
11550075.s4 | Inhibition of aromatase is an important approach for reducing growth stimulatory effects of estrogens in hormone-dependent breast cancer. | breast | {
"name": "aromatase",
"pos": [
14,
22
]
} | {
"name": "breast cancer",
"pos": [
123,
135
]
} | decreased | cancerTOnormal | causality | unidentifiable | {
"name": "\nNone\n",
"pos": null,
"type": null
} | {
"name": "Inhibition",
"pos": [
0,
9
],
"type": "Negative_regulation"
} |
18060053.s0 | Functional ablation of pRb activates Cdk2 and causes antiestrogen resistance in human breast cancer cells. | breast | {
"name": "Cdk2",
"pos": [
37,
40
]
} | {
"name": "breast cancer",
"pos": [
86,
98
]
} | increased | unidentifiable | {
"name": "\nNone\n",
"pos": null,
"type": null
} | {
"name": "activates",
"pos": [
27,
35
],
"type": "Positive_regulation"
} |
||
18270579.s0 | Induction of ErbB-3 expression by alpha6beta4 integrin contributes to tamoxifen resistance in ERbeta1-negative breast carcinomas. | breast | {
"name": "ErbB-3",
"pos": [
13,
18
]
} | {
"name": "breast carcinomas",
"pos": [
111,
127
]
} | increased | unidentifiable | {
"name": "expression",
"pos": [
20,
29
],
"type": "Gene_expression"
} | {
"name": "Induction",
"pos": [
0,
8
],
"type": "Positive_regulation"
} |
||
3524819.s4 | These results indicate that the overexpression of H-ras in human breast tumors is not correlated with alteration of the protooncogene. | breast | {
"name": "H-ras",
"pos": [
50,
54
]
} | {
"name": "breast tumors",
"pos": [
65,
77
]
} | increased | normalTOcancer | observation | unidentifiable | {
"name": "overexpression",
"pos": [
32,
45
],
"type": "Gene_expression"
} | {
"name": "overexpression",
"pos": [
32,
45
],
"type": "Positive_regulation"
} |
3524819.s8 | Correlation with clinicopathological data showed, however, that the loss of one H-ras-1 allele in breast carcinoma DNAs is significantly linked to histological Grade III tumors, the lack of estrogen and/or progesterone receptors, and the subsequent occurrence of distal metastasis. | breast | {
"name": "H-ras-1 allele",
"pos": [
80,
93
]
} | {
"name": "breast carcinoma",
"pos": [
98,
113
]
} | decreased | normalTOcancer | observation | unchanged | {
"name": "\nNone\n",
"pos": null,
"type": null
} | {
"name": "loss",
"pos": [
68,
71
],
"type": "Negative_regulation"
} |
2440556.s0 | Increase of urokinase-type plasminogen activator gene expression in human lung and breast carcinomas. | breast | {
"name": "urokinase-type plasminogen activator gene",
"pos": [
12,
52
]
} | {
"name": "breast carcinomas",
"pos": [
83,
99
]
} | increased | normalTOcancer | observation | unchanged | {
"name": "expression",
"pos": [
54,
63
],
"type": "Gene_expression"
} | {
"name": "Increase",
"pos": [
0,
7
],
"type": "Positive_regulation"
} |
22037875.s0 | Cyclin D3 compensates for the loss of cyclin D1 during ErbB2-induced mammary tumor initiation and progression. | breast | {
"name": "cyclin D1",
"pos": [
38,
46
]
} | {
"name": "mammary tumor",
"pos": [
69,
81
]
} | decreased | unidentifiable | {
"name": "\nNone\n",
"pos": null,
"type": null
} | {
"name": "loss",
"pos": [
30,
33
],
"type": "Negative_regulation"
} |
||
22037875.s4 | The lack of Cyclin D1 was associated with a compensatory upregulation of Cyclin D3, which explains why the targeted downregulation of Cyclin D1 in established mammary tumors had no effect on cancer cell proliferation. | breast | {
"name": "Cyclin D1",
"pos": [
12,
20
]
} | {
"name": "mammary tumors",
"pos": [
159,
172
]
} | decreased | unidentifiable | {
"name": "\nNone\n",
"pos": null,
"type": null
} | {
"name": "lack",
"pos": [
4,
7
],
"type": "Negative_regulation"
} |
||
22037875.s4 | The lack of Cyclin D1 was associated with a compensatory upregulation of Cyclin D3, which explains why the targeted downregulation of Cyclin D1 in established mammary tumors had no effect on cancer cell proliferation. | breast | {
"name": "Cyclin D1",
"pos": [
134,
142
]
} | {
"name": "mammary tumors",
"pos": [
159,
172
]
} | decreased | unidentifiable | {
"name": "\nNone\n",
"pos": null,
"type": null
} | {
"name": "downregulation",
"pos": [
116,
129
],
"type": "Negative_regulation"
} |
||
22037875.s4 | The lack of Cyclin D1 was associated with a compensatory upregulation of Cyclin D3, which explains why the targeted downregulation of Cyclin D1 in established mammary tumors had no effect on cancer cell proliferation. | breast | {
"name": "Cyclin D3",
"pos": [
73,
81
]
} | {
"name": "mammary tumors",
"pos": [
159,
172
]
} | increased | unidentifiable | {
"name": "\nNone\n",
"pos": null,
"type": null
} | {
"name": "upregulation",
"pos": [
57,
68
],
"type": "Positive_regulation"
} |
||
22037875.s5 | Cyclin D1 and D3 are overexpressed in human breast cancer cell lines and primary invasive breast cancers, and Cyclin D3 frequently exceeded the expression of Cyclin D1 in ErbB2-positive cases. | breast | {
