Brainscape's Knowledge GenomeTM

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


See full index

Biology of Cancer > 10) Chemotherapy > Flashcards

10) Chemotherapy Flashcards

You may prefer our related Brainscape-certified flashcards:
AP® Biology flashcards Biology 101 flashcards
1
Q

What are the different levels of tumour spread?

A

Local - surrounding structures
Lymphatic - carcinoma
Blood - sarcoma
Implantation - mechanical spread of tumour cells e.g. in chest drain

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

What are some options for chemotherapy use in patients?

A

Primary treatment (radical)
Adjuvant
Neoadjuvant
Palliative

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

When is chemotherapy used as radical treatment?

A

Lymphomas and leukaemia

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

What is adjuvant therapy?

A

Post-op treatment in a patient at high risk of microscopic metastases

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

What is neoadjuvant therapy?

A

Primary treatment of patients with a clinically localised tumour, reduce size for easier removal

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What is the fractional cell kill hypothesis?

A

Chemotherapy given in fractionated doses to minimise damage to normal cells as they have time to recover

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

Give examples of cytotoxic agent classes:

A

Antimetabolites
Alkylating agents
Intercalating agents
Spindle poisons

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

What is the mechanism of action of platinum compounds?

A

Platinated intra and interstrand adducts leading to inhibition of DNA synthesis

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

What is the mechanism of action of topoisomerase inhibitors?

A

Inhibit the toposiomerase enzyme that unravels supercoiled DNA. Induces strand breaks leading to apoptosis

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

What is the mechanism of action of anti-metabolites?

A

Interfere with purine and pyramidine synthesis

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

Describe the treatment, Xeloda (campecitabine):

A

Treatment that is only activated in the tumour to produce 5-FU

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

What is the mechanism of action of spindle poisons?

A

Inhibit polymerisation of spindle microtubules

Stimulate polymerisation and prevent depolymerisation of spindle microtubules

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

What is the aim of combination therapy?

A

To provide increased efficacy using drugs with different modes of action that require different mechanisms to become resistant

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

How is P-glycoprotein involved in resistance to chemotherapy?

A

Efflux of cytotoxic agents out of cells

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

What are some mechanisms of resistance to chemotherapy?

A

Enhanced repair of DNA lesions
Efflux of drug
Inactivation of agent in cell
Modified target

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

What are some examples of DNA repair pathways?

A

Base excision repair
Recombinational repair
Nucleotide excision repair
Mismatch repair

17
Q

How can mismatch repair status be used in bowel cancer treatment?

A

Those with mismatch repair deficient bowel tumour don’t respond to adjuvant chemotherapy

18
Q

How can PARP1 inhibitors be used in BRCA mutated patients?

A

Inhibiting PARP1 which repairs SSBs will increase double strand DNA damage (not repaired due to BRCA mutation) causing cancer cell death

19
Q

Describe the use of hormone therapy in breast cancer:

A

Anti-oestrogen - tamoxifen
Aromatase inhibitors
LHRH agonists

20
Q

Describe the use of hormone therapy in prostate cancer:

A

LHRH agonists
Anti-androgens
Oestrogens

21
Q

What is the rationale behind biologically targeted therapy?

A

Exploiting differences between normal cells and tumour cells to specifically target them

22
Q

What is the mechanism of action of imatinib?

A

Bcr-abl tyrosine kinase inhibitor - inhibits fusion protein

23
Q

What is the mechanism of action of Herceptin?

A

Monoclonal antibody against HER2 that inhibits proliferation of cancer cells and flags them for destruction

24
Q

What is the mechanism of action of cetuximab? When will it fail as a treatment?

A

Blocks EGFR dimerisation, preventing proliferation of cancer cells
If the KRAS gene is mutated, KRAS becomes active without EGFR activation

25
Q

How can angiogenesis be targeted for inhibition?

A

Anti-VEGF antibodies
Anti-VEGFR antibodies
Soluble VEGFRs

26
Q

What are some routes of administration for chemotherapy?

A

IV - PICC and Hickman line
Subcutaneous injection
Intralesional e.g. liver

27
Q

What is the mechanism of action of ipilimumab?

A

Ipilimumab is a monoclonal antibody that works to activate the immune system by targeting CTLA-4, a protein receptor that downregulates the immune system

28
Q

Why are aromatase inhibitors particularly useful in post-menopausal women?

A

They can only get oestrogen by aromatase enzyme

29
Q

What is the mechanism of action of nivolumab?

A

Anti-PD1 that allows T cells to bind and kill cancer cells

Biology of Cancer (12 decks)

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