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Determination of synthetic lethal interactions in KRAS oncogene-dependent cancer cells reveals novel therapeutic targeting strategies

Cell research, 2012-08, Vol.22 (8), p.1227-1245

2012

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PI3K Pathway Dependencies in Endometrioid Endometrial Cancer Cell Lines

Clinical cancer research, 2013-07, Vol.19 (13), p.3533-3544

2013

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Reduced NF1 expression confers resistance to EGFR inhibition in lung cancer

Cancer discovery, 2014-05, Vol.4 (5), p.606-619

2014

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Regulators of Mitotic Arrest and Ceramide Metabolism Are Determinants of Sensitivity to Paclitaxel and Other Chemotherapeutic Drugs

Cancer cell, 2007-06, Vol.11 (6), p.498-512

2007

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Role of Phosphoinositide 3-OH Kinase in Cell Transformation and Control of the Actin Cytoskeleton by Ras

Cell, 1997-05, Vol.89 (3), p.457-467

1997

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Direct interaction of Ras and the amino-terminal region of Raf-1 in vitro

Nature (London), 1993-07, Vol.364 (6435), p.352-355

1993

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Involvement of MINK, a Ste20 Family Kinase, in Ras Oncogene-Induced Growth Arrest in Human Ovarian Surface Epithelial Cells

Molecular cell, 2005-12, Vol.20 (5), p.673-685

2005

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The transcriptional response to Raf activation is almost completely dependent on Mitogen-activated Protein Kinase Kinase activity and shows a major autocrine component

Molecular biology of the cell, 2004-07, Vol.15 (7), p.3450-3463

2004

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Fibroblast Growth Factor 2-Mediated Translational Control of IAPs Blocks Mitochondrial Release of Smac/DIABLO and Apoptosis in Small Cell Lung Cancer Cells

Molecular and Cellular Biology, 2003-11, Vol.23 (21), p.7600-7610

2003

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Matrix adhesion and Ras transformation both activate a phosphoinositide 3-OH kinase and protein kinase B/Akt cellular survival pathway

The EMBO journal, 1997-05, Vol.16 (10), p.2783-2793

1997

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Phosphatidylinositol-3-OH kinase direct target of Ras

Nature (London), 1994-08, Vol.370 (6490), p.527-532

1994

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p110δ , a Novel Phosphoinositide 3-Kinase in Leukocytes

Proceedings of the National Academy of Sciences - PNAS, 1997-04, Vol.94 (9), p.4330-4336

1997

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Epithelial to mesenchymal transition in Madin-Darby canine kidney cells is accompanied by down-regulation of Smad3 expression, leading to resistance to transforming growth factor-beta-induced growth arrest

The Journal of biological chemistry, 2003-01, Vol.278 (5), p.3251-3256

2003

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Stimulation of p21ras upon T-cell activation

Nature (London), 1990-08, Vol.346 (6286), p.719-723

1990

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Binding of Ras to Phosphoinositide 3-Kinase p110α Is Required for Ras- Driven Tumorigenesis in Mice

Cell, 2007-06, Vol.129 (5), p.957-968

2007

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Phosphatidylinositol 3' kinase: one of the effectors of Ras

Philosophical transactions of the Royal Society of London. Series B. Biological sciences, 1996-02, Vol.351 (1336), p.225-232

1996

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CUTL1 is a target of TGFβ signaling that enhances cancer cell motility and invasiveness

Cancer cell, 2005-06, Vol.7 (6), p.521-532

2005

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Abstract 4472: PI3K pathway dependencies in endometrioid endometrial cancer

Cancer research (Chicago, Ill.), 2013-04, Vol.73 (8_Supplement), p.4472-4472

2013

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Activation of phosphoinositide 3‐kinase by interaction with Ras and by point mutation

The EMBO journal, 1996-05, Vol.15 (10), p.2442-2451

1996

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Abstract 4835: Genetic determinants of mTOR inhibitor response in breast and endometrial cancer

