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dict | cancer
dict | CGE
stringclasses 2
values | CCS
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values | PT
stringclasses 3
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values | expression_change_keyword_1
dict | expression_change_keyword_2
dict |
|---|---|---|---|---|---|---|---|---|---|---|
15688367.s6 | Overexpressing ID2 in the MDA-MB-468 breast cancer cell line generated a marked cytoplasmic localisation of the protein and reduced the invasive capacity of cells. | breast | {
"name": "ID2",
"pos": [
15,
17
]
} | {
"name": "breast cancer",
"pos": [
37,
49
]
} | increased | cancerTOnormal | causality | unidentifiable | {
"name": "Overexpressing",
"pos": [
0,
13
],
"type": "Gene_expression"
} | {
"name": "Overexpressing",
"pos": [
0,
13
],
"type": "Positive_regulation"
} |
15113415.s1 | The cellular retinol binding protein I gene (CRBP) is downregulated in a subset of human breast cancers and in MMTV-Myc induced mouse mammary tumors. | breast | {
"name": "CRBP",
"pos": [
45,
48
]
} | {
"name": "mammary tumors",
"pos": [
134,
147
]
} | decreased | normalTOcancer | observation | unchanged | {
"name": "\nNone\n",
"pos": null,
"type": null
} | {
"name": "downregulated",
"pos": [
54,
66
],
"type": "Negative_regulation"
} |
15113415.s1 | The cellular retinol binding protein I gene (CRBP) is downregulated in a subset of human breast cancers and in MMTV-Myc induced mouse mammary tumors. | breast | {
"name": "cellular retinol binding protein I gene",
"pos": [
4,
42
]
} | {
"name": "mammary tumors",
"pos": [
134,
147
]
} | decreased | normalTOcancer | observation | unchanged | {
"name": "\nNone\n",
"pos": null,
"type": null
} | {
"name": "downregulated",
"pos": [
54,
66
],
"type": "Negative_regulation"
} |
15113415.s2 | Functional studies suggest that CRBP downregulation contributes to breast tumor progression. | breast | {
"name": "CRBP",
"pos": [
32,
35
]
} | {
"name": "breast tumor",
"pos": [
67,
78
]
} | decreased | normalTOcancer | causality | unidentifiable | {
"name": "\nNone\n",
"pos": null,
"type": null
} | {
"name": "downregulation",
"pos": [
37,
50
],
"type": "Negative_regulation"
} |
16464948.s8 | The insLQ polymorphism increases LHR activity, thereby shortening breast cancer disease-free survival, probably by increasing estrogen exposure in female carriers. | breast | {
"name": "LHR",
"pos": [
33,
35
]
} | {
"name": "breast cancer",
"pos": [
66,
78
]
} | increased | unidentifiable | {
"name": "\nNone\n",
"pos": null,
"type": null
} | {
"name": "increases",
"pos": [
23,
31
],
"type": "Positive_regulation"
} |
||
1436241.s4 | IFN-alpha increased the cell surface expression of DR antigen only in ZR-75-1 cells. | breast | {
"name": "DR antigen",
"pos": [
51,
60
]
} | {
"name": "ZR-75-1",
"pos": [
70,
76
]
} | increased | unidentifiable | {
"name": "expression",
"pos": [
37,
46
],
"type": "Gene_expression"
} | {
"name": "increased",
"pos": [
10,
18
],
"type": "Positive_regulation"
} |
||
1436241.s5 | IL-1-alpha induced a moderate level of HLA class I antigen in ZR-75-1, BT-20 and MDA-MB-468 cells, and HLA class II (DR) expression only in ZR-75-1 cells. | breast | {
"name": "HLA class II (DR)",
"pos": [
103,
119
]
} | {
"name": "MDA-MB-468",
"pos": [
81,
90
]
} | increased | unidentifiable | {
"name": "expression",
"pos": [
121,
130
],
"type": "Gene_expression"
} | {
"name": "induced",
"pos": [
11,
17
],
"type": "Positive_regulation"
} |
||
1349318.s9 | No statistically significant association was found between increased PTPase activity and either c-erbB-2 overexpression or grade and stage of disease in primary human mammary tumors. | breast | {
"name": "PTPase",
"pos": [
69,
74
]
} | {
"name": "mammary tumors",
"pos": [
167,
180
]
} | increased | unidentifiable | {
"name": "\nNone\n",
"pos": null,
"type": null
} | {
"name": "increased",
"pos": [
59,
67
],
"type": "Positive_regulation"
} |
||
1349318.s9 | No statistically significant association was found between increased PTPase activity and either c-erbB-2 overexpression or grade and stage of disease in primary human mammary tumors. | breast | {
"name": "c-erbB-2",
"pos": [
96,
103
]
} | {
"name": "mammary tumors",
"pos": [
167,
180
]
} | increased | unidentifiable | {
"name": "overexpression",
"pos": [
105,
118
],
"type": "Gene_expression"
} | {
"name": "overexpression",
"pos": [
105,
118
],
"type": "Positive_regulation"
} |
||
21643005.s12 | Administration of exogenous LTB4 (1-10 nmol/L) was able to stimulate the promoter activity of FASN in MCF-7 cells. | breast | {
"name": "FASN",
"pos": [
94,
97
]
} | {
"name": "MCF-7",
"pos": [
102,
106
]
} | increased | unidentifiable | {
"name": "\nNone\n",
"pos": null,
"type": null
} | {
"name": "stimulate",
"pos": [
59,
67
],
"type": "Positive_regulation"
} |
||
20504320.s8 | In aggregate, these studies support the notion that TGF-beta plays an important role in both bone-and lung metastases of basal-like breast cancer, and that inhibiting TGF-beta signaling results in a therapeutic effect independently of the tissue-tropism of the metastatic cells. | breast | {
"name": "TGF-beta",
"pos": [
167,
174
]
} | {
"name": "breast cancer",
"pos": [
132,
144
]
} | decreased | cancerTOnormal | causality | unidentifiable | {
"name": "\nNone\n",
"pos": null,
"type": null
} | {
"name": "inhibiting",
"pos": [
156,
165
],
"type": "Negative_regulation"
} |
19115233.s0 | Loss of profilin-1 expression enhances breast cancer cell motility by Ena/VASP proteins. | breast | {
"name": "profilin-1",
"pos": [
8,
17
]
} | {
"name": "breast cancer",
"pos": [
39,
51
]
} | decreased | normalTOcancer | causality | unidentifiable | {
"name": "expression",
"pos": [
19,
28
],
"type": "Gene_expression"
} | {
"name": "Loss",
"pos": [
0,
3
],
"type": "Negative_regulation"
} |
19115233.s2 | Herein, we demonstrate that loss of Pfn1 expression leads to slower but more stable lamellipodial protrusion thereby enhancing the net protrusion rate and the overall motility of MDA-MB-231 breast cancer cells. | breast | {
"name": "Pfn1",
"pos": [
36,
39
]
} | {
"name": "breast cancer",
"pos": [
190,
202
]
} | decreased | normalTOcancer | causality | unidentifiable | {
"name": "expression",
"pos": [
41,
50
],
"type": "Gene_expression"
} | {
"name": "loss",
"pos": [
