Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

302 Scientific basis of medicine > Cancer 2) Hallmarks of cancer > Flashcards

Cancer 2) Hallmarks of cancer Flashcards

1
Q

Why is it important to study cancer?

A

1 in 3 people will develop cancer
1 in 4 men and 1 in 5 women will die of cancer
Incidence of cancer increases with age

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What has studying cancer revealed?

A

Growth of normal cells
Pathways of controlling normal growth
Mechanisms of cell death
Mechanisms of tissue regeneration

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What is the evidence that cancer is genetic?

A

Age evidence
Carcinogens are mutagens
DNA of tumours contains many and varied aberrations
Mutations in specific genes generate cells bearing hallmarks of cancer

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What are the features of malignancy?

A

Uncontrolled growth
Capacity to infiltrate normal or damaged tissues
Capacity to spread to other sites
Capacity to cause illness and/or death

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What are the cellular hallmarks of cancer?

A 
Autonomy from growth signals
Evasion of growth inhibitory signals
Evasion of apoptosis
Unlimited replicative potential
Angiogenesis
Invasion and metastases
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What cancer do viral HPV 16 and 18 cause?

A

Cervical cancer

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What is the role of E6 and E7 proteins in cervical cancer?

A

Both required for carcinogenesis
E6 binds p53 and targets it for degradation
E7 binds, phosphorylates and inactivates Rb protein

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What cancer does HTLV-1 cause?

A

Adult T-cell lymphoma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What virus causes Burkitt’s lymphoma?

A

EBV

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What do UV radiation and chemical carcinogens do?

A

Interact with components of DNA to cause damage
Damage can be to bases or sugar-phosphate backbone
Damage can be repaired, misrepaired or unrepaired

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What are oncogenes?

A

Mutated version of normal human proto-oncogenes

Dominant, not normally inherited

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

How can oncogenes affect gene function?

A

Increase level of expression of the gene
De-regulate expression of the gene
Alter protein product so it’s more active
Alter protein product so it’s not degraded

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What do oncogenes do to malignant pathways?

A

Increase activity of pro-malignant pathways - cell growth, replication, angiogenesis, invasion, metasases
Inhibit activity of anti-malignant pathways - apoptosis, cell cycle regulation, growth inhibition

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Give examples of oncogenes

A

erbB1
erbB2
ras

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What does erbB1 encode and what do mutations do?

A

Encodes EGFR
Oncogenic mutation means EGFR is activated in absence of EGF
Causes overactivity of RAS-MAPK pathway and over expression of growth promoting genes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What does mutated ras cause?

A

Loss of GTP-ase activity of RAS protein

RAS remains bound to GTP and is constitutively activated

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What are tumour suppressor genes?

A

Suppress pro-malignant processes: apoptosis, cell cycle checkpoints, growth inhibition, DNA repair

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Give examples of tumour suppressor genes

A

p53
BRCA1 and BRCA2
APC

19
Q

What is the consequence of mutated p53?

A

Cells proceed to mitosis with damaged DNA
Cells fail to undergo apoptosis when damaged
Incomplete DNA repair
Tumour angiogenesis persists causing tumour growth

20
Q

What is Li-Fraumeni syndrome?

A

Inherited p53 mutation
Grossly elevated cancer risk
Causes sarcoma, breast cancer, leukaemia and brain tumours at early age

21
Q

Describe APC mutations

A

Inherited mutations responsible for familial adenomatous polyposis coli
1 mutation inherited, other is spontaneous mutation in colonic epithelium

22
Q

What is FAP?

A

Develop multiple colonic polyps in early adulthood which predispose to cancer
Very high risk of colon cancer

23
Q

Describe the chain of events leading to colorectal cancer

A 
Normal colonic epithelium
APC mutation causes small adenoma
K-ras DCC mutation causes large adenoma
p53 mutation causes carcinoma
Aneuploidy causes metastases
24
Q

What do normal growth inhibitory signals do?

A

Downregulate growth receptors
Inhibit transcription
Inactivate or degrade signalling proteins
Phosphatases inhibit kinase signalling cascades
Compete with growth mediating proteins

25
Q

What is the mechanism of apoptosis?

A

Cytoplasmic shrinkage
Nuclear breakdown
Cleavage of structural proteins
Membrane blebbing, apoptotic bodies

26
Q

How can apoptosis be activated?

A

Extrinsically e.g. in response to TNF or intrinsically in response to oxidative stress or DNA damage

27
Q

Give an example of an anti-apoptotic protein

A

Bcl-2

28
Q

Give examples of pro-apoptotic proteins

A

Bax

p53

29
Q

What is the consequence of p53 mutation on apoptosis?

A

Renders cells less likely to undergo apoptosis
Mutant cells are more likely to develop further mutations
Mutant cells are more resistant to cancer treatment

30
Q

How does cancer cause unlimited replicative potential?

A

Telomerase is unregulated which maintains length of telomeres and stops them shortening so they don’t undergo cellular senescence or apoptosis

31
Q

What is a stimulant of angiogenesis?

A

Vascular endothelial growth factor (VEGF)

Hypoxia

32
Q

How do tumour cells break free from inter and extracellular connections?

A

Via abnormal expressions of integrins

Invasive capacity mediated by matrix metalloproteases and inhibited by TIMPs

33
Q

What are the emerging hallmarks of cancer?

A

Deregulating cellular energetics
Avoiding immune destruction
Genome instability and mutation
Tumour-promoting inflammation

34
Q

What drugs are given to prevent proliferative signalling?

A

EGFR inhibitors

35
Q

What drugs are given to stop evasion of growth suppressors?

A

Cyclin-dependent kinase inhibitors

36
Q

What drugs are given to stop cancer avoiding immune destruction?

A

Immune-activating CTLA4 mAb

37
Q

What drugs are given to stop cancer enabling replicative immortality?

A

Telomerase inhibitors

38
Q

What drugs are given to stop tumour promoting inflammation?

A

selective anti-inflammatory drugs

39
Q

What drugs are given to stop cancer activating invasion and metastases??

A

Imhibitors HGF/c-MET

40
Q

What drugs are given to stop cancer inducing angiogenesis?

A

Inhibitors VEGF signalling

41
Q

What drugs are given to stop genome instability and mutation?

A

PARP inhibitors

42
Q

What drugs are given to stop cancer resisting cell death?

A

Propapoptotic BH3 mimetics

43
Q

What drugs are given to stop cancer deregulating cellular energetics?

A

Aerobic glycolysis inhibitors

302 Scientific basis of medicine (28 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions