Status of PI3K inhibition and biomarker development in cancer therapeutics.
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J. Baselga | J. Tabernero | J. Pérez-García | B. Markman | F. Atzori | J Baselga | J Tabernero | B Markman | F Atzori | J Pérez-García | J. Peréz-García
[1] M. Somerfield,et al. American Society of Clinical Oncology provisional clinical opinion: testing for KRAS gene mutations in patients with metastatic colorectal carcinoma to predict response to anti-epidermal growth factor receptor monoclonal antibody therapy. , 2009, Journal of clinical oncology : official journal of the American Society of Clinical Oncology.
[2] Francesca Molinari,et al. PIK3CA mutations in colorectal cancer are associated with clinical resistance to EGFR-targeted monoclonal antibodies. , 2009, Cancer research.
[3] S. Andreola,et al. PI3KCA/PTEN deregulation contributes to impaired responses to cetuximab in metastatic colorectal cancer patients. , 2009, Annals of oncology : official journal of the European Society for Medical Oncology.
[4] G. Mills,et al. Mutations in the phosphatidylinositol-3-kinase pathway predict for antitumor activity of the inhibitor PX-866 whereas oncogenic Ras is a dominant predictor for resistance. , 2009, Cancer research.
[5] Ralph Weissleder,et al. Effective Use of PI3K and MEK Inhibitors to Treat Mutant K-Ras G12D and PIK3CA H1047R Murine Lung Cancers , 2008, Nature Medicine.
[6] Violeta Serra,et al. Phosphatidylinositol 3-kinase hyperactivation results in lapatinib resistance that is reversed by the mTOR/phosphatidylinositol 3-kinase inhibitor NVP-BEZ235. , 2008, Cancer research.
[7] J. Baselga,et al. 218 POSTER A phase I dose-escalation study of the safety, pharmacokinetics and pharmacodynamics of XL147, a novel PI3K inhibitor administered orally to patients with advanced solid tumors , 2008 .
[8] G. Demetri,et al. 223 POSTER Pharmacokinetics and pharmacodynamic biomarkers for the pan-PI3K inhibitor GDC-0941: Initial Phase I evaluation , 2008 .
[9] J. Baselga,et al. 216 POSTER A phase I dose-escalation study of the safety, pharmacokinetics and pharmacodynamics of XL765, a novel inhibitor of PI3K and mTOR, administered orally to patients with solid tumors , 2008 .
[10] J. Baselga,et al. NVP-BEZ235, a dual PI3K/mTOR inhibitor, prevents PI3K signaling and inhibits the growth of cancer cells with activating PI3K mutations. , 2008, Cancer research.
[11] P. Pandolfi,et al. Inhibition of mTORC1 leads to MAPK pathway activation through a PI3K-dependent feedback loop in human cancer. , 2008, The Journal of clinical investigation.
[12] Gary Box,et al. The identification of 2-(1H-indazol-4-yl)-6-(4-methanesulfonyl-piperazin-1-ylmethyl)-4-morpholin-4-yl-thieno[3,2-d]pyrimidine (GDC-0941) as a potent, selective, orally bioavailable inhibitor of class I PI3 kinase for the treatment of cancer . , 2008, Journal of medicinal chemistry.
[13] Zhi Hu,et al. An integrative genomic and proteomic analysis of PIK3CA, PTEN, and AKT mutations in breast cancer. , 2008, Cancer research.
[14] Daniela Gabriel,et al. Identification and characterization of NVP-BEZ235, a new orally available dual phosphatidylinositol 3-kinase/mammalian target of rapamycin inhibitor with potent in vivo antitumor activity , 2008, Molecular Cancer Therapeutics.
[15] E. Heath,et al. A phase I dose-escalation study of the safety, pharmacokinetics (PK), and pharmacodynamics (PD) of a novel PI3K inhibitor, XL765, administered orally to patients (pts) with advanced solid tumors , 2008 .
[16] M. Borad,et al. Phase 1 pharmacokinetic (PK) and pharmacodynamic(PD) evaluation of SF1126 a vascular targeted pan phosphoinositide 3- kinase (PI3K) inhibitor in patients with solid tumors , 2008 .