28,
31
],
"type": "Negative_regulation"
} |
19115233.s3 | Interestingly, MDA-MB-231 cells showed dramatic enrichment of VASP at their leading edge when Pfn1 expression was downregulated and this observation was also reproducible in other cell types including human mammary epithelial cells and vascular endothelial cells. | breast | {
"name": "Pfn1",
"pos": [
94,
97
]
} | {
"name": "MDA-MB-231",
"pos": [
15,
24
]
} | decreased | unidentifiable | {
"name": "expression",
"pos": [
99,
108
],
"type": "Gene_expression"
} | {
"name": "downregulated",
"pos": [
114,
126
],
"type": "Negative_regulation"
} |
||
19115233.s4 | We further demonstrate that Pfn1 downregulation results in a hyper-motile phenotype of MDA-MB-231 cells in an Ena/VASP-dependent mechanism. | breast | {
"name": "Pfn1",
"pos": [
28,
31
]
} | {
"name": "MDA-MB-231",
"pos": [
87,
96
]
} | decreased | normalTOcancer | causality | unidentifiable | {
"name": "\nNone\n",
"pos": null,
"type": null
} | {
"name": "downregulation",
"pos": [
33,
46
],
"type": "Negative_regulation"
} |
7917361.s8 | We conclude that c-erbB-2 protein overexpression assessed by IHC is a superior prognostic indicator in operable breast cancer compared to c-erbB-2 gene amplification analysed by the dot-blot technique. | breast | {
"name": "c-erbB-2 protein",
"pos": [
17,
32
]
} | {
"name": "breast cancer",
"pos": [
112,
124
]
} | increased | normalTOcancer | observation | unidentifiable | {
"name": "overexpression",
"pos": [
34,
47
],
"type": "Gene_expression"
} | {
"name": "overexpression",
"pos": [
34,
47
],
"type": "Positive_regulation"
} |
7949208.s0 | Effects of Fadrozole (CGS 16949A) and Letrozole (CGS 20267) on the inhibition of aromatase activity in breast cancer patients. | breast | {
"name": "aromatase",
"pos": [
81,
89
]
} | {
"name": "breast cancer",
"pos": [
103,
115
]
} | decreased | unidentifiable | {
"name": "\nNone\n",
"pos": null,
"type": null
} | {
"name": "inhibition",
"pos": [
67,
76
],
"type": "Negative_regulation"
} |
||
7949208.s6 | The inhibition of aromatase activity by these imidazole derivatives as second line therapy for patients with hormone dependent breast cancer appears to be a favorable alternative form of hormone ablative therapy and holds considerable promise for the treatment of this malignancy. | breast | {
"name": "aromatase",
"pos": [
18,
26
]
} | {
"name": "breast cancer",
"pos": [
127,
139
]
} | decreased | cancerTOnormal | causality | unidentifiable | {
"name": "\nNone\n",
"pos": null,
"type": null
} | {
"name": "inhibition",
"pos": [
4,
13
],
"type": "Negative_regulation"
} |
12861063.s3 | The analysis of E-cadherin glycoprotein expression is a powerful tool for distinguishing lobular from ductal carcinomas, because complete loss of E-cadherin expression occurs in most infiltrating lobular tumors and lobular carcinomas in situ, but not in ductal tumors. | breast | {
"name": "E-cadherin",
"pos": [
146,
155
]
} | {
"name": "lobular carcinomas",
"pos": [
215,
232
]
} | decreased | normalTOcancer | observation | unidentifiable | {
"name": "expression",
"pos": [
157,
166
],
"type": "Gene_expression"
} | {
"name": "loss",
"pos": [
138,
141
],
"type": "Negative_regulation"
} |
11156389.s7 | We show, for the first time in a transgenic mouse model, that mammary tumor progression is associated with the loss of ERalpha expression, as has been often observed in human breast cancers with important clinical significance. | breast | {
"name": "ERalpha",
"pos": [
119,
125
]
} | {
"name": "breast cancers",
"pos": [
175,
188
]
} | decreased | normalTOcancer | observation | unidentifiable | {
"name": "expression",
"pos": [
127,
136
],
"type": "Gene_expression"
} | {
"name": "loss",
"pos": [
111,
114
],
"type": "Negative_regulation"
} |
8080727.s2 | A strong association has been observed between reduced expression of the nm23 gene and acquisition of metastatic behaviour in some tumour cells, including breast cancer and melanoma, but not in others, such as neuroblastoma and colon, cervical and thyroid cancers. | breast | {
"name": "nm23 gene",
"pos": [
73,
81
]
} | {
"name": "breast cancer",
"pos": [
155,
167
]
} | decreased | normalTOcancer | observation | unidentifiable | {
"name": "expression",
"pos": [
55,
64
],
"type": "Gene_expression"
} | {
"name": "reduced",
"pos": [
47,
53
],
"type": "Negative_regulation"
} |
18181175.s3 | Here, we show that overexpression of BIRC5 induces a high proliferation level in MCF-7 breast tumor cells. | breast | {
"name": "BIRC5",
"pos": [
37,
41
]
} | {
"name": "breast tumor",
"pos": [
87,
98
]
} | increased | normalTOcancer | causality | unidentifiable | {
"name": "overexpression",
"pos": [
19,
32
],
"type": "Gene_expression"
} | {
"name": "overexpression",
"pos": [
19,
32
],
"type": "Positive_regulation"
} |
16489002.s0 | ErbB2 increases vascular endothelial growth factor protein synthesis via activation of mammalian target of rapamycin/p70S6K leading to increased angiogenesis and spontaneous metastasis of human breast cancer cells. | breast | {
"name": "vascular endothelial growth factor protein",
"pos": [
16,
57
]
} | {
"name": "breast cancer",
"pos": [
194,
206
]
} | increased | normalTOcancer | causality | unidentifiable | {
"name": "synthesis",
"pos": [
59,
67
],
"type": "Gene_expression"
} | {
"name": "increases",
"pos": [
6,
14
],
"type": "Positive_regulation"
} |
16489002.s1 | ErbB2 overexpression in breast tumors results in increased metastasis and angiogenesis and reduced survival. | breast | {
"name": "ErbB2",
"pos": [
0,
4
]
} | {
"name": "breast tumors",
"pos": [
24,
36
]
} | increased | normalTOcancer | causality | unidentifiable | {
"name": "overexpression",
"pos": [
6,
19
],
"type": "Gene_expression"
} | {
"name": "overexpression",
"pos": [
6,
19
],
"type": "Positive_regulation"
} |
18066063.s3 | Here we show that heterozygous inactivation of the tumor suppressor gene Pten leads to the formation of basal-like mammary tumors in mice, and that loss of PTEN expression is significantly associated with the BBC subtype in human sporadic and BRCA1-associated hereditary breast cancers. | breast | {
"name": "Pten",
"pos": [
73,
76
]
} | {
"name": "hereditary breast cancers",
"pos": [
260,
284
]
} | decreased | normalTOcancer | causality | unchanged | {
"name": "\nNone\n",
"pos": null,
