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Cancer > Cancer basics > Flashcards

Cancer basics Flashcards

1
Q

Neurological side-effect of chemotherapy?

A

Reduced cognition

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2
Q

Driver mutations?

A

TP53
Telomerase
RAS

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3
Q

What is offered to those with a TP53 mutation?

A

Annual whole body MRI

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4
Q

What are the normal functions of TP53?

A

Activates DNA repair
Arrests division if there’s DNA damage
Initiates apoptosis

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5
Q

What proportion of cancers have a TP53 mutation?

A

Over half

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6
Q

What are RAS oncogenes?

A

Proto-oncogenes stuck in proliferative ‘on-mode’ meaning the tumour does not need growth factor stimulation to divide

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7
Q

What does over-expression of telomerase permit?

A

Cellular immortality

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8
Q

Non-specific signs of cancer?

A 
Cachexia
Anaemia
Tachycardia
Tachypnoea
Palpable metastases
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9
Q

What does a liquid biopsy of cell free circulating DNA grant?

A

Aggregate of all tumour cells in the population

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10
Q

What is TP53

A

A tumour suppressor gene

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11
Q

Gradings of ‘T’ in TNM?

A

0, 1, 2, 3, 4

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12
Q

Gradings of ‘N’ in TNM?

A

0, 1, 2, 3

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13
Q

Gradings of ‘M’ in TNM?

A

0, 1

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14
Q

Example of a type of cancer RAS mutation is associated with?

A

Pancreatic cancer

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15
Q

What is a proto-oncogene?

A

A gene that when mutated or over expressed contributes to the development of cancer, i.e. has the potential to give rise to an oncogene

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16
Q

What is a tumour suppressor gene?

A

A gene who’s loss contributes to the development of a cancer

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17
Q

Resistance to apoptosis achieved by what?

A

Loss of p53

Upregulation of pro-survival factors like Bcl-2

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18
Q

What occurs in 85% of human carcinomas?

A

Telomerase expression/activity is gained

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19
Q

Which protein do cancer cells lose allowing them to become more motile?

A

E-cadherin

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20
Q

List some common oncogenes:

A 
Her2-neu
RAS
Myc
Src
Htert
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21
Q

List some common tumour suppressor genes:

A

P53
Rb
APC

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22
Q

Breast oncogene

A

Her2

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23
Q

Colorectal oncogene

A

Kras

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24
Q

Melanoma oncogene

A

BRAF

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25
Q

What type of mutation is an oncogene?

A

Gain of function

26
Q

What type of mutation is in a defective tumour suppressor gene?

A

Loss of function

27
Q

Mutation of which gene changes a normal colon epithelium to a small adenoma?

A

APC

28
Q

Mutation of which gene changes a small adenoma to a large adenoma?

A

RAS

29
Q

Mutation of which gene changes a large adenoma to a carcinoma?

A

PI3K
Cell cycle/apoptosis
TGF-beta

30
Q

Hereditary breast cancer:

5-10%

A

BRCA1/2 (HPOC)

P53 (LFS)

31
Q

Hereditary ovarian cancer:

15-20%

A 
BRCA1/2 (HPOC)
MMR genes (Lynch syndrome)
32
Q

Hereditary colorectal cancer:

5-10%

A 
MMR genes (Lynch syndrome)
APC (FAP)
33
Q

Hereditary melanoma:

5-10%

A

p16 (FAMM)

34
Q

Hereditary medullary thyroid:

25%

A

RET (MEN2)

35
Q

Hereditary retinoblastoma:

40%

A

RB1 (familial retinoblastoma)

36
Q

Hereditary phaeochromocytoma:

30%

A

SDHx (familial paraganglioma and phaechromocytoma syndrome)

37
Q

How does the chemotherapy carboplatin treat BRCA deficient tumours?

A

Introduces DNA cross links that the BRCA deficient cells cannot repair through homologous recombination (considered platinum therapy)

38
Q

How do PARP inhibitors kill BRCA deficient cancer cells?

A

Introduce single strand breaks which form into double strand breaks that are toxic to the BRCA deficient cancer cell

39
Q

Example of a PARP inhibitor?

A

Olaparib

40
Q

How is PARP inhibition therapy used?

A

Maintenance therapy after chemotherapy

41
Q

What causes Lynch syndrome?

A

Germline mutation in the DNA mismatch repair (MMR) genes: MLH1, MSH2, MSH6, PMS2

42
Q

What do tumour cells have in Lynch syndrome that makes them an immune target?

A

Mutator phenotype and micro-satellite instability (MSI-H, high antigenicity)

43
Q

How do MSI-H tumours avoid immune recognition?

A

Expression of immunosuppressant molecules e.g. PD1

44
Q

How do you restore the immune response to MSI-H tumours?

A

Use a PD1 inhibitor e.g. pembrolizumab

45
Q

Epidermal growth factor receptor is over expressed in which cancer?

A

Non-small cell lung cancer, especially squamous cell carcinoma

46
Q

What are Gefitinib and Erlotinib?

A

Tyrosine kinase inhibitors

47
Q

What are Gefitinib and Erlotinib used to treat?

A

Non-small cell lung cancers (squamous) to block the EGFR pathway

48
Q

What is EGFR in lung cancer?

A

Oncogene with driver mutations

49
Q

Aflatoxin (produced by aspergillus)

A

Liver - hepatocellular carcinoma

50
Q

Aniline dyes

A

Bladder - transitional cell carcinoma

51
Q

Asbestos

A

Mesothelioma

Bronchial carcinoma

52
Q

Nitrosamines

A

Oesophageal carcinoma

53
Q

Vinyl chloride

A

Hepatic angiosarcoma

54
Q

BRCA2 risks:

A 
Breast cancer 70% (8% in men)
Contralateral breast cancer 65%
Ovarian cancer 20%
Prostate cancer (25%)
Pancreatic cancer (3%)
55
Q

Action of cisplatin?

A

Targets DNA

56
Q

Action of taxanes e.g. paclitaxel?

A

Targets microtubules

57
Q

Non-cytotoxic therapies:

A

Targeting tyrosine kinase
Monoclonal Abs to cell surface receptors
Immune checkpoint inhibitors

58
Q

Action of nivolumab?

A

Anti-PDL-1 used to treat melanoma

59
Q

Side effects of EGFR-targeting drugs?

A

Rash and diarrhoea

60
Q

Side effects of trastuzumab (herceptin)?

A

Cardiac toxicity

61
Q

Side effects of checkpoint inhibitors?

A

AI colitis

Pneumonitis

62
Q

What is Li-Fraumeni syndrome?

A

Autosomal dominant
Germline mutations to the p53 tumour suppressor gene
Diagnosed when: 1st degree relative develops cancer <45 and another relative does <45/sarcoma at any time

Cancer (10 decks)

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