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1. Full Text Dependency of a therapy-resistant state of cancer cells on a lipid peroxidase pathway
by Viswanathan, Vasanthi S and Ryan, Matthew J and Dhruv, Harshil D and Gill, Shubhroz and Eichhoff, Ossia M and Seashore-Ludlow, Brinton and Kaffenberger, Samuel D and Eaton, John K and Shimada, Kenichi and Aguirre, Andrew J and Viswanathan, Srinivas R and Chattopadhyay, Shrikanta and Tamayo, Pablo and Yang, Wan Seok and Rees, Matthew G and Chen, Sixun and Boskovic, Zarko V and Javaid, Sarah and Huang, Cherrie and Wu, Xiaoyun and Tseng, Yuen-Yi and Roider, Elisabeth M and Gao, Dong and Cleary, James M and Wolpin, Brian M and Mesirov, Jill P and Haber, Daniel A and Engelman, Jeffrey A and Boehm, Jesse S and Kotz, Joanne D and Hon, Cindy S and Chen, Yu and Hahn, William C and Levesque, Mitchell P and Doench, John G and Berens, Michael E and Shamji, Alykhan F and Clemons, Paul A and Stockwell, Brent R and Schreiber, Stuart L
Nature, ISSN 0028-0836, 07/2017, Volume 547, Issue 7664, pp. 453 - 457
Plasticity of the cell state has been proposed to drive resistance to multiple classes of cancer therapies, thereby limiting their effectiveness(1-4). A... 
EPITHELIAL-MESENCHYMAL TRANSITION | METABOLISM | MULTIDISCIPLINARY SCIENCES | PROSTATE-CANCER | HUMAN-MELANOMA CELLS | SENSITIVITY | DEATH | INHIBITOR | EXPRESSION | SIGNATURE | REVEALS | Prostatic Neoplasms - metabolism | Cadherins - metabolism | Humans | Mesoderm - drug effects | Melanoma - enzymology | Male | Lipid Peroxides - metabolism | Zinc Finger E-box-Binding Homeobox 1 - genetics | Neoplasms - genetics | Mesoderm - enzymology | Cell Death | Epithelial-Mesenchymal Transition | Lipid Peroxidation - drug effects | Cell Transdifferentiation | Prostatic Neoplasms - drug therapy | Melanoma - metabolism | Glutathione Peroxidase - metabolism | Prostatic Neoplasms - pathology | Reproducibility of Results | Neoplasms - enzymology | Melanoma - pathology | Iron - metabolism | Neoplasms - drug therapy | Cell Lineage | Drug Resistance, Neoplasm - genetics | Proto-Oncogene Proteins B-raf - genetics | Melanoma - drug therapy | Proteomics | Cell Line, Tumor | Prostatic Neoplasms - enzymology | Mesoderm - metabolism | Neoplasms - pathology | Mesoderm - pathology | Peroxidase | Research | Chemical properties | Chemical synthesis | Analysis | Cancer cells | Therapy | Biotechnology | Carcinoma | Mesenchyme | Genes | Lipid peroxidation | Lipids | Iron | Genomes | Phospholipids | Kinases | Cancer therapies | Proteins | Organoids | Dissipation | Peroxides | Lipid metabolism | Glutathione | Transfer RNA | Peroxidation | Glutathione peroxidase | Enzymes | Mortality | Melanoma | Selenocysteine | Tumor cell lines | Metabolism | Substrates | Cell death | Lipoxygenase | Prostate cancer | Prostate | Tumors | Apoptosis | Cancer | Index Medicus
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2. Full Text Diverse somatic mutation patterns and pathway alterations in human cancers
by Li, Li and Waring, Paul and Stern, Howard M and Stokoe, David and Zheng, Jianbiao and Eberhard, David A and Chaudhuri, Subhra and Moorhead, Martin and Wang, Weiru and Yue, Peng and Modrusan, Zora and Pujara, Kanan and Faham, Malek and Davis, David P and Eigenbrot, Charles and Tomsho, Lynn P and Janakiraman, Vasantharajan and Stinson, Jeremy and Bourgon, Richard and Carlton, Victoria E. H and Jaiswal, Bijay S and Seshagiri, Somasekar and Kaminker, Joshua S and Schuster, Stephan C and Kan, Zhengyan and Peters, Brock A and Cordes, Shaun and Zhang, Zemin and de Sauvage, Frederic J and Bhatt, Deepali and Haverty, Peter M and Yuan, Wenlin
Nature, ISSN 0028-0836, 08/2010, Volume 466, Issue 7308, pp. 869 - 873
The systematic characterization of somatic mutations in cancer genomes is essential for understanding the disease and for developing targeted therapeutics.... 