"type": null
} | {
"name": "inactivation",
"pos": [
31,
42
],
"type": "Negative_regulation"
} |
18066063.s3 | Here we show that heterozygous inactivation of the tumor suppressor gene Pten leads to the formation of basal-like mammary tumors in mice, and that loss of PTEN expression is significantly associated with the BBC subtype in human sporadic and BRCA1-associated hereditary breast cancers. | breast | {
"name": "PTEN",
"pos": [
156,
159
]
} | {
"name": "hereditary breast cancers",
"pos": [
260,
284
]
} | decreased | normalTOcancer | observation | unchanged | {
"name": "expression",
"pos": [
161,
170
],
"type": "Gene_expression"
} | {
"name": "loss",
"pos": [
148,
151
],
"type": "Negative_regulation"
} |
18945339.s13 | HER-2 over-expression was observed in 18.1% of Tunisian breast carcinoma affecting female patients. | breast | {
"name": "HER-2",
"pos": [
0,
4
]
} | {
"name": "breast carcinoma",
"pos": [
56,
71
]
} | increased | normalTOcancer | observation | unchanged | {
"name": "over-expression",
"pos": [
6,
20
],
"type": "Gene_expression"
} | {
"name": "over-expression",
"pos": [
6,
20
],
"type": "Positive_regulation"
} |
18829495.s9 | Here, we defined a new mechanism for IMC-C225 that cross-links integrins with EGFR, leading to activation of RhoA and inhibition of breast cancer cell invasion irrespective of the level of EGFR in the cells, thus providing a rationale for using IMC-C225 in the metastatic setting independent of the levels of EGFR. | breast | {
"name": "RhoA",
"pos": [
109,
112
]
} | {
"name": "breast cancer",
"pos": [
132,
144
]
} | increased | cancerTOnormal | observation | unidentifiable | {
"name": "\nNone\n",
"pos": null,
"type": null
} | {
"name": "activation",
"pos": [
95,
104
],
"type": "Positive_regulation"
} |
15313907.s3 | Southern analysis of breast cancer profiling arrays revealed that 29 patients (group I) expressed an elevated LF, 10 patients (group II) showed decreased LF, and 8 patients (group III) had no change relative to the adjacent normal tissue. | breast | {
"name": "LF",
"pos": [
154,
155
]
} | {
"name": "breast cancer",
"pos": [
21,
33
]
} | decreased | normalTOcancer | observation | unchanged | {
"name": "\nNone\n",
"pos": null,
"type": null
} | {
"name": "decreased",
"pos": [
144,
152
],
"type": "Negative_regulation"
} |
15894658.s9 | This study suggests that the Asn allele in the SHBG gene may be related to a reduced risk of breast cancer among postmenopausal women by increasing their blood SHBG levels. | breast | {
"name": "SHBG",
"pos": [
160,
163
]
} | {
"name": "breast cancer",
"pos": [
93,
105
]
} | increased | cancerTOnormal | observation | unidentifiable | {
"name": "levels",
"pos": [
165,
170
],
"type": "Gene_expression"
} | {
"name": "increasing",
"pos": [
137,
146
],
"type": "Positive_regulation"
} |
16510571.s3 | Activated STAT3 correlated with elevated cyclin D1 protein in primary breast tumors and breast cancer-derived cell lines. | breast | {
"name": "STAT3",
"pos": [
10,
14
]
} | {
"name": "breast tumors",
"pos": [
70,
82
]
} | increased | unidentifiable | {
"name": "\nNone\n",
"pos": null,
"type": null
} | {
"name": "Activated",
"pos": [
0,
8
],
"type": "Positive_regulation"
} |
||
16510571.s3 | Activated STAT3 correlated with elevated cyclin D1 protein in primary breast tumors and breast cancer-derived cell lines. | breast | {
"name": "cyclin D1 protein",
"pos": [
41,
57
]
} | {
"name": "breast tumors",
"pos": [
70,
82
]
} | increased | unidentifiable | {
"name": "\nNone\n",
"pos": null,
"type": null
} | {
"name": "elevated",
"pos": [
32,
39
],
"type": "Positive_regulation"
} |
||
16510571.s7 | Furthermore, knockdown of cyclin D1 in breast carcinoma cells led to a reduction in anchorage-independent growth. | breast | {
"name": "cyclin D1",
"pos": [
26,
34
]
} | {
"name": "breast carcinoma",
"pos": [
39,
54
]
} | decreased | cancerTOnormal | causality | unidentifiable | {
"name": "\nNone\n",
"pos": null,
"type": null
} | {
"name": "knockdown",
"pos": [
13,
21
],
"type": "Negative_regulation"
} |
15359289.s1 | The EphA2 receptor tyrosine kinase is frequently overexpressed in invasive breast cancer cells. | breast | {
"name": "EphA2 receptor tyrosine kinase",
"pos": [
4,
33
]
} | {
"name": "invasive breast cancer",
"pos": [
66,
87
]
} | increased | normalTOcancer | observation | unchanged | {
"name": "overexpressed",
"pos": [
49,
61
],
"type": "Gene_expression"
} | {
"name": "overexpressed",
"pos": [
49,
61
],
"type": "Positive_regulation"
} |
20525379.s12 | AGR2 knockdown induced cell death in ZR-75-1 and T47 D cells, and also downregulated survivin and c-Myc. | breast | {
"name": "survivin",
"pos": [
85,
92
]
} | {
"name": "ZR-75-1",
"pos": [
37,
43
]
} | decreased | cancerTOnormal | observation | unidentifiable | {
"name": "\nNone\n",
"pos": null,
"type": null
} | {
"name": "downregulated",
"pos": [
71,
83
],
"type": "Negative_regulation"
} |
20525379.s12 | AGR2 knockdown induced cell death in ZR-75-1 and T47 D cells, and also downregulated survivin and c-Myc. | breast | {
"name": "c-Myc",
"pos": [
98,
102
]
} | {
"name": "ZR-75-1",
"pos": [
37,
43
]
} | decreased | cancerTOnormal | observation | unidentifiable | {
"name": "\nNone\n",
"pos": null,
"type": null
} | {
"name": "downregulated",
"pos": [
71,
83
],
"type": "Negative_regulation"
} |
20525379.s12 | AGR2 knockdown induced cell death in ZR-75-1 and T47 D cells, and also downregulated survivin and c-Myc. | breast | {
"name": "AGR2",
"pos": [
0,
3
]
} | {
"name": "ZR-75-1",
"pos": [
37,
43
]
} | decreased | cancerTOnormal | causality | unidentifiable | {
"name": "\nNone\n",
"pos": null,
"type": null
} | {
"name": "knockdown",
"pos": [
5,
13
],
"type": "Negative_regulation"
} |
11964084.s1 | Increased cellular activity of ornithine decarboxylase (ODC), the first and rate-limiting enzyme in polyamine (PA) synthesis, is an independent adverse prognostic factor for overall survival in human breast cancer, thus suggesting an important role for PA in tumor progression. | breast | {
"name": "ornithine decarboxylase",
"pos": [
31,
53
]
} | {
"name": "breast cancer",
"pos": [
200,
212
]
} | increased | normalTOcancer | observation | unidentifiable | {
"name": "\nNone\n",
"pos": null,
"type": null
} | {
"name": "Increased",
"pos": [
0,
8
],
"type": "Positive_regulation"
} |
