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Personalised Medicine and Cancer > Mills Questions > Flashcards

Mills Questions Flashcards

1
Q

Define apoptosis.

There’s more than one correct answer

A

A) Physiological cell death where unwanted or useless cells are eliminated during development and other normal biological processes.

B) Programmed cell death (PCD) is a mode of cell death that occurs under normal physiological conditions.

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2
Q

Define necrosis.

A

Pathological cell death which occurs when cells are exposed to a serious physical or chemical insult e.g. hypoxia, hyperthermia, ischaemia.

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3
Q

What is the ‘death domain’?

A

A cytoplasmic domain made up of about 80 amino acids.

involved in extrinsic pathway

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4
Q

Which caspase(s) is involved in the extrinsic pathway?

A

Caspase-8.

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5
Q

Which caspase(s) in involved in the intrinsic pathway?

A 
Caspase-9 = "initiator".
Caspase-3 = "executioner".
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6
Q

What is the function of p53?

A

Activates transcription.
Causes cell cycle arrest at G1/S interface (G1-checkpoint).
Involved in apoptosis pathway.

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7
Q

What is the mechanism for antibody drug conjugates (ADCs)? (6 steps)

A
  1. Circulation into bloodstream.
  2. Binding of mAb to tumour antigen.
  3. Internalisation – receptor-mediated endocytosis.
  4. Recycling – fractions recycled back out of cell.
  5. Release – lysosomes and endoscopes fuse and release active cytotoxin.
  6. Action – cytotoxin interferes with critical cell machinery.
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8
Q

Issues with ADCs?

A 
Have to limit non-target toxicity.
Have to retain high immunogenicity.
Inefficient internalisation.
Limited target antigens.
(There are others, go mental).
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9
Q

What is Besponsa?

A

Inotuzumab ozogamicin – humanised antiCD22 ADA with calicheamicin.

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10
Q

What is Besponsa licensed for?

A

Acute lymphoblastic leukaemia (ALL).

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11
Q

Adcetris MOA?

Brentuximab vedotin

A

CD30-directed antibody drug conjugate.

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12
Q

What two drugs make up Kadcyla?

A

Trastuzumab (ADC) and Emtansine (cytotoxic microtubule inhibitor).

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13
Q

What is Trastuzumab?

A

Anti-HER2 monoclonal antibody.

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14
Q

What costs more to develop generics or biosimilars?

A

Biosimilars.

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15
Q

What is SB3?

A

A biosimilar of Trastuzumab.

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16
Q

What is Maytansine?

A

Microtubule polymerisation inhibitor.

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17
Q

What is Mechlorethamine?

A

Nitrogen mustard - alkylating agent.

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18
Q

What 4 drugs make up the MOPP regimen?

A

Mechlorethamine, Oncovin, Prednisone and Procarbazine.

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19
Q

What are Cyclophosphamide and Ifosfamide?

A

Nitrogen mustards - alkylating agents.

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20
Q

What are the 4 grades of the grading system?

A

Grade I = 75-100% - highly differentiated.
Grade II = 50-75% differentiated.
Grade III = 25-50% differentiated.
Grade IV = 0-25% differentiated.

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21
Q

What is the TNM system?

Basically what is T, N and M

A

Tumour size – T0, T1, T2, T3, T4.
Nodal involvement – N0, N1, N2, N3, N4.
Distant metastasis – M0, M1, M2, M3, M4.

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22
Q

How does angiogenesis accelerate tumour progression?

A

Improves tumour uptake of oxygen and nutrients.
Removes acid metabolites.
Provides a route whereby the tumour can metastasise.

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23
Q

What is adjuvant cytotoxic chemo for?

A

To eliminate residual cells not cleared by surgery or radiotherapy, and to minimise the risk of recurrence.

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24
Q

What is neoadjuvant cytotoxic chemo for?

A

Pre-shrink the tumour prior to surgery or radiotherapy, a more complete/less mutilating resection.

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25
Q

What is induction therapy?

A

Initial therapy for pts presenting with cancer to induce remission.

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26
Q

Weight of tumour when death usually occurs?

A

1kg.

27
Q

Mechanisms of drug resistance for Cytarabine?

A

Decreased drug activation.
Increased drug inactivation.
Alternative biochemical pathways.

28
Q

Mechanisms of drug resistance for Methotrexate?

A

Decreased drug activation.
Decreased cellular uptake of drug.
Alternative biochemical pathways.
Alterations in target enzymes.

29
Q

What is the Zubrod scale?

A 
0 = normal activity.
1 = symptomatic and ambulatory – cares for self.
2 = ambulatory >50% of time – occasional  assistance.
3 = ambulatory ≤50%, nursing care needed.
4 = bedridden.
30
Q

What is the Karnofsky scale?

