Tumor microenvironment-based feed-forward regulation of NOS2 in breast cancer progression

Proceedings of the National Academy of Sciences of the United States of America

Volumn 111, Issue 17, 2014, Pages 6323-6328

  Heinecke, Julie L ^a   Ridnour, Lisa A ^a   Cheng, Robert Y S ^a   Switzer, Christopher H ^a   Lizardo, Michael M ^a   Khanna, Chand ^a   Glynn, Sharon A ^b   Hussain, S Perwez ^c   Young, Howard A ^d   Ambs, Stefan ^c   Wink, David A ^a  

^a NATIONAL INSTITUTES OF HEALTH   (United States)

^b NATIONAL UNIVERSITY OF IRELAND   (Ireland)

^c NATIONAL CANCER INSTITUTE   (United States)

^d NATIONAL CANCER INSTITUTE   (United States)

Author keywords

[No Author keywords available]

Indexed keywords

ALPHA INTERFERON; BETA INTERFERON; CALGRANULIN A; CYCLOOXYGENASE 2; ESTROGEN RECEPTOR; GAMMA INTERFERON; HERMES ANTIGEN; INDUCIBLE NITRIC OXIDE SYNTHASE; INTERLEUKIN 1BETA; INTERLEUKIN 6; INTERLEUKIN 8; MESSENGER RNA; NITRIC OXIDE; PACLITAXEL; TISSUE INHIBITOR OF METALLOPROTEINASE 1; TOLL LIKE RECEPTOR 4; TUMOR NECROSIS FACTOR ALPHA;

ANIMAL EXPERIMENT; ARTICLE; BRAIN METASTASIS; BREAST CANCER; BREAST CANCER CELL LINE; CANCER GROWTH; CANCER RESISTANCE; CELL MIGRATION; CONTROLLED STUDY; CYTOKINE RESPONSIVE ELEMENT; DISEASE COURSE; ENZYME ACTIVITY; FEMALE; HYPOXIA; MOUSE; NEGATIVE FEEDBACK; NONHUMAN; NUTRIENT UPTAKE; PHENOTYPE; PRIORITY JOURNAL; PROMOTER REGION; PROTEIN EXPRESSION; PROTEIN PROCESSING; SIGNAL TRANSDUCTION; TUMOR GROWTH; TUMOR MICROENVIRONMENT; UPREGULATION;

ANIMALS; BREAST NEOPLASMS; CELL HYPOXIA; CELL LINE, TUMOR; CELL MOVEMENT; CELL PROLIFERATION; CULTURE MEDIA, SERUM-FREE; DISEASE PROGRESSION; DRUG RESISTANCE, NEOPLASM; FEEDBACK, PHYSIOLOGICAL; FEMALE; GUANIDINES; HUMANS; INTERFERON-GAMMA; MICE; MODELS, BIOLOGICAL; NEOPLASM METASTASIS; NITRIC OXIDE; NITRIC OXIDE SYNTHASE TYPE II; SIGNAL TRANSDUCTION; TUMOR MARKERS, BIOLOGICAL; TUMOR MICROENVIRONMENT;

EID: 84899655872     PISSN: 00278424     EISSN: 10916490     Source Type: Journal    
DOI: 10.1073/pnas.1401799111     Document Type: Article

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