11964084.s1 | Increased cellular activity of ornithine decarboxylase (ODC), the first and rate-limiting enzyme in polyamine (PA) synthesis, is an independent adverse prognostic factor for overall survival in human breast cancer, thus suggesting an important role for PA in tumor progression. | breast | {
"name": "ODC",
"pos": [
56,
58
]
} | {
"name": "breast cancer",
"pos": [
200,
212
]
} | increased | normalTOcancer | observation | unidentifiable | {
"name": "\nNone\n",
"pos": null,
"type": null
} | {
"name": "Increased",
"pos": [
0,
8
],
"type": "Positive_regulation"
} |
11518717.s1 | Hyperactivation of the insulin-like growth factor I receptor (IGF-IR) contributes to primary breast cancer development, but the role of the IGF-IR in tumor metastasis is unclear. | breast | {
"name": "insulin-like growth factor I receptor",
"pos": [
23,
59
]
} | {
"name": "breast cancer",
"pos": [
93,
105
]
} | increased | normalTOcancer | causality | unidentifiable | {
"name": "\nNone\n",
"pos": null,
"type": null
} | {
"name": "Hyperactivation",
"pos": [
0,
14
],
"type": "Positive_regulation"
} |
11518717.s1 | Hyperactivation of the insulin-like growth factor I receptor (IGF-IR) contributes to primary breast cancer development, but the role of the IGF-IR in tumor metastasis is unclear. | breast | {
"name": "IGF-IR",
"pos": [
62,
67
]
} | {
"name": "breast cancer",
"pos": [
93,
105
]
} | increased | normalTOcancer | causality | unidentifiable | {
"name": "\nNone\n",
"pos": null,
"type": null
} | {
"name": "Hyperactivation",
"pos": [
0,
14
],
"type": "Positive_regulation"
} |
11518717.s3 | We found that IGF-IR overexpression markedly stimulated aggregation in E-cad-positive MCF-7 breast cancer cells, but not in E-cad-negative MDA-MB-231 cells. | breast | {
"name": "IGF-IR",
"pos": [
14,
19
]
} | {
"name": "breast cancer",
"pos": [
92,
104
]
} | increased | unidentifiable | {
"name": "overexpression",
"pos": [
21,
34
],
"type": "Gene_expression"
} | {
"name": "overexpression",
"pos": [
21,
34
],
"type": "Positive_regulation"
} |
||
2516715.s3 | All three interferons and TPA enhanced the expression of the Mr 180,000 carcinoembryonic antigen (CEA) and CEA-related TAA recognized by monoclonal antibody B1.1 in both T47D and MCF-7 human breast carcinoma cell lines. | breast | {
"name": "carcinoembryonic antigen",
"pos": [
72,
95
]
} | {
"name": "breast carcinoma",
"pos": [
191,
206
]
} | increased | unidentifiable | {
"name": "expression",
"pos": [
43,
52
],
"type": "Gene_expression"
} | {
"name": "enhanced",
"pos": [
30,
37
],
"type": "Positive_regulation"
} |
||
2516715.s3 | All three interferons and TPA enhanced the expression of the Mr 180,000 carcinoembryonic antigen (CEA) and CEA-related TAA recognized by monoclonal antibody B1.1 in both T47D and MCF-7 human breast carcinoma cell lines. | breast | {
"name": "CEA",
"pos": [
98,
100
]
} | {
"name": "breast carcinoma",
"pos": [
191,
206
]
} | increased | unidentifiable | {
"name": "expression",
"pos": [
43,
52
],
"type": "Gene_expression"
} | {
"name": "enhanced",
"pos": [
30,
37
],
"type": "Positive_regulation"
} |
||
2516715.s3 | All three interferons and TPA enhanced the expression of the Mr 180,000 carcinoembryonic antigen (CEA) and CEA-related TAA recognized by monoclonal antibody B1.1 in both T47D and MCF-7 human breast carcinoma cell lines. | breast | {
"name": "CEA-related TAA",
"pos": [
107,
121
]
} | {
"name": "breast carcinoma",
"pos": [
191,
206
]
} | increased | unidentifiable | {
"name": "expression",
"pos": [
43,
52
],
"type": "Gene_expression"
} | {
"name": "enhanced",
"pos": [
30,
37
],
"type": "Positive_regulation"
} |
||
2516715.s5 | In general, IFN-gamma was more effective than IFN-alpha, IFN-beta or TPA in augmenting the expression of TAA, CEA and BCA-225, and HLA-DR expression in T47D and MCF-7 cells. | breast | {
"name": "HLA-DR",
"pos": [
131,
136
]
} | {
"name": "MCF-7",
"pos": [
161,
165
]
} | increased | unidentifiable | {
"name": "expression",
"pos": [
138,
147
],
"type": "Gene_expression"
} | {
"name": "augmenting",
"pos": [
76,
85
],
"type": "Positive_regulation"
} |
||
19041697.s6 | In addition, Cd enhanced DNA synthesis and pS2 mRNA levels in estrogen (10 pM estradiol) treated T47D cells. | breast | {
"name": "pS2 mRNA",
"pos": [
43,
50
]
} | {
"name": "T47D",
"pos": [
97,
100
]
} | increased | unidentifiable | {
"name": "\nNone\n",
"pos": null,
"type": null
} | {
"name": "enhanced",
"pos": [
16,
23
],
"type": "Positive_regulation"
} |
||
15040833.s2 | E2 but not ICI stimulated BMP-6 reporter activity in breast cancer cells, whereas the opposite was observed in osteoblast-like cells, associated with lack of AF-2 dependence of the response, and absent intranuclear localization of ERalpha, suggesting the involvement of a distinct ERalpha-dependent response mechanism in osteoblasts. | breast | {
"name": "BMP-6",
"pos": [
26,
30
]
} | {
"name": "breast cancer",
"pos": [
53,
65
]
} | increased | unidentifiable | {
"name": "\nNone\n",
"pos": null,
"type": null
} | {
"name": "stimulated",
"pos": [
15,
24
],
"type": "Positive_regulation"
} |
||
15040833.s6 | E2, but not ICI, stimulated BMP-6 reporter activity by approximately 100% in MCF-7, T47-D cells, and HepG2 cells when transfected with ERalpha. | breast | {
"name": "ERalpha",
"pos": [
135,
141
]
} | {
"name": "MCF-7",
"pos": [
77,
81
]
} | increased | unidentifiable | {
"name": "transfected",
"pos": [
118,
128
],
"type": "Gene_expression"
} | {
"name": "transfected",
"pos": [
118,
128
],
"type": "Positive_regulation"
} |
||
10998426.s1 | We report that transfection of insulin-like growth factor-binding protein-3 (IGFBP-3) cDNA in human breast cancer cell lines expressing either mutant p53 (T47D) or wild-type p53 (MCF-7) induces apoptosis. | breast | {
"name": "insulin-like growth factor-binding protein-3",
"pos": [
31,
74
]
} | {
"name": "breast cancer",
"pos": [
100,
112
]
} | increased | cancerTOnormal | causality | unidentifiable | {
"name": "transfection",
"pos": [
15,
26
],
"type": "Gene_expression"
} | {
"name": "transfection",
"pos": [
15,
26
],
"type": "Positive_regulation"
} |
10998426.s1 | We report that transfection of insulin-like growth factor-binding protein-3 (IGFBP-3) cDNA in human breast cancer cell lines expressing either mutant p53 (T47D) or wild-type p53 (MCF-7) induces apoptosis. | breast | {