"name": "Cyclin D1",
"pos": [
0,
8
]
} | {
"name": "invasive breast cancers",
"pos": [
81,
103
]
} | increased | normalTOcancer | observation | unchanged | {
"name": "overexpressed",
"pos": [
21,
33
],
"type": "Gene_expression"
} | {
"name": "overexpressed",
"pos": [
21,
33
],
"type": "Positive_regulation"
} |
22037875.s7 | Collectively, the results of this study suggest that only the combined inhibition of Cyclin D1 and D3 might be a suitable strategy for breast cancer prevention and therapy. | breast | {
"name": "Cyclin D1",
"pos": [
85,
93
]
} | {
"name": "breast cancer",
"pos": [
135,
147
]
} | decreased | unidentifiable | {
"name": "\nNone\n",
"pos": null,
"type": null
} | {
"name": "inhibition",
"pos": [
71,
80
],
"type": "Negative_regulation"
} |
||
12036928.s4 | We had reported previously that although both BT474 and MKN7 cells overexpress ErbB2, only BT474 cells show an antiproliferative response to mAb 4D5 treatment. | breast | {
"name": "ErbB2",
"pos": [
79,
83
]
} | {
"name": "BT474",
"pos": [
46,
50
]
} | increased | normalTOcancer | observation | unchanged | {
"name": "overexpress",
"pos": [
67,
77
],
"type": "Gene_expression"
} | {
"name": "overexpress",
"pos": [
67,
77
],
"type": "Positive_regulation"
} |
17145775.s1 | The multidrug transporter breast cancer resistance protein (BCRP/ABCG2) is strongly induced in the mammary gland during pregnancy and lactation. | breast | {
"name": "BCRP/ABCG2",
"pos": [
60,
69
]
} | {
"name": "breast cancer",
"pos": [
26,
38
]
} | increased | unidentifiable | {
"name": "\nNone\n",
"pos": null,
"type": null
} | {
"name": "induced",
"pos": [
84,
90
],
"type": "Positive_regulation"
} |
||
17145775.s1 | The multidrug transporter breast cancer resistance protein (BCRP/ABCG2) is strongly induced in the mammary gland during pregnancy and lactation. | breast | {
"name": "multidrug transporter breast cancer resistance protein",
"pos": [
4,
57
]
} | {
"name": "breast cancer",
"pos": [
26,
38
]
} | increased | unidentifiable | {
"name": "\nNone\n",
"pos": null,
"type": null
} | {
"name": "induced",
"pos": [
84,
90
],
"type": "Positive_regulation"
} |
||
12231537.s1 | Maspin is a noninhibitory member of the serpin family that is down-regulated in breast carcinoma but overexpressed in pancreatic carcinoma. | breast | {
"name": "Maspin",
"pos": [
0,
5
]
} | {
"name": "breast carcinoma",
"pos": [
80,
95
]
} | increased | unidentifiable | {
"name": "overexpressed",
"pos": [
101,
113
],
"type": "Gene_expression"
} | {
"name": "overexpressed",
"pos": [
101,
113
],
"type": "Positive_regulation"
} |
||
12231537.s1 | Maspin is a noninhibitory member of the serpin family that is down-regulated in breast carcinoma but overexpressed in pancreatic carcinoma. | breast | {
"name": "Maspin",
"pos": [
0,
5
]
} | {
"name": "breast carcinoma",
"pos": [
80,
95
]
} | decreased | normalTOcancer | observation | unchanged | {
"name": "\nNone\n",
"pos": null,
"type": null
} | {
"name": "down-regulated",
"pos": [
62,
75
],
"type": "Negative_regulation"
} |
7913408.s8 | Ovarian carcinoma and breast carcinoma cells which are multiply drug resistant due to overexpression of P-glycoprotein are markedly less resistant to cryptophycin than they are to vinblastine, colchicine, and taxol. | breast | {
"name": "P-glycoprotein",
"pos": [
104,
117
]
} | {
"name": "breast carcinoma",
"pos": [
22,
37
]
} | increased | normalTOcancer | causality | unidentifiable | {
"name": "overexpression",
"pos": [
86,
99
],
"type": "Gene_expression"
} | {
"name": "overexpression",
"pos": [
86,
99
],
"type": "Positive_regulation"
} |
15072561.s2 | In several breast cancer cell lines, trichostatin A (TSA), a potent HDAC inhibitor, strongly decreases ERalpha expression in a dose-dependent manner. | breast | {
"name": "ERalpha",
"pos": [
103,
109
]
} | {
"name": "breast cancer",
"pos": [
11,
23
]
} | decreased | unidentifiable | {
"name": "expression",
"pos": [
111,
120
],
"type": "Gene_expression"
} | {
"name": "decreases",
"pos": [
93,
101
],
"type": "Negative_regulation"
} |
||
21983172.s6 | We also observed a reduction of UBR1 protein levels in geldanamycin-treated mouse embryonic fibroblasts and human breast cancer cells, suggesting that UBR1 is an Hsp90 client. | breast | {
"name": "UBR1 protein",
"pos": [
32,
43
]
} | {
"name": "breast cancer",
"pos": [
114,
126
]
} | decreased | normalTOcancer | observation | unidentifiable | {
"name": "\nNone\n",
"pos": null,
"type": null
} | {
"name": "reduction",
"pos": [
19,
27
],
"type": "Negative_regulation"
} |
9816210.s5 | One of the best examples of a correlation between high levels of a protease in a primary tumor and poor prognosis is urokinase plasminogen activation in breast cancer. | breast | {
"name": "urokinase plasminogen",
"pos": [
117,
137
]
} | {
"name": "breast cancer",
"pos": [
153,
165
]