[17] Pier Paolo Pandolfi,et al. Tenets of PTEN Tumor Suppression , 2008, Cell.
[18] Sanjay Goel,et al. PIK3CA mutation/PTEN expression status predicts response of colon cancer cells to the epidermal growth factor receptor inhibitor cetuximab. , 2008, Cancer research.
[19] Li Zhao,et al. Helical domain and kinase domain mutations in p110α of phosphatidylinositol 3-kinase induce gain of function by different mechanisms , 2008, Proceedings of the National Academy of Sciences.
[20] S. Horvath,et al. Antitumor Activity of Rapamycin in a Phase I Trial for Patients with Recurrent PTEN-Deficient Glioblastoma , 2008, PLoS medicine.
[21] Bernd Giese,et al. Targeting phosphoinositide 3-kinase: moving towards therapy. , 2008, Biochimica et biophysica acta.
[22] S. Goodman,et al. Circulating mutant DNA to assess tumor dynamics , 2008, Nature Medicine.
[23] G. Mills,et al. A vascular targeted pan phosphoinositide 3-kinase inhibitor prodrug, SF1126, with antitumor and antiangiogenic activity. , 2008, Cancer research.
[24] S. Dong,et al. Mutual exclusiveness between PIK3CA and KRAS mutations in endometrial carcinoma , 2007, International Journal of Gynecologic Cancer.
[25] G. Mills,et al. A functional genetic approach identifies the PI3K pathway as a major determinant of trastuzumab resistance in breast cancer. , 2007, Cancer cell.
[26] M. Moasser,et al. Targeting HER proteins in cancer therapy and the role of the non-target HER3 , 2007, British Journal of Cancer.
[27] Spyro Mousses,et al. A transforming mutation in the pleckstrin homology domain of AKT1 in cancer , 2007, Nature.
[28] David M Sabatini,et al. Defining the role of mTOR in cancer. , 2007, Cancer cell.
[29] D. Troyer,et al. Determining Risk of Biochemical Recurrence in Prostate Cancer by Immunohistochemical Detection of PTEN Expression and Akt Activation , 2007, Clinical Cancer Research.
[30] M. Waterfield,et al. Pharmacologic characterization of a potent inhibitor of class I phosphatidylinositide 3-kinases. , 2007, Cancer research.
[31] S. Hahn,et al. Phosphatase and tensin homologue deficiency in glioblastoma confers resistance to radiation and temozolomide that is reversed by the protease inhibitor nelfinavir. , 2007, Cancer research.
[32] M. Ringnér,et al. Poor prognosis in carcinoma is associated with a gene expression signature of aberrant PTEN tumor suppressor pathway activity , 2007, Proceedings of the National Academy of Sciences.
[33] S. Horvath,et al. Insulin growth factor-binding protein 2 is a candidate biomarker for PTEN status and PI3K/Akt pathway activation in glioblastoma and prostate cancer , 2007, Proceedings of the National Academy of Sciences.
[34] Mieke Schutte,et al. Phosphatidylinositol-3-OH Kinase or RAS Pathway Mutations in Human Breast Cancer Cell Lines , 2007, Molecular Cancer Research.
[35] S. Stein,et al. Lapatinib antitumor activity is not dependent upon phosphatase and tensin homologue deleted on chromosome 10 in ErbB2-overexpressing breast cancers. , 2007, Cancer research.
[36] Y. Song,et al. Akt Involvement in Paclitaxel Chemoresistance of Human Ovarian Cancer Cells , 2007, Annals of the New York Academy of Sciences.
[37] S. Franceschi,et al. Correlation Among Pathology, Genotype, and Patient Outcomes in Glioblastoma , 2006, Journal of neuropathology and experimental neurology.
[38] M. Perucho,et al. The relationship between microsatellite instability and PTEN gene mutations in endometrial cancer , 2006, International journal of cancer.
[39] Ji Luo,et al. The evolution of phosphatidylinositol 3-kinases as regulators of growth and metabolism , 2006, Nature Reviews Genetics.
[40] G. Mills,et al. Progress in Chemoprevention Drug Development: The Promise of Molecular Biomarkers for Prevention of Intraepithelial Neoplasia and Cancer—A Plan to Move Forward , 2006, Clinical Cancer Research.
