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1. Full Text Epirubicin, oxaliplatin, and capecitabine with or without panitumumab for patients with previously untreated advanced oesophagogastric cancer (REAL3): a randomised, open-label phase 3 trial
by Waddell, Tom, MBBCh and Chau, Ian, MD and Cunningham, David, Prof and Gonzalez, David, PhD and Okines, Alicia Frances Clare, MBBCh and Wotherspoon, Andrew, MBBCh and Saffery, Claire and Middleton, Gary, MD and Wadsley, Jonathan, MBBCh and Ferry, David, Prof and Mansoor, Wasat, PhD and Crosby, Tom, MBBS and Coxon, Fareeda, MBBS and Smith, David, MD and Waters, Justin, PhD and Iveson, Timothy, MD and Falk, Stephen, MD and Slater, Sarah, MD and Peckitt, Clare, MSc and Barbachano, Yolanda, PhD
Lancet Oncology, The, ISSN 1470-2045, 2013, Volume 14, Issue 6, pp. 481 - 489
Summary Background EGFR overexpression occurs in 27–55% of oesophagogastric adenocarcinomas, and correlates with poor prognosis. We aimed to assess addition of... 
Hematology, Oncology and Palliative Medicine | GROWTH-FACTOR RECEPTOR | 1ST-LINE TREATMENT | CETUXIMAB | PROSPECTIVE MULTICENTER | ONCOLOGY | GASTRIC-CANCER | PROGNOSTIC-SIGNIFICANCE | CELL-LINES | METASTATIC COLORECTAL-CANCER | ESOPHAGEAL ADENOCARCINOMA | III TRIAL | Multivariate Analysis | Adenocarcinoma - pathology | Capecitabine | Humans | Middle Aged | Antineoplastic Combined Chemotherapy Protocols - adverse effects | Male | Stomach Neoplasms - pathology | Epirubicin - administration & dosage | Molecular Targeted Therapy | Esophageal Neoplasms - pathology | Early Termination of Clinical Trials | Organoplatinum Compounds - administration & dosage | Receptor, Epidermal Growth Factor - metabolism | Fluorouracil - administration & dosage | Time Factors | Biomarkers, Tumor - metabolism | Esophageal Neoplasms - mortality | Female | Biomarkers, Tumor - antagonists & inhibitors | Odds Ratio | Stomach Neoplasms - enzymology | Fluorouracil - analogs & derivatives | Deoxycytidine - administration & dosage | Adenocarcinoma - enzymology | Kaplan-Meier Estimate | Proportional Hazards Models | Logistic Models | Treatment Outcome | United Kingdom | Stomach Neoplasms - drug therapy | Chi-Square Distribution | Adenocarcinoma - drug therapy | Disease-Free Survival | Protein Kinase Inhibitors - administration & dosage | Esophageal Neoplasms - enzymology | Antibodies, Monoclonal - administration & dosage | Antineoplastic Combined Chemotherapy Protocols - therapeutic use | Intention to Treat Analysis | Receptor, Epidermal Growth Factor - antagonists & inhibitors | Aged | Esophageal Neoplasms - drug therapy | Stomach Neoplasms - mortality | Deoxycytidine - analogs & derivatives | Adenocarcinoma - mortality | Care and treatment | Anthracyclines | Product development | Cancer | Index Medicus
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2. Full Text Repression of the Long Noncoding RNA-LET by Histone Deacetylase 3 Contributes to Hypoxia-Mediated Metastasis
by Yang, Fu and Huo, Xi-song and Yuan, Sheng-xian and Zhang, Ling and Zhou, Wei-ping and Wang, Fang and Sun, Shu-han
Molecular Cell, ISSN 1097-2765, 03/2013, Volume 49, Issue 6, pp. 1083 - 1096
Recently, long noncoding RNAs (lncRNAs) were found to be dysregulated in a variety of tumors. However, it remains unknown how and through what molecular... 