A 
100 = normal, no evidence of disease.
90 = able to perform normal activities with only minor symptoms.
80 = normal activity with effort, some symptoms.
70 = able to care for self but unable to do normal activities.
60 = requires occasional assistance, cares for most needs.
50 = requires considerable assistance.
40 = disabled, requires special assistance.
30 = severely disabled.
20 = v. sick, requires active support Tx.
10 = moribund.
31
Q

What is the ECOG/WHO score?

A 
0 = fully active, able to carry on all pre-disease performance without restriction.
1 = restricted in physically strenuous activity, but ambulatory and able to carry out work of a light and sedentary nature.
2 = ambulatory and capable of all self-care but unable to carry out any work activities, >50% up and about.
3 = capable of only limited self-care, confined to bed or chair >50% of waking hours.
4 = completely disabled, no self-care, totally confined to bed/chain.
5 = dead.
32
Q

What do alkylating agents covalently bind to?

A

N7 and O6 of guanine.
N1 and N3 of adenine.
N3 of cytosine.

33
Q

Alkylating agents functions (x6):

A

Inter-strand cross linking of DNA strands stops strand separation.
Intra-strand cross linking.
Base ring cleavage – strand cleavage,
De-purination – strand cleavage.
Tautomeric mutation – G pairs with T, GC to AT in daughter cells.
Ineffective repair – frameshift mutation.

34
Q

Mechanisms of alkylating agents:

A

Undergo intramolecular cyclisation forming an unstable ethylene immonium compound.
Tertiary amine is transformed into quaternery ammonium compound.
Ring opens out to form reaction carbonium ion which performs the alkylation.
Carbonium ion is unstable reacts with an electron donor.

35
Q

Why don’t nitrogen mustards cross the BBB?

A

They’re too polar.

36
Q

Resistance against Cyclophosphamide and Ifosfamide occurs from what?

A

Increased DNA repair.

Increased production of thiols (glutathione).

37
Q

What is Cyclophosphamide and Ifosfamide used for?

A

Burkitt’s lymphoma, ALL, breast etc.

38
Q

How does Bendamustine work?

A

Inhibition of checkpoint control, inefficient DNA repair and activation of “traditional” apoptosis.

39
Q

What is Chlorambucil used for?

A

Lymphocytic leukaemia especially CLL.

40
Q

What is Melphalan used for?

A

Myeloma and ovarian.

41
Q

How does resistance against nitrosureas occur?

A

DNA repair before cell death occurs.

Inactivation of the drug by thiols.

42
Q

How does cisplatin work?

A

Binds to N7 on purine residues, causing DNA damage, blocking cell division, and causing apoptosis.

43
Q

Why does cisplatin have a long half-life?

A

It’s protein bound and accumulates in tissue (esp. kidney and liver).

44
Q

Before starting cisplatin, what is the patient pre-treated with?

A

Pre-treatment forced diuresis – IV mannitol or saline.

45
Q

What is Vincristine used for?

A

Childhood ALL, Wilm’s tumour, lymphomas.

46
Q

What is Vinblastine used for?

A

Administered with bleomycin/cisplatin for metastatic testicular carcinoma and lymphomas.

47
Q

What is Vinorelbine used for?

A

Advanced non-small cell lung cancer.

48
Q

What do vinca alkaloids inhibit?

A

Microtubule - stops microtubule formation.

49
Q

What are Paclitaxel and Docetaxel examples of?

A

Microtubule inhibitors.

50
Q

What are the taxanes used in?

A

Advanced ovarian and metastatic breast, and in small cell lung cancer.

51
Q

What is Eribulin a synthetic analogue of?

A

Potent Halichondrin B.

52
Q

What is Doxorubicin used for?

A

Widely used and important cancer drug for sarcomas, breast lung, ALL and lymphomas.

53
Q

What is Daunorubicin used for?

A

Used to treat ALL and AML.

54
Q

Anthracyline mechanism?

A

Bind to DNA causing adducts.

55
Q

What is Bleomycin?

A

A mix of different metal chelating glycopeptides.

56
Q

What drug for testicular cancer is almost 100% effective in combination with cisplatin and vinblastine/etoposide?

A

Bleomycin.

57
Q

What is the role of folic acid?

A

Co-enzyme.

58
Q

What do antifolates inhibit?

A

Dihydrofolate reductase (DHFR).

59
Q

What is Methotrexate’s MOA?

A

Inhibit DHFR and indirectly inhibits folate dependent enzymes e.g. thymidylate synthase.

60
Q

What is Raltitrexed used for?

A

Advanced colon cancer.

61
Q

What is Raltitrexed used in combination with?

A

Irinotecan and oxaliplatin.

62
Q

What does Pemetrexed target?

A

Dihydrofolate reductase (DHFR), thymidylate synthase (TS) and glycinamide ribonucleotide formyl transferase (GARFT).

63
Q

How much 5-fluorouracil is activated to anticancer agent?

A

10-20%.

Personalised Medicine and Cancer (4 decks)

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