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81. Full Text Analysis of circulating DNA and protein biomarkers to predict the clinical activity of regorafenib and assess prognosis in patients with metastatic colorectal cancer: a retrospective, exploratory analysis of the CORRECT trial
by Tabernero, Josep, Dr and Lenz, Heinz-Josef, Prof and Siena, Salvatore, MD and Sobrero, Alberto, MD and Falcone, Alfredo, Prof and Ychou, Marc, Prof and Humblet, Yves, Prof and Bouché, Olivier, Prof and Mineur, Laurent, MD and Barone, Carlo, Prof and Adenis, Antoine, Prof and Yoshino, Takayuki, MD and Goldberg, Richard M, Prof and Sargent, Daniel J, Prof and Wagner, Andrea, MD and Laurent, Dirk, MD and Teufel, Michael, PhD and Jeffers, Michael, PhD and Grothey, Axel, Prof and Van Cutsem, Eric, Prof
Lancet Oncology, The, ISSN 1470-2045, 2015, Volume 16, Issue 8, pp. 937 - 948
Summary Background Tumour mutational status is an important determinant of the response of metastatic colorectal cancer to targeted treatments. However, the... 
Hematology, Oncology and Palliative Medicine | KRAS MUTATIONS | 1ST-LINE TREATMENT | LEUCOVORIN | PLUS IRINOTECAN | ONCOLOGY | RANDOMIZED PHASE-III | INHIBITS GROWTH | ACQUIRED-RESISTANCE | FLUOROURACIL | PLACEBO PLUS | TUMOR-GROWTH | Predictive Value of Tests | Proto-Oncogene Proteins p21(ras) | Colorectal Neoplasms - genetics | Humans | Middle Aged | Male | Antineoplastic Agents - therapeutic use | Clinical Trials, Phase III as Topic | Time Factors | DNA Mutational Analysis | Colorectal Neoplasms - drug therapy | Real-Time Polymerase Chain Reaction | Precision Medicine | Receptor, TIE-1 - blood | Phosphatidylinositol 3-Kinases - blood | Genetic Predisposition to Disease | Adenocarcinoma - blood | ras Proteins - blood | Adenocarcinoma - drug therapy | Adenocarcinoma - secondary | Disease Progression | Phenotype | Class I Phosphatidylinositol 3-Kinases | Biomarkers, Tumor - genetics | ras Proteins - genetics | Patient Selection | DNA, Neoplasm - blood | Female | Adenocarcinoma - genetics | Retrospective Studies | Pyridines - therapeutic use | Colorectal Neoplasms - mortality | Colorectal Neoplasms - blood | Kaplan-Meier Estimate | Proportional Hazards Models | Phenylurea Compounds - therapeutic use | Proto-Oncogene Proteins B-raf - blood | Proto-Oncogene Proteins - genetics | Treatment Outcome | Randomized Controlled Trials as Topic | Biomarkers, Tumor - blood | Phosphatidylinositol 3-Kinases - genetics | Disease-Free Survival | Proto-Oncogene Proteins B-raf - genetics | Aged | DNA, Neoplasm - genetics | Colorectal Neoplasms - pathology | Proto-Oncogene Proteins - blood | Adenocarcinoma - mortality | Medical colleges | Medical research | Cancer patients | Prognosis | Liver | DNA | Colorectal cancer | Genetic research | Medicine, Experimental | Metastasis | Life Sciences | Human health and pathology
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82. Full Text Class III PI3K Vps34 plays an essential role in autophagy and in heart and liver function
by Nadia Jaber and Zhixun Dou and Juei-Suei Chen and Joseph Catanzaro and Ya-Ping Jiang and Lisa M. Ballou and Elzbieta Selinger and Xiaosen Ouyang and Richard Z. Lin and Jianhua Zhang and Wei-Xing Zong
Proceedings of the National Academy of Sciences of the United States of America, ISSN 0027-8424, 2/2012, Volume 109, Issue 6, pp. 2003 - 2008
A critical regulator of autophagy is the Class III PI3K Vps34 (also called PIK3C3). Although Vps34 is known to play an essential role in autophagy in yeast,... 
