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Flashcards in Outline of Disease Processes Deck (48)
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1
Q

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

A

Monoclonal (arise from a single cell)

2
Q

What does monoclonal mean?

A

Arise from a single cell

3
Q

How do cancer cells divide?

A

Using the mitosis stages just like normal cells

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

5
Q

Why do cancer cells have uncontrollable growth?

A

They have no regulation

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

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

8
Q

What can you say about cancer and oncogene expression?

A

Increase in oncogene expression leads to cancer

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

10
Q

What is carcinogenesis?

A

The initiation of cancer formation

11
Q

What are the 2 stages of carcinogenesis?

A

Pre-clinical cancer

Clinical cancer

12
Q

What are the steps of pre clinical cancer in carcinogenesis?

A

Initiation

Promotion

Tumour growth

13
Q

What happens during clinical cancer in carcinogenesis?

A

Tumour progression

14
Q

When are cancers detectable?

A

Only after a certain amount of cells are present

15
Q

What are the causes of cancer seperated into?

A

Initiation

Promotion

Progression

16
Q

What can initiate cancer?

A

Chemical

Physical

Viral

17
Q

What is related to the promotion of cancer?

A

Growth factors

Oncogenes

18
Q

What is related to the progression of cancer?

A

Metastasis

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)

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