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1. Full Text Gefitinib plus chemotherapy versus placebo plus chemotherapy in EGFR -mutation-positive non-small-cell lung cancer after progression on first-line gefitinib (IMPRESS): a phase 3 randomised trial
by Soria, Jean-Charles, Prof and Wu, Yi-Long, Prof and Nakagawa, Kazuhiko, Prof and Kim, Sang-We, Prof and Yang, Jin-Ji, MD and Ahn, Myung-Ju, Prof and Wang, Jie, MD and Yang, James Chih-Hsin, Prof and Lu, You, Prof and Atagi, Shinji, MD and Ponce, Santiago, MD and Lee, Dae Ho, Prof and Liu, Yunpeng, Prof and Yoh, Kiyotaka, MD and Zhou, Jian-Ying, Prof and Shi, Xiaojin, MD and Webster, Alan, MSc and Jiang, Haiyi, MD and Mok, Tony S K, Prof
Lancet Oncology, The, ISSN 1470-2045, 2015, Volume 16, Issue 8, pp. 990 - 998
Summary Background Optimum management strategies for patients with advanced non-small-cell lung cancer (NSCLC) with acquired resistance to EGFR tyrosine-kinase... 
Hematology, Oncology and Palliative Medicine | TYROSINE KINASE INHIBITORS | MULTICENTER | ONCOLOGY | ADENOCARCINOMA | ACQUIRED-RESISTANCE | OPEN-LABEL | AFATINIB | ERLOTINIB | GEMCITABINE | Lung Neoplasms - drug therapy | Receptor, Epidermal Growth Factor - genetics | Prospective Studies | Guanine - analogs & derivatives | Lung Neoplasms - mortality | Humans | Middle Aged | Antineoplastic Combined Chemotherapy Protocols - adverse effects | Lung Neoplasms - pathology | Male | Cisplatin - administration & dosage | Receptor, Epidermal Growth Factor - metabolism | Time Factors | Adult | Female | Quinazolines - administration & dosage | Carcinoma, Non-Small-Cell Lung - pathology | Lung Neoplasms - genetics | Genetic Predisposition to Disease | Lung Neoplasms - enzymology | Drug Administration Schedule | Administration, Oral | Carcinoma, Non-Small-Cell Lung - genetics | Europe | Kaplan-Meier Estimate | Proportional Hazards Models | Treatment Outcome | Carcinoma, Non-Small-Cell Lung - mortality | Pemetrexed | Disease Progression | Disease-Free Survival | Protein Kinase Inhibitors - administration & dosage | Phenotype | Antineoplastic Combined Chemotherapy Protocols - therapeutic use | Asia | Glutamates - administration & dosage | Receptor, Epidermal Growth Factor - antagonists & inhibitors | Aged | Biomarkers, Tumor - genetics | Carcinoma, Non-Small-Cell Lung - drug therapy | Carcinoma, Non-Small-Cell Lung - enzymology | Infusions, Intravenous | Mutation | Guanine - administration & dosage | Medical colleges | Chemotherapy | Strategic planning (Business) | Genetic aspects | Product development | Lung cancer, Non-small cell | Gefitinib | Cancer
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2. Full Text Predicting Progression in Barrettʼs Esophagus: Development and Validation of the Barrettʼs Esophagus Assessment of Risk Score (BEAR Score)
by Brown, Craig S and Lapin, Brittany and Goldstein, Jay L and Linn, John G and Talamonti, Mark S and Carbray, Joann and Ujiki, Michael B
Annals of Surgery, ISSN 0003-4932, 04/2018, Volume 267, Issue 4, pp. 716 - 720
OBJECTIVE:To develop and validate a scoring tool capable of accurately predicting which patients with Barrettʼs esophagus (BE) will progress to dysplasia... 