Cancer research (Chicago, Ill.), 2012-04, Vol.72 (8_Supplement), p.4835-4835

2012

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R-Ras can activate the phosphoinositide 3-kinase but not the MAP kinase arm of the Ras effector pathways

Current biology, 1997-01, Vol.7 (1), p.63-71

1997

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Downregulation of the Ras activation pathway by MAP kinase phosphorylation of Sos

Oncogene, 1995-10, Vol.11 (7), p.1327-1331

1995

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Binding of ras to phosphoinositide 3-kinase p110alpha is required for ras-driven tumorigenesis in mice

Cell, 2007-06, Vol.129 (5), p.957-968

2007

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The Transcriptional Response to Raf Activation Is Almost Completely Dependent on Mitogen-activated Protein Kinase Kinase Activity and Shows a Major Autocrine ComponentD

Molecular biology of the cell, 2004-07, Vol.15 (7), p.3450-3463

2004

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CUTL1 is a target of TGF(beta) signaling that enhances cancer cell motility and invasiveness

Cancer cell, 2005-06, Vol.7 (6), p.521-532

2005

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Determination of synthetic lethal interactions in KRAS oncogene-dependent cancer cells reveals novel therapeutic targeting strategies

PI3K Pathway Dependencies in Endometrioid Endometrial Cancer Cell Lines

Reduced NF1 expression confers resistance to EGFR inhibition in lung cancer

Regulators of Mitotic Arrest and Ceramide Metabolism Are Determinants of Sensitivity to Paclitaxel and Other Chemotherapeutic Drugs

Role of Phosphoinositide 3-OH Kinase in Cell Transformation and Control of the Actin Cytoskeleton by Ras

Direct interaction of Ras and the amino-terminal region of Raf-1 in vitro

Involvement of MINK, a Ste20 Family Kinase, in Ras Oncogene-Induced Growth Arrest in Human Ovarian Surface Epithelial Cells

The transcriptional response to Raf activation is almost completely dependent on Mitogen-activated Protein Kinase Kinase activity and shows a major autocrine component

Fibroblast Growth Factor 2-Mediated Translational Control of IAPs Blocks Mitochondrial Release of Smac/DIABLO and Apoptosis in Small Cell Lung Cancer Cells

Matrix adhesion and Ras transformation both activate a phosphoinositide 3-OH kinase and protein kinase B/Akt cellular survival pathway

Phosphatidylinositol-3-OH kinase direct target of Ras

p110δ , a Novel Phosphoinositide 3-Kinase in Leukocytes

Epithelial to mesenchymal transition in Madin-Darby canine kidney cells is accompanied by down-regulation of Smad3 expression, leading to resistance to transforming growth factor-beta-induced growth arrest

Stimulation of p21ras upon T-cell activation

Binding of Ras to Phosphoinositide 3-Kinase p110α Is Required for Ras- Driven Tumorigenesis in Mice

Phosphatidylinositol 3' kinase: one of the effectors of Ras

CUTL1 is a target of TGFβ signaling that enhances cancer cell motility and invasiveness

Abstract 4472: PI3K pathway dependencies in endometrioid endometrial cancer

Activation of phosphoinositide 3‐kinase by interaction with Ras and by point mutation

Abstract 4835: Genetic determinants of mTOR inhibitor response in breast and endometrial cancer

R-Ras can activate the phosphoinositide 3-kinase but not the MAP kinase arm of the Ras effector pathways

Downregulation of the Ras activation pathway by MAP kinase phosphorylation of Sos

Binding of ras to phosphoinositide 3-kinase p110alpha is required for ras-driven tumorigenesis in mice

The Transcriptional Response to Raf Activation Is Almost Completely Dependent on Mitogen-activated Protein Kinase Kinase Activity and Shows a Major Autocrine ComponentD

CUTL1 is a target of TGF(beta) signaling that enhances cancer cell motility and invasiveness

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