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Principles of disease > Outline of Disease Process CANCER > Flashcards

Outline of Disease Process CANCER Flashcards

1
Q

What does “cancers are mostly monoclonal” mean?

A

Mainly arise from one cell

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2
Q

Whats different about cancer cells?

A

Increased growth factor secretion
Increased in oncogene expression
Loss of tumour supressor genes
Loss of contact inhibition

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3
Q

What are the 5 steps of carcinogenesis?

A

Carcinogen
Initiation
Promotion
Tumour Growth
Progression

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4
Q

What is a diagnostic threshhold?

A

Size at which a cancer becomes clinically detectable

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5
Q

What are the 3 types of carcinogens?

A

Chemical
Physical
Viral

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6
Q

What chemical carcinogen causes liver cancer?

A

Aflatoxin (in mouldy peanuts)

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7
Q

Most common chemical carcinogens?

A

Smoking & alcohol

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8
Q

Physical carcinogen?

A

Ionising radiation

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9
Q

How does ionising radiation cause cancer?

A
  • Translocate chromosomes
  • Amplify certain Genes
  • Activate Oncogenes
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10
Q

What viral carcinogen causes burkitts lymphoma?

A

Herpes virus

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11
Q

What viral carcinogen caues liver cancer?

A

HEP B

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12
Q

What 3 things are involved in the promotion stage?

A

Oncogenes
Tumour suppressor genes
Growth factors

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13
Q

How do oncogenes promote the progression stage?

A

Positive growth regulators, stimulate tumour growth

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14
Q

How do growth factors stimulate cell growth?

A

Bind to cell-membrane receptors & activate intracellular signal transduction pathways

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15
Q

Whats the difference between autocrine & paracrine signalling?

A

Paracrine signalling - signals act on nearby cells
Autocrine - signals acting on the same cell that produces them

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16
Q

Whats the normal function of tumor suppressor genes?

A

Promoting:

DNA repair
Apoptosis
Differentiation

17
Q

What normally induces tumor suppressor genes to act?

A

Hypoxia & DNA damage

18
Q

Name a tumor supressor gene

A

P53

19
Q

How does progression (metastasis) occur?

A

Tumour invades through basement membrane
Invades ECM/CT/other cells
Invades blood vessels
Cells arrested in distant tissue

20
Q

Describe the progression stage

A

Series of limited sequential steps involving host-tumour interactions

21
Q

At what point is angiogenesis vital for continued tumor growth?

A

New vessels must form for a tumour to grow beyond 2mm in diameter

22
Q

How does angiogenesis affect the ECM?

A

Enzymes degrade ECM to allow for new vessel growth

23
Q

How is angiogenesis related to cancer severity?

A

Higher density of blood vessels, more severe tumour malignancy/metastasis

24
Q

How is angiogenesis inhibited?

A

Avastin (anti-VEGF antibody) binds to VEGF
Prevents VEGF-receptor interaction

(VEGF = Vascular endothelial growth factor)

25
Q

What is the ultimate effect of anti-VEGF treatments?

A

Vascular regression & dormant tumours

26
Q

What is the purpose of T cell inhibition receptors?

A

Maintain self-tolerance & protect tissue during immune responses

27
Q

How do tumours blind T cells?

A

Express specific ligand and bind to T cell inhibition receptors

28
Q

What ligand/receptor combo is used by cancers to blind T cells?

A

ligand on cancer cell = PDL-1
Receptor on T cell = PD1

29
Q

Explain therapeutic options to bypass T cell blindness to cancer cells?

A

Block PDL-1 on cancer cell or PD1 on T cell
Modified artificial T cells - CAR T cells (chimeric antigen receptors)

30
Q

What is Epithelial Mesenchymal Transition (EMT)

A

Conversion of connected epithelial cells to
independent mesenchymal cells
Enables the ability to move and invade local environment
Reversible
Occurs in Embryogenesis, cancer metastasis

31
Q

What is the function of integrin

A

Allows cells to become mobile

32
Q

What is the function of proteases in cancer

A

Creates Pathway through ECM
Matrix Metalloproteins
Contributes to loss of cell junctions

Principles of disease (47 decks)

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