STATEMENT | SURGERY | MANAGEMENT | ADENOCARCINOMA INCIDENCE | risk score | DYSPLASIA | MODEL | PREVALENCE | TRENDS | esophageal adenocarcinoma | Barrett's esophagus | prediction | SURVEILLANCE | COHORT | RADIOFREQUENCY ABLATION | Risk Assessment - methods | Adenocarcinoma - pathology | Humans | Middle Aged | Endoscopy, Gastrointestinal | Male | Disease Progression | Barrett Esophagus - surgery | Esophageal Neoplasms - pathology | Algorithms | Barrett Esophagus - pathology | Radiofrequency Ablation - methods | Female | Aged | Retrospective Studies
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3. Full Text Suppression of tumour-specific CD4+ T cells by regulatory T cells is associated with progression of human colorectal cancer
by Betts, Gareth and Jones, Emma and Junaid, Syed and El-Shanawany, Tariq and Scurr, Martin and Mizen, Paul and Kumar, Mayur and Jones, Sion and Rees, Brian and Williams, Geraint and Gallimore, Awen and Godkin, Andrew
Gut, ISSN 0017-5749, 08/2012, Volume 61, Issue 8, pp. 1163 - 1171
BackgroundThere is indirect evidence that T cell responses can control the metastatic spread of colorectal cancer (CRC). However, an enrichment of CD4+Foxp3+... 
COLON-CANCER | RESPONSES | EPITOPE | CD25(+) | CARCINOEMBRYONIC ANTIGEN | MALIGNANT-TISSUES | 5T4 ANTIGEN | IDENTIFICATION | GASTROENTEROLOGY & HEPATOLOGY | EXPRESSION | LYMPHOCYTES | Immunohistochemistry | Adenocarcinoma - pathology | Prognosis | Follow-Up Studies | Humans | Middle Aged | Male | Antineoplastic Agents - therapeutic use | Colectomy | T-Lymphocytes, Regulatory - immunology | CD4-Positive T-Lymphocytes - immunology | Colorectal Neoplasms - therapy | Lymphocyte Activation - immunology | Flow Cytometry | Time Factors | Aged, 80 and over | Adult | Female | Forkhead Transcription Factors - biosynthesis | Adenocarcinoma - immunology | Neoplasm Recurrence, Local | Disease Progression | Colorectal Neoplasms - immunology | Adenocarcinoma - therapy | Aged | Colorectal Neoplasms - pathology | Neoplasm Staging | Immunity, Cellular | Physiological aspects | Development and progression | Research | T cells | Colorectal cancer | Studies | Antigens | Chemotherapy | Lymphocytes | Laboratories | Surgery | Cloning | Immunotherapy | Medical prognosis | T cell receptors | Patients | Tumors | T lymphocytes | colorectal cancer | colorectal diseases | hepatitis B | hepatitis C | histopathology | cancer immunobiology | Regulatory T cells | hepatitis | imaging | immunoregulation | Colon | 1506 | α β T cells
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4. Full Text Retinoic Acid–Induced Pancreatic Stellate Cell Quiescence Reduces Paracrine Wnt–β-Catenin Signaling to Slow Tumor Progression
by Froeling, Fieke E.M and Feig, Christine and Chelala, Claude and Dobson, Richard and Mein, Charles E and Tuveson, David A and Clevers, Hans and Hart, Ian R and Kocher, Hemant M
Gastroenterology, ISSN 0016-5085, 2011, Volume 141, Issue 4, pp. 1486 - 1497.e14
Background & Aims Patients with pancreatic ductal adenocarcinoma are deficient in vitamin A, resulting in activation of pancreatic stellate cells (PSCs). We... 
Gastroenterology and Hepatology | 9RA | Therapy | Secreted Frizzled-Related Protein 4 | 13RA | Mouse Model | ACTIVATION | CANCER CELLS | TRANSCRIPTOME | ADENOCARCINOMA | STABILIZATION | MODEL | CULTURE | IN-VITRO | GASTROENTEROLOGY & HEPATOLOGY | IMMORTALIZATION | EXPRESSION | Transcription, Genetic - drug effects | Pancreatic Neoplasms - metabolism | Apoptosis - drug effects | Humans | Pancreatic Stellate Cells - drug effects | Carcinoma, Pancreatic Ductal - metabolism | Cellular Senescence - drug effects | Wnt Proteins - metabolism | Carcinoma, Pancreatic Ductal - genetics | Dose-Response Relationship, Drug | Pancreatic Neoplasms - drug therapy | RNA Interference | Time Factors | Mice, Mutant Strains | Antineoplastic Agents - pharmacology | Gene Expression Regulation, Neoplastic - drug effects | Pancreatic Stellate Cells - pathology | Disease Models, Animal | Tretinoin - pharmacology | Proto-Oncogene Proteins - metabolism | Isotretinoin - pharmacology | Pancreatic Neoplasms - pathology | Pancreatic Neoplasms - genetics | Carcinoma, Pancreatic Ductal - pathology | beta Catenin - metabolism | Disease Progression | Carcinoma, Pancreatic Ductal - drug therapy | Cell Movement - drug effects | Animals | Signal Transduction - drug effects | Paracrine Communication - drug effects | Cell Line, Tumor | Cell Proliferation - drug effects | Mice | Pancreatic Stellate Cells - metabolism
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5. Full Text Suppression of lung adenocarcinoma progression by Nkx2-1
by Winslow, Monte M and Dayton, Talya L and Verhaak, Roel G. W and Kim-Kiselak, Caroline and Snyder, Eric L and Feldser, David M and Hubbard, Diana D and Dupage, Michel J and Whittaker, Charles A and Hoersch, Sebastian and Yoon, Stephanie and Crowley, Denise and Bronson, Roderick T and Chiang, Derek Y and Meyerson, Matthew and Jacks, Tyler
Nature, ISSN 0028-0836, 05/2011, Volume 473, Issue 7345, pp. 101 - 104
Despite the high prevalence and poor outcome of patients with metastatic lung cancer the mechanisms of tumour progression and metastasis remain largely... 
