Please use this identifier to cite or link to this item: https://doi.org/10.3402/pba.v2i0.17391
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dc.titleBreast tumors in PyMT transgenic mice expressing mitochondrial catalase have decreased labeling for macrophages and endothelial cells.
dc.contributor.authorFatemie, Sy
dc.contributor.authorGoh, Jorming
dc.contributor.authorPettan-Brewer, Christina
dc.contributor.authorLadiges, Warren
dc.date.accessioned2022-04-21T09:26:54Z
dc.date.available2022-04-21T09:26:54Z
dc.date.issued2012
dc.identifier.citationFatemie, Sy, Goh, Jorming, Pettan-Brewer, Christina, Ladiges, Warren (2012). Breast tumors in PyMT transgenic mice expressing mitochondrial catalase have decreased labeling for macrophages and endothelial cells.. Pathobiol Aging Age Relat Dis 2 (1) : 17391-17391. ScholarBank@NUS Repository. https://doi.org/10.3402/pba.v2i0.17391
dc.identifier.issn2001-0001
dc.identifier.urihttps://scholarbank.nus.edu.sg/handle/10635/219462
dc.description.abstractWe show by immunohistochemical labeling that prominent cell types in the tumor microenvironment of PyMT transgenic mice are tumor-associated macrophages (TAMs) and endothelial cells, and that both populations are decreased in the presence of mitochondrial targeted catalase (mCAT). This observation suggests that mitochondrial ROS can drive tumor invasiveness in conjunction with the presence of TAMs and increased angiogenesis. Since primary PyMT tumor cells expressing mCAT undergo increased apoptosis, mitochondrial antioxidants might be attractive anti-tumor agents.
dc.publisherInforma UK Limited
dc.sourceElements
dc.subjectendothelial cells
dc.subjectimmunohistochemistry of mouse breast cancer
dc.subjectmitochondrial catalase
dc.subjectreactive oxygen species
dc.subjecttumor associated macrophages
dc.typeArticle
dc.date.updated2022-04-21T02:17:35Z
dc.contributor.departmentDEPT OF PHYSIOLOGY
dc.description.doi10.3402/pba.v2i0.17391
dc.description.sourcetitlePathobiol Aging Age Relat Dis
dc.description.volume2
dc.description.issue1
dc.description.page17391-17391
dc.published.statePublished
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