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1. Full Text The role of TGF-β/SMAD4 signaling in cancer
by Zhao, Ming and Mishra, Lopa and Deng, Chu-Xia
International Journal of Biological Sciences, ISSN 1449-2288, 01/2018, Volume 14, Issue 2, pp. 111 - 123
Transforming growth factor beta (TGF-beta) signaling pathway plays important roles in many biological processes, including cell growth, differentiation,... 
TGF-β | SMAD4 | Mouse model | Tumorigenesis | Prognosis | mouse model | BIOCHEMISTRY & MOLECULAR BIOLOGY | TUMOR-SUPPRESSOR GENE | DPC4 EXPRESSION | MESENCHYMAL TRANSITION | prognosis | BREAST-CANCER | TGF-beta | COLORECTAL-CANCER | SMAD4 LOSS | SQUAMOUS-CELL CARCINOMA | tumorigenesis | UP-REGULATION | P21(WAF1) EXPRESSION | Neoplasms - metabolism | Signal Transduction | Smad4 Protein - physiology | Transforming Growth Factor beta - physiology | Models, Molecular | Epithelial-Mesenchymal Transition - genetics | Smad4 Protein - metabolism | Animals | Neoplasms - genetics | Smad4 Protein - genetics | DNA Repair | DNA Damage - genetics | Mice | Mutation | Transforming Growth Factor beta - metabolism | Adenocarcinoma | Deactivation | Stability | Transforming growth factor | DNA damage | Colorectal carcinoma | Inactivation | DNA repair | Smad4 protein | Biological activity | Skin cancer | Genomic instability | Adenomatous polyposis coli | Signal transduction | Signaling | Transcription activation | Skin | Pancreas | Cell migration | Deoxyribonucleic acid--DNA | Cancer | Tumors | Apoptosis
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2. Full Text Functional screening for miRNAs targeting Smad4 identified miR-199a as a negative regulator of TGF-β signalling pathway
by Zhang, Yan and Fan, Kai-Ji and Sun, Qiang and Chen, Ai-Zhong and Shen, Wen-Long and Zhao, Zhi-Hu and Zheng, Xiao-Fei and Yang, Xiao
Nucleic Acids Research, ISSN 0305-1048, 10/2012, Volume 40, Issue 18, pp. 9286 - 9297
The transforming growth factor-beta (TGF-beta) signalling pathway participates in various biological processes. Dysregulation of Smad4, a central cellular... 
GROWTH-FACTOR-BETA | HEPATOCELLULAR-CARCINOMA | GENE | DPC4/SMAD4 EXPRESSION | BIOCHEMISTRY & MOLECULAR BIOLOGY | TRANSDUCTION | ACUTE MYELOID-LEUKEMIA | CELL-GROWTH | MUTATIONS | MICRORNA EXPRESSION PATTERNS | CANCER | Stomach Neoplasms - genetics | NIH 3T3 Cells | Smad4 Protein - antagonists & inhibitors | Signal Transduction | Humans | Cells, Cultured | Gene Expression Regulation, Neoplastic | Stomach Neoplasms - metabolism | MicroRNAs - metabolism | Stomach Neoplasms - pathology | Smad4 Protein - metabolism | Cell Cycle Checkpoints | Sequence Alignment | Animals | Smad4 Protein - genetics | Base Sequence | Cell Line, Tumor | Transforming Growth Factor beta - antagonists & inhibitors | Mice | 3' Untranslated Regions | MicroRNAs - chemistry | Apoptosis | Signal transduction | Seeds | 3' Untranslated regions | Transcription | Agar | miRNA | Transforming growth factor- beta | Tumor cell lines | Bioinformatics | Gastric cancer | Smad4 protein | RNA
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3. Full Text Iron regulates phosphorylation of Smad1/5/8 and gene expression of Bmp6, Smad7, Id1, and Atoh8 in the mouse liver
by Kautz, Léon and Meynard, Delphine and Monnier, Annabelle and Darnaud, Valérie and Bouvet, Régis and Wang, Rui-Hong and Deng, Chiuxia and Vaulont, Sophie and Mosser, Jean and Coppin, Hélène and Roth, Marie-Paule
Blood, ISSN 0006-4971, 08/2008, Volume 112, Issue 4, pp. 1503 - 1509
Although hepcidin expression was shown to be induced by the BMP/Smad signaling pathway, it is not yet known how iron regulates this pathway and what its exact... 