BREAST-CANCER | ONCOGENE | METASTASIS | K-RAS | HMGI-C | MULTIDISCIPLINARY SCIENCES | EMBRYONIC STEM-CELLS | PROTEIN EXPRESSION | SELF-RENEWAL | CLINICAL-SIGNIFICANCE | P53 | Lung Neoplasms - genetics | Thyroid Nuclear Factor 1 | Adenocarcinoma of Lung | Down-Regulation | Humans | Gene Expression Regulation, Neoplastic | Nuclear Proteins - metabolism | Lung Neoplasms - physiopathology | Transcription Factors - genetics | Transcription Factors - metabolism | Animals | Adenocarcinoma - physiopathology | HMGA2 Protein - genetics | Cell Line, Tumor | Adenocarcinoma - genetics | Cell Differentiation | Mice | Nuclear Proteins - genetics | Disease Models, Animal | Adenocarcinoma | Development and progression | Care and treatment | Genetic aspects | Research | Cancer | Proteins | Rodents | Lung cancer | Genomes | Metastasis | Gene expression | Apoptosis
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6. Full Text SMAD4-dependent barrier constrains prostate cancer growth and metastatic progression
by Ding, Zhihu and Wu, Chang-Jiun and Chu, Gerald C and Xiao, Yonghong and Ho, Dennis and Zhang, Jingfang and Perry, Samuel R and Labrot, Emma S and Wu, Xiaoqiu and Lis, Rosina and Hoshida, Yujin and Hiller, David and Hu, Baoli and Jiang, Shan and Zheng, Hongwu and Stegh, Alexander H and Scott, Kenneth L and Signoretti, Sabina and Bardeesy, Nabeel and Wang, Y. Alan and Hill, David E and Golub, Todd R and Stampfer, Meir J and Wong, Wing H and Loda, Massimo and Mucci, Lorelei and Chin, Lynda and Depinho, Ronald A
Nature, ISSN 0028-0836, 02/2011, Volume 470, Issue 7333, pp. 269 - 276
Effective clinical management of prostate cancer (PCA) has been challenged by significant intratumoural heterogeneity on the genomic and pathological levels... 