} | increased | normalTOcancer | observation | unchanged | {
"name": "\nNone\n",
"pos": null,
"type": null
} | {
"name": "activation",
"pos": [
139,
148
],
"type": "Positive_regulation"
} |
16954434.s1 | Oestrogen receptor-alpha (ERalpha) is an important prognostic marker in breast cancer and endocrine therapies are designed to inhibit or prevent ERalpha activity. | breast | {
"name": "ERalpha",
"pos": [
145,
151
]
} | {
"name": "breast cancer",
"pos": [
72,
84
]
} | decreased | cancerTOnormal | causality | up-regulated | {
"name": "\nNone\n",
"pos": null,
"type": null
} | {
"name": "prevent",
"pos": [
137,
143
],
"type": "Negative_regulation"
} |
18373644.s0 | IGFBP2 and IGFBP5 overexpression correlates with the lymph node metastasis in T1 breast carcinomas. | breast | {
"name": "IGFBP5",
"pos": [
11,
16
]
} | {
"name": "breast carcinomas",
"pos": [
81,
97
]
} | increased | normalTOcancer | observation | unidentifiable | {
"name": "overexpression",
"pos": [
18,
31
],
"type": "Gene_expression"
} | {
"name": "overexpression",
"pos": [
18,
31
],
"type": "Positive_regulation"
} |
18373644.s0 | IGFBP2 and IGFBP5 overexpression correlates with the lymph node metastasis in T1 breast carcinomas. | breast | {
"name": "IGFBP2",
"pos": [
0,
5
]
} | {
"name": "breast carcinomas",
"pos": [
81,
97
]
} | increased | normalTOcancer | observation | unidentifiable | {
"name": "overexpression",
"pos": [
18,
31
],
"type": "Gene_expression"
} | {
"name": "overexpression",
"pos": [
18,
31
],
"type": "Positive_regulation"
} |
18373644.s2 | Overexpression of IGFBP2 and IGFBP5 contributes to the invasiveness and progression of several human cancers, but their roles in the metastasis of breast cancer have not been investigated in detail. | breast | {
"name": "IGFBP2",
"pos": [
18,
23
]
} | {
"name": "breast cancer",
"pos": [
147,
159
]
} | increased | unidentifiable | {
"name": "Overexpression",
"pos": [
0,
13
],
"type": "Gene_expression"
} | {
"name": "Overexpression",
"pos": [
0,
13
],
"type": "Positive_regulation"
} |
||
18373644.s2 | Overexpression of IGFBP2 and IGFBP5 contributes to the invasiveness and progression of several human cancers, but their roles in the metastasis of breast cancer have not been investigated in detail. | breast | {
"name": "IGFBP5",
"pos": [
29,
34
]
} | {
"name": "breast cancer",
"pos": [
147,
159
]
} | increased | unidentifiable | {
"name": "Overexpression",
"pos": [
0,
13
],
"type": "Gene_expression"
} | {
"name": "Overexpression",
"pos": [
0,
13
],
"type": "Positive_regulation"
} |
||
10449619.s0 | Induction of thymidine phosphorylase expression and enhancement of efficacy of capecitabine or 5'-deoxy-5-fluorouridine by cyclophosphamide in mammary tumor models. | breast | {
"name": "thymidine phosphorylase",
"pos": [
13,
35
]
} | {
"name": "mammary tumor",
"pos": [
143,
155
]
} | increased | unidentifiable | {
"name": "expression",
"pos": [
37,
46
],
"type": "Gene_expression"
} | {
"name": "Induction",
"pos": [
0,
8
],
"type": "Positive_regulation"
} |
||
10449619.s3 | In the present study, we confirmed that the administration of cytostatics used for breast cancer treatment, such as taxanes and cyclophosphamide (CPA), up-regulated the tumor level of dThdPase in mammary tumor models as well. | breast | {
"name": "dThdPase",
"pos": [
184,
191
]
} | {
"name": "mammary tumor",
"pos": [
196,
208
]
} | increased | unidentifiable | {
"name": "\nNone\n",
"pos": null,
"type": null
} | {
"name": "up-regulated",
"pos": [
152,
163
],
"type": "Positive_regulation"
} |
||
10449619.s6 | The preferential up-regulation of PyNPase activity in the tumor by CPA administration was also confirmed in mice bearing a syngeneic murine mammary adenocarcinoma, A755. | breast | {
"name": "PyNPase",
"pos": [
34,
40
]
} | {
"name": "mammary adenocarcinoma",
"pos": [
140,
161
]
} | increased | unidentifiable | {
"name": "\nNone\n",
"pos": null,
"type": null
} | {
"name": "up-regulation",
"pos": [
17,
29
],
"type": "Positive_regulation"
} |
||
3298786.s3 | Enhanced Ha-ras expression was documented in 66% of breast and 100% of colon carcinomas as compared with their normal counterparts, with levels in breast carcinomas ranging from 10.1 to 50.4 pg ras p21/micrograms protein and those in colon carcinomas ranging from 18.4 to 51.7 pg ras p21/micrograms protein. | breast | {
"name": "Ha-ras",
"pos": [
9,
14
]
} | {
"name": "breast carcinomas",
"pos": [
147,
163
]
} | increased | normalTOcancer | observation | unchanged | {
"name": "expression",
"pos": [
16,
25
],
"type": "Gene_expression"
} | {
"name": "Enhanced",
"pos": [
0,
7
],
"type": "Positive_regulation"
} |
17726528.s11 | Artesunate treatment of human CCRF-CEM leukemia and MCF7 breast cancer cells induced ABCB6 expression but repressed ABCB7 expression. | breast | {
"name": "ABCB6",
"pos": [
85,
89
]
} | {
"name": "breast cancer",