HUMAN BREAST | MELANOMA | IDENTIFICATION | MULTIDISCIPLINARY SCIENCES | INSIGHTS | REVEALS | Breast Neoplasms - classification | Lung Neoplasms - genetics | Neoplasms - metabolism | Protein Kinases - genetics | Humans | Neoplasms - enzymology | GTP-Binding Protein alpha Subunits - genetics | Male | DNA Copy Number Variations - genetics | Signal Transduction - genetics | Mutation - genetics | Ovarian Neoplasms - genetics | Lung Neoplasms - classification | Ovarian Neoplasms - classification | Breast Neoplasms - genetics | Prostatic Neoplasms - genetics | Neoplasms - genetics | DNA Mutational Analysis | Prostatic Neoplasms - classification | MAP Kinase Kinase 4 - genetics | Female | Receptors, G-Protein-Coupled - genetics | Neoplasms - pathology | Genes, Neoplasm - genetics | Care and treatment | Gene mutations | Physiological aspects | Genetic aspects | Cellular signal transduction | Research | Health aspects | Protein kinases | Cancer | Studies | Mutation | Mass spectrometry | Deoxyribonucleic acid--DNA | Index Medicus
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3. Full Text The deficiency of Akt1 is sufficient to suppress tumor development in Pten+/- mice
by Chen, Mei-Ling and Xu, Pei-Zhang and Peng, Xiao-Ding and Chen, William S and Guzman, Grace and Yang, Ximing and Di Cristofano, Antonio and Pandolfi, Pier Paolo and Hay, Nissim
Genes and Development, ISSN 0890-9369, 06/2006, Volume 20, Issue 12, pp. 1569 - 1574
The tumor suppressor PTEN is frequently inactivated in human cancers. A major downstream effector of PTEN is Akt, which is hyperactivated via PTEN... 
Intestinal polyps | PIN | Endometrium carcinoma | Thyroid and adrenal tumors | Cancer therapy | AKT/PKB | GENETICALLY-ENGINEERED MICE | PTEN | DEVELOPMENTAL BIOLOGY | PHOSPHOINOSITIDE 3-KINASE | CANCER | CELL BIOLOGY | cancer therapy | PATHWAY | thyroid and adrenal tumors | NEOPLASIA | RELEVANCE | intestinal polyps | MUTATION | GENETICS & HEREDITY | endometrium carcinoma | Prostatic Intraepithelial Neoplasia - pathology | Thyroid Neoplasms - enzymology | Proto-Oncogene Proteins c-akt - deficiency | Male | Intestinal Polyps - enzymology | Proto-Oncogene Proteins c-akt - genetics | Adrenal Gland Neoplasms - enzymology | Prostatic Neoplasms - genetics | Endometrial Neoplasms - genetics | Neoplasms - genetics | Female | Pseudolymphoma - genetics | Pseudolymphoma - enzymology | Adrenal Gland Neoplasms - pathology | PTEN Phosphohydrolase - genetics | Prostatic Neoplasms - pathology | Endometrial Neoplasms - enzymology | Neoplasms - enzymology | PTEN Phosphohydrolase - metabolism | Pseudolymphoma - pathology | Thyroid Neoplasms - genetics | Animals | Prostatic Intraepithelial Neoplasia - enzymology | Intestinal Polyps - pathology | Prostatic Neoplasms - enzymology | Endometrial Neoplasms - pathology | Heterozygote | Mice | Prostatic Intraepithelial Neoplasia - genetics | Neoplasms - pathology | Adrenal Gland Neoplasms - genetics | Thyroid Neoplasms - pathology | Index Medicus | Research Communication
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4. Full Text Asparagine bioavailability governs metastasis in a model of breast cancer
by Knott, Simon R.V and Wagenblast, Elvin and Khan, Showkhin and Kim, Sun Y and Soto, Mar and Wagner, Michel and Turgeon, Marc-Olivier and Fish, Lisa and Erard, Nicolas and Gable, Annika L and MacEli, Ashley R and DIckopf, Steffen and Papachristou, Evangelia K and D'Santos, Clive S and Carey, Lisa A and Wilkinson, John E and Harrell, J. Chuck and Perou, Charles M and Goodarzi, Hani and Poulogiannis, George and Hannon, Gregory J
Nature, ISSN 0028-0836, 02/2018, Volume 554, Issue 7692, pp. 378 - 381
Using a functional model of breast cancer heterogeneity, we previously showed that clonal sub-populations proficient at generating circulating tumour cells... 