CELLS | CHROMATIN | GENE | ANGIOGENESIS | HIF | BIOCHEMISTRY & MOLECULAR BIOLOGY | CANCER | EXPRESSION | CARCINOMA | CELL BIOLOGY | Neoplasm Transplantation | Humans | Middle Aged | Gene Expression Regulation, Neoplastic | Molecular Sequence Data | Male | Carcinoma, Hepatocellular - secondary | Cell Hypoxia | Lung Neoplasms - secondary | Base Sequence | Carcinoma, Hepatocellular - genetics | Female | Liver Neoplasms - pathology | Acetylation | Liver Neoplasms - enzymology | Lung Neoplasms - genetics | Gene Expression | Lung Neoplasms - enzymology | Liver Neoplasms - genetics | Down-Regulation | RNA, Long Noncoding - genetics | Carcinoma, Hepatocellular - enzymology | Nuclear Factor 90 Proteins - metabolism | Animals | Mice, Nude | Cell Line, Tumor | Mice | Protein Processing, Post-Translational | Histone Deacetylases - physiology | Histones - metabolism | Nuclear Factor 90 Proteins - genetics | RNA, Long Noncoding - metabolism | Cell Movement | Medical colleges | Lung cancer | Colorectal cancer | Medical genetics | Development and progression | Antisense RNA | Metastasis | Health aspects | Index Medicus
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3. Full Text Human tumor antigens Tn and sialyl Tn arise from mutations in Cosmc
by Ju, Tongzhong and Lanneau, Grainger S and Gautam, Tripti and Wang, Yingchun and Xia, Baoyun and Stowell, Sean R and Willard, Margaret T and Wang, Wenyi and Xia, Jonathan Y and Zuna, Rosemary E and Laszik, Zoltan and Benbrook, Doris M and Hanigan, Marie H and Cummings, Richard D
Cancer Research, ISSN 0008-5472, 03/2008, Volume 68, Issue 6, pp. 1636 - 1646
Neoplastic lesions typically express specific carbohydrate antigens on glycolipids, mucins, and other glycoproteins. Such antigens are often under epigenetic... 
Galactosyltransferases - deficiency | Colorectal Neoplasms - enzymology | Uterine Cervical Neoplasms - enzymology | Jurkat Cells | Colorectal Neoplasms - genetics | Humans | Molecular Chaperones - genetics | Melanoma - enzymology | Neoplasms - enzymology | Uterine Cervical Neoplasms - immunology | Galactosyltransferases - metabolism | Uterine Cervical Neoplasms - genetics | Colorectal Neoplasms - immunology | Transfection | Antigens, Tumor-Associated, Carbohydrate - genetics | Neoplasms - genetics | Melanoma - genetics | Melanoma - immunology | Neoplasms - immunology | Cell Line, Tumor | Female | Molecular Chaperones - immunology | Antigens, Tumor-Associated, Carbohydrate - biosynthesis | Index Medicus
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4. Full Text IL-4 induces cathepsin protease activity in tumor-associated macrophages to promote cancer growth and invasion
by Gocheva, Vasilena and Wang, Hao-Wei and Gadea, Bedrick B and Shree, Tanaya and Hunter, Karen E and Garfall, Alfred L and Berman, Tara and Joyce, Johanna A
Genes and Development, ISSN 0890-9369, 02/2010, Volume 24, Issue 3, pp. 241 - 255
Innate immune cells can constitute a substantial proportion of the cells within the tumor microenvironment and have been associated with tumor malignancy in... 
