Brainscape's Knowledge GenomeTM

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


See full index

YR2: MCD Cancer > Biological Basis of Cancer Therapy > Flashcards

Biological Basis of Cancer Therapy Flashcards

1
Q

What are the 5 most common cancers worldwide?

A 
Lung 
Breast 
Bowel 
Prostate  
Stomach
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What are the 4 main anti-cancer modalities?

A

Radiotherapy
Chemotherapy
Surgery
Immunotherapy

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

List 6 different types of cytotoxic chemotherapy.

A 
Alkylating agents  
Pseudoalkylating agents  
Antimetabolites 
Anthracyclines  
Vinca alkaloids + taxanes 
Topoisomerase inhibitors
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What are the main types of targeted therapy for cancer?

A

Monoclonal antibodies

Small molecule inhibitors

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

What is the term used to describe chemotherapy that is given:
Pre and post surgery

A

Pre: Neoadjuvant
Post: Adjuvant

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

How do alkylating agents work?

A

Add an alkyl groups to the guanine residues in DNA
Causes cross-linking of DNA strands + prevents DNA from uncoiling at replication
This triggers apoptosis (via a DNA checkpoint pathway)
It encourages mis-pairing

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q 
What class of anti cancer drugs includes the following:
Chlorambucil 
Cyclophosphamide 
Dacarbazine 
Temozolomide
A

Alkylating agents.

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

How do pseudoalkylating agents work?

A

Have the same mechanism as alkylating agents but use platinum instead of alkyl groups

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

What class of anti cancer drugs includes the following:
Carboplatin
Cisplatin
Oxaliplatin

A

Pseudoalkylating agents.

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

List 9 side effects of alkylating and pseudoalkylating agents

A 
Alopecia (except carboplatin)  
Nephrotoxicity 
Neurotoxicity 
Ototoxicity (platins) 
Nausea
Vomiting
Diarrhoea
Immunosuppression
Tiredness
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

How do anti-metabolites work?

A

Masquerade as purine or pyrimidines leading to inhibition of DNA replication + transcription
Leads to DNA double strand breaks + apoptosis
Can also be folate antagonists

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q 
Which class of anticancer drugs includes the following:
Methotrexate  
Capecitabine  
Gemcitabine  
5-fluorouracil 
6-mercaptopurine
Fludarabine
A

Anti-metabolites.

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

State 9 side effects of anti-metabolites.

A 
Alopecia (not 5-fluorouracil or capecitabine) 
Bone marrow suppression 
Increased risk of neutropenic sepsis 
Nausea 
Vomiting
Mucositis
Diarrhoea
Fatigue 
Palmar-plantar erythrodysesthesia (PPE)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

How do anthracyclines work?

A

Intercalate into DNA/ RNA sequences + inhibit transcription + replication
Also blocks DNA repair
Create DNA + cell membrane damaging oxygen free radicals

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

Which class of anti cancer drugs includes the following:
Doxorubicin
Epirubicin

A

Anthracyclines.

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

State 7 side effects of anthracyclines.

A 
Cardiac toxicity (probably due to free radicals) 
Alopecia  
Neutropenia 
Nausea
Vomiting
Fatigue  
Red urine (doxorubicin –‘the red devil’)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

How do vinca alkaloids and taxanes work?

A

Vinca alkaloids inhibit assembly of microtubules
Taxanes inhibit disassembly of microtubules
This forces cells into mitotic arrest

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

State 7 side effects of vinca alkaloids and taxanes

A

Nerve damage (peripheral + autonomic neuropathy)
Hair loss
Nausea
Vomiting
Bone marrow suppression
Arthralgia (severe joint pain without swelling or signs of arthritis)
Allergy

19
Q

How do topoisomerase inhibitors work?

A

Topoisomerase= enzymes that unwind DNA + induce temporary single + double strand breaks in the phosphodiester backbone
Topoisomerase inhibitors alter the binding of topoisomerase to DNA + allow permanent DNA breaks

20
Q

Which class of anti cancer drug includes the following:
Topotecan
Irinotecan
Etoposide

A

Topoisomerase inhibitors.

21
Q

State 6 side effects of topoisomerase inhibitors.

A 
Irinotecan= acute cholinergic type syndrome (diarrhoea, abdominal cramps, diaphoresis– so given atropine) 
Hair loss  
Nausea
Vomiting
Fatigue  
Bone marrow suppression
22
Q

What are the 6 hallmarks of cancer?

A 
SPINAP 
Self-sufficient  
Pro-invasive + metastatic  
Insensitive to anti-growth signals  
Non-senescent
Anti-apoptotic  
Pro-angiogenic
23
Q

What are the 4 hallmarks of cancer that have recently been added?

A 
DIE U 
Dysregulated metabolism 
Inflammation 
Evades immune system  
Unstable DNA
24
Q

Give 3 examples of receptors that are over-expressed in cancer. What is the consequence of this?

