Outline of Disease Processes Flashcards

1
Q

What are most cancers (in terms of how many cells they arise from)?

A

Monoclonal (arise from a single cell)

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2
Q

What does monoclonal mean?

A

Arise from a single cell

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3
Q

How do cancer cells divide?

A

Using the mitosis stages just like normal cells

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4
Q

What are the stages of mitosis in cancer cells?

A

1) Interphase
2) Prophase
3) Metaphase
4) Anaphase
5) Telophase
6) Daughter cells

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5
Q

Why do cancer cells have uncontrollable growth?

A

They have no regulation

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6
Q

What are some properties of cancer cell that is different to normal cells?

A

Loss of contact inhibition

Increase in growth factor secretion

Increase in oncogene expression

Loss of tumour suppresor genes

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7
Q

What can you say about tumour suppresor genes in relation to cancer?

A

Cancer is caused by a loss of tumour suppresor genes

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8
Q

What can you say about cancer and oncogene expression?

A

Increase in oncogene expression leads to cancer

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9
Q

What are properties of normal cells that are different to cancer cells?

A

Oncogene expression is rare

Intermittent or co-ordinated growth factor secretion

Presence of tumour suppressor genes

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10
Q

What is carcinogenesis?

A

The initiation of cancer formation

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11
Q

What are the 2 stages of carcinogenesis?

A

Pre-clinical cancer

Clinical cancer

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12
Q

What are the steps of pre clinical cancer in carcinogenesis?

A

Initiation

Promotion

Tumour growth

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13
Q

What happens during clinical cancer in carcinogenesis?

A

Tumour progression

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14
Q

When are cancers detectable?

A

Only after a certain amount of cells are present

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15
Q

What are the causes of cancer seperated into?

A

Initiation

Promotion

Progression

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16
Q

What can initiate cancer?

A

Chemical

Physical

Viral

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17
Q

What is related to the promotion of cancer?

A

Growth factors

Oncogenes

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18
Q

What is related to the progression of cancer?

A

Metastasis

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19
Q

What are some chemicals that can initiate cancer?

A

Hydrocarbons such as soot and tarts

Analine dyes (cause bladder cancer)

Aflatoxin (causes liver cancer)

Nitrogen mustard (causes leukaemia)

Alcohol and smoking (causes lung, head and neck, and gastrointestinal cancers)

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20
Q

What are physical causes of cancer?

A

Ionising radiation

Mechanisms (chromosome translocation, gene amplification, oncogene activation)

21
Q

What are some mechanisms that are considered a physical cause of cancer?

A

Chromosome translocation

Gene amplification

Oncogene activation

22
Q

What are some virus causes of cancer?

A

Herpes virus (causes Burkitt’s lymphoma-cervical cancer)

Hepatitis B (causes liver cancer)

Papilomavirus (causes adult T cell leukaemia/lymphoma)

23
Q

What do oncogenes do?

A

Promote cells to become cancerous

24
Q

How do oncogenes promote cells to become cancerous?

A

Transformation genes

Positive regulators of growth

25
What are growth factors that promote cancer growth?
Peptide molecules that: Regulate cell growth and function Bind to cell membrane receptors Stimulate activation of intracellular signal transduction pathways
26
What do polypeptide molecules that are growth factors promoting cancer do?
Regulate cell growth and function Bind to cell membrane receptors Stimulate activation of intracellular transduction pathways
27
What do oncogenes cause in the surrounding cells?
The cells to undergo growth by paracrine stimulation
28
What does not happen in oncogene expression that normally happens?
The feedback loop that stops growth at a certain point
29
What is the most common altered tumour suppresor gene?
P53
30
What is the normal function of P53?
Transcriptional regulator Promotes DNA repair Apoptosis Differentiation
31
What induces P53 to become altered?
DNA damage Hypoxia
32
What is hypoxia?
Deficiency in the amount of oxygen reaching the tissues
33
Why is metastasis not random?
It is a cascade of tumour-host interactions in sequential steps
34
What is the process of invasion and metastasis?
1) Tumour invades through basement membrane 2) Moves into extracellular matrix/connective tissue/surrounding cells 3) Invades blood vessels 4) Spreads to distant tissues/organs
35
What are some enzymes involved in metastasis and what do they do?
Matrix metalloproteinases (MMPs which degrade the extracellular matrix) Cahedrinks, integrins and CD44 (stop cell ahesion so the cancer cell can break away)
36
What is matrix metalloproteinases (MMPs)?
Enzymes that degrade the extracellular matrix
37
What are cahedrins, integrins and CD44?
Enzymes which stop cell adhesion so the cancer cell can break away
38
What is angiogenesis?
The formation of new blood vessels
39
What is angiogenesis a key factor in?
The maintanance and progression of malignant tumours
40
What must happen for a tumour to exceed 2mm in diameter?
New blood vessels must form
41
What is required for new blood vessels to form?
Degradation of the extracellular matrix
42
What are clinical correlations seen in relation to angiogenesis and cancer?
Vessel density Tumour malignancy Metastasis
43
What can prevent tumour growth?
Drugs that can inhibit growth factors
44
What is an example of a growth factor which can be inhibited by drugs?
Vascular endothelial growth factor (VEGF)
45
46
How does the inhibition of growth factors like vascular endothelial growth factor (VEGF) work?
Drugs block receptors on epithelial cells and prevent binding of VEGF Prevents formation of new blood vessels so the tumour cannot grow
47
Why do immune cells not recognise cancer cells?
They are self
48
In terms of receptors, why do immune cells not kill cancer cells and how can we change this?
PD1 (programmed cell death receptor) is present on T cells Ligand (PDL-1) is on tumour cells Interaction of these two suppreses T cell activation, therapeutic opportunity to block either receptor