Interleukin-4 | Cysteine cathepsin | Tumor-associated macrophage | Tumor microenvironment | Protease | Invasion | interleukin-4 | PARACRINE LOOP | RECOMBINANT HUMAN INTERLEUKIN-4 | CELL LINES | DEVELOPMENTAL BIOLOGY | CYSTEINE CATHEPSINS | MULTISTAGE TUMORIGENESIS | CELL BIOLOGY | protease | PHASE-II TRIAL | MAMMARY-TUMORS | invasion | SOUTHWEST-ONCOLOGY-GROUP | COLORECTAL-CANCER | cysteine cathepsin | MOUSE MODEL | GENETICS & HEREDITY | tumor microenvironment | Neoplasm Invasiveness | Interleukin-4 - metabolism | Pancreatic Neoplasms - pathology | Neoplasms - enzymology | Lung Neoplasms - pathology | Mice, Transgenic | Macrophages - enzymology | Neovascularization, Pathologic - pathology | Neovascularization, Pathologic - enzymology | Macrophages - metabolism | Animals | Cathepsins - metabolism | Mammary Neoplasms, Experimental | Biomarkers, Tumor - metabolism | Cell Line, Tumor | Female | Mice | Neoplasms - pathology | Pancreatic cancer | Physiological aspects | Cathepsins | Genetic aspects | Research | Health aspects | Index Medicus | Research Paper
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5. Full Text TMPRSS4 promotes invasion, migration and metastasis of human tumor cells by facilitating an epithelial-mesenchymal transition
by Jung, H and Lee, K.P and Park, S.J and Park, J.H and Jang, Y.-S and Choi, S.-Y and Jung, J.-G and Jo, K and Park, D.Y and Yoon, J.H and Park, J.-H and Lim, D.-S and Hong, G.-R and Choi, C and Park, Y.-K and Lee, J.W and Hong, H.J and Kim, S and Park, Y.W
Oncogene, ISSN 0950-9232, 04/2008, Volume 27, Issue 18, pp. 2635 - 2647
TMPRSS4 is a novel type II transmembrane serine protease found at the cell surface that is highly expressed in pancreatic, colon and gastric cancer tissues.... 
Serine protease | Metastasis | E-cadherin | EMT | Invasion | TMPRSS4 | PROSTATE | MATRIPTASE | SURFACE PROTEOLYTIC-ENZYMES | PROTEIN | BIOCHEMISTRY & MOLECULAR BIOLOGY | serine protease | CELL BIOLOGY | BREAST-CANCER CELLS | MATRIX METALLOPROTEINASES | invasion | PLASMINOGEN-ACTIVATOR | ONCOLOGY | metastasis | GENETICS & HEREDITY | TRANSMEMBRANE SERINE PROTEASES | EXPRESSION | RNA, Small Interfering - genetics | Cadherins - metabolism | Humans | Neoplasm Proteins - antagonists & inhibitors | Cell Movement - genetics | Neoplasm Metastasis | Serine Endopeptidases - genetics | Liver Neoplasms - pathology | Cadherins - genetics | Liver Neoplasms - enzymology | Liver Neoplasms - secondary | Neoplasm Proteins - genetics | Gene Expression Regulation, Neoplastic - genetics | Lung Neoplasms - enzymology | Liver Neoplasms - genetics | Serine Endopeptidases - biosynthesis | Membrane Proteins - genetics | Epithelial Cells - pathology | Lung Neoplasms - therapy | Gastrointestinal Neoplasms - enzymology | Gastrointestinal Neoplasms - therapy | Cell Adhesion | Cell Movement - drug effects | Membrane Proteins - biosynthesis | Membrane Proteins - antagonists & inhibitors | Gene Expression Regulation, Enzymologic - genetics | Mice, Nude | Cell Communication - drug effects | Epithelial Cells - enzymology | Cell Line, Tumor | Biomarkers, Tumor - genetics | Cadherins - antagonists & inhibitors | Mice | RNA-Binding Proteins - metabolism | Gene Expression Regulation, Enzymologic - drug effects | Neoplasm Transplantation | RNA-Binding Proteins - genetics | Gastrointestinal Neoplasms - genetics | Lung Neoplasms - pathology | Liver Neoplasms - therapy | Gastrointestinal Neoplasms - pathology | Gene Expression Regulation, Neoplastic - drug effects | Lung Neoplasms - genetics | Neoplasm Invasiveness | Neoplasm Proteins - biosynthesis | Cell Communication - genetics | Nerve Tissue Proteins - genetics | Nerve Tissue Proteins - metabolism | Animals | Biomarkers, Tumor - biosynthesis | Care and treatment | Control | Proteases | Cancer cells | Physiological aspects | Genetic aspects | Research | Risk factors | Oncology | Genetics | Cellular biology | Pancreatic cancer | Colorectal cancer | Index Medicus
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6. Full Text BRAF and RAS mutations as prognostic factors in metastatic colorectal cancer patients undergoing liver resection
by Schirripa, M and Bergamo, F and Cremolini, C and Casagrande, M and Lonardi, S and Aprile, G and Yang, Dongyun and Marmorino, F and Pasquini, G and Sensi, E and Lupi, C and De Maglio, G and Borrelli, N and Pizzolitto, S and Fasola, G and Bertorelle, R and Rugge, M and Fontanini, G and Zagonel, V and Loupakis, F and Falcone, A
British Journal of Cancer, ISSN 0007-0920, 06/2015, Volume 112, Issue 12, pp. 1921 - 1928
Background: Despite major advances in the management of metastatic colorectal cancer (mCRC) with liver-only involvement, relapse rates are high and reliable... 