SIGNAL-TRANSDUCTION | ANTIMICROBIAL PEPTIDE HEPCIDIN | CELLS | MESSENGER-RNA EXPRESSION | JUVENILE HEMOCHROMATOSIS | INFLAMMATION | DIFFERENTIATION | IDENTIFICATION | HEMATOLOGY | HEMOJUVELIN | MICROARRAY EXPERIMENTS | Bone Morphogenetic Protein 6 | Phosphorylation | Basic Helix-Loop-Helix Transcription Factors - genetics | Iron Overload - genetics | Signal Transduction | Liver - metabolism | Smad4 Protein - physiology | Male | Smad Proteins - genetics | Gene Expression Profiling | Mice, Knockout | Animals | Iron - physiology | Diet | Smad5 Protein - metabolism | Smad1 Protein - metabolism | Transcription, Genetic | Mice | Smad4 Protein - deficiency | Active Transport, Cell Nucleus | Smad8 Protein - metabolism | Smad7 Protein - genetics | Bone Morphogenetic Proteins - genetics | Smad Proteins - metabolism | Smad7 Protein | Liver | Smad4 Protein | Iron | Cellular Biology | Smad5 Protein | Life Sciences | Smad1 Protein | Smad Proteins | Bone Morphogenetic Proteins | Basic Helix-Loop-Helix Transcription Factors | Smad8 Protein | Iron Overload
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4. 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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5. Full Text Smad4 Deficiency in Smooth Muscle Cells Initiates the Formation of Aortic Aneurysm
by Zhang, Peng and Hou, Siyuan and Chen, Jicheng and Zhang, Jishuai and Lin, Fuyu and Ju, Renjie and Cheng, Xuan and Ma, Xiaowei and Song, Yao and Zhang, Youyi and Zhu, Minsheng and Du, Jie and Lan, Yu and Yang, Xiao
Circulation Research, ISSN 0009-7330, 02/2016, Volume 118, Issue 3, pp. 388 - 399
RATIONALE:Aortic aneurysm is a life-threatening cardiovascular disorder caused by the predisposition for dissection and rupture. Genetic studies have proved... 
Smooth muscle | Myocytes | Macrophages | Aortic aneurysm | Aortic rupture | Smad4 protein | myocytes, smooth muscle | CARDIAC & CARDIOVASCULAR SYSTEMS | HEREDITARY HEMORRHAGIC TELANGIECTASIA | ENDOTHELIAL SMAD4 | ATHEROSCLEROSIS | RECEPTOR | JUVENILE POLYPOSIS SYNDROME | aortic aneurysm | macrophages | GROWTH-FACTOR-BETA | aortic rupture | PERIPHERAL VASCULAR DISEASE | MUTATIONS | METALLOELASTASE | HEMATOLOGY | EXPRESSION | CONTRIBUTES | Protein-Serine-Threonine Kinases - deficiency | Up-Regulation | Receptors, Transforming Growth Factor beta - genetics | Aortic Aneurysm - metabolism | Muscle, Smooth, Vascular - metabolism | Myocytes, Smooth Muscle - pathology | Male | Aorta - metabolism | Transfection | RNA Interference | Smad4 Protein - genetics | Time Factors | Proteolysis | Female | Aortic Aneurysm - pathology | Myocytes, Smooth Muscle - metabolism | Aortic Aneurysm - prevention & control | Cell Line | Elastin - metabolism | Genetic Predisposition to Disease | Mice, Inbred C57BL | Protein-Serine-Threonine Kinases - genetics | Rats | Matrix Metalloproteinase 12 - metabolism | Chemotaxis | Smad4 Protein - metabolism | Mice, Knockout | Aorta - pathology | Macrophages - metabolism | Muscle, Smooth, Vascular - pathology | Phenotype | Animals | Cathepsins - metabolism | Chemokines - metabolism | Smad4 Protein - deficiency | Aortic Aneurysm - genetics | Receptors, Transforming Growth Factor beta - deficiency
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6. Full Text MicroRNA-183 is an oncogene targeting Dkk-3 and SMAD4 in prostate cancer
by Ueno, K and Hirata, H and Shahryari, V and Deng, G and Tanaka, Y and Tabatabai, Z.L and Hinoda, Y and Dahiya, R
British Journal of Cancer, ISSN 0007-0920, 04/2013, Volume 108, Issue 8, pp. 1659 - 1667
Background: The purpose of this study was to identify prostate cancer (PC) oncogenic microRNAs (miRs) based on miR microarray and to investigate whether these... 