[41] L. Cantley,et al. Loss of class IA PI3K signaling in muscle leads to impaired muscle growth, insulin response, and hyperlipidemia. , 2006, Cell metabolism.
[42] G. Hortobagyi,et al. Mechanisms of Disease: understanding resistance to HER2-targeted therapy in human breast cancer , 2006, Nature Clinical Practice Oncology.
[43] Tak W. Mak,et al. Beyond PTEN mutations: the PI3K pathway as an integrator of multiple inputs during tumorigenesis , 2006, Nature Reviews Cancer.
[44] B. Vanhaesebroeck,et al. Oncogenic transformation induced by the p110β, -γ, and -δ isoforms of class I phosphoinositide 3-kinase , 2006, Proceedings of the National Academy of Sciences of the United States of America.
[45] B. Vanhaesebroeck,et al. Oncogenic transformation induced by the p110beta, -gamma, and -delta isoforms of class I phosphoinositide 3-kinase. , 2006, Proceedings of the National Academy of Sciences of the United States of America.
[46] C. Warneke,et al. Examination of mutations in BRAF, NRAS, and PTEN in primary cutaneous melanoma. , 2006, The Journal of investigative dermatology.
[47] Yiling Lu,et al. Exploiting the PI3K/AKT Pathway for Cancer Drug Discovery , 2005, Nature Reviews Drug Discovery.
[48] Li Zhao,et al. Oncogenic PI3K deregulates transcription and translation , 2005, Nature Reviews Cancer.
[49] M. Skinner,et al. Inhibition of phosphatidylinositol 3-kinase sensitizes ovarian cancer cells to carboplatin and allows adjunct chemotherapy treatment , 2005, Molecular Cancer Therapeutics.
[50] Lewis C Cantley,et al. Feedback inhibition of Akt signaling limits the growth of tumors lacking Tsc2. , 2005, Genes & development.
[51] A. Balmain,et al. Crosstalk Between Pten and Ras Signaling Pathways in Tumor Development , 2005, Cell cycle.
[52] D. Polsky,et al. PTEN Expression in Melanoma: Relationship with Patient Survival, Bcl-2 Expression, and Proliferation , 2005, Clinical Cancer Research.
[53] S. Schwartz,et al. The prevalence of PIK3CA mutations in gastric and colon cancer. , 2005, European journal of cancer.
[54] T. Kawabe,et al. Functional analysis of PIK3CA gene mutations in human colorectal cancer. , 2005, Cancer research.
[55] Carlo Rago,et al. Mutant PIK3CA promotes cell growth and invasion of human cancer cells. , 2005, Cancer cell.
[56] Paul Tempst,et al. Phosphorylation and Functional Inactivation of TSC2 by Erk Implications for Tuberous Sclerosisand Cancer Pathogenesis , 2005, Cell.
[57] J. Baselga,et al. Critical update and emerging trends in epidermal growth factor receptor targeting in cancer. , 2005, Journal of clinical oncology : official journal of the American Society of Clinical Oncology.
[58] Cristina M. Pinto,et al. Retracted: Frequent genetic and biochemical alterations of the PI 3‐K/AKT/PTEN pathway in head and neck squamous cell carcinoma , 2005, International journal of cancer.
[59] D. Guertin,et al. Phosphorylation and Regulation of Akt/PKB by the Rictor-mTOR Complex , 2005, Science.
[60] Suk Woo Nam,et al. PIK3CA gene is frequently mutated in breast carcinomas and hepatocellular carcinomas , 2005, Oncogene.
[61] R. Chibbar,et al. Reduced PTEN expression predicts relapse in patients with breast carcinoma treated by tamoxifen , 2005, Modern Pathology.
[62] P. Vogt,et al. Phosphatidylinositol 3-kinase mutations identified in human cancer are oncogenic. , 2005, Proceedings of the National Academy of Sciences of the United States of America.
[63] J. Nakamura,et al. PKB/Akt mediates radiosensitization by the signaling inhibitor LY294002 in human malignant gliomas , 2005, Journal of Neuro-Oncology.