Heart | Starvation | Hepatocytes | Liver | Cell aggregates | Amino acids | Gene expression regulation | Directional control | Vacuoles | Phosphatidylinositols | 3-MA | SQSTM1/p62 | Transferrin | LC3 | Epidermal growth factor receptor | ACTIVATION | epidermal growth factor receptor | PHOSPHATIDYLINOSITOL 3-KINASE | MULTIDISCIPLINARY SCIENCES | transferrin | HVPS34 | CANCER | METABOLISM | PATHWAY | PHOSPHOINOSITIDE 3-KINASES | EARLY ENDOSOMES | MICE | SELF-DIGESTION | Fibroblasts - enzymology | Liver - pathology | Liver - enzymology | Phosphatidylinositol Phosphates - metabolism | TOR Serine-Threonine Kinases - metabolism | Liver - physiopathology | Autophagy | Amino Acids - metabolism | Gene Deletion | Electrocardiography | Phagosomes - ultrastructure | Liver - ultrastructure | Signal Transduction | Phagosomes - metabolism | Class III Phosphatidylinositol 3-Kinases - metabolism | Myocardium - pathology | Fibroblasts - pathology | Phagosomes - pathology | Mice, Knockout | Class III Phosphatidylinositol 3-Kinases - deficiency | Myocardium - enzymology | Animals | Embryo, Mammalian - cytology | Mice | Enzyme Activation | Autophagy (Cytology) | Physiological aspects | Genetic aspects | Research | Gene expression | Growth factors | Biological Sciences | SQSTM1 | p62
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83. Full Text AKT-Independent Signaling Downstream of Oncogenic PIK3CA Mutations in Human Cancer
by Vasudevan, Krishna M and Barbie, David A and Davies, Michael A and Rabinovsky, Rosalia and McNear, Chontelle J and Kim, So Young and Kim, Jessica J and Hennessy, Bryan T and Tseng, Hsiuyi and Pochanard, Panisa and Dunn, Ian F and Schinzel, Anna C and Sandy, Peter and Hoersch, Sebastian and Sheng, Qing and Gupta, Piyush B and Boehm, Jesse S and Reiling, Jan H and Silver, Serena and Lu, Yiling and Stemke-Hale, Katherine and Dutta, Bhaskar and Joy, Corwin and Sahin, Aysegul A and Gonzalez-Angulo, Ana Maria and Lluch, Ana and Rameh, Lucia E and Jacks, Tyler and Root, David E and Lander, Eric S and Mills, Gordon B and Hahn, William C and Sellers, William R and Garraway, Levi A
Cancer Cell, ISSN 1535-6108, 2009, Volume 16, Issue 1, pp. 21 - 32
Dysregulation of the phosphatidylinositol 3-kinase (PI3K) signaling pathway occurs frequently in human cancer. tumor suppressor or oncogene mutations both... 
CELLCYCLE | BREAST-CANCER | ACTIVATION | CAENORHABDITIS-ELEGANS | 3-PHOSPHOINOSITIDE-DEPENDENT PROTEIN KINASE-1 | PHOSPHATIDYLINOSITOL 3-KINASES | HOMOLOGY DOMAIN | ONCOLOGY | HYDROPHOBIC MOTIF PHOSPHORYLATION | HIGH-FREQUENCY | MTOR COMPLEX | MAMMARY EPITHELIAL-CELLS | CELL BIOLOGY | Neoplasms - metabolism | PTEN Phosphohydrolase - genetics | PTEN Phosphohydrolase - deficiency | Humans | Protein-Serine-Threonine Kinases - genetics | Cell Survival - genetics | Gene Expression Profiling | Phosphatidylinositol 3-Kinases - metabolism | Proto-Oncogene Proteins c-akt - physiology | Signal Transduction - genetics | Breast Neoplasms - physiopathology | Proto-Oncogene Proteins c-akt - genetics | Breast Neoplasms - metabolism | Phosphatidylinositol 3-Kinases - genetics | Breast Neoplasms - enzymology | Breast Neoplasms - genetics | Class I Phosphatidylinositol 3-Kinases | Neoplasms - genetics | Cell Line, Tumor | Female | Enzyme Activation | Mutation | Protein-Serine-Threonine Kinases - metabolism | Medical colleges | Phosphatidylinositol | Oncology, Experimental | Genetic research | Genetic aspects | Research | Cancer | PTEN | AKT | SGK3 | cancer | PI3 kinase | PDK1
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84. Full Text PIK3CA mutations are associated with decreased benefit to neoadjuvant human epidermal growth factor receptor 2-targeted therapies in breast cancer
by Majewski, Ian J and Nuciforo, Paolo and Mittempergher, Lorenza and Bosma, Astrid J and Eidtmann, Holger and Holmes, Eileen and Sotiriou, Christos and Fumagalli, Debora and Jimenez, Jose and Aura, Claudia and Prudkin, Ludmila and Díaz-Delgado, Maria Carmen and de la Peña, Lorena and Loi, Sherene and Ellis, Catherine and Schultz, Nikolaus and de Azambuja, Evano and Harbeck, Nadia and Piccart-Gebhart, Martine and Bernards, René and Baselga, José
Journal of Clinical Oncology, ISSN 0732-183X, 04/2015, Volume 33, Issue 12, pp. 1334 - 1339
PURPOSE: We investigated whether mutations in the gene encoding the phosphatidylinositol 3-kinase (PI3K) catalytic subunit (PIK3CA) correlates with response to... 