"pos": [
57,
69
]
} | increased | unidentifiable | {
"name": "expression",
"pos": [
91,
100
],
"type": "Gene_expression"
} | {
"name": "induced",
"pos": [
77,
83
],
"type": "Positive_regulation"
} |
||
17726528.s11 | Artesunate treatment of human CCRF-CEM leukemia and MCF7 breast cancer cells induced ABCB6 expression but repressed ABCB7 expression. | breast | {
"name": "ABCB7",
"pos": [
116,
120
]
} | {
"name": "breast cancer",
"pos": [
57,
69
]
} | decreased | unidentifiable | {
"name": "expression",
"pos": [
122,
131
],
"type": "Gene_expression"
} | {
"name": "repressed",
"pos": [
106,
114
],
"type": "Negative_regulation"
} |
||
20305816.s7 | Using multiple primer sets and controls, we found that neither mature BORIS transcripts nor spliced variants are commonly expressed at detectable levels in malignant breast cells or tissues, although endogenous BORIS transcripts can be induced in MCF-7 cells following 5-aza-2'-deoxycytidine treatment. | breast | {
"name": "BORIS transcripts",
"pos": [
211,
227
]
} | {
"name": "MCF-7",
"pos": [
247,
251
]
} | increased | unidentifiable | {
"name": "\nNone\n",
"pos": null,
"type": null
} | {
"name": "induced",
"pos": [
236,
242
],
"type": "Positive_regulation"
} |
||
7840509.s6 | The elevated testosterone levels and the increased levels of insulin, IGF-I, and IGF-II that are seen in PCOS and abdominal obesity could favor the development of breast cancer in several ways, all of which have been demonstrated experimentally: binding of testosterone to cancer cells bearing testosterone receptors, with direct stimulation; intratissular aromatization of testosterone to estradiol, with stimulation of estrogen-sensitive cells; stimulation of the production of epithelial growth factor (EGF) by testosterone, with direct mitogenic effect of EGF on cancer cells; stimulation of aromatase by insulin and IGF-I; direct mitogenic stimulation of cancer cells by insulin, IGF-I, and IGF-II; and stimulation by IGF-I and IGF-II of the intratissular reduction of estrone to estradiol. | breast | {
"name": "epithelial growth factor",
"pos": [
480,
503
]
} | {
"name": "breast cancer",
"pos": [
163,
175
]
} | increased | normalTOcancer | causality | unidentifiable | {
"name": "production",
"pos": [
466,
475
],
"type": "Gene_expression"
} | {
"name": "stimulation",
"pos": [
447,
457
],
"type": "Positive_regulation"
} |
7840509.s6 | The elevated testosterone levels and the increased levels of insulin, IGF-I, and IGF-II that are seen in PCOS and abdominal obesity could favor the development of breast cancer in several ways, all of which have been demonstrated experimentally: binding of testosterone to cancer cells bearing testosterone receptors, with direct stimulation; intratissular aromatization of testosterone to estradiol, with stimulation of estrogen-sensitive cells; stimulation of the production of epithelial growth factor (EGF) by testosterone, with direct mitogenic effect of EGF on cancer cells; stimulation of aromatase by insulin and IGF-I; direct mitogenic stimulation of cancer cells by insulin, IGF-I, and IGF-II; and stimulation by IGF-I and IGF-II of the intratissular reduction of estrone to estradiol. | breast | {
"name": "EGF",
"pos": [
506,
508
]
} | {
"name": "breast cancer",
"pos": [
163,
175
]
} | increased | normalTOcancer | causality | unidentifiable | {
"name": "production",
"pos": [
466,
475
],
"type": "Gene_expression"
} | {
"name": "stimulation",
"pos": [
447,
457
],
"type": "Positive_regulation"
} |
11839580.s5 | Those patients that progressed to breast cancer (cases) showed significantly higher ER-alpha [median, 57.00% of cells within individual HUT foci; interquartile range (IQ), 33.48 to 67.78] and Ki-67 (median, 3.82%; IQ, 0.85 to 11.28) expression in their HUT foci compared with controls (ER-alpha median, 30.27%; IQ, 19.75 to 52.50 and Ki-67 median, 0.77%; IQ, 0.0458 to 1.72, P = 0.008 and <0.001). | breast | {
"name": "ER-alpha",
"pos": [
84,
91
]
} | {
"name": "breast cancer",
"pos": [
34,
46
]
} | increased | normalTOcancer | observation | unidentifiable | {
"name": "\nNone\n",
"pos": null,
"type": null
} | {
"name": "higher",
"pos": [
77,
82
],
"type": "Positive_regulation"
} |
11839580.s5 | Those patients that progressed to breast cancer (cases) showed significantly higher ER-alpha [median, 57.00% of cells within individual HUT foci; interquartile range (IQ), 33.48 to 67.78] and Ki-67 (median, 3.82%; IQ, 0.85 to 11.28) expression in their HUT foci compared with controls (ER-alpha median, 30.27%; IQ, 19.75 to 52.50 and Ki-67 median, 0.77%; IQ, 0.0458 to 1.72, P = 0.008 and <0.001). | breast | {
"name": "ER-alpha",
"pos": [
84,
91
]
} | {
"name": "breast cancer",
"pos": [
34,
46
]
} | increased | normalTOcancer | observation | unidentifiable | {
"name": "expression",
"pos": [
233,
242
],
"type": "Gene_expression"
} | {