HETEROGENEITY | EXPRESSION | MULTIDISCIPLINARY SCIENCES | MAMMARY-TUMOR | Prostatic Neoplasms - metabolism | Prognosis | Humans | Lung Neoplasms - metabolism | Biological Availability | Lung Neoplasms - pathology | Male | Epithelial-Mesenchymal Transition - genetics | Breast Neoplasms - metabolism | Breast Neoplasms - enzymology | Prostatic Neoplasms - genetics | Lung Neoplasms - secondary | RNA Interference | Neoplasm Invasiveness - pathology | Female | Asparaginase - therapeutic use | Aspartate-Ammonia Ligase - metabolism | Disease Models, Animal | Asparagine - deficiency | Prostatic Neoplasms - pathology | Reproducibility of Results | Asparaginase - metabolism | Lung Neoplasms - enzymology | Aspartate-Ammonia Ligase - genetics | Disease Progression | Animals | Breast Neoplasms - genetics | Breast Neoplasms - pathology | Neoplasm Metastasis - pathology | Asparagine - metabolism | Cell Line, Tumor | Prostatic Neoplasms - enzymology | Mice | Oncology, Experimental | Asparagine | Breast cancer | Cancer invasiveness | Research | Metastasis | Cancer | Mesenchyme | Invasiveness | RNA-mediated interference | L-asparaginase | Amino acids | Genomes | Bioavailability | Gene expression | Ribonucleic acid--RNA | Patients | Metastases | Proteins | Aspartate-ammonia ligase | Diet | Asparaginase | Tumors | Index Medicus
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5. Full Text MnSOD upregulation sustains the Warburg effect via mitochondrial ROS and AMPK-dependent signalling in cancer
by Hart, Peter C and Mao, Mao and De Abreu, Andre Luelsdorf P and Ansenberger-Fricano, Kristine and Ekoue, Dede N and Ganini, Douglas and Kajdacsy-Balla, Andre and Diamond, Alan M and Minshall, Richard D and Consolaro, Marcia E. L and Santos, Janine H and Bonini, Marcelo G
Nature Communications, ISSN 2041-1723, 2015, Volume 6, Issue 1, pp. 6053 - 6053
Manganese superoxide dismutase (MnSOD/SOD2) is a mitochondria-resident enzyme that governs the types of reactive oxygen species egressing from the organelle to... 
