Oncogenic properties of the endogenous fatty acid metabolism: molecular pathology of fatty acid synthase in cancer cells

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Pharmacological inhibitors of mammalian fatty acid synthase suppress DNA replication and induce apoptosis in tumor cell lines.

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Transcriptome analysis of HER2 reveals a molecular connection to fatty acid synthesis.

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Pharmacological inhibition of fatty acid synthase activity produces both cytostatic and cytotoxic effects modulated by p53.

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Fatty Acid Synthase Is Expressed Mainly in Adult Hormone-sensitive Cells or Cells with High Lipid Metabolism and in Proliferating Fetal Cells¹

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Regulation of sterol regulatory-element binding protein 1 gene expression in liver: role of insulin and protein kinase B/cAkt

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BRCA1 Affects Lipid Synthesis through Its Interaction with Acetyl-CoA Carboxylase

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Novel signaling molecules implicated in tumor-associated fatty acid synthase-dependent breast cancer cell proliferation and survival: Role of exogenous dietary fatty acids, p53-p21WAF1/CIP1, ERK1/2 MAPK, p27KIP1, BRCA1, and NF-κB

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Pharmacological and small interference RNA‐mediated inhibition of breast cancer‐associated fatty acid synthase (oncogenic antigen‐519) synergistically enhances Taxol (paclitaxel)‐induced cytotoxicity

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Structural organization of the multifunctional animal fatty‐acid synthase

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Nutritional Control of Rat Liver Fatty Acid Synthase and S14 mRNA Abundance

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In support of fatty acid synthase (FAS) as a metabolic oncogene: Extracellular acidosis acts in an epigenetic fashion activating FAS gene expression in cancer cells

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Pharmacological inhibition of fatty acid synthase (FAS): A novel therapeutic approach for breast cancer chemoprevention through its ability to suppress Her‐2/neu (erbB‐2) oncogene‐induced malignant transformation

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Inhibition of Tumor-associated Fatty Acid Synthase Hyperactivity Induces Synergistic Chemosensitization of HER-2/neu-Overexpressing Human Breast Cancer Cells to Docetaxel (taxotere)

2004 • 81 citations

Overexpression and hyperactivity of breast cancer-associated fatty acid synthase (oncogenic antigen-519) is insensitive to normal arachidonic fatty acid-induced suppression in lipogenic tissues but it is selectively inhibited by tumoricidal alpha-linolenic and gamma-linolenic fatty acids: a novel mechanism by which dietary fat can alter mammary tumorigenesis.

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Fatty acid synthase-catalyzed de novo fatty acid biosynthesis: from anabolic-energy-storage pathway in normal tissues to jack-of-all-trades in cancer cells.

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Why does tumor-associated fatty acid synthase (oncogenic antigen-519) ignore dietary fatty acids?

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Targeting Fatty Acid Synthase: Potential for Therapeutic Intervention in Her-2/neu-Overexpressing Breast Cancer

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HER-2 Gene Amplification Correlates with Higher Levels of Angiogenesis and Lower Levels of Hypoxia in Primary Breast Tumors

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Expression of Fatty Acid Synthase Is Closely Linked to Proliferation and Stromal Decidualization in Cycling Endometrium

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Inhibition of tumor-associated fatty acid synthase activity antagonizes estradiol- and tamoxifen-induced agonist transactivation of estrogen receptor (ER) in human endometrial adenocarcinoma cells

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Progestin Increases Gene Transcription and Messenger Ribonucleic Acid Stability of Fatty Acid Synthetase in Breast Cancer Cells

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Inhibition of tumor-associated fatty acid synthase activity enhances vinorelbine (Navelbine®)-induced cytotoxicity and apoptotic cell death in human breast cancer cells

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The antiobesity drug Orlistat induces cytotoxic effects, suppresses Her-2/neu (erbB-2) oncogene overexpression, and synergistically interacts with trastuzumab (Herceptintm) in chemoresistant ovarian cancer cells

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Orlistat: From Antiobesity Drug to Anticancer Agent in Her-2/neu (erbB-2)-Overexpressing Gastrointestinal Tumors?

2005 • 35 citations

Acetyl-CoA carboxylase gene and breast cancer susceptibility

2004 • 31 citations

The estrogenic activity of synthetic progestins used in oral contraceptives enhances fatty acid synthase-dependent breast cancer cell proliferation and survival

2005 • 30 citations

RNA interference-mediated silencing of the p53 tumor-suppressor protein drastically increases apoptosis after inhibition of endogenous fatty acid metabolism in breast cancer cells

2005 • 29 citations

Does endogenous fatty acid metabolism allow cancer cells to sense hypoxia and mediate hypoxic vasodilatation? Characterization of a novel molecular connection between fatty acid synthase (FAS) and hypoxia-inducible factor-1? (HIF-1?)-related expression of vascular endothelial growth factor (VEGF) in cancer cells overexpressing her-2/neu oncogene

2005 • 29 citations

Transcriptional targeting of the HER-2/neu oncogene

2000 • 22 citations