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MOD > Cancer > Flashcards

Cancer Flashcards

1
Q

2 types of benign epithelial tumours

A

Papilloma

Adenoma

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2
Q

Papillloma

A

Benign epithelial tumour, non glandular, non secretory

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3
Q

4 exceptions of the benign epithelial tumour rule

A

Melanoma, lymphoma, seminoma, mesothelioma

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4
Q

2 types of malignancy epithelial tumours

A

Carcinomas

Adenocarcinomas

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5
Q

Benign mesenchymal tumour suffix and prefix

A

Suffix- oma

Prefix- tusse or cell of origin e.g osteoma

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6
Q

Smooth muscle benign tumour

A

Leiomyoma

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7
Q

Skeletal muscle benign tumour

A

Rhabdomyoma

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8
Q

Adipose benign tumour

A

Lipoma

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9
Q

Blood vessel benign tumour

A

Angioma

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10
Q

Cartialge benign tumour

A

Chondroma

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11
Q

Fribous benign tumour

A

Fibroma

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12
Q

Suffix for malignant mesenchymal tumours

A

sarcoma e.g. liposarcoma

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13
Q

Exceptions of the benign mesenchymal tumour rules

A

Melanocytic nevus-benign tumour or melanocytes

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14
Q

Exceptions of the malignant mesenchymal tumour rule

A

Melanoma
Leukaemia
Lymphoma
Myeloma

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15
Q

CNS tumours

A

Meningioma
Astrocytoma (glioblastoma multiforme)
Ependymoma
Medulloblastoma

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16
Q

Where do germ cell tumours arise?

A

From germ cells in the gonads

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17
Q

Embryonal tumours

A

Occur in v. young (

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18
Q

Where do you find carcinosarcomas

A

Ovaries

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19
Q

Non-neoplastic overgrowth of normal tissue. Indigenous to the site of occurrence e.g lung hamartoma

A

Hamartoma

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20
Q

Nodules of organ parenchyma in another organ e.g. normal (non neoplastic) pancreas nodule in stomach

A

Choristoma

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21
Q

Initiators

A

Often genotoxic-can chemically modify or damage DNA

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22
Q

Promotors

A

Often non-genotoxic. Induce proliferation and DNA replication

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23
Q

Complete carcinogens

A

Can initiate and promote e.g UV light

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24
Q

What are the 2 ways in which promotors work?

A
  1. Stimulate more than 2 rounds of DNA replication required for mutation fixation
  2. Stimulate clonal expansion of mutated cells, whcih allows the accumulation of further mutations
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25
Q

Direct acting carcinogens

A

Do not require enzymatic (metabolic) activation before they react with the DNA e.g oxygen radicals, nitrosamines, UV light, ionising radiation

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26
Q

Procarcinogens

A

Require enzymatic (metabolic) activation before they react with DNA e.g. aromatic amines, polycyclic aromatic hydrocarbons (PAH)

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27
Q

Describe the action of benzopyrene

A

A procarcinogen which can be generated in the combustion of most organic material e.g. meat, tobacco, fuel. Requires metabolic activation before it’s able to react with DNA. Throm a series of enzymatic reactions, benzopyrene is converted to BPDE-reacts with TP53 gene in lung tumours of smokers.

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28
Q

Consequence of damage to nucleotide excision repair

A

Xeroderma pigmentosum -AR inherited skin disorder-sensitivity to UV light, increase frequency of skin cancer and abnormal pigmentation

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29
Q

Consequence of damage to recombinational repair

A

Ataxia telangiectasia (AT) AR inherited increases incidence of cancers.

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30
Q

How many carinogens are there in tobacco smoke?

A

19

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31
Q

Name some carcinogens of tobacco smoke

A

Polycyclinc aromatic hydrocarbons e.g. benzopyrene, require metabolic activation
Acrolein-acrid smell
Nitrosamine- formed during curing of the leaves
Radioactive lead and polonium
Heavy metals-cadmium, chromium

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32
Q

Tobacco, in combination with alcohol, leads to what increase in head and neck cancer?

A

x100 increased risk (alcohol is a good solvent)

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33
Q

What is the potent chemical that alcohol is converted to?

A

Acetaldehyde- liked to oral, oesophageal, bowel and liver cancer

34
Q

List 4 ways in which alcohol can increase the risk of cancer

A

Increased levels of oestrogen and testosterone (liver can no longer metabolise)
Increase uptake of carcinogenic chemicals into our cells within the upper GI.
Decrease levels of folate- needed for accurate DNA replication
Can kill surface epithelium leading to unscheduled proliferation

35
Q

How does oestrogen act as a carcinogen

A

Initiator (induces DNA damage) and promotor (stimulates cell division)

36
Q

How does HRT increase the risk of oestrogen associated cancers

A

Both HRT and oestrogen bind to mitogenic genes involved in proliferation

37
Q

How does alcohol consumption increase the risk of oestrogen associated cancers?

A

Oestrogen and alcohol can be converted to estradiol -3,4, quinone that can be incorporated into DNA and causes damage that can be replicated

38
Q

How does chronic inflammation induce cancer?

A

Initiation-DNA damage from release of free radicals by immune cells
Promotion- growth factor induced cell division to repair tissue damage

39
Q

Carcinogenesis consists of what 2 processes?

A

Oncogene activation

TSG inactivation

40
Q

Gatekeeper genes

A

Play an important role in regulating normal growth; negative regulators of the cell cycle and proliferation
Positive regulators of apoptosis
Positive regulators of cell differentiation

41
Q

Li fraumeni is an inherited cancer of what gene and results in cancer of what tissue?