"name": "IGFBP-3",
"pos": [
77,
83
]
} | {
"name": "breast cancer",
"pos": [
100,
112
]
} | increased | cancerTOnormal | causality | unidentifiable | {
"name": "transfection",
"pos": [
15,
26
],
"type": "Gene_expression"
} | {
"name": "transfection",
"pos": [
15,
26
],
"type": "Positive_regulation"
} |
10998426.s3 | In MCF-7, an increase in Bad and Bax protein expression and a decrease in Bcl-x(L) protein and Bcl-2 protein and mRNA were observed. | breast | {
"name": "Bcl-x(L) protein",
"pos": [
74,
89
]
} | {
"name": "MCF-7",
"pos": [
3,
7
]
} | decreased | normalTOcancer | observation | unchanged | {
"name": "\nNone\n",
"pos": null,
"type": null
} | {
"name": "decrease",
"pos": [
62,
69
],
"type": "Negative_regulation"
} |
10998426.s3 | In MCF-7, an increase in Bad and Bax protein expression and a decrease in Bcl-x(L) protein and Bcl-2 protein and mRNA were observed. | breast | {
"name": "Bcl-2 protein",
"pos": [
95,
107
]
} | {
"name": "MCF-7",
"pos": [
3,
7
]
} | decreased | normalTOcancer | observation | unchanged | {
"name": "\nNone\n",
"pos": null,
"type": null
} | {
"name": "decrease",
"pos": [
62,
69
],
"type": "Negative_regulation"
} |
10998426.s3 | In MCF-7, an increase in Bad and Bax protein expression and a decrease in Bcl-x(L) protein and Bcl-2 protein and mRNA were observed. | breast | {
"name": "Bad",
"pos": [
25,
27
]
} | {
"name": "MCF-7",
"pos": [
3,
7
]
} | increased | normalTOcancer | observation | unchanged | {
"name": "\nNone\n",
"pos": null,
"type": null
} | {
"name": "increase",
"pos": [
13,
20
],
"type": "Positive_regulation"
} |
10998426.s3 | In MCF-7, an increase in Bad and Bax protein expression and a decrease in Bcl-x(L) protein and Bcl-2 protein and mRNA were observed. | breast | {
"name": "Bad",
"pos": [
25,
27
]
} | {
"name": "MCF-7",
"pos": [
3,
7
]
} | increased | normalTOcancer | observation | unchanged | {
"name": "expression",
"pos": [
45,
54
],
"type": "Gene_expression"
} | {
"name": "increase",
"pos": [
13,
20
],
"type": "Positive_regulation"
} |
10998426.s3 | In MCF-7, an increase in Bad and Bax protein expression and a decrease in Bcl-x(L) protein and Bcl-2 protein and mRNA were observed. | breast | {
"name": "Bax protein",
"pos": [
33,
43
]
} | {
"name": "MCF-7",
"pos": [
3,
7
]
} | increased | normalTOcancer | observation | unchanged | {
"name": "expression",
"pos": [
45,
54
],
"type": "Gene_expression"
} | {
"name": "increase",
"pos": [
13,
20
],
"type": "Positive_regulation"
} |
10998426.s4 | In T47D, Bax and Bad proteins were up-regulated; Bcl-2 protein is undetectable in these cells. | breast | {
"name": "Bad proteins",
"pos": [
17,
28
]
} | {
"name": "T47D",
"pos": [
3,
6
]
} | increased | normalTOcancer | observation | unchanged | {
"name": "\nNone\n",
"pos": null,
"type": null
} | {
"name": "up-regulated",
"pos": [
35,
46
],
"type": "Positive_regulation"
} |
10998426.s4 | In T47D, Bax and Bad proteins were up-regulated; Bcl-2 protein is undetectable in these cells. | breast | {
"name": "Bax",
"pos": [
9,
11
]
} | {
"name": "T47D",
"pos": [
3,
6
]
} | increased | normalTOcancer | observation | unchanged | {
"name": "\nNone\n",
"pos": null,
"type": null
} | {
"name": "up-regulated",
"pos": [
35,
46
],
"type": "Positive_regulation"
} |
10998426.s8 | Transfection of IGFBP-3 increased the radiosensitivity of T47D and increased IR-induced apoptosis but did not effect a rapid G(1) arrest. | breast | {
"name": "IGFBP-3",
"pos": [
16,
22
]
} | {
"name": "T47D",
"pos": [
58,
61
]
} | increased | cancerTOnormal | causality | unidentifiable | {
"name": "Transfection",
"pos": [
0,
11
],
"type": "Gene_expression"
} | {
"name": "Transfection",
"pos": [
0,
11
],
"type": "Positive_regulation"
} |
17595766.s6 | HGF induces Dgk activation in MDA-MB-231 cells that is required for cell invasiveness. | breast | {
"name": "Dgk",
"pos": [
12,
14
]
} | {
"name": "MDA-MB-231",
"pos": [
30,
39
]
} | increased | normalTOcancer | causality | unidentifiable | {
"name": "\nNone\n",
"pos": null,
"type": null
} | {
"name": "activation",
"pos": [
16,
25
],
"type": "Positive_regulation"
} |
21070441.s0 | Complete response of brain metastases from breast cancer overexpressing Her-2/neu to radiation and concurrent Lapatinib and Capecitabine. | breast | {
"name": "Her-2/neu",
"pos": [
72,
80
]
} | {
"name": "breast cancer",
"pos": [
43,
55
]
} | increased | normalTOcancer | observation | unidentifiable | {
"name": "overexpressing",
"pos": [
57,
70
],
"type": "Gene_expression"
} | {
"name": "overexpressing",
"pos": [
57,
70
],
"type": "Positive_regulation"
} |
15609126.s0 | Increased frequency of long androgen receptor CAG repeats in male breast cancers. | breast | {
"name": "androgen receptor CAG repeats",
"pos": [
28,
56
]
} | {
"name": "male breast cancers",
"pos": [
61,
79
]
} | increased | normalTOcancer | observation | unchanged | {
"name": "\nNone\n",
"pos": null,
"type": null
} | {
"name": "Increased",
"pos": [
0,
8
],
"type": "Positive_regulation"
} |
7814146.s10 | Stimulation of SKBR3 cells and HCII RI#11 mouse mammary epithelial cells expressing the human erbB-2 with EGF led to an increase in scFv(FRP5)-ETA activity, showing that the EGF-induced activation of erbB-2 can potentiate the action of the erbB-2-directed toxin. | breast | {
"name": "FRP5",
"pos": [
137,
140
]
} | {
"name": "SKBR3",
"pos": [
15,
19
]
} | increased | unidentifiable | {
"name": "\nNone\n",
"pos": null,
"type": null
} | {
"name": "increase",
"pos": [
120,
127
],
"type": "Positive_regulation"
} |
||
7814146.s10 | Stimulation of SKBR3 cells and HCII RI#11 mouse mammary epithelial cells expressing the human erbB-2 with EGF led to an increase in scFv(FRP5)-ETA activity, showing that the EGF-induced activation of erbB-2 can potentiate the action of the erbB-2-directed toxin. | breast | {
"name": "erbB-2",
"pos": [
200,
205
]
} | {
"name": "SKBR3",
"pos": [
15,
19
]
} | increased | unidentifiable | {
"name": "\nNone\n",
"pos": null,
"type": null
} | {
"name": "activation",
"pos": [
186,
195
],
"type": "Positive_regulation"
} |
||
7814146.s10 | Stimulation of SKBR3 cells and HCII RI#11 mouse mammary epithelial cells expressing the human erbB-2 with EGF led to an increase in scFv(FRP5)-ETA activity, showing that the EGF-induced activation of erbB-2 can potentiate the action of the erbB-2-directed toxin. | breast | {
