Functional genomics reveal that the serine synthesis pathway is essential in breast cancer

By 이연수. 2011

783 citations recorded by the source corpus.

View Paper: https://www.semanticscholar.org/paper/b9cf0fcb8ba8fb78eb7697b08824d9ec5ed5473d

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Citations in the corpus

One-Carbon Metabolism in Health and Disease. (2017, background): “In both breast cancer and melanoma, PHGDH is overexpressed at the protein level, due in part to genomic amplification of the locus (Locasale et al., 2011; Possemato et al., 2011).”
Cancer Cell Metabolism: One Hallmark, Many Faces (2012, background): “Increases in PHGDH expression at both the mRNA and protein levels were observed in nearly 70% of estrogen receptor (ER)negative breast cancers, despite the lack of PHGDH amplification among a fraction of cell lines within this subtype (99).”
Targeting Metabolism for Cancer Therapy (2017, background): “…in plasma and can be taken up by cells via amino acid transporters, yet PHGDH expression and increased serine biosynthesis have been shown to be important for supporting cancer cell proliferation and survival in both in vitro and in vivo settings (Locasale et al., 2011; Possemato et al., 2011).”
Hexokinase 2 is required for tumor initiation and maintenance and its systemic deletion is therapeutic in mouse models of cancer (2013, background): “Although this reaction can be catalyzed by many enzymes, including glutamate dehydrogenase, glutamate-aspartate aminotransferase, and alanine transaminase, it was previously reported that, in cells expressing high 3-phosphoglycerate dehydrogenase, approximately half of aKG is generated by the transa”
Fueling Immunity: Insights into Metabolism and Lymphocyte Function (2013, background): “Amplification of PHGDH has been observed in breast cancer and melanoma (65), and increased PHGDH expression can promote both enhanced serine biosynthesis and the proliferation of cancer cells (65, 66).”
Understanding the intersections between metabolism and cancer biology (2017, unknown): “Genomic alterations can also result in copy number gains and losses of genes encoding metabolic enzymes, and this may induce vulnerabilities (Li et al., 2014; Locasale et al., 2011; Possemato et al., 2011).”