EXAM 3

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  1. What are the 4 types of cyclin CdK's?
    • G1-CdK
    • G/S-CdK
    • S-CdK
    • M-Cdk
  2. What activates a CdK?
    • Binding of:
    • Cyclin
    • Phosphorylation
  3. Which two CdK's are triggered by mitogen?
    • G1-CdK
    • G1/S-CdK
  4. What gets phosphorylated and releases E2F?
    Rb
  5. What two genes activated by myc lead to Rb phosphorylation?
    • Cyclin D gene
    • SCF gene
  6. What ubiquitin ligase degrades p53?
    Mdm2
  7. What does protein kinase ATM do?
    Phosphorylates p53 so Mdm2 can no longer bind to it and degrade it
  8. How can p53 halt the cell cycle?
    Once p53 is active it binds to p21--p21 levels increase and the inhibitor protein binds (hugs) the G1/S-CdK and the G1-CdK keeping it in an inactive state
  9. Is CAK or Wee1 the activating phosphatase when activating M-CdK?
    CAK
  10. How does CDC25 remove the inhibiting phosphate?
    CDC25 is phosphorylated via S-CdK and removes it
  11. How many checkpoints are in the cell cycle?
    3 total
  12. When does the G2 checkoint occur?
    Right before M phase
  13. How does M-CdK activate the APC?
    It phosphorylates the APC allowing CdC20 to bind to it
  14. What does APC do when it is active?
    It ubiquinates the securin--the securin degredation activates seperase
  15. What does seperase do?
    It cleaves the cohesions and allows the sister chromatids to be pulled apart
  16. What 7 genes could you knock out that would lead to cell proliferation?
    p1, p21, p27, p53, securin, ATM, Rb
  17. What is necrosis?
    Accidental cell death
  18. What are the characteristics of apoptosis?
    • Cell shrinks & membrane blebbing occurs
    • The nucleus condenses
    • DNA fragments into mono & oglionucleosomes
    • Apoptotic bodies are ingested by macrophages
  19. What signals phagocytosis of the apoptoic bodies?
    phosphatidylserine on the outer layer of the plasma membrane
  20. Name 2 examples of apoptosis in health?
    • Shedding of the endometrium during mensturation
    • Neutrophils during an acute inflammatory response
  21. Name two post- mitotic cells that undergo apoptosis due to aging?
    • cardiac myocytes
    • skeletal myocytes
  22. Is procaspase active or inactive?
    Inactive
  23. Mitochondrial medicated signaling is induced if there is mitochondrial dysfunction, what are two signals that tell the cell the mitochondria is dysfunctioning?
    • Increased ROS/RNS
    • Decreased ATP
  24. What makes up the apoptosome?
    • Cytochrome c
    • dATP
    • Apaf-1
    • Procaspase 9
  25. What triggers the release of cytochrome-c?
    • Bax
    • t-Bid
  26. What activates Procaspase 9?
    It cleaves itself causing activation
  27. What inhibits the release of cytochrome-c?
    Bcl-2
  28. What does XIAP inhibit?
    The activity of caspase 9 & caspase 3, inhibiting apotosis
  29. What does Smac/Diabloe & OmiHtrA2 do?
    Inhibits XIAP allowing Caspase 9 and 3 to continue apoptosis
  30. What does Caspase 3 do after it is active?
    Cleaves and degrades ICAD, also Caspases 6 & 7, and the cytoskeleton (causing blebbing)