CELLS | APOPTOSIS | SMAD4 | miRNA-183 | RISK | DEATH | prostate cancer | GROWTH-FACTOR-BETA | GENE | ONCOLOGY | Dkk-3 | DPC4 SMAD4 | EXPRESSION | CARCINOMA | PROGRESSION | Prostatic Neoplasms - metabolism | Prostatic Neoplasms - pathology | MicroRNAs - antagonists & inhibitors | Humans | Intercellular Signaling Peptides and Proteins - genetics | Intercellular Signaling Peptides and Proteins - biosynthesis | Male | MicroRNAs - biosynthesis | Wnt Proteins - metabolism | beta Catenin - metabolism | Gene Knockdown Techniques | In Situ Hybridization | Prostatic Neoplasms - genetics | Transfection | Smad4 Protein - genetics | Cell Line, Tumor | MicroRNAs - genetics | Cell Growth Processes - genetics | Smad4 Protein - biosynthesis | Wnt Signaling Pathway | Molecular Diagnostics
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7. Chemoresistance to doxorubicin induces epithelial-mesenchymal transition via upregulation of transforming growth factor β signaling in HCT116 colon cancer cells
by Li, Jinpeng and Liu, Hao and Yu, Jieping and Yu, Honggang
Molecular Medicine Reports, ISSN 1791-2997, 07/2015, Volume 12, Issue 1, pp. 192 - 198
Doxorubicin (Dox) is a commonly used chemotherapeutic drug in human colon cancer. However, it becomes increasingly ineffective with tumor progression, the... 
Epithelial-mesenchymal transition | Transforming growth factor β/Smad4 signaling | Colon cancer | Doxorubicin chemoresistance | RNA interference | RNA, Small Interfering - genetics | Smad4 Protein - antagonists & inhibitors | Antibiotics, Antineoplastic - pharmacology | Cadherins - metabolism | Signal Transduction | Vimentin - metabolism | HCT116 Cells | Humans | Gene Expression Regulation, Neoplastic | Epithelial-Mesenchymal Transition - drug effects | Transcription Factors - genetics | Epithelial-Mesenchymal Transition - genetics | Smad4 Protein - metabolism | Transcription Factors - metabolism | Drug Resistance, Neoplasm - genetics | Transforming Growth Factor beta - genetics | Smad4 Protein - genetics | Vimentin - genetics | Cadherins - genetics | Snail Family Transcription Factors | Transforming Growth Factor beta - metabolism | Doxorubicin - pharmacology | Drug Resistance, Neoplasm - drug effects | RNA, Small Interfering - metabolism
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8. Full Text Genistein downregulates onco-miR-1260b and upregulates sFRP1 and Smad4 via demethylation and histone modification in prostate cancer cells
by Hirata, H and Hinoda, Y and Shahryari, V and Deng, G and Tanaka, Y and Tabatabai, Z.L and Dahiya, R
British Journal of Cancer, ISSN 0007-0920, 03/2014, Volume 110, Issue 6, pp. 1645 - 1654
Background: Recently several microRNAs (miRNAs) have been found to be regulated by genistein in cancer cells. In this study, we focused on the gene regulatory... 
