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British Journal of Cancer, ISSN 0007-0920, 02/2018, Volume 118, Issue 3, pp. 428 - 434
Background: Periodontal pathogens have been linked to oral and gastrointestinal (orodigestive) carcinogenesis. However, the exact mechanisms remain unknown.... 
chymotrypsin-like proteinase | Treponema denticola | periodontopathogen | COLLAGENASE-2 MMP-8 | PORPHYROMONAS-GINGIVALIS | PANCREATIC-CANCER | TISSUE INHIBITORS | PERIODONTAL-DISEASE | METALLOPROTEINASES | ONCOLOGY | gastrointestinal cancer | ALPHA-1-ANTITRYPSIN | EXPRESSION | oral cancer | HUMAN NEUTROPHIL | PROGRESSION | Digestive System Neoplasms - metabolism | Pancreatic Neoplasms - chemistry | Adenocarcinoma - pathology | Pancreatic Neoplasms - metabolism | Carcinoma, Squamous Cell - metabolism | Carcinoma, Squamous Cell - pathology | Humans | Treponema denticola - enzymology | Mouth Neoplasms - metabolism | Stomach Neoplasms - pathology | Tonsillar Neoplasms - chemistry | Complement C1q - metabolism | Colonic Neoplasms - metabolism | Head and Neck Neoplasms - metabolism | Esophageal Neoplasms - pathology | Tonsillar Neoplasms - metabolism | Tissue Inhibitor of Metalloproteinase-1 - metabolism | Tissue Inhibitor of Metalloproteinase-2 - metabolism | Head and Neck Neoplasms - chemistry | Matrix Metalloproteinase 9 - metabolism | Adenocarcinoma - metabolism | Matrix Metalloproteinase 8 - metabolism | Esophageal Neoplasms - metabolism | Digestive System Neoplasms - pathology | Colonic Neoplasms - chemistry | Stomach Neoplasms - chemistry | Adenocarcinoma - chemistry | Esophageal Neoplasms - chemistry | Tonsillar Neoplasms - pathology | Pancreatic Neoplasms - pathology | Carcinoma, Squamous Cell - chemistry | Mouth Neoplasms - chemistry | Head and Neck Neoplasms - pathology | Cell Transformation, Neoplastic - immunology | Digestive System Neoplasms - chemistry | alpha 1-Antichymotrypsin - metabolism | Colonic Neoplasms - pathology | Chymases - analysis | Mouth Neoplasms - pathology | Immunohistochemistry | Proteinase | Virulence | Tissue inhibitor of metalloproteinase 2 | Tissues | Tissue inhibitor of metalloproteinase 1 | Carcinogenesis | Proteins | Carcinogens | Pancreatic carcinoma | Bacteria | Colon | Pancreas | Gastric cancer | Squamous cell carcinoma | Tonsil | Immunomodulation | Teeth | Proteinase inhibitors | Esophagus | Complement component C1q | Chymotrypsin | Periodontitis | Neutrophil collagenase | Tumors | Index Medicus | Molecular Diagnostics
Journal Article
Gut, ISSN 0017-5749, 06/2012, Volume 61, Issue 6, pp. 847 - 854
ObjectiveColorectal cancer is typically classified into proximal colon, distal colon and rectal cancer. Tumour genetic and epigenetic features differ by tumour... 
ISLAND METHYLATOR PHENOTYPE | COLON-CANCER | POPULATION-BASED SAMPLE | DNA METHYLATION | LINE-1 HYPOMETHYLATION | BRAF MUTATION | MICROSATELLITE INSTABILITY | BODY-MASS INDEX | GASTROENTEROLOGY & HEPATOLOGY | EXPRESSION | P-GLYCOPROTEIN | ras Proteins - genetics | Colonic Neoplasms - genetics | Microsatellite Instability | Proto-Oncogene Proteins p21(ras) | Cecal Neoplasms - pathology | Colorectal Neoplasms - genetics | Humans | Long Interspersed Nucleotide Elements - genetics | Male | Colonic Neoplasms - metabolism | Sigmoid Neoplasms - genetics | Rectal Neoplasms - genetics | Female | Rectal Neoplasms - pathology | Colorectal Neoplasms - metabolism | Cecal Neoplasms - genetics | Mutation Rate | Proto-Oncogene Proteins - genetics | DNA Methylation - genetics | Mutation - genetics | Phosphatidylinositol 3-Kinases - genetics | Class I Phosphatidylinositol 3-Kinases | Proto-Oncogene Proteins B-raf - genetics | Colonic Neoplasms - pathology | CpG Islands - genetics | Aged | Rectal Neoplasms - metabolism | DNA, Neoplasm - genetics | Colorectal Neoplasms - pathology | Sigmoid Neoplasms - pathology | Development and progression | Genetic aspects | Colon (Anatomy) | Research | Gene mutations | Colorectal cancer | Medical personnel | Studies | Hypotheses | Hospitals | Biopsy | Rodents | Epigenetics | Mutation | Data bases | Tumors | Index Medicus | Abridged Index Medicus
Journal Article
Journal Article
Molecular Cell, ISSN 1097-2765, 08/2010, Volume 39, Issue 4, pp. 493 - 506
A transient inflammatory signal can initiate an epigenetic switch from nontransformed to cancer cells via a positive feedback loop involving NF-κB, Lin28,... 