"name": "higher",
"pos": [
77,
82
],
"type": "Positive_regulation"
} |
18702457.s5 | Several of the analogues elicit stronger growth inhibitory activity against prostate (PC-3) and breast (MDA-MB-468) carcinoma cells, which contain elevated basal IKK activity; this antiproliferative activity correlates with increased inhibition of recombinant IKKbeta in vitro, suggesting that the anticancer activities of these AdArs might be related to the inhibition of IKK/NFkappaB signaling. | breast | {
"name": "IKK",
"pos": [
162,
164
]
} | {
"name": "MDA-MB-468",
"pos": [
104,
113
]
} | increased | normalTOcancer | observation | unchanged | {
"name": "\nNone\n",
"pos": null,
"type": null
} | {
"name": "elevated",
"pos": [
147,
154
],
"type": "Positive_regulation"
} |
18702457.s5 | Several of the analogues elicit stronger growth inhibitory activity against prostate (PC-3) and breast (MDA-MB-468) carcinoma cells, which contain elevated basal IKK activity; this antiproliferative activity correlates with increased inhibition of recombinant IKKbeta in vitro, suggesting that the anticancer activities of these AdArs might be related to the inhibition of IKK/NFkappaB signaling. | breast | {
"name": "IKK/NFkappaB",
"pos": [
373,
384
]
} | {
"name": "MDA-MB-468",
"pos": [
104,
113
]
} | decreased | cancerTOnormal | observation | unidentifiable | {
"name": "\nNone\n",
"pos": null,
"type": null
} | {
"name": "inhibition",
"pos": [
359,
368
],
"type": "Negative_regulation"
} |
19087284.s12 | Our findings show, for the first time, that DC is a natural tumor promoter by elevating Flk-1 and decreasing ceramide-mediated apoptosis of breast cancer progenitor cells. | breast | {
"name": "Flk-1",
"pos": [
88,
92
]
} | {
"name": "breast cancer",
"pos": [
140,
152
]
} | increased | normalTOcancer | causality | unidentifiable | {
"name": "\nNone\n",
"pos": null,
"type": null
} | {
"name": "elevating",
"pos": [
78,
86
],
"type": "Positive_regulation"
} |
1317462.s0 | Accumulation of p53 tumor suppressor gene protein: an independent marker of prognosis in breast cancers. | breast | {
"name": "p53 tumor suppressor gene protein",
"pos": [
16,
48
]
} | {
"name": "breast cancers",
"pos": [
89,
102
]
} | increased | normalTOcancer | observation | unchanged | {
"name": "\nNone\n",
"pos": null,
"type": null
} | {
"name": "Accumulation",
"pos": [
0,
11
],
"type": "Positive_regulation"
} |
1317462.s1 | Mutations of the tumor suppressor gene p53 have been identified in breast cancer cell lines, and some breast carcinomas are detectable by immunohistochemical assay because of p53 protein accumulation. | breast | {
"name": "p53 protein",
"pos": [
175,
185
]
} | {
"name": "breast carcinomas",
"pos": [
102,
118
]
} | increased | normalTOcancer | observation | unchanged | {
"name": "\nNone\n",
"pos": null,
"type": null
} | {
"name": "accumulation",
"pos": [
187,
198
],
"type": "Positive_regulation"
} |
15075673.s4 | In MDA-MB-231 breast carcinoma cells, Taxo did not interfere with the re-activation of E-cadherin and maspin genes by 5-AZA-CdR. | breast | {
"name": "maspin genes",
"pos": [
102,
113
]
} | {
"name": "breast carcinoma",
"pos": [
14,
29
]
} | increased | unidentifiable | {
"name": "\nNone\n",
"pos": null,
"type": null
} | {
"name": "re-activation",
"pos": [
70,
82
],
"type": "Positive_regulation"
} |
||
15075673.s4 | In MDA-MB-231 breast carcinoma cells, Taxo did not interfere with the re-activation of E-cadherin and maspin genes by 5-AZA-CdR. | breast | {
"name": "E-cadherin",
"pos": [
87,
96
]
} | {
"name": "breast carcinoma",
"pos": [
14,
29
]
} | increased | unidentifiable | {
"name": "\nNone\n",
"pos": null,
"type": null
} | {
"name": "re-activation",
"pos": [
70,
82
],
"type": "Positive_regulation"
} |
||
16176813.s6 | While expression of Bcl-2, Bcl-X(L), Hsp 70 and 90 was increased, expression of Bax and caspases 8 and 3 was significantly lower in both human as well as canine mammary tumor tissues compared to corresponding adjacent tissues. | breast | {
"name": "Bcl-2",
"pos": [
20,
24
]
} | {
"name": "mammary tumor",
"pos": [
161,
173
]
} | increased | normalTOcancer | observation | unchanged | {
"name": "expression",
"pos": [
6,
15
],
"type": "Gene_expression"
} | {
"name": "increased",
"pos": [
55,
63
],
"type": "Positive_regulation"
} |
16176813.s6 | While expression of Bcl-2, Bcl-X(L), Hsp 70 and 90 was increased, expression of Bax and caspases 8 and 3 was significantly lower in both human as well as canine mammary tumor tissues compared to corresponding adjacent tissues. | breast | {
"name": "Bcl-X",
"pos": [
27,
31
]
} | {
"name": "mammary tumor",
"pos": [
161,
173
]
} | increased | normalTOcancer | observation | unchanged | {
"name": "expression",
"pos": [
6,
15
],
"type": "Gene_expression"
} | {
"name": "increased",
"pos": [
55,
63
],
"type": "Positive_regulation"
} |
