Outline of Disease Process CANCER Flashcards

1
Q

What does “cancers are mostly monoclonal” mean?

A

They 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

The 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

Ionising radiation:
- Translocate chromosomes
- Amplify certain Genes
- Activate Oncogenes

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10
Q

What viral carcinogen causes burkitts lymphoma?

A

Herpes virus causes burkitts lymphoma

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11
Q

What viral carcinogen caues liver cancer?

A

HEP B can cause liver cancer.

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12
Q

What 3 things are involved in the promotion stage?

A

Oncogens
Tumour supresser genes
Growth factors

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13
Q

How do oncogenes promote the progression stage?

A

Oncogenes are positive regulaters of growth, they 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

Define autocrine signaling?

A

When a cell secretes a substance (i.e. growth factor) that acts on receptors on the same cell inducin changes in it

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16
Q

Whats the difference between autocrine & paracrine signalling?

A

Paracrine signalling involves signals acting on nearby cells, autocrine involves signals acting on the same cell that produces them

17
Q

Whats the normal function of tumor suppressor genes?

A

Promoting DNA repair, Apoptosis & differentiation

18
Q

What normally induces tumor suppressor genes to act?

A

Hypoxia & DNA damage

19
Q

Name a tumor supressor gene

A

P53

20
Q

How does progression (metastasis) occur?

A

Tumour invades through basement membrane.
Invades into ECM/connective tissue/other cells
Invades blood vessles
Finally cells arressted in a distant tissue

21
Q

IS the progression stage random?

A

No its a series of limited sequential steps involivng host-tumor interactions

22
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

23
Q

How does angiogenesis affect the ECM?

A

Enzymes degrade the ECM to allow for new vessel growth

24
Q

How is angiogenesis related to cancer severity?

A

Theres a correlation between vessel density and tumour malignancy/metastasis.

25
Q

How is angiogenesis inhibited?

A

-> Avastin (anti-VEGF antibody) binds to VEGF
-> prevents VEGF-receptor interaction

26
Q

What is the ultimate effect of anti-VEGF treatments?

A

Vascular regression & dormant tumours

27
Q

What is the purpose of T cell inhibition receptors?

A

TO maintain self-tolerance & protect tissue duing immune responses

28
Q

How do tumours blind T cells to them?

A

They express a specific ligand and bind to T cell inhibition receptors

29
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

30
Q

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

A

Block PDL-1 on cancer cell or PD1 on T cell.
Or use modified aritifical T cells (chimeric antigen receptors, CAR T cells)