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Flashcards in Biological Basis of Cancer Therapy Deck (42)
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1

What are the five most common cancers worldwide?

Lung
Breast
Bowel
Prostate
Stomach

2

What are the four main anti-cancer modalities?

Radiotherapy
Chemotherapy
Surgery
Immunotherapy

3

List the different types of cytotoxic chemotherapy.

Alkylating agents
Pseudoalkylating agents
Antimetabolites
Anthracyclines
Vinca alkaloids and taxanes
Topoisomerase inhibitors

4

What are the main types of targeted therapy for cancer?

Monoclonal antibodies
Small molecule inhibitors

5

hat is the term used to describe chemotherapy that is given:
a. Following surgery
b. Before surgery

Adjuvant
Neoadjuvant

6

How do alkylating agents work?

They add an alkyl group to the guanine residues in DNA
This causes cross-linking of the DNA strands and prevents DNA from uncoiling at replication
This then triggers apoptosis (via a DNA checkpoint pathway)
It encourages mis-pairing

7

Name four alkylating agents.

Chlorambucil
Cyclophosphamide
Dacarbazine
Temozolomide

8

How do pseudoalkylating agents work?

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

9

Name three pseudoalkylating agents.

Carboplatin
Cisplatin
Oxaliplatin

10

What are some side effects of alkylating and pseudoalkylating agents?

Alopecia (except carboplatin)
Nephrotoxicity
Neurotoxicity
Ototoxicity (platins)
Nausea, Vomiting, Diarrhoea, Immunosuppression, Tiredness

11

How do anti-metabolites work?

They masquerade as purine or pyrimidines leading to inhibition of DNA replication and transcription
They can also be folate antagonists (dihydrofolate reductase inhibitors)
This blocks DNA replication and transcription

12

Give six examples of anti-metabolites.

Methotrexate
Capecitabine
Gemcitabine
5-fluorouracil
6-mercaptopurine
Fludarabine

13

State some side effects of anti-metabolites.

Alopecia (not 5-fluorouracil or capecitabine)
Bone marrow suppression
Increased risk of neutropenic sepsis
Nausea, Vomiting, Mucositis, Diarrhoea, Fatigue
Palmar-plantar erythrodysesthesia (PPE)

14

How do anthracyclines work?

They intercalate into DNA or RNA sequences and inhibit transcription and replication
It also blocks DNA repair
They create DNA damaging and cell membrane damaging oxygen free radicals

15

Give two examples of anthracyclines.

Doxorubicin
Epirubicin

16

State some side effects of anthracyclines.

Cardiac toxicity (probably due to the free radicals)
Alopecia
Neutropenia
Nausea, Vomiting, Fatigue
Red urine (doxorubicin –‘the red devil’)

17

How do vinca alkaloids and taxanes work?

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

18

State some side effects of these drugs.

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

19

How do topoisomerase inhibitors work?

Topoisomerase is responsible for the unwinding of DNA and they induce temporary single and double strand breaks in the phosphodiester backbone
Topoisomerase inhibitors alter the binding of topoisomerase to DNA and allow permanent breaks in the DNA

20

Give three examples of topoisomerase inhibitors.

Topotecan
Irinotecan
Etoposide

21

State some side effects of topoisomerase inhibitors.

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

22

What are the six hallmarks of cancer?

SPINAP
Self-sufficient
Pro-invasive and metastatic
Insensitive to anti-growth signals
Non-senescent
Anti-apoptotic
Pro-angiogenic

23

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

DIE U
Dysregulated metabolism
Inflammation
Evades the immune system
Unstable DNA

24

Give three examples of receptors that are over-expressed in cancer.

EGFR – over-expressed in many breast and colorectal cancers
HER2 – breast
PDGFR – glioma (brain)

25

Give an example of a ligand that is over-expressed in some cancers.

VEGF – prostate, kidney and breast cancer

26

Give two examples of constitutive (ligand independent) receptor activation in cancer.

EGFR – lung cancer
FGFR – head and neck cancers, myeloma

27

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
b.–ximab
Chimeric antibody
c.–zumab
Humanised antibody
d.–mumab
Fully human antibody

28

Describe the structure of humanised monoclonal antibodies.

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

29

Describe the structure of chimeric monoclonal antibodies.

The murine component of the variable region of the Fab section is maintained integrally

30

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

They target the extracellular component of receptors and can prevent receptor dimerization, neutralise the ligand and cause internalisation of the receptor
NOTE: they also activate Fc-receptor-dependent phagocytosis or cytolysis induced complement-dependent cytotoxicity or antibody-dependent cellular cytotoxicity (ADCC)