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0. Foundations of Medicine > Tumour Pathology 4 > Flashcards

Tumour Pathology 4 Flashcards

1
Q

<p>What is mitosis?</p>

A

<p>Mechanism of cellular replication</p>

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2
Q

<p>What does mitotic division generate?</p>

A

<p>Two genetically identical daughter cells</p>

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3
Q

<p>What is a cell cycle?</p>

A

<p>Time interval between miotic division</p>

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4
Q

<p>What is the cell cycle made up of?</p>

A

<p>G0</p>

<p>G1</p>

<p>S</p>

<p>G2</p>

<p>M</p>

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5
Q

<p>What happens during G0?</p>

A

<p>Left cell cycle and stopped dividing</p>

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6
Q

<p>What happens during G1?</p>

A

<p>Synthesis of components needed for DNA synthesis</p>

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7
Q

<p>What happens during S?</p>

A

<p>DNA synthesis</p>

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8
Q

<p>What happens during G2?</p>

A

<p>Preparation for mitosis</p>

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9
Q

<p>What happens during M?</p>

A

<p>Mitosis and cell division</p>

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10
Q

<p>How much cell divisions occur per second in humans?</p>

A

<p>25 x 106</p>

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11
Q

<p>How many cells are in the body?</p>

A

<p>1013</p>

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12
Q

<p>What does quality control insure?</p>

A

<p>Genetic fidelity:</p>

<p></p>

<p>Each cell must recieve a full chromosome compliment</p>

<p>Mutations in DNA sequences must not pass on</p>

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13
Q

<p>What factors is the cell cycle control by?</p>

A

<p>External factors</p>

<p>Intrinsic factors</p>

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14
Q

<p>What external factors control the cell cycle?</p>

A

<p>Hormones</p>

<p>Growth factors</p>

<p>Cytokines</p>

<p>Stroma</p>

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15
Q

<p>What intrinsic factor controls the cell cycle?</p>

A

<p>Critical checkpoints (restriction point R)</p>

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16
Q

<p>What does progress before and after restriction point R depend on?</p>

A

<p>Prior depends on external factors</p>

<p>After becomes autonomous</p>

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17
Q

<p>Where is R?</p>

A

<p>At the end of G1</p>

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18
Q

<p>What does G1 control mechanism ensure?</p>

A

<p>Everything is ready for DNA synthesis</p>

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19
Q

<p>What does G2 control mechanism ensure?</p>

A

<p>Everything is ready for cell division</p>

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20
Q

<p>What do checkpoints in G1 check?</p>

A

<p>Cell size is inadequete</p>

<p>Nutrition supply inadequete</p>

<p>Essential external stimulus lacking</p>

<p>DNA damage detected</p>

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21
Q

<p>What do checkpoints in S check?</p>

A

<p>DNA is not replicated</p>

<p>Chromosome mis-alignment</p>

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22
Q

<p>What do checkpoints in G2 do?</p>

A

<p>Cell size is inadequete</p>

<p>DNA damage is detected</p>

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23
Q

<p>What are checkpoints?</p>

A

<p>Systems of cyclically active and inactive enzymes</p>

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24
Q

<p>What is a catalytic subunit activated by?</p>

A

<p>Regulatory subunit</p>

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25
Q

<p>What are cyclin dependant kinases (CDK)?</p>

A

<p>Catalytic subunits</p>

26
Q

<p>What are the catalytic subunits?</p>

A

<p>Cyclin-dependent kinases (CDK)</p>

27
Q

<p>What are cyclines?</p>

A

<p>Regulatory subunits</p>

28
Q

<p>What are the active enzyme component of checkpoints called?</p>

A

<p>CDK/cyclin complex</p>

29
Q

<p>What is the process of cyclines and cyclin dependant kinases?</p>

A

<p>1) Different CDKs and cyclines operate at sequential stages of the cycle</p>

<p>2) Active CDK/cyclin complex phosphorylates target proteins</p>

<p>3) Phosphorylation results in activation/inactivation</p>

<p>4) Substrates regulate events in the next cycle phase</p>

30
Q

<p>How are CDKs regulated?</p>

A

<p>CDKs are constitutively expressed in an inactive form, whereas cyclines accumulate and are destroyed as cycle progresses</p>

<p>CDKs inhibitors (CKIs)</p>

31
Q

<p>What are the 2 families of CKIs?</p>

A

<p>INK4A family</p>

<p>CIP/KIP family</p>

32
Q

<p>What do molecules of the INK4A family do?</p>

A

<p>Bind to CDK4 and 6 and prevent association of these with their cyclin regulatory proteins</p>