miR-1260b | apoptosis | Smad4 | genistein | sFRP1 | UNITED-STATES | METHYLATION | ISOFLAVONES | ONCOLOGY | EPIGENETIC INACTIVATION | ALTERS GROWTH | GENES | PROMOTER | SOY | EXPRESSION | INCIDENCE TRENDS | Prostatic Neoplasms - metabolism | Prostatic Neoplasms - pathology | Ataxia Telangiectasia Mutated Proteins - metabolism | Tissue Array Analysis | Down-Regulation | Humans | In Situ Hybridization, Fluorescence | Male | MicroRNAs - metabolism | Smad4 Protein - metabolism | Up-Regulation - drug effects | Histones - genetics | Prostatic Neoplasms - genetics | Smad4 Protein - genetics | Ataxia Telangiectasia Mutated Proteins - biosynthesis | Genistein - pharmacology | MicroRNAs - genetics | Gene Expression Regulation, Neoplastic - drug effects | Histones - metabolism | Ataxia Telangiectasia Mutated Proteins - genetics | Smad4 Protein - biosynthesis | Anticarcinogenic Agents - pharmacology | DNA Methylation - drug effects | Prostatic Neoplasms - drug therapy | Molecular Diagnostics
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9. Full Text AMP-activated protein kinase (AMPK) activation inhibits nuclear translocation of Smad4 in mesangial cells and diabetic kidneys
by Zhao, Jinghong and Miyamoto, Satoshi and You, Young-Hyun and Sharma, Kumar
American Journal of Physiology - Renal Physiology, ISSN 0363-6127, 05/2015, Volume 308, Issue 10, pp. F1167 - F1177
Diabetic nephropathy is characterized by diffuse mesangial matrix expansion and is largely dependent on the TGF-beta/Smad signaling pathway. Smad4 is required... 
Diabetic nephropathy | AICAR | Smad4 | AMP-activated protein kinase | High glucose | PHYSIOLOGY | TGF-BETA | TUMOR-SUPPRESSOR SMAD4 | RENAL HYPERTROPHY | GROWTH-FACTOR-BETA | high glucose | INFLAMMATION | IN-VIVO | DISEASE | GENE-EXPRESSION | UROLOGY & NEPHROLOGY | TRANSCRIPTION FACTOR | diabetic nephropathy | AMP-Activated Protein Kinases - metabolism | Smad4 Protein - antagonists & inhibitors | Male | AMP-Activated Protein Kinases - drug effects | Aminoimidazole Carboxamide - pharmacology | Mesangial Cells - drug effects | Ribonucleotides - pharmacology | Smad4 Protein - drug effects | Cell Nucleus - metabolism | Diabetes Mellitus, Experimental - chemically induced | Diabetes Mellitus, Experimental - complications | Streptozocin - adverse effects | Disease Models, Animal | Cell Line | Diabetic Nephropathies - pathology | Diabetic Nephropathies - metabolism | Mice, Inbred C57BL | Glucose - pharmacology | Mesangial Cells - metabolism | Smad4 Protein - metabolism | Hypoglycemic Agents - pharmacology | Transforming Growth Factor beta - pharmacology | Animals | Aminoimidazole Carboxamide - analogs & derivatives | Mesangial Cells - pathology | Signal Transduction - physiology | Biological Transport - physiology | Mice | In Vitro Techniques | Transforming Growth Factor beta - metabolism | Transcription factors | Biological transport | Diabetic nephropathies | Development and progression | Genetic aspects | Properties | Protein kinases
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10. Full Text MicroRNA-20a-5p promotes colorectal cancer invasion and metastasis by downregulating Smad4
by Cheng, Dantong and Zhao, Senlin and Tang, Huamei and Zhang, Dongyuan and Sun, Hongcheng and Yu, Fudong and Jiang, Weiliang and Yue, Ben and Wang, Jingtao and Zhang, Meng and Yu, Yang and Liu, Xisheng and Sun, Xiaofeng and Zhou, Zongguang and Qin, Xuebin and Zhang, Xin and Yan, Dongwang and Wen, Yugang and Peng, Zhihai and Medicinska fakulteten and Region Östergötland and Linköpings universitet and Institutionen för klinisk och experimentell medicin and Onkologiska kliniken US and Avdelningen för kliniska vetenskaper and Centrum för kirurgi, ortopedi och cancervård and Avdelningen för Kirurgi, Ortopedi och Onkologi
Oncotarget, ISSN 1949-2553, 2016, Volume 7, Issue 29, pp. 45199 - 45213
Background: Tumor metastasis is one of the leading causes of poor prognosis for colorectal cancer (CRC) patients. Loss of Smad4 contributes to aggression... 