[64] B. Manning. Balancing Akt with S6K , 2004, The Journal of cell biology.
[65] Wayne A. Phillips,et al. Mutation of the PIK3CA Gene in Ovarian and Breast Cancer , 2004, Cancer Research.
[66] Y. Marie,et al. Distinct Responses of Xenografted Gliomas to Different Alkylating Agents Are Related to Histology and Genetic Alterations , 2004, Cancer Research.
[67] J. Ptak,et al. High Frequency of Mutations of the PIK3CA Gene in Human Cancers , 2004, Science.
[68] Ming Tan,et al. PTEN activation contributes to tumor inhibition by trastuzumab, and loss of PTEN predicts trastuzumab resistance in patients. , 2004, Cancer cell.
[69] Charis Eng,et al. PTEN: One Gene, Many Syndromes , 2003, Human mutation.
[70] Kyucheol Cho,et al. Frequent monoallelic deletion of PTEN and its reciprocal associatioin with PIK3CA amplification in gastric carcinoma , 2003, International journal of cancer.
[71] Pier Paolo Pandolfi,et al. PTEN and p53: who will get the upper hand? , 2003, Cancer cell.
[72] Satoshi Matsumoto,et al. Frequent somatic mutations in PTEN and TP53 are mutually exclusive in the stroma of breast carcinomas , 2002, Nature Genetics.
[73] K. Inoki,et al. TSC2 is phosphorylated and inhibited by Akt and suppresses mTOR signalling , 2002, Nature Cell Biology.
[74] J. Litz,et al. Inhibition of phosphatidylinositol 3-kinase-Akt signaling blocks growth, promotes apoptosis, and enhances sensitivity of small cell lung cancer cells to chemotherapy. , 2002, Molecular cancer therapeutics.
[75] P. Dennis,et al. Constitutive and inducible Akt activity promotes resistance to chemotherapy, trastuzumab, or tamoxifen in breast cancer cells. , 2002, Molecular cancer therapeutics.
[76] Ajay N. Jain,et al. Genomic copy number analysis of non-small cell lung cancer using array comparative genomic hybridization: implications of the phosphatidylinositol 3-kinase pathway. , 2002, Cancer research.
[77] Lewis C Cantley,et al. The phosphoinositide 3-kinase pathway. , 2002, Science.
[78] I. Campbell,et al. The phosphatidylinositol 3'-kinase p85alpha gene is an oncogene in human ovarian and colon tumors. , 2001, Cancer research.
[79] R. Stein. Prospects for phosphoinositide 3-kinase inhibition as a cancer treatment. , 2001, Endocrine-related cancer.
[80] C. James,et al. PTEN mutation, EGFR amplification, and outcome in patients with anaplastic astrocytoma and glioblastoma multiforme. , 2001, Journal of the National Cancer Institute.
[81] P. Depowski,et al. Loss of Expression of the PTEN Gene Protein Product Is Associated with Poor Outcome in Breast Cancer , 2001, Modern Pathology.
[82] P. Dennis,et al. Akt/protein kinase B is constitutively active in non-small cell lung cancer cells and promotes cellular survival and resistance to chemotherapy and radiation. , 2001, Cancer research.
[83] T. Fleming,et al. Use of chemotherapy plus a monoclonal antibody against HER2 for metastatic breast cancer that overexpresses HER2. , 2001, The New England journal of medicine.
[84] C. Eng. Will the real Cowden syndrome please stand up: revised diagnostic criteria , 2000, Journal of medical genetics.
[85] M. Peacocke,et al. Identification of PTEN mutations in metastatic melanoma specimens , 2000, Journal of medical genetics.
[86] A. Sakurada,et al. Anticorresponding mutations of the KRAS and PTEN genes in human endometrial cancer. , 2000, Oncology reports.
[87] M. Wolter,et al. Allelic losses on chromosome arm 10q and mutation of the PTEN (MMAC1) tumour suppressor gene in primary and metastatic malignant melanomas , 2000, Virchows Archiv.
[88] P. Guldberg,et al. Mutation and allelic loss of the PTEN/MMAC1 gene in primary and metastatic melanoma biopsies. , 2000, The Journal of investigative dermatology.