Humans | Middle Aged | Antineoplastic Combined Chemotherapy Protocols | Quinazolines | Breast Neoplasms | Molecular Targeted Therapy | Randomized Controlled Trial | Phosphatidylinositol 3-Kinases | Journal Article | Antibodies, Monoclonal, Humanized | Clinical Trial, Phase III | Research Support, Non-U.S. Gov't | Female | Neoadjuvant Therapy | Multicenter Study | Aged | Receptor, ErbB-2 | Chemotherapy, Adjuvant | Mutation | Neoplasm Staging | Trastuzumab | ADJUVANT CHEMOTHERAPY | LAPATINIB | SURVIVAL | MULTICENTER | ACTIVATION | ONCOLOGY | COLORECTAL-CANCER | PHASE-3 TRIAL | OPEN-LABEL | TRASTUZUMAB RESISTANCE | PLUS | Receptor, ErbB-2 - metabolism | Breast Neoplasms - drug therapy | Phosphatidylinositol 3-Kinases - genetics | Breast Neoplasms - enzymology | Antibodies, Monoclonal, Humanized - administration & dosage | Breast Neoplasms - genetics | Class I Phosphatidylinositol 3-Kinases | Antineoplastic Combined Chemotherapy Protocols - therapeutic use | Breast Neoplasms - pathology | Quinazolines - administration & dosage | Receptor, ErbB-2 - antagonists & inhibitors | To14 | Bc6 | To8 | ORIGINAL REPORTS | Bc8 | To2
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85. Full Text Biomarker Analyses in CLEOPATRA: A phase III, placebo-controlled study of pertuzumab in human epidermal growth factor receptor 2-positive, first-line metastatic breast cancer
by Baselga, José and Cortés, Javier and Im, Seock-Ah and Clark, Emma and Ross, Graham and Kiermaier, Astrid and Swain, Sandra M
Journal of Clinical Oncology, ISSN 0732-183X, 11/2014, Volume 32, Issue 33, pp. 3753 - 3761
Purpose To explore the prognostic and/or predictive value of human epidermal growth factor receptor 2 (HER2) pathway-related biomarkers in the phase III... 
SURVIVAL | CELLS | COMPLEX | IMPACT | TRASTUZUMAB | ONCOLOGY | RESISTANCE | ANTIBODY | DOCETAXEL | Antibodies, Monoclonal, Humanized - therapeutic use | Prognosis | Prospective Studies | Double-Blind Method | Biomarkers, Tumor - analysis | Humans | Antineoplastic Agents - therapeutic use | Receptors, Estrogen - analysis | Breast Neoplasms - drug therapy | Phosphatidylinositol 3-Kinases - genetics | Breast Neoplasms - chemistry | Neoplasm Metastasis | Class I Phosphatidylinositol 3-Kinases | Breast Neoplasms - blood | Breast Neoplasms - mortality | Female | Mutation | Receptor, ErbB-2 - analysis
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86. Full Text Somatic Activating PIK3CA Mutations Cause Venous Malformation
by Limaye, Nisha and Kangas, Jaakko and Mendola, Antonella and Godfraind, Catherine and Schlögel, Matthieu J and Helaers, Raphael and Eklund, Lauri and Boon, Laurence M and Vikkula, Miikka
The American Journal of Human Genetics, ISSN 0002-9297, 12/2015, Volume 97, Issue 6, pp. 914 - 921
Somatic mutations in , the gene encoding endothelial cell tyrosine kinase receptor TIE2, cause more than half of sporadically occurring unifocal venous... 