A

p53-gate/care

Sarcomas/breast

42
Q

Proto-oncogenes

A

promote cell proliferation, survival, angiogenesis and negative replication of apoptosis

43
Q

Oncogenes

A

Mutations lead to activated versions or increased expression of proto-oncogenes.

44
Q

How does the activation of oncogenes/inhibition of TSGs vary with regards to the number of muations

A

2 hit hypothesis for TSGs
Only 1 copy of the gene needs to be activated to induce a gain of function- mutated gene is dominant to the other normal parental gene.

45
Q

3 mechanisms of oncogene activation

A

Translocation-of protooncogene from a low transcriptionall active site to an active site-aberrent expression of the oncogene.
Point mutation- substitution of a single base pair can alter an amino acid in the protein causing it to become hyperactive
Amplification-by insertion of multiple copies of an oncogene which increases expression

46
Q

Multi-step tumorigenesis

A

3 genetic alterations are requred to transform a normal cell into a neoplastic cell (2 inactivations of TSGs, 1 inactivation of oncogene)

47
Q

APC

A

Adematous polyposis gene

48
Q

6 hallmarks of cancer cells

A 
Self sufficiency in growth signals
Insensitivity to antigrowth signals
Tissue invasion and metastasis
Limitless potential for replication
Sustained angiogenesis
Evading apoptosis
49
Q

Signal transduction

A

Cascade of signal from growth factor receptors to expression of genes in the nucleus

50
Q

Give 3 examples of mutations to the signal transduction pathway to trigger growth, regardless of growth signals

A

EGFR mutation or expression-colorectal cancer
Ras mutation-pancreatic cancer
B-Raf mutation

51
Q

Give an example of a gene that is activated by negative growth factors to regulate the cell cycle by preventing progression from G1 to S phase

A

Retinoblastoma gene (RB1)

52
Q

What happens when you get a mutation in the RB1 gene

A

Resistance to negative growth factors

53
Q

How do tumour cells act to achieve limitless potential for replication

A

Overexpression of the telomerase enzyme maintains the normal telomere length- normal cells have a finite replicative lifespan due to shortening of the chromosome ends (telomeres)

54
Q

Describe the action of the TP53 gene

A

Kep player in apoptosis; codes for p53 protein that induces cell cycle arrest to allow repair of DNA damage and induces apoptosis if too much damage. TP53 inactivation is common in over 50% tumours. Inherited mutation results in Li-Fraumeni cancer syndrome

55
Q

What size do tumours have to be before they require a good blood supply?

A

over 2mm

56
Q

How do cancer cells create their own blood supply?

A

Hypoxia stabilizes HIF1 transcription factor, which induces vascular endothelial growth factor (VEGF)-actively recruits endothelial cells that proced to construct new capillaries and vessels.

57
Q

How do cancer cells invade and metastasize

A

Epithelial cells are held tightly together by adhesion molecule E.cadherin. Loss of E.cadherin in tumour cells results in epithelial-mesnchymal transition (EMT). Mesenchymal cells are motile and secrete proteases that allow them to break through basement membrane and invade the underlying stroma.

58
Q

Marker for diagnosis and monitoring of response to treatment in ovarian cancer

A

CA-125

59
Q

Another name for herceptin

A

Traztuzumab

60
Q

Metastatic disease kills what proportion of patients

A

50% patients. Majority of lung cancer patients. 30% breast cancer patients.

61
Q

What changes bring about invasion of tumour cells

A

Increased motility- production of proteolytic enzymes

Decreased adhesion and mechanical pressure

62
Q

Cadherins

A

Cell to cell adhesion molecules

63
Q

Integrins

A

Cell to matrix adhesion molecules

64
Q

Epithelial-mesenchymal transition

A

Epithelial cells are thightly connected, polarised and tethered. Mesenchymal cells are loosely connected and able to migrate. In cancer, epithelial cells gain mesenchymal properties and can invade and migrate

65
Q

Name 3 proteolytic enzymes that are secreted by tumour cells and degrade extracellular matrix

A

Interstitial collagenases
Gelatinases
Stomolysins

66
Q

What do interstitial collagenases break down?

A

Collagen types 1, 2, 3

67
Q

What do gelatinases break down?

A

Collagen type 4 , gelatin

68
Q

What do stomolysins break down?

A

Collagen type 4, proteoglycans

69
Q

Normal tissue witholds a balance between what 2 things that control ECM breakdown?

A

Matrix metalloproteinases

Inhibitors of metalloproteinases

70
Q

5 stages of metastasis

A 
Intravasation
Detachment invasion
Survival against host defences
Adherence extravasation
Growth
71
Q

Carcinomas generally spread by what means first?

A

Lymphatic

72
Q

Sarcomas generally spread by what means first?

A

Blood

73
Q

Which tumours generally spread to the bone

A

Breast, prostate, lung, kidney, thyroid

74
Q

2 patterns of metastasis

A

Mechanical hypothesis

Seed and Soil hypothesis

75
Q

Pattern of metastasis: dicated by anatomy e.g. lymphatic drainage. Liver mets in GI cancer.

A

Mechanical hypothesis

76
Q

Pattern of metastasis: seeds are carried in all directions but only grow in favourable conditions

A

Seed and soild hypothesis

77
Q

3 examples of promotors of angiogenesis

A

VEGF
PDGF
TGFbeta

78
Q

3 examples of inhibitors of angiogensis

A

ECM proteins
Thrombospondin
Canstatin
Endostatin

79
Q

How many stages are there in the TNM staging system?

A

4

80
Q

What staging system is used for colorectal cancer?

A

Duke’s staging

81
Q

How do you determine the grade of a tumour?

A

Done by histopathologists- subjective. Takes into account differentiation, nuclear pleomorphism and size, mitotic activity, necrosis

MOD (4 decks)

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