prognostic | metastatic colorectal cancer | BRAF | liver | RAS | SURVIVAL | SURGERY | HEPATECTOMY | MICROSATELLITE INSTABILITY | KRAS STATUS | PATTERNS | HEPATIC RESECTION | PANITUMUMAB | CETUXIMAB | ONCOLOGY | RECURRENCE | ras Proteins - genetics | Colorectal Neoplasms - enzymology | Prognosis | Liver Neoplasms - genetics | Colorectal Neoplasms - genetics | Humans | Middle Aged | Liver Neoplasms - surgery | Male | Disease-Free Survival | Proto-Oncogene Proteins B-raf - genetics | Female | Aged | Biomarkers, Tumor - genetics | Mutation | Colorectal Neoplasms - pathology | Genes, ras | Liver Neoplasms - enzymology | Liver Neoplasms - secondary | Index Medicus | Molecular Diagnostics
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7. Full Text COX‐2 is expressed in human pulmonary, colonic, and mammary tumors
by Soslow, Robert A and Dannenberg, Andrew J and Rush, Demaretta and Woerner, B. M and Khan, K. Nasir and Masferrer, J and Koki, Alane T
Cancer, ISSN 0008-543X, 12/2000, Volume 89, Issue 12, pp. 2637 - 2645
BACKGROUND. The cyclooxygenase (COX) enzyme catalyzes the formation of prostaglandins, which can affect cell proliferation and alter the response of the immune... 
colon carcinoma | cancer prevention | lung carcinoma | breast carcinoma | COX‐2 | cyclooxygenase | immunohistochemistry | Immunohistochemistry | Breast carcinoma | Cyclooxygenase | COX-2 | Cancer prevention | Lung carcinoma | Colon carcinoma | CYCLOOXYGENASE-2 GENE-EXPRESSION | HUMAN BREAST-CANCER | CARCINOGENESIS | INHIBITION | EPITHELIAL-CELLS | ONCOLOGY | CHEMOPREVENTIVE ACTIVITY | COLORECTAL-CANCER | ANTIINFLAMMATORY AGENT | PHORBOL ESTER | UP-REGULATION | Prostaglandin-Endoperoxide Synthases - biosynthesis | Colon - enzymology | Lung - pathology | Lung Neoplasms - enzymology | Breast - enzymology | Colon - pathology | Cyclooxygenase 2 | Humans | Cyclooxygenase 1 | Neoplasms - enzymology | Lung Neoplasms - pathology | Lung - enzymology | Membrane Proteins | Breast Neoplasms - enzymology | Breast Neoplasms - pathology | Colonic Neoplasms - pathology | Colonic Neoplasms - enzymology | Isoenzymes - biosynthesis | Neoplasms - pathology | Breast - pathology | Index Medicus | Abridged Index Medicus
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8. Full Text mTORC1 and mTORC2 regulate EMT, motility, and metastasis of colorectal cancer via RhoA and Rac1 signaling pathways
by Gulhati, Pat and Bowen, Kanika A and Liu, Jianyu and Stevens, Payton D and Rychahou, Piotr G and Chen, Min and Lee, Eun Y and Weiss, Heidi L and O'Connor, Kathleen L and Gao, Tianyan and Evers, B. Mark
Cancer Research, ISSN 0008-5472, 05/2011, Volume 71, Issue 9, pp. 3246 - 3256
Activation of phosphoinositide 3-kinase (PI3K)/Akt signaling is associated with growth and progression of colorectal cancer (CRC). We have previously shown... 
