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Cell Pathology > Cancer > Flashcards

Cancer Flashcards

1
Q

How was the Viral Theory of Cancer created? What is the theory?

A

Lecture 10, slide 7

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2
Q

What is the Somatic Mutation Theory of Cancer? What is the DNA Provirus Hypothesis of cancer?

A

Lecture 10, slide 8

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3
Q

Summarise the early observations of cancer

A

Lecture 10, slide 10

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4
Q

What are the original Hallmarks of Cancer? Give an example mechanism for each hallmark.

A

Lecture 10, slide 11-12

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5
Q

What additional hallmarks were added in the Hallmarks of Cancer: Next Generation?

A

Lecture 10, slide 14

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6
Q

What general components/cells make up a tumour microenvironment?

A

Lecture 10, slide 15

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7
Q

Discuss the signals in a tumour microenvironment.

A

Lecture 10, slide 16

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8
Q

What are cancer stem cells?

A

Lecture 10, slide 18-19

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9
Q

How can you measure human cancer stem cells?

A

Lecture 10, slide 22-23

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10
Q

What general aspects of cancer stem cell biology are potentially susceptible to therapeutically intervention?

A

Lecture 10, slide 24

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11
Q

What general treatments can be used to cure cancer?

A
  • surgery
  • chemotherapy
  • radiotherapy
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12
Q

Give some examples of cytotoxic drug classes. What is their general mode of action? What partly determines their effectiveness?

A

Lecture 11, slide 4

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13
Q

What does tumour growth rate depend on? What is the overall aim of systemic cancer therapies?

A

Lecture 11, slide 5

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14
Q

What is a major challenge when designing systemic chemotherapies?

A

Lecture 11, slide 6-7

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15
Q

Give an example of a chemotherapy strategy.

A

Lecture 11, slide 8

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16
Q

What are the different types of curative chemotherapy? What are the aims of curative chemotherapy? What are the aims of palliative chemotherapy?

A

Lecture 11, slide 9

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17
Q

Briefly discuss the chemosensitivity of tumours.

A

Lecture 11, slide 10

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18
Q

Give methotrexate as an example of an antimetabolite. What is the role of 5-FU?

A

Lecture 11, slide 12

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19
Q

Give some examples of DNA damage-based therapies. What are their consequences?

A

Lecture 11, slide 13

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20
Q

Give cyclophosphamide as an example of an alkylating agent.

A

Lecture 11, slide 15

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21
Q

Give cisplatin as an example of a platinum drug.

A

Lecture 11, slide 16

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22
Q

Give doxorubicin as an example of a topoisomerase inhibitor. What is it’s cytotoxicity partly determined by?

A

Lecture 11, slide 18

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23
Q

Give vincristine as an example of an anti-mitotic agent

A

Lecture 11, slide 21

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24
Q

What are taxanes?

A

Lecture 11, slide 22

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25
Q

What are some side effects of chemotherapy? What does toxicity limit?

A

Lecture 11, slide 23

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26
Q

What is bone marrow toxicity? How is it treated?

A

Lecture 11, slide 24

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27
Q

What is alopecia? How may it be limited?

A

Lecture 11, slide 25

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28
Q

What is the extravasation of cytotoxic drugs?

A

Lecture 11, slide 26

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29
Q

How can the risk of extravasation be decreased?

A

Lecture 11, slide 27

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30
Q

What is hand-foot syndrome?

A

Lecture 11, slide 28

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31
Q

What, how and why are a combination of chemotherapies used. Give an example of combined chemotherapy.

A

Lecture 11, slide 29

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32
Q

What is therapy-induced tumourigenesis?

A

Lecture 11, slide 30

33
Q

Give tamoxifen as an example of hormonal therapy.

A

Lecture 11, slide 32

34
Q

What chromosomal translocation drives chronic myeloid leukaemia (CML)? What does this translocation cause?

A

Lecture 11, slide 33

35
Q

Give imatinib as an example of treatment for CML

A

Lecture 11, slide 34

36
Q

What is HER2 and how may it be implicated in cancer?

A

Lecture 11, slide 35

37
Q

Give trastuzumab as an example of treatment for HER2-positive tumours

A

Lecture 11, slide 36

38
Q

What are some cell cycle checkpoints?

A

Lecture 11, slide 37

39
Q

What effects do different therapies have on the cell cycle?

A

Lecture 11, slide 38

40
Q

What are some mechanisms of drug resistance?

