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

What are cyclin dependant kinases (CDK)?

Catalytic subunits

26

What are the catalytic subunits?

Cyclin-dependent kinases (CDK)

27

What are cyclines?

Regulatory subunits

28

What are the active enzyme component of checkpoints called?

CDK/cyclin complex

29

What is the process of cyclines and cyclin dependant kinases?

1) Different CDKs and cyclines operate at sequential stages of the cycle

2) Active CDK/cyclin complex phosphorylates target proteins

3) Phosphorylation results in activation/inactivation

4) Substrates regulate events in the next cycle phase

30

How are CDKs regulated?

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

CDKs inhibitors (CKIs)

31

What are the 2 families of CKIs?

INK4A family

CIP/KIP family

32

What do molecules of the INK4A family do?

Bind to CDK4 and 6 and prevent association of these with their cyclin regulatory proteins

33

What are the members of the INK4A family?

P16INK4A

P15INK4B

P18INK4C

P19INK4D

34

What is a member of the CIP/KIP family?

P21CIP1

35

What do CDK inhibitors do?

Bind to the cyclin/CDK complexes

36

What does the Retinoblastoma gene do?

Encodes a 110kDa phophoprotein (pRb) which is hypophosphorylated

37

What does hypophosphorylated mean?

Phosphorylated to a less than normal extent

38

What does phosphorylation do?

Increases a cells progress through the cycle

39

What is pRb phosphorylated by?

Active cyclin D/CDK complex

40

What does pRb target?

E2F transcription factor

41

What does a hypphosphorylated/active Rb do?

Inactivates E2F

42

What does a phosphorylated/inactive Rb do?

Loses affinity for E2F

43

When is Rb active?

When it is hypophosphorylated

44

When is Rb inactive?

When it is phosphorylated

45

What does E2F do?

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

46

What does pRb binding to E2F do to the cell cycle?

Stops it

47

What is carcinogenesis?

The initiation of cancer formation

48

What is carcinogenesis caused by?

Mutation of genetic material that upsets the normal balance between proliferation and apoptosis

49

What does uncontrolled proliferation lead to?

Tumours

50

Loss of the ability to control proliferation is due to mutations in genes regulating?

Cell division

Apoptosis

DNA

51

What is carcinogenesis caused by specifically?

Envrionmental agents

Inherited

52

What environmental agents can cause carcinogenesis?

Chemicals

Radiation

Oncogene viruses

53

What is the process of chemical carcinogenesis?

1) Purine and pyrimidine bases in DNA are critically damaged by oxidising and alkylating agents

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

54

What are critical targets for radiation damage?

Purines and pyrimidine bases in DNA

55

What is the primary defect in cancer?

Uncontrolled proliferation due to cell cycle dysregulation

56

What are 2 regulatory pathways that frequently cause cancer?

Cyclin D-pRb-E2F pathway

P53 pathway

57

What genes are the cause of dysregulation at G1 to S causing most cancers?

Rb

CDK4

Cyclin D

P16

58

What is the function of P53?

Maintain genetic integrity

59

How do P53 levels change in damaged cells?

They increase

60

What does the increase of P53 in damaged cells do?

Induces a cycle arrest at G1

Facilitates DNA repair

Severe damage of P53 leads to P53-induced apoptosis

61

What happens if there is no P53 present?

No cell arrest

Genetically damaged cells proliferate and form malignant tumours