Genetic and pharmacological inhibition of TTK impairs pancreatic cancer cell line growth by inducing lethal chromosomal instability

Keyphrases

• Pancreatic Ductal Adenocarcinoma 100%
• Chromosomal Instability 100%
• Pharmacological Inhibitors 100%
• Pancreatic Cancer Cell Lines 100%
• Ubiquitin-specific Peptidase 75%
• Primary Tumor 50%
• Pancreatic Cancer 50%
• Spindle Assembly Checkpoint 50%
• Catalytic Inhibition 50%
• Phosphorylation 25%
• Overexpression 25%
• Cell Cycle Arrest 25%
• Cell Proliferation 25%
• Protein Kinase 25%
• Cell Death 25%
• Normal Pancreas 25%
• Gene Expression Profile 25%
• UCHL1 25%
• Small Interfering RNA (siRNA) 25%
• Apoptosis Induction 25%
• Therapeutic Potential 25%
• Primary Cells 25%
• Molecular Characteristics 25%
• Proteasomal Degradation 25%
• Potential Therapeutic Strategies 25%
• Condensation 25%
• Potential Identification 25%
• Genomic Profiling 25%
• Lethal Infection 25%
• Heterogeneous Landscape 25%
• Phosphomimetic 25%
• Multinucleation 25%
• G2-M Transition 25%
• Replication Error 25%
• MPS1 25%
• Co-overexpression 25%
• Cell Cycle Profile 25%
• Transforming Growth 25%
• Deubiquitination 25%
• H2AX Phosphorylation 25%
• Complex Landscapes 25%
• Selective Catalysts 25%
• Aberrant Cells 25%
• Polo-like Kinase 1 25%
• Nucleation Induction Time 25%

Biochemistry, Genetics and Molecular Biology

• Genetics 100%
• Cancer Cell 100%
• Chromosome Instability 100%
• Ubiquitin 100%
• Peptidase 100%
• Spindle Checkpoint 66%
• Gene Expression 33%
• Cell Cycle Arrest 33%
• Protein Kinases 33%
• Cell Death 33%
• Cell Proliferation 33%
• Cell Cycle 33%
• Phosphomimetics 33%
• Cell Cycle Checkpoint 33%
• Histone H2A 33%
• Chromosome Condensation 33%
• Genomics 33%
• Polo-Like Kinase 1 33%
• Programmed Cell Death 33%
• Deubiquitylating Enzyme 33%
• Small Interfering RNA 33%
• phosphorylation 33%