Dynamical Systems Biology of Cancer Metastasis by Mohit Kumar Jolly

Dynamical Systems Biology of Cancer Metastasis by Mohit Kumar Jolly

International Centre for Theoretical Sciences via YouTube Direct link

Notch-Jagged signaling can form CTC clusters

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31 of 38

Notch-Jagged signaling can form CTC clusters

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Classroom Contents

Dynamical Systems Biology of Cancer Metastasis by Mohit Kumar Jolly

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  1. 1 Dynamical systems biology of cancer metastasis
  2. 2 uncontrolled growth of abnormal cells
  3. 3 Stages of cancer progression
  4. 4 Metastasis : the cause of 90 percent of all cancer deaths
  5. 5 What traits cells need to successfully metastasize?
  6. 6 Is genetics the answer? Not always
  7. 7 Can cancer proceed without mutations? Perhaps!
  8. 8 Can a 'systems' view help 'understand' cancer?
  9. 9 Example of 'systems' approach
  10. 10 We are...
  11. 11 EMT/MET: The engine of metastasis
  12. 12 Metastasis: a journey taken in groups
  13. 13 How do clusters reconcile with binary EMT?
  14. 14 Systems biology model for EMT/MET
  15. 15 Toggle switch: A systems biology model
  16. 16 Theoretical framework for miRNA-based circuits
  17. 17 Tristability in the underlying EMT network
  18. 18 Hybrid E/M can be a stable phenotype
  19. 19 Co-existence of phenotypes seen experimentally
  20. 20 Quantifying the EMT spectrum of states
  21. 21 Identifying 'phenotypic stability factors' PSFs
  22. 22 Knockdown of PSFs can drive a complete EMT
  23. 23 Spontaneous switching among phenotypes
  24. 24 Is EMT always reversible?
  25. 25 How EMT alters tumor-initiation ability stemness?
  26. 26 Hybrid E/M cells can form many more tumors
  27. 27 In vivo spontaneous EMT model highlights the aggressive behavior of hybrid E/M phenotypes
  28. 28 Hybrid E/M phenotype may form CTC clusters
  29. 29 How are CTC clusters formed?
  30. 30 Crosstalk between EMT and Notch pathways
  31. 31 Notch-Jagged signaling can form CTC clusters
  32. 32 JAG1 knockdown diminishes emboli formation
  33. 33 Why do hybrid E/M cells matter in the clinic?
  34. 34 Hybrid E/M: the 'fittest' for metastasis?
  35. 35 Conclusion
  36. 36 Ongoing questions/debate
  37. 37 Fifty or more shades of cellular plasticity
  38. 38 Acknowledgements

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