4.26.2010 2
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  • 1. 4.26.2010 – Cancer<br />
    • Mutations
    • 2. Most mutations occur after birth
    • 3. Environmental mutations
    • 4. P53 – prevents DNA damage or drives apoposis
    • 5. No safeguards now to recognize damage and shut cell proliferation down
    • 6. Benzoapyrene from smoking
    • 7. Deamination
    • 8. Replace for thymine –
    • 9. Andogenous process – liver metabolism
    • 10. About 50% of cancers are from a mutation in the p53 gene
    • 11. P53
    • 12. Tumor suppressor gene (not a protooncogene)
    • 13. Helps suppress cell proliferation that is abnormal
    • 14. Retinoblastoma – RB
    • 15. Holds on to and inhibits transcription factors that drive production of cyclins that move past G1 until phosphorylated by Ras pathway for gene transcription regulation
    • 16. Restricts mitosis and regulates cell growth in unaltered state
    • 17. Proto-oncogenes
    • 18. APC
    • 19. Ras (ras pathway)
    • 20. In an overexpressed state, will drive
    • 21. Src – SH2 domains
    • 22. Kinase, has SH2 domain, activated in response to RTK
    • 23. If there is is single allel in a protooncogene that is mutated, it will cause that cell to divide uncontrollably and unregulated
    • 24. If there is a normal copy on the other allele, a normal cell will divide correctly. However, if both alleles are mutated, that single cell may divide uncontrollably.
    • 25. Pathways
    • 26. Ras
    • 27. GFs activated RTK
    • 28. Recruit SH2 to activate Ras
    • 29. Ras activates gene transcription pathways
    • 30. Myc, when Pi, will lead to enhanced gene expression and enhance cell mitosis
    • 31. Protonocogene – leads to favored gene expression and poliferation
    • 32. P16, like p21, inhibits cyclin that binds to cyclin and keeps it from Pi Rb
    • 33. P16 is a tumor suppressor, restricts cell mitosis
    • 34. Anti growth factors
    • 35. TNS – tumor necrosis factor
    • 36. Growth factor that regulates growth – restricting it
    • 37. Activates a pathway that turns on inhibitors of cyclins
    • 38. Binds to RTK
    • 39. Attacks
    • 40. Secreted by activated immune cells
    • 41. P53
    • 42. Upregulates p21 function
    • 43. Drives inhibits cyclin dependent kinases and cells stop dividing – senescence – G0
    • 44. PUMA
    • 45. Activated by p53 that leads to cells death
    • 46. Inhibits Bcl2
    • 47. Makes mitochondrial membrane more unstable
    • 48. Cytocochrome c is released
    • 49. Apotosome and caspase 9
    • 50. Apoptosis
    • 51. Checkpoints within mitosis
    • 52. What is regulating G2 and metaphase checkpoints and drive to S phase and see what is required and see if they act as tumor suppressors or proto oncogenes
    • 53. Examples of Oncogenes
    • 54. GFs
    • 55. Overexpression can cause cancers
    • 56. PDGF – platelet derived growth factor
    • 57. Sarcomas
    • 58. Fibrosarcomas
    • 59. There are two genes (oncogenes) that express amounts of PDGF
    • 60. V-sis
    • 61. TRK receptor
    • 62. Binds to JrK – Nerve Growth factor, neurotrophins, brain derived nuerotrophic factor (BDNF)
    • 63. Thyroid
    • 64. Breast
    • 65. Ras – inability to hydrolzyze GTP to GDp – making it on all the time
    • 66. Single point mutations
    • 67. Raf
    • 68. Src kinase – v-src – sarcomas
    • 69. Myc – regulated by ras – translocation, aplification, inserional mutagensis – 3 types of cancer
    • 70. Cyclins – Bcl2 –
    • 71. Types of Cancer
    • 72. Carcinomas – Epithelium
    • 73. Throat lining, skin, intestines
    • 74. Sarcomas
    • 75. Muscles or Connective Tissue
    • 76. Leukias/Lymphomas
    • 77. Hematopoietic System
    • 78. Nervous System
    • 79. Neuromas
    • 80. Gliomas
    • 81. Astrocytomas
    • 82. What types of Mutations are taking place?
    • 83. Gene amplification
    • 84. Some muation has caused gene to be respresnted in multiple ways, causing an overexpression of that gene product
    • 85. Chromsomes rearrangement
    • 86. Overexpression of proteins that enhance production of that particular gene of interest
    • 87. Fusio nevent – gene made is on all the time
    • 88. Her2 receptor
    • 89. Single mutation in transmembrane region
    • 90. Thinks bound to GF
    • 91. Deletion – receptor is always on signaling for cell to divide
    • 92. TRK receptor
    • 93. RTK, bound by GFs, autphosphorylation
    • 94. Mutations: gene rearragnement replaces EXdomain of receptor ith a muscle tropomysoin protein involved in smooth muscle contraction, losing resulatory EXC domain and TRPM is sticking out.
    • 95. Links with trasmembrane