Prognosis | Smad4 | Metastasis | miR-20a-5p | Colorectal cancer | CELLS | MORPHOGENETIC PROTEIN PATHWAY | NETWORK | colorectal cancer | TUMOR PROGRESSION | prognosis | CELL BIOLOGY | COLON-CANCER | metastasis | EXPRESSION | CARCINOMA | Colorectal Neoplasms - mortality | Smad4 Protein - antagonists & inhibitors | Neoplasm Invasiveness | Down-Regulation | Humans | Middle Aged | Proportional Hazards Models | Male | Neoplasm Metastasis | Animals | Smad4 Protein - genetics | Colorectal Neoplasms - drug therapy | Epithelial-Mesenchymal Transition | Cell Line, Tumor | Adult | Female | Aged | Mice | Mice, Inbred BALB C | MicroRNAs - physiology | 3' Untranslated Regions | Colorectal Neoplasms - pathology | Clinical Medicine | Medical and Health Sciences | Medicin och hälsovetenskap | Cancer and Oncology | Klinisk medicin | miR-20a-5p; colorectal cancer; metastasis; prognosis; Smad4 | Cancer och onkologi
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11. Full Text Smad4 inactivation promotes malignancy and drug resistance of colon cancer
by Papageorgis, Panagiotis and Cheng, Kuanghung and Ozturk, Sait and Gong, Yi and Lambert, Arthur W and Abdolmaleky, Hamid M and Zhou, Jin-Rong and Thiagalingam, Sam
Cancer Research, ISSN 0008-5472, 02/2011, Volume 71, Issue 3, pp. 998 - 1008
SMAD4 is localized to chromosome 18q21, a frequent site for loss of heterozygosity in advanced stage colon cancers. Although Smad4 is regarded as a signaling... 
CHROMOSOME 18Q | CELLS | GROWTH-FACTOR-BETA | TGF-BETA | ONCOLOGY | COLORECTAL-CANCER | MICROSATELLITE INSTABILITY | LIVER METASTASIS | UP-REGULATION | DPC4 | II RECEPTOR GENE | Vascular Endothelial Growth Factor A - biosynthesis | Colonic Neoplasms - genetics | Colonic Neoplasms - drug therapy | Humans | Gene Expression Regulation, Neoplastic | Drug Resistance, Neoplasm | Vascular Endothelial Growth Factor A - antagonists & inhibitors | Cell Movement - genetics | Colonic Neoplasms - metabolism | Neovascularization, Pathologic - pathology | Matrix Metalloproteinase 9 - metabolism | Neoplasm Metastasis | Receptor, Transforming Growth Factor-beta Type II | Smad4 Protein - genetics | Cell Transformation, Neoplastic - genetics | Smad4 Protein - biosynthesis | Protein-Serine-Threonine Kinases - metabolism | Colonic Neoplasms - blood supply | HCT116 Cells | Gene Silencing | Cell Transformation, Neoplastic - metabolism | Smad4 Protein - metabolism | Receptors, Transforming Growth Factor beta - metabolism | Neovascularization, Pathologic - genetics | Fluorouracil - pharmacology | Neovascularization, Pathologic - metabolism | Cell Hypoxia - genetics | Cell Transformation, Neoplastic - pathology | Transforming Growth Factor beta - metabolism | GLUT1 | Chromosome 18q21 | Smad4 | LOH | VEGF | colon cancer
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12. Full Text Smad4-Mediated Signaling Inhibits Intestinal Neoplasia by Inhibiting Expression of β-Catenin
by Freeman, Tanner J and Smith, J. Joshua and Chen, Xi and Washington, M. Kay and Roland, Joseph T and Means, Anna L and Eschrich, Steven A and Yeatman, Timothy J and Deane, Natasha G and Beauchamp, R. Daniel
Gastroenterology, ISSN 0016-5085, 2012, Volume 142, Issue 3, pp. 562 - 571.e2
Background & Aims Mutational inactivation of adenomatous polyposis coli (APC) is an early event in colorectal cancer (CRC) progression that affects the... 
