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Cancer discovery, ISSN 2159-8274, 04/2016, Volume 6, Issue 4, pp. 353 - 367
Journal Article
The Journal of experimental medicine, ISSN 0022-1007, 2014, Volume 211, Issue 7, pp. 1379 - 1391
Journal Article
Nature (London), ISSN 1476-4687, 2018, Volume 562, Issue 7725, pp. 69 - 75
Primary liver cancer represents a major health problem. It comprises hepatocellular carcinoma (HCC) and intrahepatic cholangiocarcinoma (ICC), which differ... 
PATHOGENESIS | HEPATOCELLULAR-CARCINOMA | READ ALIGNMENT | HEPATOCYTES | DNA | INFLAMMATION | PACKAGE | MULTIDISCIPLINARY SCIENCES | FRAMEWORK | BINDING | DISCOVERY | Humans | Tumor Microenvironment | Apoptosis - genetics | Hepatocytes - pathology | Male | Gene Expression Profiling | Genes, myc | Hepatocytes - metabolism | Proto-Oncogene Proteins c-akt - genetics | DNA-Binding Proteins - metabolism | Carcinoma, Hepatocellular - genetics | DNA Transposable Elements - genetics | Female | Liver Neoplasms - pathology | Cell Differentiation | Cell Lineage - genetics | Disease Models, Animal | Cyclin-Dependent Kinase Inhibitor p16 - deficiency | Cytokines - metabolism | Liver Neoplasms - genetics | Carcinogenesis - genetics | Transcription Factors - genetics | DNA-Binding Proteins - genetics | T-Box Domain Proteins - genetics | T-Box Domain Proteins - metabolism | Transcription Factors - metabolism | Cholangiocarcinoma - pathology | Animals | Epigenesis, Genetic - genetics | Carcinoma, Hepatocellular - pathology | Cholangiocarcinoma - genetics | Mosaicism | Mice | Necrosis - genetics | Genes, ras | Liver cancer | Research | Carcinogenesis | Oncology, Experimental | Apoptosis | Cancer | Animal models | Cytokines | Liver | Hepatocellular carcinoma | Genomes | Metastasis | Risk analysis | Gene expression | Risk factors | Metastases | Hepatocytes | Morphology | DNA methylation | Tumorigenesis | Bioinformatics | Cholangiocarcinoma | Deoxyribonucleic acid--DNA | Tumors | T-Box Domain Proteins/metabolism | Hepatocytes/pathology | DNA-Binding Proteins/metabolism | Life Sciences | Cholangiocarcinoma/pathology | Transcription Factors/metabolism | Necrosis/genetics | Cytokines/metabolism | Epigenesis, Genetic/genetics | Cyclin-Dependent Kinase Inhibitor p16/deficiency | Carcinoma, Hepatocellular/pathology | DNA Transposable Elements/genetics | Cell Lineage/genetics | T-Box Domain Proteins/genetics | Transcription Factors/genetics | Apoptosis/genetics | Proto-Oncogene Proteins c-akt/genetics | Liver Neoplasms/genetics | Cholangiocarcinoma/genetics | Liver Neoplasms/pathology | DNA-Binding Proteins/genetics | Hepatocytes/metabolism | Carcinoma, Hepatocellular/genetics | Carcinogenesis/genetics
Journal Article
The Journal of clinical investigation, ISSN 0021-9738, 2015, Volume 125, Issue 5, pp. 1998 - 2006
Journal Article
Pathology, ISSN 0031-3025, 08/2006, Volume 38, Issue 4, pp. 287 - 301
.... Current data indicate that alterations of cyclin kinase inhibitor (cdki) levels are implicated in the pathogenesis of melanoma and may be useful prognostic markers. However, large validation studies linked to comprehensive clinical follow up data are necessary to clarify the prognostic significance of cell cycle regulatory proteins in individual patients. 
pRb | pathogenesis | p16 | p27 | melanoma | cyclin D1 | immunohistochemistry | prognosis | p21 | p53 | Immunohistochemistry | Prognosis | Pathogenesis | Melanoma | Cyclin D1 | CUTANEOUS MALIGNANT-MELANOMA | P53 PROTEIN | TUMOR-SUPPRESSOR GENE | SUN-EXPOSED SKIN | PATHOLOGY | DEPENDENT KINASE INHIBITOR | UVEAL MELANOMA | RETINOBLASTOMA PROTEIN | SPORADIC PRIMARY MELANOMAS | VERTICAL GROWTH-PHASE | MELANOCYTIC LESIONS | Cell Cycle - genetics | Cyclin D1 - metabolism | Cell Proliferation | Humans | Tumor Suppressor Protein p53 - genetics | Cyclin-Dependent Kinase Inhibitor p27 - metabolism | Cyclin-Dependent Kinase Inhibitor p21 - genetics | Cell Transformation, Neoplastic - genetics | Melanoma - genetics | Cell Cycle Proteins - genetics | Cyclin-Dependent Kinase Inhibitor p21 - metabolism | Gene Expression Regulation, Neoplastic - physiology | Gene Expression Regulation, Neoplastic - genetics | Melanoma - physiopathology | Retinoblastoma Protein - metabolism | Tumor Suppressor Protein p53 - metabolism | Cyclin-Dependent Kinase Inhibitor p16 - genetics | Disease Progression | Skin Neoplasms - physiopathology | Animals | Cyclin D1 - genetics | Retinoblastoma Protein - genetics | Skin Neoplasms - genetics | Cell Cycle - physiology | Cyclin-Dependent Kinase Inhibitor p16 - metabolism | Cell Transformation, Neoplastic - pathology | Cell Cycle Proteins - physiology | Cyclin-Dependent Kinase Inhibitor p27 - genetics | Cell Cycle Proteins, genetics | Melanoma, physiopathology | Cyclin-Dependent Kinase Inhibitor p16, genetics | Cell Transformation, Neoplastic, pathology | Cell Transformation, Neoplastic, genetics | Gene Expression Regulation, Neoplastic, genetics | Cyclin-Dependent Kinase Inhibitor p27, genetics | Skin Neoplasms, genetics | Cyclin-Dependent Kinase Inhibitor p21, metabolism | Tumor Suppressor Protein p53, metabolism | Melanoma, genetics | Tumor Suppressor Protein p53, genetics | Cell Cycle, genetics | Skin Neoplasms, physiopathology | Cyclin D1, genetics | Cyclin D1, metabolism | Cell Cycle, physiology | Retinoblastoma Protein, genetics | Cyclin-Dependent Kinase Inhibitor p16, metabolism | Cyclin-Dependent Kinase Inhibitor p27, metabolism | Gene Expression Regulation, Neoplastic, physiology | Retinoblastoma Protein, metabolism | Cyclin-Dependent Kinase Inhibitor p21, genetics | Cell Cycle Proteins, physiology
Journal Article
Nature medicine, ISSN 1546-170X, 2017, Volume 23, Issue 6, pp. 775 - 781
Journal Article
The lancet oncology, ISSN 1470-2045, 2015, Volume 16, Issue 1, pp. 25 - 35
Summary Background Palbociclib (PD-0332991) is an oral, small-molecule inhibitor of cyclin-dependent kinases (CDKs... 