DIAGNOSIS | OVERGROWTH | GENE | PI3K | LYMPHATIC ENDOTHELIAL-CELLS | GENETICS & HEREDITY | Humans | Vascular Malformations - enzymology | Phosphatidylinositol 3-Kinases - metabolism | Phosphatidylinositol 3-Kinases - antagonists & inhibitors | Neovascularization, Pathologic - pathology | Neovascularization, Pathologic - enzymology | Transfection | Veins - enzymology | Receptor, TIE-2 - metabolism | Receptor, TIE-2 - antagonists & inhibitors | Human Umbilical Vein Endothelial Cells - drug effects | Genetic Association Studies | Signal Transduction | Gene Frequency | Gene Expression Regulation | Vascular Malformations - pathology | Receptor, TIE-2 - genetics | Phosphatidylinositol 3-Kinases - genetics | Class I Phosphatidylinositol 3-Kinases | Human Umbilical Vein Endothelial Cells - enzymology | Alleles | Human Umbilical Vein Endothelial Cells - pathology | Neovascularization, Pathologic - genetics | High-Throughput Nucleotide Sequencing | Protein Kinase Inhibitors - pharmacology | Thiazoles - pharmacology | Mutation | Vascular Malformations - genetics | Veins - pathology | Arteriovenous malformations | Causes of | Genetic aspects | Gene mutations | Health aspects | Phosphotransferases | Report
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87. Full Text Molecular alterations and everolimus efficacy in human epidermal growth factor receptor 2-overexpressing metastatic breast cancers: Combined exploratory biomarker analysis from BOLERO-1 and BOLERO-3
by André, Fabrice and Hurvitz, Sara and Fasolo, Angelica and Tseng, Ling-Ming and Jerusalem, Guy and Wilks, Sharon and O'Regan, Ruth and Isaacs, Claudine and Toi, Masakazu and Burris, Howard and He, Wei and Robinson, Douglas and Riester, Markus and Taran, Tetiana and Chen, David and Slamon, Dennis
Journal of Clinical Oncology, ISSN 0732-183X, 06/2016, Volume 34, Issue 18, pp. 2115 - 2124
Purpose Two recent phase III trials, BOLERO-1 and BOLERO-3 (Breast Cancer Trials of Oral Everolimus), evaluated the addition of everolimus to trastuzumab and... 
MULTICENTER | ONCOLOGY | PHASE-3 TRIAL | DOUBLE-BLIND | PTEN | OPEN-LABEL | PERTUZUMAB | TRASTUZUMAB RESISTANCE | CHEMOTHERAPY | PLUS | PACLITAXEL | PTEN Phosphohydrolase - genetics | Signal Transduction | Biomarkers, Tumor - analysis | Humans | Middle Aged | Antineoplastic Agents - therapeutic use | Breast Neoplasms - drug therapy | Phosphatidylinositol 3-Kinases - genetics | Breast Neoplasms - chemistry | Class I Phosphatidylinositol 3-Kinases | Aged, 80 and over | Phosphatidylinositol 3-Kinases - physiology | Adult | Everolimus - therapeutic use | Female | Aged | Mutation | Receptor, ErbB-2 - analysis
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88. Full Text AXL Mediates Resistance to PI3Kα Inhibition by Activating the EGFR/PKC/mTOR Axis in Head and Neck and Esophageal Squamous Cell Carcinomas
by Elkabets, Moshe and Pazarentzos, Evangelos and Juric, Dejan and Sheng, Qing and Pelossof, Raphael A and Brook, Samuel and Benzaken, Ana Oaknin and Rodon, Jordi and Morse, Natasha and Yan, Jenny Jiacheng and Liu, Manway and Das, Rita and Chen, Yan and Tam, Angela and Wang, Huiqin and Liang, Jinsheng and Gurski, Joseph M and Kerr, Darcy A and Rosell, Rafael and Teixidó, Cristina and Huang, Alan and Ghossein, Ronald A and Rosen, Neal and Bivona, Trever G and Scaltriti, Maurizio and Baselga, José
Cancer Cell, ISSN 1535-6108, 04/2015, Volume 27, Issue 4, pp. 533 - 546
Phosphoinositide-3-kinase (PI3K)-α inhibitors have shown clinical activity in squamous cell carcinomas (SCCs) of head and neck (H&N) bearing mutations or... 