Gastroenterology and Hepatology | Carcinoma | Signal Transduction | Colon Cancer | Mouse Model | Intestinal Epithelium | STEM-CELLS | SMAD4 | MICROSATELLITE INSTABILITY | C-MYC | HUMAN COLORECTAL-CANCER | COLON-CANCER | EPITHELIAL-CELLS | GENE | JUVENILE POLYPOSIS | MUTATIONS | GASTROENTEROLOGY & HEPATOLOGY | Adenocarcinoma - pathology | Oligonucleotide Array Sequence Analysis | Adenomatous Polyposis Coli - prevention & control | Colorectal Neoplasms - genetics | Humans | Middle Aged | Laser Capture Microdissection | Male | RNA Polymerase II - metabolism | RNA, Messenger - metabolism | Adenomatous Polyposis Coli - pathology | Genes, APC | Bone Morphogenetic Proteins - metabolism | Adenocarcinoma - metabolism | Smad4 Protein - genetics | HEK293 Cells | Female | Adenocarcinoma - genetics | Adenomatous Polyposis Coli - genetics | Binding Sites | Colorectal Neoplasms - metabolism | Down-Regulation | HCT116 Cells | Colorectal Neoplasms - prevention & control | Mice, Transgenic | Smad4 Protein - metabolism | beta Catenin - metabolism | beta Catenin - genetics | Adenomatous Polyposis Coli - metabolism | Mice, Knockout | Adenocarcinoma - prevention & control | Animals | Wnt Signaling Pathway - genetics | Aged | Mice | Smad4 Protein - deficiency | Colorectal Neoplasms - pathology | signal transduction | carcinoma
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13. Full Text SMAD4 Loss triggers the phenotypic changes of pancreatic ductal adenocarcinoma cells
by Chen, Yu-Wen and Hsiao, Pi-Jung and Weng, Ching-Chieh and Kuo, Kung-Kai and Kuo, Tzu-Lei and Wu, Deng-Chyang and Hung, Wen-Chun and Cheng, Kuang-Hung
BMC Cancer, ISSN 1471-2407, 03/2014, Volume 14, Issue 1, p. 181
Background: SMAD4 is a gastrointestinal malignancy-specific tumor suppressor gene found mutated in one third of colorectal cancer specimens and half of... 
Pancreatic cancer | EGFR | SMAD4/DPC4 | TGFβ1 pathway | CD133 | CANCER-CELLS | NAB-PACLITAXEL | TUMOR-SUPPRESSOR GENE | P38 MAPK | DOWN-REGULATION | BETA SIGNALING PATHWAYS | RECEPTOR | LUNG-CANCER | TGF beta 1 pathway | ONCOLOGY | IN-VIVO | EXPRESSION | Cell Proliferation | Pancreatic Neoplasms - metabolism | Humans | Mice, Inbred C57BL | Pancreatic Neoplasms - pathology | Carcinoma, Pancreatic Ductal - metabolism | Pancreatic Neoplasms - genetics | Cell Migration Inhibition - genetics | Mice, SCID | Carcinoma, Pancreatic Ductal - pathology | Smad4 Protein - metabolism | Cell Movement - genetics | Carcinoma, Pancreatic Ductal - genetics | Gene Knockdown Techniques | Phenotype | Animals | Smad4 Protein - genetics | HEK293 Cells | Cell Line, Tumor | Female | Mice | Smad4 Protein - deficiency | Smad proteins | Research | Analysis
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