Cancer type-dependent genetic interactions between cancer driver alterations indicate plasticity of epistasis across cell types

Molecular Systems Biology

Volumn 11, Issue 7, 2015, Pages

  Park, Solip ^a,b   Lehner, Ben ^a,b,c  

^a CENTRE FOR GENOMIC REGULATION CRG   (Spain)

^b UNIVERSITAT POMPEU FABRA   (Spain)

^c INSTITUCIÓ CATALANA DE RECERCA I ESTUDIS AVANÇATS ICREA   (Spain)

Author keywords

cancer; epistasis; evolution; genetic interaction networks; tissue specificity

Indexed keywords

B RAF KINASE; CYCLIN DEPENDENT KINASE 4; CYCLIN DEPENDENT KINASE INHIBITOR 2A; K RAS PROTEIN; PROTEIN P53;

ARTICLE; CELL CYCLE REGULATION; CELLS BY BODY ANATOMY; COPY NUMBER VARIATION; DNA METHYLATION; EPISTASIS; GENE INTERACTION; GENETIC DISORDER; GENOME; GENOMICS; GLIOBLASTOMA; HUMAN; MALIGNANT NEOPLASTIC DISEASE; PRIORITY JOURNAL; PROMOTER REGION; SINGLE NUCLEOTIDE POLYMORPHISM; CELL PLASTICITY; GENE EXPRESSION REGULATION; GENETIC PREDISPOSITION; GENETICS; NEOPLASM; TUMOR GENE;

CELL PLASTICITY; EPISTASIS, GENETIC; GENE EXPRESSION REGULATION, NEOPLASTIC; GENES, NEOPLASM; GENETIC PREDISPOSITION TO DISEASE; HUMANS; NEOPLASMS; POLYMORPHISM, SINGLE NUCLEOTIDE;

EID: 84938097500     PISSN: None     EISSN: 17444292     Source Type: Journal    
DOI: 10.15252/msb.20156102     Document Type: Article

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