PHOSPHOLIPASE C-GAMMA-1 | RECEPTOR TYROSINE KINASES | PLUS CETUXIMAB | PIK3CA | ONCOLOGY | PATHWAY | GROWTH | PLATINUM-BASED CHEMOTHERAPY | TUMOR-CELLS | PROTEINS | EGFR | CELL BIOLOGY | TOR Serine-Threonine Kinases - metabolism | Carcinoma, Squamous Cell - metabolism | Humans | Receptor Protein-Tyrosine Kinases - physiology | Drug Resistance, Neoplasm | Phosphatidylinositol 3-Kinases - metabolism | Phosphatidylinositol 3-Kinases - antagonists & inhibitors | Head and Neck Neoplasms - metabolism | Protein Kinase C - metabolism | Antibodies, Monoclonal, Humanized - pharmacology | Esophageal Neoplasms - metabolism | Cetuximab | Esophageal Squamous Cell Carcinoma | Proto-Oncogene Proteins - metabolism | Signal Transduction | Proto-Oncogene Proteins - genetics | Receptor Protein-Tyrosine Kinases - metabolism | Phosphatidylinositol 3-Kinases - genetics | Xenograft Model Antitumor Assays | Animals | Class I Phosphatidylinositol 3-Kinases | Receptor Protein-Tyrosine Kinases - genetics | Proto-Oncogene Proteins - physiology | Cell Line, Tumor | Mice | Protein Kinase Inhibitors - pharmacology | Thiazoles - pharmacology
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89. Full Text BRAF mutation predicts for poor outcomes after metastasectomy in patients with metastatic colorectal cancer
by Yaeger, Rona and Cercek, Andrea and Chou, Joanne F and Sylvester, Brooke E and Kemeny, Nancy E and Hechtman, Jaclyn F and Ladanyi, Marc and Rosen, Neal and Weiser, Martin R and Capanu, Marinela and Solit, David B and D'Angelica, Michael I and Vakiani, Efsevia and Saltz, Leonard B
Cancer, ISSN 0008-543X, 08/2014, Volume 120, Issue 15, pp. 2316 - 2324
BACKGROUND BRAF mutations occur in 5% to 11% of patients with metastatic colorectal cancer (mCRC) and have been associated with poor prognosis. The current... 
liver resection | colorectal cancer | 5‐bisphosphate 3‐kinase | BRAF | catalytic subunit alpha | prognosis | PIK3CA (phosphatidylinositol‐4 | 5-bisphosphate 3-kinase | PIK3CA (phosphatidylinositol-4 | SURVIVAL | POPULATION | MICROSATELLITE INSTABILITY | STAGE | PIK3CA MUTATION | ISLAND METHYLATOR PHENOTYPE | COLON-CANCER | ONCOLOGY | RAS MUTATIONS | PIK3CA (phosphatidylinositol-4, 5-bisphosphate 3-kinase, catalytic subunit alpha) | KRAS | PROGNOSTIC ROLE | Colorectal Neoplasms - surgery | Colorectal Neoplasms - enzymology | Prognosis | Colorectal Neoplasms - genetics | Humans | Middle Aged | Male | Treatment Outcome | Phosphatidylinositol 3-Kinases - metabolism | Phosphatidylinositol 3-Kinases - genetics | Metastasectomy | Class I Phosphatidylinositol 3-Kinases | Proto-Oncogene Proteins B-raf - genetics | Survival Analysis | Aged, 80 and over | Adult | Female | Aged | Mutation | Colorectal Neoplasms - pathology | Proto-Oncogene Proteins B-raf - metabolism | Care and treatment | Gene mutations | Patient outcomes | Colorectal cancer | Development and progression | Genetic aspects | Research
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90. Full Text PIK3C2B inhibition improves function and prolongs survival in myotubular myopathy animal models
by Sabha, Nesrin and Volpatti, Jonathan R and Gonorazky, Hernan and Reifler, Aaron and Davidson, Ann E and Li, Xingli and Eltayeb, Nadine M and Dall'Armi, Claudia and Di Paolo, Gilbert and Brooks, Susan V and Buj-Bello, Ana and Feldman, Eva L and Dowling, James J
Journal of Clinical Investigation, ISSN 0021-9738, 09/2016, Volume 126, Issue 9, pp. 3613 - 3625
Myotubular myopathy (MTM) is a devastating pediatric neuromuscular disorder of phosphoinositide (PIP) metabolism resulting from mutations of the PIP... 
