An outline of the Cancer Process Lectures 1,2,3 Flashcards

1
Q

What does a monoclonal cancer mean?

A

Arises from a single cell

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2
Q

Which stage of the cell cycle can give rise to non-proliferating cells?

A

G1

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3
Q

Describe the activity of cancer cells

A

Frequent mitosis
Increase in growth factor secretion
Loss of contact inhibition

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4
Q

Describe the structure of cancer cells

A

Lots of blood vessels
Increase in oncogene expression
Loss of tumour suppressor genes

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5
Q

What are the initiation causes of cancer?

A

Chemical
Physical
Viral

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6
Q

Give an example of chemicals which cause cancer

A

Nitrogen mustard gas - leukaemia

Aninline dyes - bladder cancer

Alcohol and smoking - Lung, head and neck, GI

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7
Q

Give an example of physical carcinogens

A

Ionising radiation - Radon source is mainly in buildings, risk increased by smoking, ventilation reduces risk

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8
Q

What is the mechanism of ionising radiation to cause cancer?

A

Chromosome translocation
Gene amplification
Oncogene activation

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9
Q

Give an example of Viral carcinogens

A

Papillomavirus - cervical cancer

Hepatitis B - Livercancer

Herpes Virus - Burkitt’s lymphoma

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10
Q

What are growth factors and what are their effects?

A

Polypeptide molecules

Regulate cell growth and function, bind to cell membrane receptors, stimulate activation of intracellular signal transduction pathways

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11
Q

Define autocrine stimulation

A

Cell carries the receptor and secretes growth factor

Cell escapes normal control mechanism

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12
Q

Define paracrine stimuation

A

GF’s are produced by local neighbour

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13
Q

Describe the process of invasion and metastasis

A

Tumour invades through basement membrane
Moves into extracellular matrix/connective tissue/surrounding cells
Invades blood vessels
Tumour cells ‘arrested’ in distant organ

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14
Q

What is the effect of Matrix metalloproteinases, Plasmin and Cathepsin on Invasion and metastasis?

A

Increase the likelihood of the cell coming into the extracellular matrix and metastasising

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15
Q

What is the role of enzymes involved in cell adhesion (cahedrins, Integrins, CD 44) on Invasion and metastasis?

A

makes the cell less sticky so it is more likely to invade other cells

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16
Q

What is the cost of angiogenesis in the maintenance and progression of tumours?

A

Degradation of the extracellular matrix - necessary for new blood vessel formation to occur

17
Q

What is the most commonly altered gene in human tumours?

A

P53 which is a tumour suppressor gene

18
Q

What is the normal function of the p53 gene?

A

Transcriptional regulator, promotes DNA repair, apoptosis, diffrerentiation

It is the G1/S checkpoint control gene

19
Q

What stimulates p53?

A

Induced by DNA damage and hypoxia

20
Q

Give an example of a growth factor

A

Vascular endothelial growth factor VEGF - leads to the growth, proliferation, migration and survival of endothelial cells

21
Q

What is the effect of Anti-VEGF?

A

Prevents the action of VEGF on receptors.

Reduces microvascular growth, inhibits the progression of metastatic disease and reduces intratumoral pressure, which may improve the delivery of cytotoxic agents.

22
Q

What is the function of the PD-1 protein?

A

Expressed on T cels and pro-B cells.

Plays an important role in down-regulating the immune system by preventing the activation of T-cells, reducing autoimmunity and promotes self-tolerance.

23
Q

What is the effect of the binding between PDL-1 (found on the surface of cells in various tissues) and PD-1?

A

Promotes immunosuppression to various mechanisms including apoptosis

24
Q

How can a PD-1 inhibitor treat cancer?

A

Prevents the binding interaction between PD-1 and PDL-1 and so activates the immune system to attack tumours

25
Q

How does the presence of PDL-1 in cancer cells affect survival?

A

PDL-1 stops the immune system recognising the cancer cells - reduced survival rates.