"name": "scFv",
"pos": [
132,
135
]
} | {
"name": "SKBR3",
"pos": [
15,
19
]
} | increased | unidentifiable | {
"name": "\nNone\n",
"pos": null,
"type": null
} | {
"name": "increase",
"pos": [
120,
127
],
"type": "Positive_regulation"
} |
||
17079470.s5 | By using 5' deletion mutant constructs of MMP-2 promoter, we showed that deletion of the region containing activator protein-1 (AP-1) site caused the greatest reduction of MMP-2 promoter activity both in MKK6- and H-Ras-activated MCF10A cells, suggesting that the AP-1 binding site is critical for the MMP-2 promoter activation. | breast | {
"name": "MMP-2 promoter",
"pos": [
302,
315
]
} | {
"name": "MCF10A",
"pos": [
230,
235
]
} | increased | unidentifiable | {
"name": "\nNone\n",
"pos": null,
"type": null
} | {
"name": "activation",
"pos": [
317,
326
],
"type": "Positive_regulation"
} |
||
17079470.s8 | Activation of ATF2, which depended on p38 activity, was crucial for MMP-2 promoter activity as well as induction of invasive and migrative phenotypes in MCF10A cells. | breast | {
"name": "ATF2",
"pos": [
14,
17
]
} | {
"name": "MCF10A",
"pos": [
153,
158
]
} | increased | normalTOcancer | causality | unidentifiable | {
"name": "\nNone\n",
"pos": null,
"type": null
} | {
"name": "Activation",
"pos": [
0,
9
],
"type": "Positive_regulation"
} |
10323669.s2 | It has been shown recently that 17beta-estradiol (E2) can stimulate the Src/p21ras/mitogen-activated protein kinase pathway in breast cancer cells, and this effect is supposed to mediate the E2-induced stimulation of breast cancer cell proliferation, possibly via activation of the c-fos and c-jun early genes or of genes involved in cell cycle control. | breast | {
"name": "c-jun early genes",
"pos": [
292,
308
]
} | {
"name": "breast cancer",
"pos": [
127,
139
]
} | increased | normalTOcancer | causality | unidentifiable | {
"name": "\nNone\n",
"pos": null,
"type": null
} | {
"name": "activation",
"pos": [
264,
273
],
"type": "Positive_regulation"
} |
10323669.s2 | It has been shown recently that 17beta-estradiol (E2) can stimulate the Src/p21ras/mitogen-activated protein kinase pathway in breast cancer cells, and this effect is supposed to mediate the E2-induced stimulation of breast cancer cell proliferation, possibly via activation of the c-fos and c-jun early genes or of genes involved in cell cycle control. | breast | {
"name": "c-fos",
"pos": [
282,
286
]
} | {
"name": "breast cancer",
"pos": [
127,
139
]
} | increased | normalTOcancer | causality | unidentifiable | {
"name": "\nNone\n",
"pos": null,
"type": null
} | {
"name": "activation",
"pos": [
264,
273
],
"type": "Positive_regulation"
} |
10323669.s2 | It has been shown recently that 17beta-estradiol (E2) can stimulate the Src/p21ras/mitogen-activated protein kinase pathway in breast cancer cells, and this effect is supposed to mediate the E2-induced stimulation of breast cancer cell proliferation, possibly via activation of the c-fos and c-jun early genes or of genes involved in cell cycle control. | breast | {
"name": "Src/p21ras/mitogen-activated protein kinase",
"pos": [
72,
114
]
} | {
"name": "breast cancer",
"pos": [
127,
139
]
} | increased | normalTOcancer | causality | unidentifiable | {
"name": "\nNone\n",
"pos": null,
"type": null
} | {
"name": "stimulate",
"pos": [
58,
66
],
"type": "Positive_regulation"
} |
2521857.s2 | We now show that the MDA468 breast cancer cells express the mRNA for the EGF-like molecule, transforming growth factor-alpha (TGF-alpha), and demonstrate that TPA or EGF cause an accumulation of both EGF receptor and TGF-alpha mRNA. | breast | {
"name": "TGF-alpha mRNA",
"pos": [
217,
230
]
} | {
"name": "breast cancer",
"pos": [
28,
40
]
} | increased | normalTOcancer | observation | unchanged | {
"name": "\nNone\n",
"pos": null,
"type": null
} | {
"name": "accumulation",
"pos": [
179,
190
],
"type": "Positive_regulation"
} |
12824874.s2 | It has, however, been reported that expression of connexin26 (Cx26) protein is induced in human ductal carcinomas of the breast and that its amount increases in proportion to the grade of malignancy. | breast | {
"name": "connexin26 (Cx26) protein",
"pos": [
50,
74
]
} | {
"name": "ductal carcinomas",
"pos": [
96,
112
]
} | increased | normalTOcancer | observation | unchanged | {
"name": "expression",
"pos": [
36,
45
],
"type": "Gene_expression"
} | {
"name": "induced",
"pos": [
79,
85
],
"type": "Positive_regulation"
} |
12824874.s9 | Our results strongly suggest that the induction of Cx26 protein observed in human breast cancers, reported previously, may not be very relevant to the development of breast cancers, and that Cx26 can function as a tumor suppressor in breast cancer cells. | breast | {
"name": "Cx26 protein",
"pos": [
51,
62
]
} | {
"name": "breast cancers",
"pos": [
82,
95
]
} | increased | unidentifiable | {
"name": "\nNone\n",
"pos": null,
"type": null
} | {
"name": "induction",
"pos": [
38,
46
],
"type": "Positive_regulation"
} |
||
16145051.s5 | These results support the hypothesis that EMSY overexpression can play a role in the genesis of human breast cancer. | breast | {
"name": "EMSY",
"pos": [
42,
45
]
} | {
"name": "breast cancer",
"pos": [
102,
114
]
} | increased | normalTOcancer | causality | unchanged | {
"name": "overexpression",
"pos": [
47,
60
],
"type": "Gene_expression"
} | {
"name": "overexpression",
"pos": [
47,
60
],
"type": "Positive_regulation"
} |
16234819.s6 | In this study we show that oestradiol decreased secreted sVEGFR-1, increased secreted VEGF, and decreased the ratio of sVEGFR-1/VEGF in MCF-7 human breast cancer cells. | breast | {
"name": "sVEGFR-1",
"pos": [
57,
64
]
} | {
"name": "breast cancer",
"pos": [
148,
160
]
} | decreased | unidentifiable | {
"name": "\nNone\n",
"pos": null,
"type": null
} | {
"name": "decreased",
"pos": [
38,
46
],
"type": "Negative_regulation"
} |
||
16234819.s6 | In this study we show that oestradiol decreased secreted sVEGFR-1, increased secreted VEGF, and decreased the ratio of sVEGFR-1/VEGF in MCF-7 human breast cancer cells. | breast | {
"name": "VEGF",
"pos": [
86,
89
]
} | {
"name": "breast cancer",
"pos": [
148,
160
]
} | increased | unidentifiable | {
"name": "\nNone\n",
"pos": null,
"type": null
} | {