INACTIVATION | APOPTOSIS | SMAD4 | OSTEOPONTIN | TGF-BETA | MULTIDISCIPLINARY SCIENCES | TRANSCRIPTION | PTEN | DIFFERENTIATION | PHYSICIANS HEALTH | EXPRESSION | Osteopontin - genetics | Cyclin D1 - metabolism | Cell Proliferation | Prognosis | Humans | Gene Expression Regulation, Neoplastic | Male | Gene Expression Profiling | Osteopontin - metabolism | Prostatic Neoplasms - diagnosis | Prostate - metabolism | Bone Morphogenetic Proteins - metabolism | Prostatic Neoplasms - genetics | Lung Neoplasms - secondary | Smad4 Protein - genetics | Neoplasm Invasiveness - pathology | Genes, Tumor Suppressor - physiology | Prostate-Specific Antigen - metabolism | Transforming Growth Factor beta | PTEN Phosphohydrolase - genetics | Prostatic Neoplasms - pathology | PTEN Phosphohydrolase - deficiency | Mice, Transgenic | Penetrance | Lymphatic Metastasis | Smad4 Protein - metabolism | Disease Progression | Neoplasm Metastasis - genetics | Animals | Cyclin D1 - genetics | Models, Biological | Neoplasm Metastasis - pathology | Mice | Smad4 Protein - deficiency | Neoplasm Invasiveness - genetics | Adenocarcinoma | Care and treatment | Genetic aspects | Prostate cancer | Proteins | Genotype & phenotype | Cell cycle | Apoptosis | Tumors
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7. Full Text The advanced glycation end‐product Nϵ‐carboxymethyllysine promotes progression of pancreatic cancer: implications for diabetes‐associated risk and its prevention
by Menini, Stefano and Iacobini, Carla and de Latouliere, Luisa and Manni, Isabella and Ionta, Vittoria and Blasetti Fantauzzi, Claudia and Pesce, Carlo and Cappello, Paola and Novelli, Francesco and Piaggio, Giulia and Pugliese, Giuseppe
The Journal of Pathology, ISSN 0022-3417, 06/2018, Volume 245, Issue 2, pp. 197 - 208
Diabetes is an established risk factor for pancreatic cancer (PaC), together with obesity, a Western diet, and tobacco smoking. The common mechanistic link... 
bioluminescence imaging | pancreatic cancer | Kras mutation | RAGE | advanced glycation end‐products | diabetes | advanced glycation end-products | DUCTAL ADENOCARCINOMA | RECEPTOR | PATHOLOGY | N-EPSILON-(CARBOXYMETHYL)LYSINE | ONCOLOGY | INFLAMMATION | SERUM-LEVELS | THERAPEUTIC TARGETS | MICE | PROTEINS | TUMOR-GROWTH | Adenocarcinoma | Bioluminescence | Downstream effects | Tobacco smoking | Homology | Accumulation | Risk factors | Cell adhesion molecules | Cell adhesion & migration | Prevention | Signal transduction | Cell adhesion | Age | Invasiveness | Diabetes mellitus | Health risks | Histology | Glycosylation | Tumor cell lines | Molecular chains | White blood cells | Tobacco | Carboxymethyllysine | Pancreatic cancer | Cell lines | Mice | Diabetes | Risk management | Cancer | Tumors | Smoking
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8. Full Text Inactivation of p16, RUNX3, and HPP1 occurs early in Barrett's-associated neoplastic progression and predicts progression risk
by Schulmann, Karsten and Sterian, Anca and Berki, Agnes and Yin, Jing and Sato, Fumiaki and Xu, Yan and Olaru, Andreea and Wang, Suna and Mori, Yuriko and Deacu, Elena and Hamilton, James and Kan, Takatsugu and Krasna, Mark J and Beer, David G and Pepe, Margaret S and Abraham, John M and Feng, Ziding and Schmiegel, Wolff and Greenwald, Bruce D and Meltzer, Stephen J
Oncogene, ISSN 0950-9232, 06/2005, Volume 24, Issue 25, pp. 4138 - 4148
Patients with Barrett's esophagus ( BE) are at increased risk of developing esophageal adenocarcinoma (EAC). Clinical neoplastic progression risk factors, such... 
Cancer biomarkers | Neoplastic progression | Early cancer detection | Hypermethylation | Esophageal cancer | Barrett's esophagus | PROMOTER HYPERMETHYLATION | ENDOSCOPIC SURVEILLANCE | esophageal cancer | early cancer detection | HIGH-GRADE DYSPLASIA | BIOCHEMISTRY & MOLECULAR BIOLOGY | hypermethylation | CPG ISLAND HYPERMETHYLATION | ULCERATIVE-COLITIS | neoplastic progression | TUMOR-SUPPRESSOR GENE | FOLLOW-UP | cancer biomarkers | ESOPHAGEAL ADENOCARCINOMA | CELL BIOLOGY | ONCOLOGY | GASTRIC-CARCINOMA | GENETICS & HEREDITY | ESOPHAGOGASTRIC JUNCTION | Promoter Regions, Genetic | Membrane Proteins - genetics | Humans | Risk Factors | Cyclin-Dependent Kinase Inhibitor p16 - genetics | DNA, Neoplasm - isolation & purification | RNA, Neoplasm - isolation & purification | Transcription Factors - genetics | DNA-Binding Proteins - genetics | Reverse Transcriptase Polymerase Chain Reaction | Core Binding Factor Alpha 3 Subunit | Disease Progression | DNA Methylation | Esophageal Neoplasms - genetics | Polymerase Chain Reaction | Cell Line, Tumor | RNA, Neoplasm - genetics | Adenocarcinoma - genetics | DNA, Neoplasm - genetics | Neoplasm Proteins - genetics | Barrett Esophagus - genetics
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9. Full Text Wnt β-Catenin activation promotes prostate tumor progression in a mouse model
by Yu, X and Wang, Y and Degraff, D.J and Wills, M.L and Matusik, R.J
Oncogene, ISSN 0950-9232, 04/2011, Volume 30, Issue 16, pp. 1868 - 1879
Our previous studies have found that activation of Wnt/beta-catenin signaling resulted in mouse prostatic intraepithelial neoplasia (mPIN). In the large... 