16176813.s6 | While expression of Bcl-2, Bcl-X(L), Hsp 70 and 90 was increased, expression of Bax and caspases 8 and 3 was significantly lower in both human as well as canine mammary tumor tissues compared to corresponding adjacent tissues. | breast | {
"name": "Hsp 70",
"pos": [
37,
42
]
} | {
"name": "mammary tumor",
"pos": [
161,
173
]
} | increased | normalTOcancer | observation | unchanged | {
"name": "expression",
"pos": [
6,
15
],
"type": "Gene_expression"
} | {
"name": "increased",
"pos": [
55,
63
],
"type": "Positive_regulation"
} |
9857236.s7 | In conclusion, physiological elevation of the bFGF during normal menstruation can influence the precise interpretation of the pathological elevation of the bFGF in pre-menopausal breast cancer patients. | breast | {
"name": "bFGF",
"pos": [
46,
49
]
} | {
"name": "breast cancer",
"pos": [
179,
191
]
} | increased | unidentifiable | {
"name": "\nNone\n",
"pos": null,
"type": null
} | {
"name": "elevation",
"pos": [
29,
37
],
"type": "Positive_regulation"
} |
||
9857236.s7 | In conclusion, physiological elevation of the bFGF during normal menstruation can influence the precise interpretation of the pathological elevation of the bFGF in pre-menopausal breast cancer patients. | breast | {
"name": "bFGF",
"pos": [
156,
159
]
} | {
"name": "breast cancer",
"pos": [
179,
191
]
} | increased | unidentifiable | {
"name": "\nNone\n",
"pos": null,
"type": null
} | {
"name": "elevation",
"pos": [
139,
147
],
"type": "Positive_regulation"
} |
||
16643892.s1 | Many advanced human tumors including breast cancer overproduce plasmin that is known to promote angiogenesis and metastasis. | breast | {
"name": "plasmin",
"pos": [
63,
69
]
} | {
"name": "breast cancer",
"pos": [
37,
49
]
} | increased | normalTOcancer | causality | unidentifiable | {
"name": "overproduce",
"pos": [
51,
61
],
"type": "Gene_expression"
} | {
"name": "overproduce",
"pos": [
51,
61
],
"type": "Positive_regulation"
} |
16643892.s8 | MDA-MB231 cell membranes induced plasmin generation in a time-dependent manner while those from MCF-7 cells failed to convert plasminogen to plasmin. | breast | {
"name": "plasmin",
"pos": [
33,
39
]
} | {
"name": "MDA-MB231",
"pos": [
0,
8
]
} | increased | unidentifiable | {
"name": "\nNone\n",
"pos": null,
"type": null
} | {
"name": "induced",
"pos": [
25,
31
],
"type": "Positive_regulation"
} |
||
20635137.s0 | GRB7 protein over-expression and clinical outcome in breast cancer. | breast | {
"name": "GRB7 protein",
"pos": [
0,
11
]
} | {
"name": "breast cancer",
"pos": [
53,
65
]
} | increased | normalTOcancer | observation | unchanged | {
"name": "over-expression",
"pos": [
13,
27
],
"type": "Gene_expression"
} | {
"name": "over-expression",
"pos": [
13,
27
],
"type": "Positive_regulation"
} |
20635137.s14 | GRB7 protein over-expression is an independent adverse prognostic factor in human breast cancer. | breast | {
"name": "GRB7 protein",
"pos": [
0,
11
]
} | {
"name": "breast cancer",
"pos": [
82,
94
]
} | increased | normalTOcancer | observation | unchanged | {
"name": "over-expression",
"pos": [
13,
27
],
"type": "Gene_expression"
} | {
"name": "over-expression",
"pos": [
13,
27
],
"type": "Positive_regulation"
} |
9654650.s10 | All of the test compounds (10 nM) substantially inhibited estrogen sulfatase activity of intact MDA-MB-231 cells. | breast | {
"name": "estrogen sulfatase",
"pos": [
58,
75
]
} | {
"name": "MDA-MB-231",
"pos": [
96,
105
]
} | decreased | unidentifiable | {
"name": "\nNone\n",
"pos": null,
"type": null
} | {
"name": "inhibited",
"pos": [
48,
56
],
"type": "Negative_regulation"
} |
||
9654650.s14 | Our data indicate the utility of the new compounds for inhibition of breast cancer cell estrone sulfatase activity. | breast | {
"name": "breast cancer cell estrone sulfatase",
"pos": [
69,
104
]
} | {
"name": "breast cancer",
"pos": [
69,
81
]
} | decreased | unidentifiable | {
"name": "\nNone\n",
"pos": null,
"type": null
} | {
"name": "inhibition",
"pos": [
55,
64
],
"type": "Negative_regulation"
} |
||
22179838.s2 | Experimentally, we found that reducing expression of SCRIB by short-hairpin RNAs (shRNAs) reduces the growth of human breast cancer cells in xenograft assays. | breast | {
"name": "SCRIB",
"pos": [
53,
57
]
} | {
"name": "breast cancer",
"pos": [
118,
130
]
} | decreased | cancerTOnormal | causality | unidentifiable | {
"name": "expression",
"pos": [
39,
48
],
"type": "Gene_expression"
} | {
"name": "reducing",
"pos": [
30,
37
],
"type": "Negative_regulation"
} |
10885804.s10 | We found that the functional disruption of IGF-1R markedly influences breast cancer metastasis in nude mice by suppressing cellular adhesion, invasion, and metastasis of breast cancer cells to the lung, lymph nodes, and lymph vessels. | breast | {
"name": "IGF-1R",
"pos": [
43,
48
]
} | {
"name": "breast cancer",
"pos": [
70,
