Ketone body utilization drives tumor growth and metastasis.
about
Oncogenes induce the cancer-associated fibroblast phenotype: metabolic symbiosis and "fibroblast addiction" are new therapeutic targets for drug discoveryEvaluation and prognostic significance of ACAT1 as a marker of prostate cancer progressionEthanol exposure induces the cancer-associated fibroblast phenotype and lethal tumor metabolism: implications for breast cancer preventionA gene expression estimator of intramuscular fat percentage for use in both cattle and sheepThe nutritional phenome of EMT-induced cancer stem-like cellsDeregulation of the EGFR/PI3K/PTEN/Akt/mTORC1 pathway in breast cancer: possibilities for therapeutic intervention.FABP7 and HMGCS2 are novel protein markers for apocrine differentiation categorizing apocrine carcinoma of the breast.The ketogenic diet and hyperbaric oxygen therapy prolong survival in mice with systemic metastatic cancer.Identification of Serum Markers of Esophageal Adenocarcinoma by Global and Targeted Metabolic ProfilingHydroxycarboxylic acid receptors are essential for breast cancer cells to control their lipid/fatty acid metabolismA network-based pathway-expanding approach for pathway analysis.Mitochondria "fuel" breast cancer metabolism: fifteen markers of mitochondrial biogenesis label epithelial cancer cells, but are excluded from adjacent stromal cellsMitochondrial dysfunction in breast cancer cells prevents tumor growth: understanding chemoprevention with metformin.Cigarette smoke metabolically promotes cancer, via autophagy and premature aging in the host stromal microenvironment.Compartment-specific activation of PPARγ governs breast cancer tumor growth, via metabolic reprogramming and symbiosis.Intermittent energy restriction induces changes in breast gene expression and systemic metabolismAutophagy in breast cancer and its implications for therapyCould Intermittent Energy Restriction and Intermittent Fasting Reduce Rates of Cancer in Obese, Overweight, and Normal-Weight Subjects? A Summary of EvidenceOncogenes and inflammation rewire host energy metabolism in the tumor microenvironment: RAS and NFκB target stromal MCT4.Discovery of genes from feces correlated with colorectal cancer progressionThe action of β-hydroxybutyrate on the growth, metabolism and global histone H3 acetylation of spontaneous mouse mammary tumours: evidence of a β-hydroxybutyrate paradoxMolecular and diagnostic features of apocrine breast lesions.Fibroblast activation and senescence in oral cancer.Multi-dimensional Roles of Ketone Bodies in Fuel Metabolism, Signaling, and Therapeutics.Ketone supplementation decreases tumor cell viability and prolongs survival of mice with metastatic cancerCell-surface G-protein-coupled receptors for tumor-associated metabolites: A direct link to mitochondrial dysfunction in cancer.Metabolic Plasticity of Stem Cells and Macrophages in Cancer.Inactivation of HMGCL promotes proliferation and metastasis of nasopharyngeal carcinoma by suppressing oxidative stress.Age-related changes in the transcriptome of antibody-secreting cells.Vitamin C and Doxycycline: A synthetic lethal combination therapy targeting metabolic flexibility in cancer stem cells (CSCs).Synergy of Dendritic Cell Vaccines and Avasimibe in Treatment of Head and Neck Cancer in Mice.Cancer metabolism: new validated targets for drug discovery.Response to commentary by Champ and Klement: Is a ketogenic diet the solution for the hyperglycemia problem in glioblastoma therapy?Mitoketoscins: Novel mitochondrial inhibitors for targeting ketone metabolism in cancer stem cells (CSCs).Preliminary investigation of blood concentrations of insulin-like growth factor, insulin, lactate and β-hydroxybutyrate in dogs with lymphoma as compared with matched controls.Discovery and validation of urinary metabotypes for the diagnosis of hepatocellular carcinoma in West Africans.Tracking cellular and molecular changes in a species-specific manner during experimental tumor progression in vivo.Cancer stem cells (CSCs): metabolic strategies for their identification and eradication.Insulin promotes progression of colon cancer by upregulation of ACAT1.Beta-hydroxybutyrate (3-OHB) can influence the energetic phenotype of breast cancer cells, but does not impact their proliferation and the response to chemotherapy or radiation.
P2860
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P2860
Ketone body utilization drives tumor growth and metastasis.
description
2012 nî lūn-bûn
@nan
2012 թուականի Սեպտեմբերին հրատարակուած գիտական յօդուած
@hyw
2012 թվականի սեպտեմբերին հրատարակված գիտական հոդված
@hy
2012年の論文
@ja
2012年論文
@yue
2012年論文
@zh-hant
2012年論文
@zh-hk
2012年論文
@zh-mo
2012年論文
@zh-tw
2012年论文
@wuu
name
Ketone body utilization drives tumor growth and metastasis.
@ast
Ketone body utilization drives tumor growth and metastasis.
@en
Ketone body utilization drives tumor growth and metastasis.
@nl
type
label
Ketone body utilization drives tumor growth and metastasis.
@ast
Ketone body utilization drives tumor growth and metastasis.
@en
Ketone body utilization drives tumor growth and metastasis.
@nl
prefLabel
Ketone body utilization drives tumor growth and metastasis.
@ast
Ketone body utilization drives tumor growth and metastasis.
@en
Ketone body utilization drives tumor growth and metastasis.
@nl
P2093
P2860
P50
P356
P1433
P1476
Ketone body utilization drives tumor growth and metastasis.
@en
P2093
Anthony Howell
Ubaldo E Martinez-Outschoorn
P2860
P304
P356
10.4161/CC.22137
P577
2012-09-19T00:00:00Z