prostate | T-antigen | Wnt/β-catenin | Foxa2 | TRANSCRIPTION FACTORS | METASTASIS | BIOCHEMISTRY & MOLECULAR BIOLOGY | NEUROENDOCRINE DIFFERENTIATION | BETA-CATENIN | CELL BIOLOGY | ONCOLOGY | WNT PATHWAY | COLORECTAL-CANCER | Wnt/beta-catenin | GROWTH | GENETICS & HEREDITY | SMALL-CELL CARCINOMA | ANDROGEN | TRANSGENIC MICE | Prostatic Neoplasms - metabolism | Prostatic Neoplasms - pathology | Adenocarcinoma - metabolism | Adenocarcinoma - pathology | Animals | Signal Transduction | Receptors, Androgen - metabolism | Male | Mice | Wnt Proteins - metabolism | beta Catenin - metabolism | Disease Progression | β-Catenin | Wnt | Prostate
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10. Full Text Cyclooxygenases, prostanoids, and tumor progression
by Wang, Man-Tzu and Honn, Kenneth V and Nie, Daotai
Cancer and Metastasis Reviews, ISSN 0167-7659, 12/2007, Volume 26, Issue 3, pp. 525 - 534
In response to various growth factors, hormones or cytokines, arachidonic acid can be mobilized from phospholipids pools and converted to bioactive eicosanoids... 
Cyclooxygenase | Biomedicine | Tumor progression | Cancer Research | Oncology | Metastasis | Biomedicine general | Prostanoids | PROSTAGLANDIN-E SYNTHASE | cyclooxygenase | ACTIVATED RECEPTOR-DELTA | THROMBOXANE SYNTHASE | BREAST-CANCER | tumor progression | prostanoids | ONCOLOGY | metastasis | NONSTEROIDAL ANTIINFLAMMATORY DRUGS | COLORECTAL-CANCER | SQUAMOUS-CELL CARCINOMA | GENE-EXPRESSION | GROWTH-FACTOR | HUMAN ENDOMETRIAL ADENOCARCINOMA | Dinoprostone - physiology | Prostaglandins - physiology | Animals | Thromboxane A2 - physiology | Humans | Receptors, Prostaglandin - physiology | Neoplasms - enzymology | Neoplasms - pathology | Disease Progression | Prostaglandin-Endoperoxide Synthases - physiology | Development and progression | Tumors
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11. Full Text Complement activation via a C3a receptor pathway alters CD4+ T lymphocytes and mediates lung cancer progression
by Kwak, Jeff W and Laskowski, Jennifer and Li, Howard Y and McSharry, Maria V and Sippel, Trisha R and Bullock, Bonnie L and Johnson, Amber M and Poczobutt, Joanna M and Neuwelt, Alexander J and Malkoski, Stephen P and Weiser-Evans, Mary C and Lambris, John D and Clambey, Eric T and Thurman, Joshua M and Nemenoff, Raphael A
Cancer Research, ISSN 0008-5472, 01/2018, Volume 78, Issue 1, pp. 143 - 156
The complement cascade is a part of the innate immune system that acts primarily to remove pathogens and injured cells. However, complement activation is also... 
SYSTEM | HOMEOSTASIS | THERAPY | METASTASIS | CELL RESPONSES | MICROENVIRONMENT | ONCOLOGY | TUMOR | ANTITUMOR IMMUNITY | C5A | MODULATION | Adenocarcinoma - pathology | Adenocarcinoma of Lung |