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Cancer LCRS > Biological Basis of Cancer Therapy > Flashcards

Biological Basis of Cancer Therapy Flashcards

1
Q

Which of the pseudoalkylating agents does not cause alopecia?

A

Carboplatin

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2
Q

Besides nausea and vomiting and tiredness, what side effects do alkylating and pseudoalkylating agents have?

A

Toxicity - Ototoxicity, neurotoxicity and nephrotoxicity
Diarrhoea
Alopecia (except for carboplatin)

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3
Q

Besides nausea and vomiting and tiredness, what side effects do anti-metabolites have?

A 
BM suppression; anaemia, neutropenia, thrombocytopenia 
Mucositis 
Diarrhoea 
Palmar-plantar erythrodysesthesia 
Alopecia
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4
Q

Name an antimetabolite which pretends to be a purine

A

Dacarbazine
6-mercaptopurine
Fludarabine

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5
Q

Name an antimetabolite which pretends to be a pyrimidine

A

5-Fluorouracil
Capecitabine
Gemcitabine

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6
Q

Name two cytosine analogues

A

Capecitabine

Gemcitabine

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7
Q

How does methotrexate work?

A

Folate antagonist therefore interferes with DNA synthesis

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8
Q

Name two anthracyclines

A

Doxorubicin

Epirubicin

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9
Q

Besides nausea and vomiting and fatigue, what side effects do anthracyclines cause?

A 
Cardiac toxicity 
Alopecia 
Neutropenia 
Red urine 
Skin changes
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10
Q

What is the anthracycline-induced cardiac toxicity thought to be due to?

A

Free radicals

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11
Q

What side effects do vinca alkaloids and taxanes cause besides nausea and vomiting?

A 
Peripheral and autonomic neuropathy 
Alopecia 
Arthralgia (joint pain)
BM suppression 
Allergic reaction
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12
Q

What are the two topoisomerases and what do they do?

A

Topo 1 - normally prevents single stranded DNA tortional strain during replication and transcription

Topo 2 - prevents double stranded DNA torsional strain

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13
Q

Give examples of topoisomerase 1 inhibitors

A

Topotecan

Irinotecan

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14
Q

Give examples of topoisomerase 2 inhibitors

A

Etoposide

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15
Q

What side effect does irinotecan specifically cause and what is the treatment for this?

A

Acute cholinergic syndrome (diarrhoea, cramping, diaphoresis)
Anticholinergics e.g. atropine

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16
Q

What is diaphoresis?

A

Increased sweating

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17
Q

Give three mechanisms of resistance to cancer therapy

A

Upregulation of DNA repair
Base excision repair (to remove drug) using ‘PARP’
Removal of drug from cell using ABC (ATP-binding cassette transporters)

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18
Q

Which receptor is overexpressed in gliomas?

A

PDGFR

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19
Q

Which receptor is overexpressed in breast and colorectal cancers?

A

EGFR

20
Q

VEGF is overexpressed in which cancers?

A

Prostate, kidney and breast cancer

21
Q

What name is given to the activation of receptors independent of ligands?

A

Constitutive receptor activation

22
Q

Give an example of two receptors in cancer which can be activated independent of ligands, and where these are found

A

EGFR - lung cancer

FGFR - head and neck cancers and myelomas

23
Q

What do the -momab suffix for monoclonal antibodies mean?

A

MOuse antibodies = MOmab

24
Q

What do the -zumab suffix for monoclonal antibodies mean?

A

Zumab = humaniZed

25
Q

What do the -mumab suffix for monoclonal antibodies mean?

A

MUmab = hUMan

26
Q

What do the -ximab suffix for monoclonal antibodies mean?

A

Ximab = chimeric antibodies

27
Q

How do monoclonal antibodies work in cancer?

A 
They target the extracellular domain of receptors, thereby: 
Neutralising ligands
Preventing receptor dimerization 
Causes internalisation of the receptor 
Stimulating cell death via complement or
Antibody dependent cellular toxicity
28
Q

Which drug targets the EGFR receptor?

A

Cetuximab - for bowel cancer

29
Q

Which drug targets VEGF?

A

Bevacizumab - also for colorectal cancer

30
Q

How do small molecule inhibitors work?

A

They bind to tyrosine kinases and prevent phosphorylation and downstream signalling

31
Q

Give an example of a small molecule inhibitor

A

Glivec

32
Q

How does Glivec work and what is it used in?

A

It targets the ATP binding region within the kinase domain.

Used in CML due to Bcr-Abl gene

33
Q

What are the mechanisms of resistance to targeted therapies?

A

Mutations in the ATP binding domain
Intrinsic resistance e.g. the cancer produces a different product
Intragenic mutations
Upregulation of downstream pathways

34
Q

How do anti-sense oligonucleotides work?

A

They bind to completementary RNA sequence and prevent translation by recruiting RNAse H to cleave the target mRNA

35
Q

What mutation do 60% of melanomas have?

A

B-Raf mutation - substitution of glutamic acid for valine

36
Q

Why is this mutation in melanomas significant in therapy?

A

B-Raf inhibitors have been successful in treatment - life span extended by 7 months

37
Q

Give an example of a B-Raf inhibitor

A

Vemurafenib

38
Q

How does RNA interreference work?

A

Single stranded complementary RNA

39
Q

Name something which can bind to T-cells to prevent them from recognising cancer

A

PD-1 (programmed-death 1)

40
Q

Which drug has been used to block PD-1?

A

Nivolumab

41
Q

Which cancers have been targeted by Nivolumab?

A

Melanoma
Non-small cell lung cancer
Renal cell carcinoma

42
Q

What are humanised monoclonal antibodies?

A

Antibodies from non-human species are taken. Their protein sequences are modified to increase similarity ot human antibodies.

43
Q

Explain how humanised monoclonal antibodies work

A

The murine (mouse) regions are interspersed with light and heavy chains of Fab portion

44
Q

What are chimeric monoclonal antibodies?

A

Antibodies from various species are taken and spliced together

45
Q

What do mAbs activate which causes phagocytosis of the target cells?

A

Fc gamma-receptor

46
Q

What else can Fc gamma-receptor binding cause?

A

Cytolysis

47
Q

What are the two downstream effects of cytolysis or phagocytosis induced by Fc-gamma receptor binding of monoclonal antibodies?

A

Antibody-dependent cellular cytotoxicity

Complement dependent cytotoxicity

Cancer LCRS (10 decks)

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