82
]
} | decreased | cancerTOnormal | causality | unidentifiable | {
"name": "\nNone\n",
"pos": null,
"type": null
} | {
"name": "disruption",
"pos": [
29,
38
],
"type": "Negative_regulation"
} |
9092801.s4 |
In T-47D cells, PRG1 mRNA was rapidly and transiently induced by progestins, expression peaking between 2 and 4 h and returning to control levels by 12 h. | breast | {
"name": "PRG1 mRNA",
"pos": [
16,
24
]
} | {
"name": "T-47D",
"pos": [
3,
7
]
} | increased | unidentifiable | {
"name": "\nNone\n",
"pos": null,
"type": null
} | {
"name": "induced",
"pos": [
54,
60
],
"type": "Positive_regulation"
} |
||
21607411.s1 | Both elevated protein-tyrosine kinase activity of pp60(c-src) and the association of its high activity with a short disease-free period have been reported in patients with human breast cancer. | breast | {
"name": "pp60(c-src)",
"pos": [
50,
60
]
} | {
"name": "breast cancer",
"pos": [
178,
190
]
} | increased | unidentifiable | {
"name": "\nNone\n",
"pos": null,
"type": null
} | {
"name": "elevated",
"pos": [
5,
12
],
"type": "Positive_regulation"
} |
||
21607411.s5 |
In 60% of breast cancers, the pp60(c-src) level was increased, the reaction intensity was elevated, and a positive reaction was seen in cytoplasma and in the nuclear area. | breast | {
"name": "pp60(c-src)",
"pos": [
30,
40
]
} | {
"name": "breast cancers",
"pos": [
10,
23
]
} | increased | normalTOcancer | observation | unidentifiable | {
"name": "\nNone\n",
"pos": null,
"type": null
} | {
"name": "increased",
"pos": [
52,
60
],
"type": "Positive_regulation"
} |
20736065.s0 | Selective inhibition of human 3β-hydroxysteroid dehydrogenase type 1 as a potential treatment for breast cancer. | breast | {
"name": "human 3β-hydroxysteroid dehydrogenase type 1",
"pos": [
24,
67
]
} | {
"name": "breast cancer",
"pos": [
98,
110
]
} | decreased | cancerTOnormal | causality | unidentifiable | {
"name": "\nNone\n",
"pos": null,
"type": null
} | {
"name": "inhibition",
"pos": [
10,
19
],
"type": "Negative_regulation"
} |
20630060.s14 | We showed that treatment of MCF-7 and triple-negative MDA-MB-231 human breast cancer cells with a GnRH-II antagonist results in apoptotic cell death in vitro via activation of stress-activated MAPK p38 and loss of mitochondrial membrane potential. | breast | {
"name": "p38",
"pos": [
198,
200
]
} | {
"name": "breast cancer",
"pos": [
71,
83
]
} | increased | cancerTOnormal | causality | unidentifiable | {
"name": "\nNone\n",
"pos": null,
"type": null
} | {
"name": "activation",
"pos": [
162,
171
],
"type": "Positive_regulation"
} |
20630060.s15 | In addition, we showed GnRH-II antagonist-induced activation of caspase-3 in MDA-MB-231 human breast cancer cells. | breast | {
"name": "caspase-3",
"pos": [
64,
72
]
} | {
"name": "breast cancer",
"pos": [
94,
106
]
} | increased | unidentifiable | {
"name": "\nNone\n",
"pos": null,
"type": null
} | {
"name": "activation",
"pos": [
50,
59
],
"type": "Positive_regulation"
} |
||
20390342.s0 | CTEN (C-terminal tensin-like), a novel oncogene overexpressed in invasive breast carcinoma of poor prognosis. | breast | {
"name": "CTEN (C-terminal tensin-like)",
"pos": [
0,
28
]
} | {
"name": "invasive breast carcinoma",
"pos": [
65,
89
]
} | increased | normalTOcancer | observation | unchanged | {
"name": "overexpressed",
"pos": [
48,
60
],
"type": "Gene_expression"
} | {
"name": "overexpressed",
"pos": [
48,
60
],
"type": "Gene_expression"
} |
17608728.s0 | The DNA-binding epidermal growth factor-receptor inhibitor PD153035 and other DNA-intercalating cytotoxic drugs reactivate the expression of the retinoic acid receptor-beta tumor-suppressor gene in breast cancer cells. | breast | {
"name": "retinoic acid receptor-beta tumor-suppressor gene",
"pos": [
145,
193
]
} | {
"name": "breast cancer",
"pos": [
198,
210
]
} | increased | unidentifiable | {
"name": "expression",
"pos": [
127,
136
],
"type": "Gene_expression"
} | {
"name": "reactivate",
"pos": [
112,
121
],
"type": "Positive_regulation"
} |
||
17608728.s4 | Here, we demonstrate that the EGFR inhibitor PD153035 specifically induces RAR-beta2, but not the other two isoforms (RAR-beta1, RAR-beta4) in MDA-MB-468 and MDA-MB-453 human breast cancer cells. | breast | {
"name": "RAR-beta2",
"pos": [
75,
83
]
} | {
"name": "breast cancer",
"pos": [
175,
187
]
} | increased | unidentifiable | {
"name": "\nNone\n",
"pos": null,
"type": null
} | {
"name": "induces",
"pos": [
67,
73
],
"type": "Positive_regulation"
} |
||
16630134.s0 | MTA1 overexpression correlates significantly with tumor grade and angiogenesis in human breast cancers. | breast | {
"name": "MTA1",
"pos": [
0,
3
]
} | {
"name": "breast cancers",
"pos": [
88,
101
]
} | increased | normalTOcancer | causality | unchanged | {
"name": "overexpression",
"pos": [
5,
18
],
"type": "Gene_expression"
} | {