EPITHELIAL-MESENCHYMAL TRANSITION | RAPAMYCIN | OVEREXPRESSION | ACTIVATION | CYTOSKELETON | ONCOLOGY | CELL-MIGRATION | REORGANIZATION | COLON | RICTOR | EXPRESSION | Colorectal Neoplasms - enzymology | Signal Transduction | HCT116 Cells | Humans | Multiprotein Complexes | Actins - metabolism | rhoA GTP-Binding Protein - metabolism | Cell Movement - physiology | Mechanistic Target of Rapamycin Complex 1 | Transcription Factors - metabolism | Neoplasm Metastasis | Proteins - metabolism | Epithelial-Mesenchymal Transition | Cell Line, Tumor | Cytoskeleton - metabolism | TOR Serine-Threonine Kinases | Colorectal Neoplasms - pathology | Colorectal Neoplasms - metabolism | rac1 GTP-Binding Protein - metabolism | Index Medicus | mTOR | Rictor | Metastasis | EMT | Colorectal cancer
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9. Full Text Phase II Study of Cediranib, an Oral Pan–Vascular Endothelial Growth Factor Receptor Tyrosine Kinase Inhibitor, in Patients With Recurrent Glioblastoma
by Tracy T. Batchelor and Dan G. Duda and Emmanuelle di Tomaso and Marek Ancukiewicz and Scott R. Plotkin and Elizabeth Gerstner and April F. Eichler and Jan Drappatz and Fred H. Hochberg and Thomas Benner and David N. Louis and Kenneth S. Cohen and Houng Chea and Alexis Exarhopoulos and Jay S. Loeffler and Marsha A. Moses and Percy Ivy and A. Gregory Sorensen and Patrick Y. Wen and Rakesh K. Jain
Journal of Clinical Oncology, ISSN 0732-183X, 06/2010, Volume 28, Issue 17, pp. 2817 - 2823
Purpose Glioblastoma is an incurable solid tumor characterized by increased expression of vascular endothelial growth factor (VEGF). We performed a phase II... 
MALIGNANT GLIOMA | ANTIANGIOGENIC THERAPY | RESPONSE CRITERIA | ANGIOGENESIS | ONCOLOGY | BEVACIZUMAB | COLORECTAL-CANCER | CLINICAL-TRIALS | NORMALIZATION | PROGRESSION | BRAIN-TUMORS | Glioblastoma - enzymology | Humans | Middle Aged | Brain Neoplasms - pathology | Neoplasm Recurrence, Local - drug therapy | Male | Antineoplastic Agents - therapeutic use | Protein Kinase Inhibitors - adverse effects | Neoplasm Recurrence, Local - enzymology | Young Adult | Antineoplastic Agents - adverse effects | Brain Neoplasms - blood | Receptors, Vascular Endothelial Growth Factor - antagonists & inhibitors | Adult | Female | Neoplasm Recurrence, Local - blood | Brain Neoplasms - enzymology | Glioblastoma - blood | Brain Neoplasms - drug therapy | Biomarkers, Tumor - blood | Disease-Free Survival | Protein Kinase Inhibitors - therapeutic use | Quinazolines - therapeutic use | Glioblastoma - pathology | Quinazolines - adverse effects | Aged | Glioblastoma - drug therapy | Index Medicus | Neur6 | Original Reports | Neur8 | Neur1 | To1
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10. Full Text Elevated cleaved caspase-3 is associated with shortened overall survival in several cancer types
by Hu, Qian and Hu, Qian and Peng, Jing and Peng, Jing and Liu, Weiping and He, Xiaoli and Cui, Ling and Cui, Ling and Chen, Xinlian and Chen, Xinlian and Yang, Mei and Yang, Mei and Liu, Hongqian and Liu, Hongqian and Liu, Shanling and Liu, Shanling and Wang, He and Wang, He
International Journal of Clinical and Experimental Pathology, ISSN 1936-2625, 2014, Volume 7, Issue 8, pp. 5057 - 5070
Emerging evidence has indicated that apoptotic cells have a compensatory effect on the proliferation of neighboring cells. Recent studies have shown that... 