Motor Skills - drug effects | Animals, Genetically Modified | Male | Muscle, Skeletal - metabolism | Myopathies, Structural, Congenital - genetics | Zebrafish | Mice, Knockout | Class II Phosphatidylinositol 3-Kinases - physiology | Phosphatidylinositol 3-Kinases - genetics | Androstadienes - chemistry | Phenotype | Animals | Myopathies, Structural, Congenital - therapy | Protein Tyrosine Phosphatases, Non-Receptor - metabolism | Class II Phosphatidylinositol 3-Kinases - genetics | Phosphatidylinositol 3-Kinases - physiology | Female | Mice | Disease Models, Animal | Usage | Care and treatment | Muscle diseases | Genetic aspects | Models | Enzyme inhibitors | Studies | Musculoskeletal system | Genotype & phenotype | Disease | Rodents | Software | Mutation | Metabolism | Experiments
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91. Full Text PIK3CA, BRAF, and PTEN status and benefit from cetuximab in the treatment of advanced colorectal cancer-results from NCIC CTG/AGITG CO.17
by Karapetis, Christos S and Jonker, Derek and Daneshmand, Manijeh and Hanson, Jennifer E and O'Callaghan, Christopher J and Marginean, Celia and Zalcberg, John R and Simes, John and Moore, Malcolm J and Tebbutt, Niall C and Price, Timothy J and Shapiro, Jeremy D and Pavlakis, Nick and Gibbs, Peter and Van Hazel, Guy A and Lee, Ursula and Haq, Rashida and Virk, Shakeel and Tu, Dongsheng and Lorimer, Ian A.J and Australasian Gastro-Intestinal and NCIC Clinical Trials Grp and NCIC Clinical Trials Group and the Australasian Gastro-Intestinal Trials Group and for the NCIC Clinical Trials Group and the Australasian Gastro-Intestinal Trials Group
Clinical Cancer Research, ISSN 1078-0432, 2014, Volume 20, Issue 3, pp. 744 - 753
Purpose: Cetuximab improves survival in patients with K-ras wild-type advanced colorectal cancer. We examined the predictive and prognostic significance of... 
COLON-CANCER | PRIMARY TUMORS | 1ST-LINE TREATMENT | PLUS IRINOTECAN | ONCOLOGY | CLINICAL BENEFIT | RECEPTOR INHIBITOR CETUXIMAB | KRAS WILD-TYPE | TARGETED MONOCLONAL-ANTIBODIES | MUTATIONS | EXPRESSION | Immunohistochemistry | Prognosis | Tissue Array Analysis | Colorectal Neoplasms - genetics | Humans | PTEN Phosphohydrolase - analysis | Antineoplastic Agents - therapeutic use | Proto-Oncogene Proteins B-raf - analysis | DNA Mutational Analysis | Colorectal Neoplasms - drug therapy | Phosphatidylinositol 3-Kinases - analysis | Cetuximab | Phosphatidylinositol 3-Kinases - biosynthesis | Colorectal Neoplasms - mortality | PTEN Phosphohydrolase - genetics | Antibodies, Monoclonal, Humanized - therapeutic use | Biomarkers, Tumor - analysis | Kaplan-Meier Estimate | PTEN Phosphohydrolase - biosynthesis | Treatment Outcome | Phosphatidylinositol 3-Kinases - genetics | Disease-Free Survival | Class I Phosphatidylinositol 3-Kinases | Proto-Oncogene Proteins B-raf - biosynthesis | Proto-Oncogene Proteins B-raf - genetics
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92. Full Text Rare Cancer-Specific Mutations in PIK3CA Show Gain of Function
by Marco Gymnopoulos and Marc-André Elsliger and Peter K. Vogt
Proceedings of the National Academy of Sciences of the United States of America, ISSN 0027-8424, 3/2007, Volume 104, Issue 13, pp. 5569 - 5574
Fifteen rare cancer-derived mutants of PIK3CA, the gene coding for the catalytic subunit p110α of phosphatidylinositol 3-kinase (PI3K), were examined for their... 