HYPOXIA-INDUCIBLE FACTOR | LIFE-SPAN | OXIDATIVE STRESS | ACTIVATED PROTEIN-KINASE | EPITHELIAL-CELLS | MANGANESE SUPEROXIDE-DISMUTASE | MULTIDISCIPLINARY SCIENCES | INHIBIT APOPTOSIS | C-MYC | CELL-CYCLE PROGRESSION | BREAST | Mitochondria - enzymology | RNA, Small Interfering - genetics | AMP-Activated Protein Kinases - metabolism | Colonic Neoplasms - genetics | Superoxide Dismutase - genetics | Reactive Oxygen Species - metabolism | Humans | Transcriptional Activation | Gene Expression Regulation, Neoplastic | Phosphofructokinase-1 - genetics | Superoxide Dismutase - antagonists & inhibitors | Male | Glycolysis - genetics | Breast Neoplasms - enzymology | Prostatic Neoplasms - genetics | Mitochondria - genetics | Female | Hexokinase - genetics | Superoxide Dismutase - metabolism | Prostatic Neoplasms - pathology | Oxidation-Reduction | Pyruvate Kinase - metabolism | Signal Transduction | AMP-Activated Protein Kinases - antagonists & inhibitors | Hydrogen Peroxide - metabolism | Breast Neoplasms - genetics | Breast Neoplasms - pathology | Colonic Neoplasms - pathology | Cell Line, Tumor | Prostatic Neoplasms - enzymology | Colonic Neoplasms - enzymology | Hexokinase - metabolism | Neoplasm Staging | Phosphofructokinase-1 - metabolism | Pyruvate Kinase - genetics | AMP-Activated Protein Kinases - genetics | RNA, Small Interfering - metabolism | Index Medicus
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6. Full Text MTOR regulates the pro-tumorigenic senescence-associated secretory phenotype by promoting IL1A translation
by Laberge, Remi-Martin and Sun, Yu and Orjalo, Arturo V and Patil, Christopher K and Freund, Adam and Zhou, Lili and Curran, Samuel C and Davalos, Albert R and Wilson-Edell, Kathleen A and Liu, Su and Limbad, Chandani and Demaria, Marco and Li, Patrick and Hubbard, Gene B and Ikeno, Yuji and Javors, Martin and Desprez, Pierre-Yves and Benz, Christopher C and Kapahi, Pankaj and Nelson, Peter S and Campisi, Judith
Nature Cell Biology, ISSN 1465-7392, 08/2015, Volume 17, Issue 8, pp. 1049 - 1061
The TOR (target of rapamycin) kinase limits longevity by poorly understood mechanisms. Rapamycin suppresses the mammalian TORC1 complex, which regulates... 
EPITHELIAL-CELL LINE | GROWTH ARREST | DNA-DAMAGE | IN-VIVO | INFLAMMATORY CYTOKINE SECRETION | HUMAN FIBROBLASTS | TUMOR-CELLS | CANCER-THERAPY | REPLICATIVE SENESCENCE | P53 | CELL BIOLOGY | Up-Regulation | Fibroblasts - enzymology | Cell Proliferation | TOR Serine-Threonine Kinases - metabolism | Humans | Gene Expression Regulation, Neoplastic | Interleukin-1alpha - metabolism | Male | NF-kappa B - metabolism | RNA, Messenger - metabolism | Prostatic Neoplasms - secretion | Prostatic Neoplasms - immunology | Dose-Response Relationship, Drug | TOR Serine-Threonine Kinases - antagonists & inhibitors | Prostatic Neoplasms - genetics | TOR Serine-Threonine Kinases - genetics | Transfection | RNA Interference | Time Factors | Cellular Senescence | Inflammation Mediators - metabolism | Transcription, Genetic | Antineoplastic Agents - pharmacology | Interleukin-1alpha - genetics | Interleukin-6 - metabolism | Prostatic Neoplasms - drug therapy | Prostatic Neoplasms - pathology | Anti-Inflammatory Agents - pharmacology | Interleukin-1alpha - secretion | Sirolimus - metabolism | Tumor Burden | Mice, SCID | Sirolimus - pharmacology | Xenograft Model Antitumor Assays | Phenotype | Animals | Fibroblasts - drug effects | Cell Line, Tumor | Prostatic Neoplasms - enzymology | Mitoxantrone - pharmacology | Interleukins | Aging | Genetic aspects | Properties | Phosphotransferases | Carcinogenesis | Health aspects | Cells | Index Medicus
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7. Full Text Five different anti-prostate-specific membrane antigen (PSMA) antibodies confirm PSMA expression in tumor-associated neovasculature
by Chang, Sam S and Reuter, Victor E and Heston, W.D.W and Bander, Neil H and Grauer, Lana S and Gaudin, Paul B
Cancer Research, ISSN 0008-5472, 07/1999, Volume 59, Issue 13, pp. 3192 - 3198
Prostate-specific membrane antigen (PSMA) is a type II integral membrane glycoprotein that was initially characterized by the monoclonal antibody (mAb) 7E11.... 
