Molecular or metabolic reprograming: What triggers tumor subtypes?

Cancer Research

Volumn 76, Issue 18, 2016, Pages 5195-5200

  Eason, Katherine ^a   Sadanandam, Anguraj ^a  

^a INSTITUTE OF CANCER RESEARCH   (United Kingdom)

Author keywords

[No Author keywords available]

Indexed keywords

ERLOTINIB; GEMCITABINE; ISOCITRATE DEHYDROGENASE 1; PACLITAXEL; PROTEIN TYROSINE KINASE INHIBITOR; PYRUVATE KINASE; SUCCINATE DEHYDROGENASE; TAMOXIFEN; TEMOZOLOMIDE; TRASTUZUMAB;

BREAST CANCER; CANCER RESISTANCE; CELL HETEROGENEITY; CITRIC ACID CYCLE; COLORECTAL CANCER; ENERGY METABOLISM; EPIGENETICS; EPITHELIAL MESENCHYMAL TRANSITION; GENE MUTATION; GLYCOLYSIS; HUMAN; HYPOXIA; METABOLIC REPROGRAMMING; METABOLISM; METABOLOMICS; NONHUMAN; ONCOGENE; ONCOGENE K RAS; OXIDATIVE PHOSPHORYLATION; PANCREAS ADENOCARCINOMA; PANCREATIC NEUROENDOCRINE TUMOR; PARAGANGLIOMA; PERSONALIZED MEDICINE; PHENOTYPIC VARIATION; PHEOCHROMOCYTOMA; PRIORITY JOURNAL; REVIEW; SOLID TUMOR; TRANSCRIPTOMICS; TUMOR MICROENVIRONMENT; TUMOR VASCULARIZATION; ANIMAL; GENETICS; GENOTYPE; NEOPLASM; PATHOLOGY; PHENOTYPE;

ANIMALS; GENOTYPE; HUMANS; NEOPLASMS; PHENOTYPE;

EID: 84988971872     PISSN: 00085472     EISSN: 15387445     Source Type: Journal    
DOI: 10.1158/0008-5472.CAN-16-0141     Document Type: Review

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