RNA | HUMDISEASE | SIGNALING | Signaling | Humdisease | BREAST-CANCER | MICRORNA MIR-21 | TARGET | TRANSFORMATION | BIOCHEMISTRY & MOLECULAR BIOLOGY | EMBRYONIC STEM-CELLS | LET-7 | IDENTIFICATION | NF-KAPPA-B | EXPRESSION | BINDING | CELL BIOLOGY | Colonic Neoplasms - genetics | Cell Proliferation | Epigenesis, Genetic | Humans | Transcriptional Activation | MicroRNAs - metabolism | NF-kappa B - metabolism | Colonic Neoplasms - metabolism | Inflammation - metabolism | Adenocarcinoma - metabolism | RNA Interference | Cell Transformation, Neoplastic - genetics | Proto-Oncogene Proteins c-akt - metabolism | Binding Sites | Colonic Neoplasms - therapy | Tumor Suppressor Proteins - metabolism | Signal Transduction | HCT116 Cells | Computational Biology | Mammary Glands, Human - pathology | Tumor Burden | Breast Neoplasms - genetics | Adenocarcinoma - therapy | Mice, Nude | Mice | Proto-Oncogene Proteins c-myc - genetics | Kinetics | Cell Movement | Deubiquitinating Enzyme CYLD | Gene Expression Regulation, Neoplastic | Mammary Glands, Human - metabolism | Breast Neoplasms - metabolism | Transfection | Tumor Suppressor Proteins - genetics | Inflammation Mediators - metabolism | Female | Adenocarcinoma - genetics | STAT3 Transcription Factor - metabolism | Promoter Regions, Genetic | Receptors, Estrogen - genetics | Neoplasm Invasiveness | PTEN Phosphohydrolase - metabolism | Cell Transformation, Neoplastic - metabolism | Proto-Oncogene Proteins c-myc - metabolism | HT29 Cells | Xenograft Model Antitumor Assays | Algorithms | Animals | Breast Neoplasms - pathology | Inflammation - genetics | Cell Transformation, Neoplastic - pathology | Genes, src | Medical colleges | Inflammation | Colon cancer | Cancer | Adenocarcinoma | Index Medicus | microRNAs | cancer | transformation | transcription factors | inflammation | STAT3
Journal Article
Cancer Research, ISSN 0008-5472, 10/2010, Volume 70, Issue 19, pp. 7710 - 7722
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Journal Article
Journal Article
by Zhang, Bing and Zhang, Bing and Wang, Jing and Wang, Jing and Wang, Xiaojing and Wang, Xiaojing and Zhu, Jing and Zhu, Jing and Liu, Q and Liu, Qi and Shi, Zhiao and Shi, Zhiao and Chambers, Matthew C and Chambers, Matthew C and Zimmerman, Lisa J and Zimmerman, Lisa J and Shaddox, Kent F and Shaddox, Kent F and Kim, Sangtae and Kim, Sangtae and Davies, Sherri R and Davies, Sherri R and Wang, Sean and Wang, Sean and Wang, Pei and Wang, Pei and Kinsinger, Christopher R and Kinsinger, Christopher R and Rivers, Robert C and Rivers, Robert C and Rodriguez, Henry and Rodriguez, Henry and Townsend, R. Reid and Townsend, R Reid and Ellis, Matthew J. C and Ellis, Matthew J C and Carr, Steven A and Carr, Steven A and Tabb, David L and Tabb, David L and Coffey, Robert J and Coffey, Robert J and Slebos, Robbert J C and Slebos, Robbert J. C and Liebler, Daniel C and Liebler, Daniel C and NCI CPTAC, CPTAC and Gillette, Michael A and Klauser, Karl R and Kuhn, Eric and Mani, D.R and Mertins, Philipp and Ketchum, Karen A and Paulovich, Amanda G and Whiteaker, Jeffrey R and Edwards, Nathan J and McGarvey, Peter B and Madhavan, Subha and Chan, Daniel and Pandey, Akhilesh and Shih, Ie-Ming and Zhang, Hui and Zhang, Zhen and Zhu, Heng and Whiteley, Gordon A and Skates, Steven J and White, Forest M and Levine, Douglas A and Boja, Emily S and Hiltke, Tara and Mesri, Mehdi and Shaw, Kenna M and Stein, Stephen E and Fenyo, David and Liu, Tao and McDermott, Jason E and Payne, Samuel H and Rodland, Karin D and Smith, Richard D and Rudnick, Paul and Snyder, Michael and Zhao, Yingming and Chen, Xian and Ransohoff, David F and Hoofnagle, Andrew N and Sanders, Melinda E and Wang, Yue and Ding, Li and NCI CPTAC and the NCI CPTAC
Nature, ISSN 0028-0836, 2014, Volume 513, Issue 7518, pp. 382 - 387
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