CYT-356 | LOCALIZATION | CARCINOMA CELL-LINE | THERAPY | ANGIOGENESIS | GENE | ONCOLOGY | EXTRACELLULAR DOMAIN | RADICAL PROSTATECTOMY | MONOCLONAL-ANTIBODIES | CANCER RECURRENCE | Humans | Urinary Bladder Neoplasms - enzymology | Male | Testicular Neoplasms - enzymology | Testicular Neoplasms - pathology | Neovascularization, Pathologic - enzymology | Breast Neoplasms - enzymology | Transfection | Carboxypeptidases - immunology | Urinary Bladder Neoplasms - pathology | Carcinoma, Renal Cell - enzymology | Female | Antigens, Neoplasm - analysis | Tumor Cells, Cultured | Carcinoma, Renal Cell - blood supply | Prostatic Neoplasms - blood supply | Antigens, Neoplasm - genetics | Prostatic Neoplasms - pathology | Carcinoma, Renal Cell - pathology | Neoplasms - enzymology | Neoplasms - blood supply | Carboxypeptidases - genetics | Antibodies, Monoclonal | Breast Neoplasms - blood supply | Urinary Bladder Neoplasms - blood supply | Breast Neoplasms - pathology | Testicular Neoplasms - blood supply | Prostatic Neoplasms - enzymology | Antigens, Surface | Prostate - enzymology | Neoplasms - pathology | Carboxypeptidases - analysis | Glutamate Carboxypeptidase II | Index Medicus
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8. Full Text Hyaluronan synthase HAS2 promotes tumor progression in bone by stimulating the interaction of breast cancer stem-like cells with macrophages and stromal cells
by Okuda, Hiroshi and Kobayashi, Aya and Xia, Bo and Watabe, Misako and Pai, Sudha K and Hirota, Shigeru and Xing, Fei and Liu, Wen and Pandey, Puspa R and Fukuda, Koji and Modur, Vishnu and Ghosh, Arnab and Wilber, Andrew and Watabe, Kounosuke
Cancer Research, ISSN 0008-5472, 01/2012, Volume 72, Issue 2, pp. 537 - 547
The molecular mechanisms that operate within the organ microenvironment to support metastatic progression remain unclear. Here, we report that upregulation of... 
METASTASIS | ACID | ONCOLOGY | PROSTATE-CANCER | 4-METHYLUMBELLIFERONE | SOIL | GROWTH-FACTOR | INTERLEUKIN-6 | EXPRESSION | SIGNATURE | CARCINOMA | Up-Regulation | Stromal Cells - pathology | Humans | Gene Expression Regulation, Neoplastic | Bone Neoplasms - secondary | Gene Expression Profiling | Bone Neoplasms - pathology | Cell Movement - physiology | Hymecromone - analogs & derivatives | Breast Neoplasms - enzymology | Stromal Cells - enzymology | Neoplastic Stem Cells - pathology | Female | Bone Neoplasms - genetics | Hyaluronan Synthases | Hymecromone - pharmacology | Bone Neoplasms - enzymology | Macrophages - pathology | Neoplasm Invasiveness | Disease Progression | Macrophages - enzymology | Animals | Breast Neoplasms - genetics | Glucuronosyltransferase - metabolism | Breast Neoplasms - pathology | Cell Adhesion - physiology | Mice, Nude | Glucuronosyltransferase - antagonists & inhibitors | Mice | Neoplastic Stem Cells - enzymology | Index Medicus | Bone cancer | microenvironment | tumor associated macrophages | HAS2
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9. Full Text Aldehyde dehydrogenase 3A1 associates with prostate tumorigenesis
by Yan, J and De Melo, J and Cutz, J.-C and Aziz, T and Tang, D
British Journal of Cancer, ISSN 0007-0920, 05/2014, Volume 110, Issue 10, pp. 2593 - 2603
Background: Accumulating evidence demonstrates high levels of aldehyde dehydrogense (ALDH) activity in human cancer types, in part, because of its association... 