"name": "overexpression",
"pos": [
5,
18
],
"type": "Positive_regulation"
} |
21247495.s1 | Osteopontin (OPN) is a secreted phosphoprotein often overexpressed at high levels in the blood and primary tumors of breast cancer patients. | breast | {
"name": "Osteopontin",
"pos": [
0,
10
]
} | {
"name": "breast cancer",
"pos": [
117,
129
]
} | increased | normalTOcancer | observation | unchanged | {
"name": "overexpressed",
"pos": [
53,
65
],
"type": "Gene_expression"
} | {
"name": "overexpressed",
"pos": [
53,
65
],
"type": "Positive_regulation"
} |
7438115.s6 | These findings support the assumption that induction of PGR by estrogen in human breast cancer is mediated by a mechanism involving nuclear receptors. | breast | {
"name": "PGR",
"pos": [
56,
58
]
} | {
"name": "breast cancer",
"pos": [
81,
93
]
} | increased | unidentifiable | {
"name": "\nNone\n",
"pos": null,
"type": null
} | {
"name": "induction",
"pos": [
43,
51
],
"type": "Positive_regulation"
} |
||
14629195.s0 | Activated Src increases adhesion, survival and alpha2-integrin expression in human breast cancer cells. | breast | {
"name": "Src",
"pos": [
10,
12
]
} | {
"name": "breast cancer",
"pos": [
83,
95
]
} | increased | normalTOcancer | causality | unidentifiable | {
"name": "\nNone\n",
"pos": null,
"type": null
} | {
"name": "Activated",
"pos": [
0,
8
],
"type": "Positive_regulation"
} |
14629195.s0 | Activated Src increases adhesion, survival and alpha2-integrin expression in human breast cancer cells. | breast | {
"name": "alpha2-integrin",
"pos": [
47,
61
]
} | {
"name": "breast cancer",
"pos": [
83,
95
]
} | increased | normalTOcancer | observation | unidentifiable | {
"name": "expression",
"pos": [
63,
72
],
"type": "Gene_expression"
} | {
"name": "increases",
"pos": [
14,
22
],
"type": "Positive_regulation"
} |
14629195.s4 | We have shown that overexpression of an activated form of the Src tyrosine kinase suppressed the loss of adhesion induced by dominant-negative; adenoviral FAK-CD and decreased the apoptotic response in BT474 and MCF-7 breast cancer cell lines. | breast | {
"name": "Src tyrosine kinase",
"pos": [
62,
80
]
} | {
"name": "breast cancer",
"pos": [
218,
230
]
} | increased | normalTOcancer | causality | unidentifiable | {
"name": "overexpression",
"pos": [
19,
32
],
"type": "Gene_expression"
} | {
"name": "overexpression",
"pos": [
19,
32
],
"type": "Positive_regulation"
} |
14629195.s6 | We have also shown that expression of activated Src in breast cancer cells increased the expression of alpha2-integrin and that overexpression of alpha2-integrin suppressed FAK-CD-mediated loss of adhesion. | breast | {
"name": "alpha2-integrin",
"pos": [
103,
117
]
} | {
"name": "breast cancer",
"pos": [
55,
67
]
} | increased | unidentifiable | {
"name": "expression",
"pos": [
89,
98
],
"type": "Gene_expression"
} | {
"name": "increased",
"pos": [
75,
83
],
"type": "Positive_regulation"
} |
||
14629195.s6 | We have also shown that expression of activated Src in breast cancer cells increased the expression of alpha2-integrin and that overexpression of alpha2-integrin suppressed FAK-CD-mediated loss of adhesion. | breast | {
"name": "alpha2-integrin",
"pos": [
146,
160
]
} | {
"name": "breast cancer",
"pos": [
55,
67
]
} | increased | unidentifiable | {
"name": "overexpression",
"pos": [
128,
141
],
"type": "Gene_expression"
} | {
"name": "overexpression",
"pos": [
128,
141
],
"type": "Positive_regulation"
} |
||
14629195.s6 | We have also shown that expression of activated Src in breast cancer cells increased the expression of alpha2-integrin and that overexpression of alpha2-integrin suppressed FAK-CD-mediated loss of adhesion. | breast | {
"name": "Src",
"pos": [
48,
50
]
} | {
"name": "breast cancer",
"pos": [
55,
67
]
} | increased | unidentifiable | {
"name": "\nNone\n",
"pos": null,
"type": null
} | {
"name": "activated",
"pos": [
38,
46
],
"type": "Positive_regulation"
} |
||
7947821.s4 | Cell-surface expression of galectin-3 was reduced following treatment of viable T47D human breast carcinoma cells with gelatinase A. | breast | {
"name": "galectin-3",
"pos": [
27,
36
]
} | {
"name": "breast carcinoma",
"pos": [
91,
106
]
} | decreased | unidentifiable | {
"name": "expression",
"pos": [
13,
22
],
"type": "Gene_expression"
} | {
"name": "reduced",
"pos": [
42,
48
],
"type": "Negative_regulation"
} |
||
20495363.s11 | Thus, pharmacologically-induced metabolic restriction (via treatment with glycolysis inhibitors) may be a promising new therapeutic strategy for breast cancer patients that lack stromal Cav-1 expression. | breast | {
"name": "Cav-1",
"pos": [
186,
190
]
} | {
"name": "breast cancer",
"pos": [
145,
157
]
} | decreased | unidentifiable | {
"name": "expression",
"pos": [
192,
201
],
"type": "Gene_expression"
} | {
"name": "lack",
"pos": [
173,
176
],
"type": "Negative_regulation"
} |