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
Q

What are growth factors that promote cancer growth?

A

Peptide molecules that:

Regulate cell growth and function
Bind to cell membrane receptors
Stimulate activation of intracellular signal transduction pathways

26
Q

What do polypeptide molecules that are growth factors promoting cancer do?

A

Regulate cell growth and function

Bind to cell membrane receptors

Stimulate activation of intracellular transduction pathways

27
Q

What do oncogenes cause in the surrounding cells?

A

The cells to undergo growth by paracrine stimulation

28
Q

What does not happen in oncogene expression that normally happens?

A

The feedback loop that stops growth at a certain point

29
Q

What is the most common altered tumour suppresor gene?

A

P53

30
Q

What is the normal function of P53?

A

Transcriptional regulator

Promotes DNA repair

Apoptosis

Differentiation

31
Q

What induces P53 to become altered?

A

DNA damage

Hypoxia

32
Q

What is hypoxia?

A

Deficiency in the amount of oxygen reaching the tissues

33
Q

Why is metastasis not random?

A

It is a cascade of tumour-host interactions in sequential steps

34
Q

What is the process of invasion and metastasis?

A

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
Q

What are some enzymes involved in metastasis and what do they do?

A

Matrix metalloproteinases (MMPs which degrade the extracellular matrix)

Cahedrinks, integrins and CD44 (stop cell ahesion so the cancer cell can break away)

36
Q

What is matrix metalloproteinases (MMPs)?

A

Enzymes that degrade the extracellular matrix

37
Q

What are cahedrins, integrins and CD44?

A

Enzymes which stop cell adhesion so the cancer cell can break away

38
Q

What is angiogenesis?

A

The formation of new blood vessels

39
Q

What is angiogenesis a key factor in?

A

The maintanance and progression of malignant tumours

40
Q

What must happen for a tumour to exceed 2mm in diameter?

A

New blood vessels must form

41
Q

What is required for new blood vessels to form?

A

Degradation of the extracellular matrix

42
Q

What are clinical correlations seen in relation to angiogenesis and cancer?

A

Vessel density

Tumour malignancy

Metastasis

43
Q

What can prevent tumour growth?

A

Drugs that can inhibit growth factors

44
Q

What is an example of a growth factor which can be inhibited by drugs?

A

Vascular endothelial growth factor (VEGF)

45
Q
A
46
Q

How does the inhibition of growth factors like vascular endothelial growth factor (VEGF) work?

A

Drugs block receptors on epithelial cells and prevent binding of VEGF

Prevents formation of new blood vessels so the tumour cannot grow

47
Q

Why do immune cells not recognise cancer cells?

A

They are self

48
Q

In terms of receptors, why do immune cells not kill cancer cells and how can we change this?

A

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