Beyond PTEN mutations: The PI3K pathway as an integrator of multiple inputs during tumorigenesis

Nature Reviews Cancer

Volumn 6, Issue 3, 2006, Pages 184-192

  Cully, Megan ^a,b   You, Han ^a   Levine, Arnold J ^c   Mak, Tak W ^a  

^a PRINCESS MARGARET HOSPITAL   (Canada)

^b IMPERIAL CANCER RESEARCH FUND   (United Kingdom)

^c RUTGERS CANCER INSTITUTE OF NEW JERSEY   (United States)

Author keywords

[No Author keywords available]

Indexed keywords

AP 23573; EVEROLIMUS; GROWTH FACTOR RECEPTOR; IMATINIB; PHOSPHATIDYLINOSITOL 3 KINASE; PHOSPHATIDYLINOSITOL 3 KINASE INHIBITOR; PHOSPHATIDYLINOSITOL 3,4,5 TRISPHOSPHATE 3 PHOSPHATASE; PROTEIN KINASE INHIBITOR; PROTEIN P53; RAS PROTEIN; RECEPTOR BLOCKING AGENT; TARGET OF RAPAMYCIN KINASE; TEMSIROLIMUS;

BREAST CARCINOMA; CANCER THERAPY; CARCINOGENESIS; CELL SURVIVAL; CLINICAL TRIAL; DEREGULATION; DRUG ACTIVITY; DRUG EFFICACY; DRUG SAFETY; ENDOMETRIUM TUMOR; GENE DELETION; GENE MUTATION; HUMAN; KIDNEY CARCINOMA; NONHUMAN; PHEOCHROMOCYTOMA; PRIORITY JOURNAL; REGULATORY MECHANISM; REVIEW; SIGNAL TRANSDUCTION; UNSPECIFIED SIDE EFFECT;

1-PHOSPHATIDYLINOSITOL 3-KINASE; ANIMALS; CELL TRANSFORMATION, NEOPLASTIC; HUMANS; MUTATION; NEOPLASMS; PTEN PHOSPHOHYDROLASE; SIGNAL TRANSDUCTION; TUMOR SUPPRESSOR PROTEINS;

EID: 33644513730     PISSN: 1474175X     EISSN: None     Source Type: Journal    
DOI: 10.1038/nrc1819     Document Type: Review

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