Cleaved caspase-3 expression | Prognosis | Overall survival of cancer patients | Multivariate Cox proportional hazards model analysis | CLINICAL-TRIAL | CELL-PROLIFERATION | PATHOLOGY | prognosis | multivariate Cox proportional hazards model analysis | ONCOLOGY | APOPTOTIC CELLS | COMPENSATORY PROLIFERATION | REPOPULATION | INHIBITOR | CARCINOMA | overall survival of cancer patients | Immunohistochemistry | Humans | Middle Aged | Caspase 3 - metabolism | Ovarian Neoplasms - pathology | Male | Stomach Neoplasms - pathology | Uterine Cervical Neoplasms - pathology | Ovarian Neoplasms - mortality | Young Adult | Aged, 80 and over | Adult | Female | Uterine Cervical Neoplasms - mortality | Colorectal Neoplasms - mortality | Stomach Neoplasms - enzymology | Colorectal Neoplasms - enzymology | Uterine Cervical Neoplasms - enzymology | Biomarkers, Tumor - analysis | Risk Factors | Kaplan-Meier Estimate | Proportional Hazards Models | Neoplasms - enzymology | Neoplasms - mortality | Disease Progression | Ovarian Neoplasms - enzymology | Adolescent | Caspase 3 - analysis | Aged | Apoptosis - physiology | Colorectal Neoplasms - pathology | Neoplasms - pathology | Stomach Neoplasms - mortality | Index Medicus
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11. Full Text EphA2 promotes epithelial-mesenchymal transition through the Wnt/β-catenin pathway in gastric cancer cells
by Huang, J and Xiao, D and Li, G and Ma, J and Chen, P and Yuan, W and Hou, F and Ge, J and Zhong, M and Tang, Y and Xia, X and Chen, Z
Oncogene, ISSN 0950-9232, 05/2014, Volume 33, Issue 21, pp. 2737 - 2747
This study aims to investigate the significance of erythropoietin-producing hepatocellular (Eph)A2 expression and the mechanism by which EphA2 is involved in... 
epithelial-mensenchymal transition | gastric cancer | Wnt/β-catenin | EphA2 | ACTIVATION | DEPENDENT TRANSCRIPTION | BIOCHEMISTRY & MOLECULAR BIOLOGY | RECEPTOR | CELL BIOLOGY | ONCOLOGY | COLORECTAL-CANCER | Wnt/beta-catenin | GENETICS & HEREDITY | EXPRESSION | Neoplasm Transplantation | Up-Regulation | Cell Proliferation | Cadherins - metabolism | Humans | Middle Aged | Gene Expression Regulation, Neoplastic | Male | Stomach Neoplasms - pathology | Gastric Mucosa - metabolism | Antigens, CD - metabolism | Lung Neoplasms - secondary | Epithelial-Mesenchymal Transition | Adult | Female | Snail Family Transcription Factors | Wnt Signaling Pathway | Stomach Neoplasms - enzymology | Lung Neoplasms - enzymology | Receptor, EphA2 - physiology | Tumor Burden | beta Catenin - metabolism | Transcription Factors - metabolism | Animals | Mice, Nude | Cell Line, Tumor | Aged | Mice | Mice, Inbred BALB C | Cell Movement | Index Medicus
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12. Full Text Aldehyde dehydrogenase-expressing colon stem cells contribute to tumorigenesis in the transition from colitis to cancer
by Carpentino, Joseph E and Hynes, Mark J and Appelman, Henry D and Tong, Zheng and Steindler, Dennis A and Scott, Edward W and Huang, Emina H
Cancer Research, ISSN 0008-5472, 10/2009, Volume 69, Issue 20, pp. 8208 - 8215
Patients with chronic ulcerative colitis are at increased risk of developing colorectal cancer. Although current hypotheses suggest that sporadic colorectal... 