[89] M. Loda,et al. Loss of PTEN expression in paraffin-embedded primary prostate cancer correlates with high Gleason score and advanced stage. , 1999, Cancer research.
[90] C Eng,et al. PTEN mutation spectrum and genotype-phenotype correlations in Bannayan-Riley-Ruvalcaba syndrome suggest a single entity with Cowden syndrome. , 1999, Human molecular genetics.
[91] W. Liu,et al. Up-regulation of Akt3 in Estrogen Receptor-deficient Breast Cancers and Androgen-independent Prostate Cancer Lines* , 1999, The Journal of Biological Chemistry.
[92] M. Greenberg,et al. Akt Promotes Cell Survival by Phosphorylating and Inhibiting a Forkhead Transcription Factor , 1999, Cell.
[93] H. Feilotter,et al. Analysis of the 10q23 chromosomal region and the PTEN gene in human sporadic breast carcinoma , 1999, British Journal of Cancer.
[94] A. Berchuck,et al. PTEN mutation in endometrial cancers is associated with favorable clinical and pathologic characteristics. , 1998, Clinical cancer research : an official journal of the American Association for Cancer Research.
[95] M. Roussel,et al. Glycogen synthase kinase-3beta regulates cyclin D1 proteolysis and subcellular localization. , 1998, Genes & development.
[96] Carlos Cordon-Cardo,et al. Pten is essential for embryonic development and tumour suppression , 1998, Nature Genetics.
[97] H. Hibshoosh,et al. Allelic loss of chromosome 10q23 is associated with tumor progression in breast carcinomas , 1998, Oncogene.
[98] Y. Yonekawa,et al. PTEN (MMAC1) Mutations Are Frequent in Primary Glioblastomas (de novo) but not in Secondary Glioblastomas , 1998, Journal of neuropathology and experimental neurology.
[99] C Eng,et al. Mutation spectrum and genotype-phenotype analyses in Cowden disease and Bannayan-Zonana syndrome, two hamartoma syndromes with germline PTEN mutation. , 1998, Human molecular genetics.
[100] J. Cheng,et al. Amplification and overexpression of the AKT2 oncogene in a subset of human pancreatic ductal adenocarcinomas , 1998, Molecular carcinogenesis.
[101] L. Cantley,et al. Phosphoinositide kinases. , 1998, Annual review of biochemistry.
[102] J. Herman,et al. Frequent inactivation of PTEN/MMAC1 in primary prostate cancer. , 1997, Cancer research.
[103] R. McLendon,et al. PTEN gene mutations are seen in high-grade but not in low-grade gliomas. , 1997, Cancer research.
[104] J. Bruce,et al. Somatic mutations of PTEN in glioblastoma multiforme. , 1997, Cancer research.
[105] Kathleen R. Cho,et al. Mutations in PTEN are frequent in endometrial carcinoma but rare in other common gynecological malignancies. , 1997, Cancer research.
[106] P. Guldberg,et al. Disruption of the MMAC1/PTEN gene by deletion or mutation is a frequent event in malignant melanoma. , 1997, Cancer research.
[107] J. Boyd,et al. Mutation analysis of the putative tumor suppressor gene PTEN/MMAC1 in primary breast carcinomas. , 1997, Cancer research.
[108] Jing Li,et al. Germline mutations of the PTEN gene in Cowden disease, an inherited breast and thyroid cancer syndrome , 1997, Nature Genetics.
[109] M. Wigler,et al. PTEN, a Putative Protein Tyrosine Phosphatase Gene Mutated in Human Brain, Breast, and Prostate Cancer , 1997, Science.
[110] J. Cheng,et al. Molecular alterations of the AKT2 oncogene in ovarian and breast carcinomas , 1995, International journal of cancer.
[111] Michael J. Fry,et al. Phosphatidylinositol-3-OH kinase direct target of Ras , 1994, Nature.
[112] S. Staal. Molecular cloning of the akt oncogene and its human homologues AKT1 and AKT2: amplification of AKT1 in a primary human gastric adenocarcinoma. , 1987, Proceedings of the National Academy of Sciences of the United States of America.