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Cancer Flashcards

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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
What are some side effects of chemotherapy? What does toxicity limit?
Lecture 11, slide 23
26
What is bone marrow toxicity? How is it treated?
Lecture 11, slide 24
27
What is alopecia? How may it be limited?
Lecture 11, slide 25
28
What is the extravasation of cytotoxic drugs?
Lecture 11, slide 26
29
How can the risk of extravasation be decreased?
Lecture 11, slide 27
30
What is hand-foot syndrome?
Lecture 11, slide 28
31
What, how and why are a combination of chemotherapies used. Give an example of combined chemotherapy.
Lecture 11, slide 29
32
What is therapy-induced tumourigenesis?
Lecture 11, slide 30
33
Give tamoxifen as an example of hormonal therapy.
Lecture 11, slide 32
34
What chromosomal translocation drives chronic myeloid leukaemia (CML)? What does this translocation cause?
Lecture 11, slide 33
35
Give imatinib as an example of treatment for CML
Lecture 11, slide 34
36
What is HER2 and how may it be implicated in cancer?
Lecture 11, slide 35
37
Give trastuzumab as an example of treatment for HER2-positive tumours
Lecture 11, slide 36
38
What are some cell cycle checkpoints?
Lecture 11, slide 37
39
What effects do different therapies have on the cell cycle?
Lecture 11, slide 38
40
What are some mechanisms of drug resistance?
Lecture 11, slide 39
41
What does the future look like for cancer treatment?
Lecture 11, slide 41
42
What is a neoplasm? What is neoplasmic growth characterised by?
Lecture 12, slide 3
43
What molecular changes are required in cancer development?
Lecture 12, slide 5 | -mutation
44
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?
Lecture 12, slide 6
45
Give xeroderma pigmentosum as an example of familial cancer syndrome.
Lecture 12, slide 7
46
Why are so many mutations required in the development of a tumour?
Lecture 12, slide 8
47
What are the two types of mutation that contribute to cancer development?
Lecture 12, slide 11
48
What techniques have been used to identify oncogenes?
Lecture 12, slide 12-15
49
Discuss how dominant mutations can sustain proliferative signalling?
Lecture 12, slide 16-18 | MAPK/ERK pathway
50
What is BRAF V600E? How can it be therapeutically targeted?
Lecture 12, slide 20-23
51
What are some applications of next-generation sequencing? Give an example that is related to cancer genomes.
Lecture 12, slide 24-29
52
Give some examples of personalised medicine based on tumour genotype.
Lecture 12, slide 30
53
What is the role of telomerase?
Lecture 12, slide 33
54
What does telomerase activation do?
Lecture 12, slide 33-35
55
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?
Lecture 13, slide 3-5
56
Give some examples of loss-of-function mutations in human cancer.
Lecture 13, slide 6
57
Discuss the role of RB.
Lecture 13, slide 8-9
58
How may the R point be deregulation in cancer? What does this lead to?
Lecture 13, slide 10 - sustaining proliferative signalling - evading growth suprressors
59
Discuss how recessive mutations may induce angiogenesis.
Lecture 13, slide 11-12
60
What is the role of p53?
Lecture 13, slide 13-17
61
Give an example of a condition defined by germline p53 mutations.
Lecture 13, slide 18
62
How is the activation of p53 regulated?
Lecture 13, slide 19-20
63
Discuss defective p53 regulation in cancer.
Lecture 13, slide 21
64
What are the most common types of p53 mutations?
Lecture 13, slide 23-24
65
Discuss whether p53 mutations are loss or gain of function.
Lecture 13, slide 25-26
66
What are the consequences of loss of p53 function?
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
What are the differences between benign and malignant tumours?
Lecture 14, slide 2
68
What are the multiple steps to metastatic disease? Discuss how microenvironment changes contribute to metastatic disease.
Lecture 14, slide 6
69
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?
Lecture 14, slide 7
70
What is epithelial-to-mesenchymal transitions?
Lecture 14, slide 8-10
71
How is life in cirulation for cancer cells?
Lecture 14, slide 11
72
Give examples of distant accomplacines in metastatic disease.
Lecture 14, slide 12 | -exosomes
73
What are exosomes? How are they involved in metastasis?
Lecture 14, slide 13-15
74
What is involved in the homing of metastases?
Lecture 14, slide 16-17
75
Describe the process of cancer cell extravasation.
Lecture 14, slide 18
76
Discuss micrometastasis? How may this affect cancer treatment and why is the establishment of secondary metastases more efficient?
Lecture 14, slide 19-22
77
What is the angiogenic switch?
Lecture 14, slide 23
78
Discuss BRAC1 and its role in metastasis.
Lecture 14, slide 24-28
79
What are some therapeutic approaches to prevention of metastasis?
Lecture 14, slide 29

Cell Pathology (10 decks)

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