PRISMΔDB

Analyze how specific documents activate the features of the SAE. Select a dataset, a run and a document to begin.

Active Features

1487

0.0
Details List
#302 Feature 302
3.0
#1731 Feature 1731
2.5
#2460 Feature 2460
2.4
#1802 Feature 1802
2.4
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2.2
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2.2
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2.2
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2.2
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2.2
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2.2
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2.1
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2.1
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2.1
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2.1
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2.1
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2.0
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2.0
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2.0
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1.8
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1.8
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1.8
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1.8
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1.8
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1.8
#85 Feature 85
1.7
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1.7
#11 Feature 11
1.7
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1.7
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1.7
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1.7
#2309 Feature 2309
1.6
#2790 Feature 2790
1.6
#708 Drug Resistance Mechanisms in Cancer
1.6
#437 Feature 437
1.6
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1.5
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1.5
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1.5
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1.5
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1.5
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1.5
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1.4
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1.4
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1.4
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1.4
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1.4
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1.4
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1.4
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1.4
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1.4
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1.4
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1.4
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1.4
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1.4
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1.4
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1.4
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1.4
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1.4
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1.3
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1.3
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1.3
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1.3
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1.3
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1.3
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1.3
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1.3
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1.3
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1.3
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1.3
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1.3
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1.3
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1.3
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1.3
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1.3
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1.3
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1.3
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1.2
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1.2
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1.2
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1.2
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1.2
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1.2
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1.2
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1.2
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1.2
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1.2
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1.2
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1.2
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1.2
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1.2
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1.2
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1.2
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1.2
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1.2
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1.2
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1.2
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1.2
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1.2
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1.2
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1.2
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1.2
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1.2
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1.2
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1.2
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1.2
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1.2
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1.2
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1.2
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1.2
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1.2
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1.2
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1.2
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1.1
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1.1
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1.1
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1.1
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1.1
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1.1
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1.1
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1.1
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1.1
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1.1
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1.1
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1.1
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1.1
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1.1
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1.1
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1.1
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1.1
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1.1
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1.1
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1.1
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1.1
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1.1
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1.1
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1.1
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1.1
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1.1
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1.1
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1.1
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1.1
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1.1
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1.1
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1.1
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1.1
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1.1
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1.1
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1.1
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1.1
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1.1
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1.1
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1.1
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1.1
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1.0
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1.0
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1.0
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1.0
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1.0
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1.0
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1.0
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1.0
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1.0
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1.0
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1.0
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1.0
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1.0
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1.0
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1.0
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1.0
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1.0
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1.0
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1.0
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1.0
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1.0
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1.0
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1.0
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1.0
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1.0
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1.0
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1.0
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1.0
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1.0
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1.0
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1.0
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1.0
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1.0
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1.0
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1.0
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1.0
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1.0
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1.0
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1.0
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1.0
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1.0
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1.0
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1.0
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1.0
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1.0
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1.0
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1.0
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1.0
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1.0
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1.0
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1.0
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1.0
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1.0
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1.0
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1.0
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1.0
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1.0
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1.0
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0.9
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0.9
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0.9
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0.9
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0.9
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0.9
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0.9
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0.9
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0.9
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0.9
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0.9
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0.9
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0.9
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0.9
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0.9
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0.9
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0.9
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0.9
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0.9
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0.9
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0.9
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0.9
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0.9
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0.9
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0.9
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0.9
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0.9
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0.9
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0.9
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0.9
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0.9
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0.9
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0.9
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0.9
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0.9
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0.9
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0.9
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0.9
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0.9
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0.9
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0.9
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0.9
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0.9
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0.9
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0.9
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0.9
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0.9
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0.9
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0.9
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0.9
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0.9
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0.9
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0.9
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0.9
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0.9
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0.9
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0.9
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0.9
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0.9
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0.9
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0.9
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0.9
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0.9
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0.9
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0.9
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0.9
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0.9
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0.9
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0.8
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0.8
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0.8
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0.8
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0.8
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0.8
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0.8
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0.8
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0.8
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0.8
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0.8
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0.8
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0.8
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0.8
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0.8
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0.8
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0.8
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0.8
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0.8
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0.8
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0.8
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0.8
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0.8
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0.8
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0.8
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0.8
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0.8
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0.8
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0.8
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0.8
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0.8
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0.8
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0.8
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0.8
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0.8
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0.8
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0.8
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0.8
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0.8
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0.8
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0.8
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0.8
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0.8
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0.8
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0.8
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0.8
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0.8
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0.8
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0.8
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0.8
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0.8
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0.8
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0.8
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0.8
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0.8
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0.7
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Document Content

Part III. Molecular changes induced by high nitric oxide adaptation in human breast cancer cell line BT-20 (BT-20-HNO): a switch from aerobic to anaerobic metabolism.
Nutrient deprivation and reactive oxygen species (ROS) play an important role in breast cancer mitochondrial adaptation. Adaptations to these conditions allow cells to survive in the stressful microenvironment of the tumor bed. This study is directed at defining the consequences of High Nitric Oxide (HNO) exposure to mitochondria in human breast cancer cells. The breast cancer cell line BT-20 (parent) was adapted to HNO as previously reported, resulting in the BT-20-HNO cell line. Both cell lines were analyzed by a variety of methods including MTT, LDH leakage assay, DNA sequencing, and Western blot analysis. The LDH assay and the gene chip data showed that BT-20-HNO was more prone to use the glycolytic pathway than the parent cell line. The BT-20-HNO cells were also more resistant to the apoptotic inducing agent salinomycin, which suggests that p53 may be mutated in these cells. Polymerase chain reaction (PCR) followed by DNA sequencing of the p53 gene showed that it was, in fact, mutated at the DNA-binding site (L194F). Western blot analysis showed that p53 was significantly upregulated in these cells. These results suggest that free radicals, such as nitric oxide (NO), pressure human breast tumor cells to acquire an aggressive phenotype and resistance to apoptosis. These data collectively provide a mechanism by which the dysregulation of ROS in the mitochondria of breast cancer cells can result in DNA damage.