Proteins | Cell growth | Phosphorylation | Phenotypes | Maps | Lipids | Cell membranes | Mathematical functions | Genetic mutation | Phosphatidylinositols | Phosphatidylinositol 3-kinase | Protein-protein interaction | Lipid membrane | Molecular model | Activation loop | molecular model | P110-ALPHA | MULTIDISCIPLINARY SCIENCES | lipid membrane | PHOSPHOINOSITIDE 3-KINASE | activation loop | BREAST-CANCER | PHOSPHATIDYLINOSITOL 3-KINASES | GENE | HIGH-FREQUENCY | TARGETS | OVARIAN | protein-protein interaction | phosphatidylinositol 3-kinase | MAMMARY EPITHELIAL-CELLS | SUBUNIT | Protein Structure, Tertiary | Catalytic Domain | Protein Structure, Secondary | Signal Transduction | Humans | Models, Molecular | Phosphatidylinositol 3-Kinases - metabolism | Chick Embryo | Phosphatidylinositol 3-Kinases - genetics | Lipids - chemistry | Animals | Class I Phosphatidylinositol 3-Kinases | Neoplasms - genetics | Enzyme Activation | Mutation | Proto-Oncogene Proteins c-akt - metabolism | Phosphatidylinositol | Lipid membranes | Genetic aspects | Research | Protein-protein interactions | Cancer | protein–protein interaction | Biological Sciences
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93. Full Text Reactivation of multipotency by oncogenic PIK3CA induces breast tumour heterogeneity
by Van Keymeulen, Alexandra and Lee, May Yin and Ousset, Marielle and Brohée, Sylvain and Rorive, Sandrine and Giraddi, Rajshekhar R and Wuidart, Aline and Bouvencourt, Gaëlle and Dubois, Christine and Salmon, Isabelle and Sotiriou, Christos and Phillips, Wayne A and Blanpain, Cédric
Nature, ISSN 0028-0836, 09/2015, Volume 525, Issue 7567, pp. 119 - 123
Breast cancer is the most frequent cancer in women and consists of heterogeneous types of tumours that are classified into different histological and molecular... 
STEM-CELLS | ACTIVATION | ETV6-NTRK3 | MAMMARY-GLAND DEVELOPMENT | PACKAGE | MULTIDISCIPLINARY SCIENCES | MOUSE MODEL | MUTATIONS | IDENTIFICATION | FATE | CANCER | Receptors, Estrogen - metabolism | Humans | Phosphatidylinositol 3-Kinases - metabolism | Genes, p53 - genetics | Mutation - genetics | Breast Neoplasms - metabolism | Receptors, Progesterone - metabolism | Phosphatidylinositol 3-Kinases - genetics | Cell Differentiation - genetics | Cell Lineage | Mammary Neoplasms, Animal - pathology | Phenotype | Animals | Breast Neoplasms - genetics | Class I Phosphatidylinositol 3-Kinases | Breast Neoplasms - pathology | Cell Transformation, Neoplastic | Cell Division | Mammary Neoplasms, Animal - metabolism | Female | Mice | Neoplasm Invasiveness - genetics | Mammary Neoplasms, Animal - genetics | Breast tumors | Genetic aspects | Gene mutations | Health aspects | Oncogenes | Rodents | Medical prognosis | Mortality | Principal components analysis | Breast cancer | Mutation | Gene expression | Tumors | Life Sciences | Cellular Biology | Cancer
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