"name": "increased",
"pos": [
67,
75
],
"type": "Positive_regulation"
} |
||
20535861.s2 | The synergistic action of unopposed oestrogen and leptin, compounded by increasing insulin, cortisol and xeno-oestrogen exposure directly initiate, promote and exacerbate obesity, type 2 diabetes, uterine overgrowth, prostatic enlargement, prostate cancer and breast cancer. | breast | {
"name": "insulin",
"pos": [
83,
89
]
} | {
"name": "breast cancer",
"pos": [
260,
272
]
} | increased | normalTOcancer | causality | unidentifiable | {
"name": "\nNone\n",
"pos": null,
"type": null
} | {
"name": "increasing",
"pos": [
72,
81
],
"type": "Positive_regulation"
} |
16755107.s0 | Activation of PI3K/Akt signaling and hormone resistance in breast cancer. | breast | {
"name": "PI3K/Akt",
"pos": [
14,
21
]
} | {
"name": "breast cancer",
"pos": [
59,
71
]
} | increased | normalTOcancer | observation | unidentifiable | {
"name": "\nNone\n",
"pos": null,
"type": null
} | {
"name": "Activation",
"pos": [
0,
9
],
"type": "Positive_regulation"
} |
16755107.s2 | Recent studies show that aberrant activation of Akt in breast carcinoma is associated with a poor prognosis and resistance to endocrine therapy and chemotherapy. | breast | {
"name": "Akt",
"pos": [
48,
50
]
} | {
"name": "breast carcinoma",
"pos": [
55,
70
]
} | increased | normalTOcancer | observation | unidentifiable | {
"name": "\nNone\n",
"pos": null,
"type": null
} | {
"name": "activation",
"pos": [
34,
43
],
"type": "Positive_regulation"
} |
16755107.s13 | These findings therefore suggest that Akt activation induces endocrine resistance in metastatic breast cancer, irrespective of the kind of endocrine agents that were administered. | breast | {
"name": "Akt",
"pos": [
38,
40
]
} | {
"name": "metastatic breast cancer",
"pos": [
85,
108
]
} | increased | normalTOcancer | causality | unidentifiable | {
"name": "\nNone\n",
"pos": null,
"type": null
} | {
"name": "activation",
"pos": [
42,
51
],
"type": "Positive_regulation"
} |
16755107.s14 | Our findings indicate that the activation of Akt in the downstream pathway of HER2 plays an important role in resistance to endocrine therapy for breast cancer. | breast | {
"name": "Akt",
"pos": [
45,
47
]
} | {
"name": "breast cancer",
"pos": [
146,
158
]
} | increased | normalTOcancer | causality | unidentifiable | {
"name": "\nNone\n",
"pos": null,
"type": null
} | {
"name": "activation",
"pos": [
31,
40
],
"type": "Positive_regulation"
} |
16755107.s15 | Our findings suggest that pAkt may be a useful predictor of resistance to endocrine therapy for breast cancer, while also suggesting that the inhibition of Akt may increase the efficacy of endocrine therapy. | breast | {
"name": "Akt",
"pos": [
156,
158
]
} | {
"name": "breast cancer",
"pos": [
96,
108
]
} | decreased | cancerTOnormal | causality | unidentifiable | {
"name": "\nNone\n",
"pos": null,
"type": null
} | {
"name": "inhibition",
"pos": [
142,
151
],
"type": "Negative_regulation"
} |
19432961.s13 | Decreased expression of miR-342 in the therapeutically challenging triple-negative breast tumours, increased miR-342 expression in the luminal B tumours, and downregulated miR-520g in ER and PR-positive tumours indicates that not only is dysregulated miRNA expression a marker for poorer prognosis breast cancer, but that it could also present an attractive target for therapeutic intervention. | breast | {
"name": "miR-520g",
"pos": [
172,
179
]
} | {
"name": "breast tumours",
"pos": [
83,
96
]
} | decreased | normalTOcancer | observation | unidentifiable | {
"name": "\nNone\n",
"pos": null,
"type": null
} | {
"name": "downregulated",
"pos": [
158,
170
],
"type": "Negative_regulation"
} |
19432961.s13 | Decreased expression of miR-342 in the therapeutically challenging triple-negative breast tumours, increased miR-342 expression in the luminal B tumours, and downregulated miR-520g in ER and PR-positive tumours indicates that not only is dysregulated miRNA expression a marker for poorer prognosis breast cancer, but that it could also present an attractive target for therapeutic intervention. | breast | {
"name": "miR-342",
"pos": [
109,
115
]
} | {
"name": "breast tumours",
"pos": [
83,
96
]
} | increased | normalTOcancer | observation | unidentifiable | {
"name": "expression",
"pos": [
117,
126
],
"type": "Gene_expression"
} | {
"name": "increased",
"pos": [
99,
107
],
"type": "Positive_regulation"
} |
19432961.s13 | Decreased expression of miR-342 in the therapeutically challenging triple-negative breast tumours, increased miR-342 expression in the luminal B tumours, and downregulated miR-520g in ER and PR-positive tumours indicates that not only is dysregulated miRNA expression a marker for poorer prognosis breast cancer, but that it could also present an attractive target for therapeutic intervention. | breast | {
"name": "miR-342",
"pos": [
24,
30
]
} | {
"name": "breast tumours",
"pos": [
83,
96
]
} | decreased | normalTOcancer | observation | unidentifiable | {
"name": "expression",
"pos": [
10,
19
],
"type": "Gene_expression"
} | {
"name": "Decreased",
"pos": [
0,
8
],
"type": "Negative_regulation"
} |
12459033.s2 | In nuclear run-on assays, 17beta-estradiol (E2) increased the rate of Tf gene expression approximately 3-fold within 1 h after treatment and reporter gene activity was also induced in MCF-7 cells transfected with a construct containing a -3600 to +39 Tf gene promoter insert. | breast | {
"name": "Tf gene",
"pos": [
70,
76
]
} | {
"name": "MCF-7",
"pos": [
184,
188
]
} | increased | unidentifiable | {
"name": "expression",
"pos": [
78,
87
],
"type": "Gene_expression"
} | {
"name": "increased",
"pos": [
48,
56
],
"type": "Positive_regulation"
} |
||
21855113.s0 | SCARA3 mRNA is overexpressed in ovarian carcinoma compared with breast carcinoma effusions. | breast | {
"name": "SCARA3 mRNA",
"pos": [
0,
10
]
} | {
"name": "breast carcinoma",
"pos": [
64,
79
]
} | increased | unidentifiable | {
"name": "overexpressed",
"pos": [
15,
27
],
"type": "Gene_expression"
} | {
"name": "overexpressed",
"pos": [
15,
27
],
"type": "Positive_regulation"
} |
||
21855113.s1 | Scavenger receptor class A, member 3 (SCARA3) was previously found to be overexpressed in ovarian/primary peritoneal carcinoma (OC/PPC) compared with breast carcinoma effusions by global gene expression analysis. | breast | {