INITIATING CELLS | TUMOR PROGRESSION | CANCER STEM-CELLS | BREAST-CANCER | LUNG-CANCER | prostate cancer | HEMATOPOIETIC PROGENITOR CELLS | EPITHELIAL-CELLS | ONCOLOGY | FUNCTIONAL MARKER | aldehyde dehydrogenase 3A1 | GENE-EXPRESSION | BONE METASTASIS | prostate cancer stem cells | Neoplasm Transplantation | Prostatic Intraepithelial Neoplasia - pathology | Adenocarcinoma - pathology | Aldehyde Dehydrogenase - analysis | Humans | Aldehyde Dehydrogenase - biosynthesis | Gene Expression Regulation, Neoplastic | Bone Neoplasms - secondary | Male | Lung Neoplasms - secondary | Neoplasms, Hormone-Dependent - enzymology | Neoplasm Proteins - genetics | Prostatic Neoplasms - pathology | Bone Neoplasms - enzymology | Lung Neoplasms - enzymology | Neoplasm Proteins - biosynthesis | Adenocarcinoma - enzymology | Enzyme Induction | Aldehyde Dehydrogenase - genetics | Lymphatic Metastasis | Mice, SCID | Disease Progression | Androgens | Animals | Cell Transformation, Neoplastic | Neoplasms, Hormone-Dependent - pathology | Prostatic Intraepithelial Neoplasia - enzymology | Epithelial Cells - enzymology | Cell Line, Tumor | Prostatic Neoplasms - enzymology | Mice, Inbred NOD | Neoplasm Proteins - analysis | Mice | Neoplastic Stem Cells - enzymology | Cell Line, Transformed | Index Medicus | Molecular Diagnostics
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10. Full Text PTEN-Deficient Cancers Depend on PIK3CB
by Susan Wee and Dmitri Wiederschain and Sauveur-Michel Maira and Alice Loo and Christine Miller and Rosalie deBeaumont and Frank Stegmeier and Yung-Mae Yao and Christoph Lengauer
Proceedings of the National Academy of Sciences of the United States of America, ISSN 0027-8424, 9/2008, Volume 105, Issue 35, pp. 13057 - 13062
Deregulation of the PI3K signaling pathway is observed in many human cancers and occurs most frequently through loss of PTEN phosphatase tumor suppressor... 
Protein isoforms | Cell growth | HCT116 cells | Cell lines | Lipids | Down regulation | Genetic mutation | Heterologous transplantation | Tumors | Cancer | BREAST-CARCINOMA | B-CELL | GENE | PATHWAY | MULTIDISCIPLINARY SCIENCES | PROSTATE-CANCER | DRUG DISCOVERY | HIGH-FREQUENCY | TUMOR-SUPPRESSOR | PHOSPHOINOSITIDE 3-KINASES | MUTATIONS | Cell Proliferation | Humans | Male | Transplantation, Heterologous | Phosphatidylinositol 3-Kinases - metabolism | Phosphoproteins - metabolism | Phosphatidylinositol 3-Kinases - deficiency | Proto-Oncogene Proteins c-akt - metabolism | Prostatic Neoplasms - pathology | PTEN Phosphohydrolase - deficiency | Signal Transduction | Cell Survival | Down-Regulation | Neoplasms - enzymology | PTEN Phosphohydrolase - metabolism | Mutation - genetics | Animals | Class I Phosphatidylinositol 3-Kinases | Mice, Nude | Colonic Neoplasms - pathology | Cell Line, Tumor | Prostatic Neoplasms - enzymology | Colonic Neoplasms - enzymology | Mice | Neoplasms - pathology | Physiological aspects | Phosphatidylinositol | Tumor suppressor genes | Genetic aspects | Health aspects | Index Medicus | Biological Sciences
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11. 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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