Hematology, Oncology and Palliative Medicine | SURVIVAL | EXEMESTANE | ONCOLOGY | CELL-CYCLE | POSTMENOPAUSAL WOMEN | HER2 | PLUS | Cyclin-Dependent Kinase 6 - antagonists & inhibitors | Piperazines - administration & dosage | Triazoles - administration & dosage | Receptor, ErbB-2 - genetics | Humans | Middle Aged | Antineoplastic Combined Chemotherapy Protocols - adverse effects | Receptors, Estrogen - analysis | Molecular Targeted Therapy | North America | Nitriles - administration & dosage | Breast Neoplasms - enzymology | Time Factors | Postmenopause | Female | Cyclin-Dependent Kinase 4 - antagonists & inhibitors | Republic of Korea | Aromatase Inhibitors - administration & dosage | Pyridines - administration & dosage | Drug Administration Schedule | Administration, Oral | Biomarkers, Tumor - analysis | Europe | Proportional Hazards Models | Cyclin-Dependent Kinase Inhibitor p16 - genetics | Treatment Outcome | Cyclin-Dependent Kinase 6 - metabolism | Cyclin-Dependent Kinase 4 - metabolism | Breast Neoplasms - drug therapy | Disease-Free Survival | Protein Kinase Inhibitors - administration & dosage | Breast Neoplasms - genetics | Cyclin D1 - genetics | Antineoplastic Combined Chemotherapy Protocols - therapeutic use | Breast Neoplasms - pathology | Intention to Treat Analysis | South Africa | Aged | Biomarkers, Tumor - genetics | Receptor, ErbB-2 - analysis | Antimitotic agents | Care and treatment | Oncology, Experimental | Estrogen | Breast cancer | Research | Antineoplastic agents | Phosphotransferases | Cancer
Journal Article
Nature (London), ISSN 1476-4687, 2010, Volume 464, Issue 7287, pp. 374 - 379
Cellular senescence has been recently shown to have an important role in opposing tumour initiation and promotion. Senescence induced by oncogenes or by loss... 
BOX PROTEIN SKP2 | COMPLEX | TUMOR SUPPRESSION | MULTIDISCIPLINARY SCIENCES | PTEN | RESTORATION | ACCUMULATION | ONCOGENE-INDUCED SENESCENCE | INHIBITOR | EXPRESSION | P53 | Proto-Oncogene Proteins p21(ras) - genetics | Cellular Senescence - drug effects | Male | Prostate - metabolism | Cyclin-Dependent Kinase Inhibitor p27 - metabolism | S-Phase Kinase-Associated Proteins - antagonists & inhibitors | Adenovirus E1A Proteins - metabolism | Cyclin-Dependent Kinase Inhibitor p21 - metabolism | Fibroblasts | Prostatic Neoplasms - prevention & control | Prostatic Neoplasms - drug therapy | Proto-Oncogene Proteins p21(ras) - metabolism | PTEN Phosphohydrolase - genetics | Prostatic Neoplasms - pathology | Cyclin-Dependent Kinase Inhibitor p16 - deficiency | PTEN Phosphohydrolase - deficiency | Cells, Cultured | Tumor Suppressor Protein p53 - metabolism | Cyclin-Dependent Kinase Inhibitor p16 - genetics | PTEN Phosphohydrolase - metabolism | SKP Cullin F-Box Protein Ligases - metabolism | S-Phase Kinase-Associated Proteins - metabolism | Tumor Suppressor Protein p53 - deficiency | Animals | Activating Transcription Factor 4 - metabolism | Adenovirus E1A Proteins - genetics | Prostate - cytology | Cyclin-Dependent Kinase Inhibitor p16 - metabolism | S-Phase Kinase-Associated Proteins - genetics | Mice | Cell Transformation, Neoplastic - drug effects | Prevention | Care and treatment | Physiological aspects | Aging | Tumor suppressor genes | Genetic aspects | Research | Cells | Tumors | Cell cycle | Apoptosis
Journal Article