"name": "SCARA3",
"pos": [
38,
43
]
} | {
"name": "breast carcinoma",
"pos": [
150,
165
]
} | increased | unidentifiable | {
"name": "overexpressed",
"pos": [
73,
85
],
"type": "Gene_expression"
} | {
"name": "overexpressed",
"pos": [
73,
85
],
"type": "Positive_regulation"
} |
||
21855113.s1 | Scavenger receptor class A, member 3 (SCARA3) was previously found to be overexpressed in ovarian/primary peritoneal carcinoma (OC/PPC) compared with breast carcinoma effusions by global gene expression analysis. | breast | {
"name": "Scavenger receptor class A, member 3",
"pos": [
0,
35
]
} | {
"name": "breast carcinoma",
"pos": [
150,
165
]
} | increased | unidentifiable | {
"name": "overexpressed",
"pos": [
73,
85
],
"type": "Gene_expression"
} | {
"name": "overexpressed",
"pos": [
73,
85
],
"type": "Positive_regulation"
} |
||
22310293.s2 | miR-9 is overexpressed in several cancer forms, including brain tumours, hepatocellular carcinomas, breast cancer and Hodgkin lymphoma (HL). | breast | {
"name": "miR-9",
"pos": [
0,
4
]
} | {
"name": "breast cancer",
"pos": [
100,
112
]
} | increased | normalTOcancer | observation | unchanged | {
"name": "overexpressed",
"pos": [
9,
21
],
"type": "Gene_expression"
} | {
"name": "overexpressed",
"pos": [
9,
21
],
"type": "Positive_regulation"
} |
17342334.s5 | It was found that there were both significant overexpression of Wnt5A and underexpression of Wnt10B in the metastasis-derived finite life-span breast cancer cells when they were compared to the finite life-span normal and established normal and breast tumor cells. | breast | {
"name": "Wnt5A",
"pos": [
64,
68
]
} | {
"name": "breast cancer",
"pos": [
143,
155
]
} | increased | normalTOcancer | observation | unchanged | {
"name": "overexpression",
"pos": [
46,
59
],
"type": "Gene_expression"
} | {
"name": "overexpression",
"pos": [
46,
59
],
"type": "Positive_regulation"
} |
21176537.s9 | Compared with that of the vector control and naïve MCF7 cell group, there was a significant decrease of BCSG-1 protein expression in the four experimental groups by immuno-histochemistry staining (P<0.01). | breast | {
"name": "BCSG-1 protein",
"pos": [
104,
117
]
} | {
"name": "MCF7",
"pos": [
51,
54
]
} | decreased | normalTOcancer | observation | unidentifiable | {
"name": "expression",
"pos": [
119,
128
],
"type": "Gene_expression"
} | {
"name": "decrease",
"pos": [
92,
99
],
"type": "Negative_regulation"
} |
21176537.s11 | BCSG1-siRNA down-regulates the expression of BCSG1 and inhibits effectively growth of the transplaned human breast cancer cell line in nude mice. | breast | {
"name": "BCSG1",
"pos": [
45,
49
]
} | {
"name": "breast cancer",
"pos": [
108,
120
]
} | decreased | cancerTOnormal | observation | unidentifiable | {
"name": "expression",
"pos": [
31,
40
],
"type": "Gene_expression"
} | {
"name": "down-regulates",
"pos": [
12,
25
],
"type": "Negative_regulation"
} |
11891846.s1 | We have previously reported that glucocorticoids markedly increase and anti-glucocorticoids (such as RU-486) block c-fms RNA and protein expression in some breast cancer cell lines, but not in others, and that this increase is the consequence of increased transcription from the first, epithelial cell-specific promoter of the c-fms gene (encoding CSF-1R, macrophage colony-stimulating factor receptor). | breast | {
"name": "c-fms RNA",
"pos": [
115,
123
]
} | {
"name": "breast cancer",
"pos": [
156,
168
]
} | decreased | unidentifiable | {
"name": "expression",
"pos": [
137,
146
],
"type": "Gene_expression"
} | {
"name": "block",
"pos": [
109,
113
],
"type": "Negative_regulation"
} |
||
9472634.s4 | In MDA-MB-231, TGF-beta1 had no effect on cell proliferation but increased uPA activity and PAI-1 antigen level; sodium butyrate inhibited both cell proliferation and uPA activity but had no effect on PAI-1 level. | breast | {
"name": "PAI-1 antigen",
"pos": [
92,
104
]
} | {
"name": "MDA-MB-231",
"pos": [
3,
12
]
} | increased | unidentifiable | {
"name": "\nNone\n",
"pos": null,
"type": null
} | {
"name": "increased",
"pos": [
65,
73
],
"type": "Positive_regulation"
} |
||
9472634.s4 | In MDA-MB-231, TGF-beta1 had no effect on cell proliferation but increased uPA activity and PAI-1 antigen level; sodium butyrate inhibited both cell proliferation and uPA activity but had no effect on PAI-1 level. | breast | {
"name": "uPA",
"pos": [
75,
77
]
} | {
"name": "MDA-MB-231",
"pos": [
3,
12
]
} | increased | unidentifiable | {
"name": "\nNone\n",
"pos": null,
"type": null
} | {
"name": "increased",
"pos": [
65,
73
],
"type": "Positive_regulation"
} |
||
9472634.s4 | In MDA-MB-231, TGF-beta1 had no effect on cell proliferation but increased uPA activity and PAI-1 antigen level; sodium butyrate inhibited both cell proliferation and uPA activity but had no effect on PAI-1 level. | breast | {
"name": "uPA",
"pos": [
167,
169
]
} | {
"name": "MDA-MB-231",
"pos": [
3,
12
]
} | decreased | unidentifiable | {
"name": "\nNone\n",
"pos": null,
"type": null
} | {
"name": "inhibited",
"pos": [
129,
137
],
"type": "Negative_regulation"
} |
||
20622894.s7 | The proliferation of certain human HER2-positive breast cancer lines also requires HSF1, as its knockdown led to upregulation of p21 and/or decrease in survivin, precipitating growth arrest. | breast | {
"name": "p21",
"pos": [
129,
131
]
} | {
"name": "breast cancer",
"pos": [
49,
61
]
} | increased | cancerTOnormal | causality | unidentifiable | {
"name": "\nNone\n",
"pos": null,
"type": null
} | {
"name": "upregulation",
"pos": [
113,
124
],
"type": "Positive_regulation"
} |
20711231.s1 | The activation of receptor tyrosine kinases, particularly ErbB2, has an important role in the genesis of breast cancer. | breast | {
"name": "ErbB2",
"pos": [
58,
62
]
} | {
"name": "breast cancer",
"pos": [
105,
117
]
} | increased | normalTOcancer | causality | unchanged | {
"name": "\nNone\n",
"pos": null,
"type": null
} | {
"name": "activation",
"pos": [
4,
13
],
"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": "Akt",
"pos": [
355,
357
]
} | {
"name": "breast tumor",
"pos": [
106,
117
]
} | increased | unidentifiable | {
"name": "\nNone\n",
"pos": null,
"type": null
} | {
"name": "activation",
"pos": [
329,
338
],
"type": "Positive_regulation"
} |