A

EGFR: over-expressed in many breast + colorectal cancers
HER2: breast
PDGFR: glioma (brain)
Increased kinase cascade + signal amplification

25
Q

Give an example of a ligand that is over-expressed in some cancers. What is the consequence of this?

A

VEGF: prostate, kidney + breast cancer

Increased kinase cascade + signal amplification

26
Q

Give two examples of constitutive (ligand independent) receptor activation in cancer. What is the consequence of this?

A

EGFR: lung cancer
FGFR: head + neck cancers, myeloma
Increased kinase cascade + signal amplification

27
Q

What do each of the following suffixes mean in relation to monoclonal antibodies:

a. -momab
b. -ximab
c. -zumab
d. -mumab

A

–momab: Derived from mouse antibodies
–ximab: Chimeric antibody
–zumab: Humanised antibody
–mumab: Fully human antibody

28
Q

Describe the structure of humanised monoclonal antibodies.

A

Murine regions are interspersed within the light + heavy chains of the Fab portion

29
Q

Describe the structure of chimeric monoclonal antibodies.

A

Murine component of the variable region of the Fab section is maintained integrally

30
Q

What effect can monoclonal antibodies have on receptors and their activation?

A

Target extracellular component of receptors + can prevent receptor dimerization, neutralise the ligand + cause internalisation of the receptor
Also activate Fc-receptor-dependent phagocytosis or cytolysis induced complement-dependent cytotoxicity or antibody-dependent cellular cytotoxicity (ADCC)

31
Q

Give two examples of monoclonal antibodies used in oncology.

A

Bevacizumab: binds + neutralises VEGF
Cetuximab: targets EGFR

32
Q

How do small molecule inhibitors work?

A

Bind to kinase domain of tyrosine kinase receptors within the cytoplasm + block autophosphorylation + downstream signalling

33
Q

What was the 1st targeted treatment for cancer and how did it work?

A

Glivec (imatinib): a small molecule inhibitor that targets the ATP binding region within the kinase domain of BCR-ABL1
This inhibits kinase activity of ABL1

34
Q

Give four examples of small molecule inhibitors that inhibit receptors.

A

Erlotinib (EGFR)
Gefitinib (EGFR)
Lapatinib (EGFR/HER2)
Sorafenib (VEGFR)

35
Q

Give three examples of small molecule inhibitors that inhibit intracellular kinases.

A

Sorafenib (Raf kinase): in addition to its anti-VEGFR effects
Dasatinib (Src kinase)
Torcinibs (mTOR inhibitors)

36
Q

State 6 advantages and 7 disadvantages of monoclonal antibodies.

A

Advantages:
High target specificity
Cause ADCC, complement-mediated cytotoxicity + apoptosis induction
Can be radiolabelled
Cause target receptor internalisation
Long half-life (lower dosing frequency)
Good for haematological malignancies
Disadvantages:
Large + complex structure (lower penetration)
Less useful against bulky tumours
Only useful against targets with extracellular domains
Not useful for constitutively activated receptors
Cause immunogenicity + allergy
IV administration
Expensive

37
Q

State 5 advantages and 2 disadvantages of small molecule inhibitors.

A

Advantages:
Can target tyrosine kinases without an extracellular domain or which are constitutively activated
Pleiotropic targets (useful in heterogenic tumours/cross-talk)
Oral administration
Good tissue penetration
Cheap
Disadvantages:
Shorter half-life, more frequent administration
Pleiotropic targets (more unexpected toxicity)

38
Q

State 4 resistance mechanisms to targeted therapies.

A

Mutations in ATP binding domain
Intrinsic resistance
Intragenic mutations
Upregulation of downstream signalling/ parallel pathways

39
Q

Explain how anti-sense oligonucleotides work.

A

Short, single-stranded DNA-like molecules
Bind to complementary sequence on mRNA + hinder its translation
Recruits RNase H to cleave the target mRNA

40
Q

Name a successful B-Raf inhibitor and list 3 side effects

A

Vemurafenib

Side effects: arthralgia, skin rash + photosensitivity

41
Q

Explain how the PD-1 receptor-PDL1 ligand system works.

A

PD-1 receptor on surface of cancer cells
When PDL-1 binds to the PD-1 receptor, the body’s T cells can no longer recognise tumours as foreign
So blocking the PD-1 receptor will stimulate the immune system

42
Q

Name a drug that inhibiting PD-1.

A

Nivolumab (anti-PD1 antibody)

43
Q

List 6 genetic mutations that can cause cancer

A

Chromosome translocation
Gene amplification
Point mutations with promoter/ enhancer regions of genes
Deletions/ insertions
Epigenetic alterations to gene expression
Inherited

44
Q

What is the target of cytotoxic chemotherapy?

A

Targets all rapidly dividing cells in the body (inc. gut mucosa + bone marrow cells)

YR2: MCD Cancer (18 decks)

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