A

Lecture 11, slide 39

41
Q

What does the future look like for cancer treatment?

A

Lecture 11, slide 41

42
Q

What is a neoplasm? What is neoplasmic growth characterised by?

A

Lecture 12, slide 3

43
Q

What molecular changes are required in cancer development?

A

Lecture 12, slide 5

-mutation

44
Q

What can increased rates of mutation or chromosomal instability be a result of? How were many of the genes found to be mutated in sporadic cancer identified?

A

Lecture 12, slide 6

45
Q

Give xeroderma pigmentosum as an example of familial cancer syndrome.

A

Lecture 12, slide 7

46
Q

Why are so many mutations required in the development of a tumour?

A

Lecture 12, slide 8

47
Q

What are the two types of mutation that contribute to cancer development?

A

Lecture 12, slide 11

48
Q

What techniques have been used to identify oncogenes?

A

Lecture 12, slide 12-15

49
Q

Discuss how dominant mutations can sustain proliferative signalling?

A

Lecture 12, slide 16-18

MAPK/ERK pathway

50
Q

What is BRAF V600E? How can it be therapeutically targeted?

A

Lecture 12, slide 20-23

51
Q

What are some applications of next-generation sequencing? Give an example that is related to cancer genomes.

A

Lecture 12, slide 24-29

52
Q

Give some examples of personalised medicine based on tumour genotype.

A

Lecture 12, slide 30

53
Q

What is the role of telomerase?

A

Lecture 12, slide 33

54
Q

What does telomerase activation do?

A

Lecture 12, slide 33-35

55
Q

What has provided evidence for cancer as a recessive trait? What is the 2 hit hypothesis? What strategies have be used to identify tumour suppressor genes?

A

Lecture 13, slide 3-5

56
Q

Give some examples of loss-of-function mutations in human cancer.

A

Lecture 13, slide 6

57
Q

Discuss the role of RB.

A

Lecture 13, slide 8-9

58
Q

How may the R point be deregulation in cancer? What does this lead to?

A

Lecture 13, slide 10

  • sustaining proliferative signalling
  • evading growth suprressors
59
Q

Discuss how recessive mutations may induce angiogenesis.

A

Lecture 13, slide 11-12

60
Q

What is the role of p53?

A

Lecture 13, slide 13-17

61
Q

Give an example of a condition defined by germline p53 mutations.

A

Lecture 13, slide 18

62
Q

How is the activation of p53 regulated?

A

Lecture 13, slide 19-20

63
Q

Discuss defective p53 regulation in cancer.

A

Lecture 13, slide 21

64
Q

What are the most common types of p53 mutations?

A

Lecture 13, slide 23-24

65
Q

Discuss whether p53 mutations are loss or gain of function.

A

Lecture 13, slide 25-26

66
Q

What are the consequences of loss of p53 function?

A

Lecture 13, slide 27

  • failure of telomere-induced, which leads to chromosome instability
  • avoiding apoptosis in response to DNA damage or oncogene activation
  • evading tumour suppressors
  • sustaining proliferative capacity
67
Q

What are the differences between benign and malignant tumours?

A

Lecture 14, slide 2

68
Q

What are the multiple steps to metastatic disease? Discuss how microenvironment changes contribute to metastatic disease.

A

Lecture 14, slide 6

69
Q

What are some of the prerequistes of metastatic disease? What is the difference between cells in an epithelial state and cells in a mesenchymal state?

A

Lecture 14, slide 7

70
Q

What is epithelial-to-mesenchymal transitions?

A

Lecture 14, slide 8-10

71
Q

How is life in cirulation for cancer cells?

A

Lecture 14, slide 11

72
Q

Give examples of distant accomplacines in metastatic disease.

A

Lecture 14, slide 12

-exosomes

73
Q

What are exosomes? How are they involved in metastasis?

A

Lecture 14, slide 13-15

74
Q

What is involved in the homing of metastases?

A

Lecture 14, slide 16-17

75
Q

Describe the process of cancer cell extravasation.

A

Lecture 14, slide 18

76
Q

Discuss micrometastasis? How may this affect cancer treatment and why is the establishment of secondary metastases more efficient?

A

Lecture 14, slide 19-22

77
Q

What is the angiogenic switch?

A

Lecture 14, slide 23

78
Q

Discuss BRAC1 and its role in metastasis.

A

Lecture 14, slide 24-28

79
Q

What are some therapeutic approaches to prevention of metastasis?

A

Lecture 14, slide 29

Cell Pathology (10 decks)

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