33
Q

<p>What are the members of the INK4A family?</p>

A

<p>P16INK4A</p>

<p>P15INK4B</p>

<p>P18INK4C</p>

<p>P19INK4D</p>

34
Q

<p>What is a member of the CIP/KIP family?</p>

A

<p>P21CIP1</p>

35
Q

<p>What do CDK inhibitors do?</p>

A

<p>Bind to the cyclin/CDK complexes</p>

36
Q

<p>What does the Retinoblastoma gene do?</p>

A

<p>Encodes a 110kDa phophoprotein (pRb) which is hypophosphorylated</p>

37
Q

<p>What does hypophosphorylated mean?</p>

A

<p>Phosphorylated to a less than normal extent</p>

38
Q

<p>What does phosphorylation do?</p>

A

<p>Increases a cells progress through the cycle</p>

39
Q

<p>What is pRb phosphorylated by?</p>

A

<p>Active cyclin D/CDK complex</p>

40
Q

<p>What does pRb target?</p>

A

<p>E2F transcription factor</p>

41
Q

<p>What does a hypphosphorylated/active Rb do?</p>

A

<p>Inactivates E2F</p>

42
Q

<p>What does a phosphorylated/inactive Rb do?</p>

A

<p>Loses affinity for E2F</p>

43
Q

<p>When is Rb active?</p>

A

<p>When it is hypophosphorylated</p>

44
Q

<p>When is Rb inactive?</p>

A

<p>When it is phosphorylated</p>

45
Q

<p>What does E2F do?</p>

A

<p>It is a potent stimulator of cell cycle entry. free E2F transcription factor activates vital target genes</p>

46
Q

<p>What does pRb binding to E2F do to the cell cycle?</p>

A

<p>Stops it</p>

47
Q

<p>What is carcinogenesis?</p>

A

<p>The initiation of cancer formation</p>

48
Q

<p>What is carcinogenesis caused by?</p>

A

<p>Mutation of genetic material that upsets the normal balance between proliferation and apoptosis</p>

49
Q

<p>What does uncontrolled proliferation lead to?</p>

A

<p>Tumours</p>

50
Q

<p>Loss of the ability to control proliferation is due to mutations in genes regulating?</p>

A

<p>Cell division</p>

<p>Apoptosis</p>

<p>DNA</p>

51
Q

<p>What is carcinogenesis caused by specifically?</p>

A

<p>Envrionmental agents</p>

<p>Inherited</p>

52
Q

<p>What environmental agents can cause carcinogenesis?</p>

A

<p>Chemicals</p>

<p>Radiation</p>

<p>Oncogene viruses</p>

53
Q

<p>What is the process of chemical carcinogenesis?</p>

A

<p>1) Purine and pyrimidine bases in DNA are critically damaged by oxidising and alkylating agents</p>

<p>2) Chemical carcinogens or their active metabolites react with DNA forming covalent bound productes (DNA adducts)<br></br>3) Adduct formation at particular chromosome sites cause cancer</p>

54
Q

<p>What are critical targets for radiation damage?</p>

A

<p>Purines and pyrimidine bases in DNA</p>

55
Q

<p>What is the primary defect in cancer?</p>

A

<p>Uncontrolled proliferation due to cell cycle dysregulation</p>

56
Q

<p>What are 2 regulatory pathways that frequently cause cancer?</p>

A

<p>Cyclin D-pRb-E2F pathway</p>

<p>P53 pathway</p>

57
Q

<p>What genes are the cause of dysregulation at G1 to S causing most cancers?</p>

A

<p>Rb</p>

<p>CDK4</p>

<p>Cyclin D</p>

<p>P16</p>

58
Q

<p>What is the function of P53?</p>

A

<p>Maintain genetic integrity</p>

59
Q

<p>How do P53 levels change in damaged cells?</p>

A

<p>They increase</p>

60
Q

<p>What does the increase of P53 in damaged cells do?</p>

A

<p>Induces a cycle arrest at G1</p>

<p>Facilitates DNA repair</p>

<p>Severe damage of P53 leads to P53-induced apoptosis</p>

61
Q

<p>What happens if there is no P53 present?</p>

A

<p>No cell arrest</p>

<p>Genetically damaged cells proliferate and form malignant tumours</p>

0. Foundations of Medicine (167 decks)

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