PHENOTYPIC CHARACTERIZATION | SURVEILLANCE COLONOSCOPY | INFLAMMATORY-BOWEL-DISEASE | EPITHELIAL-CELLS | ONCOLOGY | COLORECTAL-CANCER | ULCERATIVE-COLITIS | CRYPT | DYSPLASIA | STROMA | IDENTIFICATION | Precancerous Conditions - etiology | Colon - enzymology | Adenocarcinoma - pathology | Stromal Cells - pathology | Adenocarcinoma - etiology | Humans | Spheroids, Cellular - pathology | Colitis - pathology | Spheroids, Cellular - enzymology | Immunoenzyme Techniques | Stromal Cells - enzymology | Flow Cytometry | Neoplastic Stem Cells - pathology | Precancerous Conditions - pathology | Aldehyde Dehydrogenase - metabolism | Colonic Neoplasms - etiology | Precancerous Conditions - enzymology | Cytokines - metabolism | Colon - pathology | Adenocarcinoma - enzymology | Mice, SCID | Xenograft Model Antitumor Assays | Animals | Colitis - enzymology | Colonic Neoplasms - pathology | Fluorescent Antibody Technique | Protein Array Analysis | Mice, Inbred NOD | Colonic Neoplasms - enzymology | Mice | Neoplastic Stem Cells - enzymology | Index Medicus | Xenograft | Colitis | tumor microenvironment | Aldehyde dehydrogenase | Colon Cancer | Colon sphere
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13. Full Text Unresponsiveness of colon cancer to BRAF(V600E) inhibition through feedback activation of EGFR
by Prahallad, Anirudh and Sun, Chong and Huang, Sidong and Di Nicolantonio, Federica and Salazar, Ramon and Zecchin, Davide and Beijersbergen, Roderick L and Bardelli, Alberto and Bernards, René
Nature, ISSN 0028-0836, 03/2012, Volume 483, Issue 7387, pp. 100 - 104
Inhibition of the BRAF(V600E) oncoprotein by the small-molecule drug PLX4032 (vemurafenib) is highly effective in the treatment of melanoma(1). However, colon... 
PANITUMUMAB | TARGET | CETUXIMAB | MELANOMA | BRAF MUTATIONS | MULTIDISCIPLINARY SCIENCES | PAPILLARY THYROID-CARCINOMA | KRAS | METASTATIC COLORECTAL-CANCER | Erlotinib Hydrochloride | Receptor, Epidermal Growth Factor - agonists | Apoptosis - drug effects | Colorectal Neoplasms - genetics | Humans | Antineoplastic Agents - therapeutic use | Antibodies, Monoclonal, Humanized | Receptor, Epidermal Growth Factor - metabolism | RNA Interference | Colorectal Neoplasms - drug therapy | HEK293 Cells | Female | Indoles - pharmacology | Antineoplastic Agents - pharmacology | Cetuximab | Proto-Oncogene Proteins B-raf - metabolism | Proto-Oncogene Proteins B-raf - chemistry | Melanoma - metabolism | Colorectal Neoplasms - enzymology | Antibodies, Monoclonal - pharmacology | Enzyme Activation - drug effects | Sulfonamides - pharmacology | Drug Synergism | Proto-Oncogene Proteins B-raf - antagonists & inhibitors | Xenograft Model Antitumor Assays | Animals | Sulfonamides - therapeutic use | Protein Kinase Inhibitors - therapeutic use | Proto-Oncogene Proteins B-raf - genetics | Quinazolines - therapeutic use | Melanoma - drug therapy | Cell Line, Tumor | Receptor, Epidermal Growth Factor - antagonists & inhibitors | Feedback, Physiological - drug effects | Indoles - therapeutic use | Cell Proliferation - drug effects | Mice | Protein Kinase Inhibitors - pharmacology | Colorectal Neoplasms - pathology | Quinazolines - pharmacology | Drug Resistance, Neoplasm - drug effects | Proteins | Library collections | Studies | Phosphorylation | Kinases | Tumors | Index Medicus
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