  31. Name 4 things p53 can do.
    • halt the cell cycle
    • stimulate DNA repair
    • induce apoptosis
    • alters transcription of pro/anti apoptotic genes
  32. True or false, the cell expressing the Fas Ligand will undergo apoptosis.
    False-the cell expressing the Fas RECEPTOR will undergo apoptosis
  33. Fas is also known as?
    CD95
  34. Fas-L is also known as?
    CD95L
  35. What is on the cytosolic side of the Fas receptor?
    FADD (Fas associated death domain) protein
  36. What does FADD do?
    It recruits Procaspase 8 inducing self cleavage and activation
  37. What dose cFLIP do?
    Inhibits the activation of Procapase 8
  38. What is a DISC?
    • death inducing signaling complex
    • it is made up of: Fas receptor, FADD, procaspase 8
  39. What does malignant mean?
    tending to infiltrate, metastasize and terminate fatally
  40. What is it called when a tumor changes from benign to malignant?
    Transformation
  41. What does activation mean?
    conversion of a proto-oncogene to an oncogene
  42. What advantage does abnormality or a genetic defect have?
    a replicative advantage over other cells
  43. What are the 7 hallmarks of cancer?
    • 1-genetic instability,
    • 2-self-sufficiency in growth signals,
    • 3-insensitivity to growth inhibitory signals,
    • 4-evasion of apoptosis,
    • 5-limitless replicative potential,
    • 6-sustained angiogenesis,
    • 7-tissue invasion & metastasis
  44. Explain self-sufficiency in growth signals .
    There is an increase in the number of GF receptors and the mutant ones begin to transmit signals without GF
  45. What types of mutations must occur to acquire an insensitivity to growth inhibitory signals?
    mutations blocking receptors for growth inhibitory signals, also mutated p53 and Rb
  46. What allows for limitless replicative potential?
    cancer cells reactivate telomerase which allows the cells to divide indefinitely
  47. Tumor suppressor genes cause a loss of function mutation, is it dominant or recessive?
    Recessive and requires the loss of both alleles
  48. Oncogenes cause a gain of function mutation is it dominant or recessive?
    Dominant and requires the loss of only one allele
  49. What is nondisjunction?
    chromosome loss that occurs during replication when one daughter cell gets both sets of chromosomes and the other cell gets none
  50. Which receptor is responsible for ~25% of breast cancer?
    HER-2
  51. What is a deletion mutation?
    removal of one or more base pairs
  52. How does HER-2 cause breast cancer?
    overexpression of the HER-2 receptor will begin to homodimerize without any ligand binding, thus, activating itself and cause excessive cell proliferation
  53. How does Herceptin treat breast cancer?
    it is an antibody that inactivates the receptor and inhibits the signal that causes the excessive cell proliferation
  54. What causes chronic myelogenous leukemia?
    There is a translocation of Bcr/Abl gene that leads to excessive cell proliferation
  55. What is overexpressed in B-cell lymphoma?
    Bcl-2 (gain of function mutation)
  56. How does anti-sense therapy work?
    it makes a complimentary mRNA strand that will bind to the RNA molecule and both will be degraded, this process could inhibit the overexpression of all the genes that are anti-apoptotic
  57. What is angiogenesis?
    Making of new blood vessels from existing blood vessels
  58. What causes the onset of angiogenesis?
    imbalance between upregulation of pro-angiogenic factors and downregulation of anti-angiogenic factors
  59. What does VEGF do?
    potent stimulus for angiogenesis
  60. What does VEGF stand for?
    vascular endothelial growth factor
  61. What three things stimulate VEGF?
    • hypoxia (HIF binds to VEGF and induces transcription),
    • mutations (in p53 results in an overexpression of VEGF), activation (of Ras leads to overexpression)
  62. What can degrade VEGF?
    MMP’s (matrix metalloproteinase) degrade the basement membrane
  63. What do pericytes do?
    they detach from the blood vessel while angiogenesis is occurring then they reattach after the basement membrane is formed
  64. What are pericytes?
    they are cells related to vascular smooth muscle located adjacent to & surround the endothelium
  65. True or false, soluble VEGF receptors are NOT a natural part of the body?
    False, they are a natural part of the body
  66. What is invasion?
    migration of cancer cells break through the barrier that keeps them localized
  67. What must cancer cells acquire to become malignant and survive in circulation?
    the invasive phenotype
  68. Name the 7 steps of metastasis.
    • 1-tumorigenesis,
    • 2-angiogenic switch,
    • 3-acquire invasive phenotype,
    • 4-survival in circulation,
    • 5-extravasation & growth at secondary site,
    • 6-angiogenesis in secondary tumor,
    • 7-evasion of immune response
  69. What is the angiogenic switch?
    the tumor is now secreting VEGF and is stimulating angiogenesis
  70. What is tumorigenesis?
    tumor formation that has acquired many mutations and has a proliferative advantage
  71. What is this called when the tumor cells kill the immune cells?
    immune privilege
  72. What does HPV (Human papilloma virus) do?
    inactivates p53 and Rb
  73. Are the cells infected with Epstein-Barr virus (EBV) more or less resistant to apoptosis?
    Less resistant, there is an increased expression of survival proteins
  74. Tumor cells with low Fas ____ apoptosis by cytotoxic T cells.
    resist
  75. Tumor cells with FasL expression _____ apoptosis in cytotoxic T cells.
    induce

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Author:
 dr.fizzle
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 43552
Filename:
 EXAM 3
Updated:
2010-10-20 01:45:17
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EXAM #3
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