L01 - What is Cancer? Flashcards

1
Q

Define cancer.

A

The uncontrolled growth of abnormal cells in a tissue, which are invasive and metastasising

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2
Q

From where do the majority of tumours originate?

A

Epithelial tissues

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3
Q

List 4 types of cancer and where they arise from.

A

1 - Carcinoma (epithelium)

2 - Sarcomas (mesenchymal cells)

3 - Leukaemias & lymphoid/myeloid tumours (haematopoietic tissue and immune cells)

4 - Neuroectodermal tumours (CNS and PNS)

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4
Q

List 3 mechanisms that cause mutations in DNA.

A

1 - Copying errors during DNA replication

2 - Spontaneous depurination

3 - Exposure to carcinogenic agents

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5
Q

What is the function of tumour suppressor genes?

A

Negative regulation of cell growth

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6
Q

How many alleles of a tumour suppressor gene must be disrupted for tumour suppressor function to be lost?

Why?

A

Both alleles must be disrupted to lose the suppressor effect because protein produced from one of the two alleles is enough to prevent cell growth

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7
Q

What is the function of oncogenes?

A

Positive regulation of cell growth

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8
Q

How many alleles of an oncogene must be disrupted to lose oncogenetic function?

Why?

A

Both alleles must be disrupted to lose the oncogenetic effect because protein produced from one of the two alleles is enough to promote cell growth

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9
Q

List the stages of development of a carcinoma.

Give an example of a protein involved in each stage.

A

1 - Normal cells become early adenomas (APC protein)

2 - Early adenomas become late adenomas (K-ras protein)

3 - Late adenomas become carcinomas (p53)

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10
Q

What are gate-keeper mutations and driver mutations?

A

Gate-keeper mutations start tumour development -> irregular growth regulation + differentiation

Driver mutations allow tumour to continue growth -> gives a selective advantage to a clone in its microenvironment, through either increasing its survival or reproduction;
tend to cause clonal expansions

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11
Q

List 6 hallmarks of cancer.

A

1 - Self-sufficiency in growth signals

2 - Insensitivity to anti-growth signals

3 - Evasion of apoptosis

4 - Limitless replicative potential

5 - Sustained angiogenesis

6 - Tissue invasion & metastasis

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12
Q

What processes are involved in sustaining proliferative signalling?

A

1 - Alterations of extracellular growth signals

2 - Alterations of transmembrane transducers of growth signals

3 - Alterations of intracellular circuits that translate growth signals

4 - Ability of cancer cells to produce own growth factor to activate own receptors (autocrine signalling)

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13
Q

Describe a mechanism that enables evasion of growth suppressors.

A

Disruption of pRb (TSG) pathway, leading to a loss of control over progression from G1 into S phase (restriction point)

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14
Q

What is the function of pRb?

A

Prevents progression of the cell division cycle from the G1 (first gap phase) to S (synthesis phase) phase - the restriction point

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15
Q

Describe a mechanism that enables evasion of apoptosis.

A

Loss or mutation of p53 (TSG), which is a proapoptotic regulator, therefore there is a reduction in apoptosis of a cancer cell

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16
Q

List 5 p53-activating signals.

A

1 - Lack of nucleotides

2 - UV/Ionising radiation

3 - Oncogene signalling

4 - Hypoxia

5 - Blockage of transcription

17
Q

List 4 effects of p53.

A

1 - Cell cycle arrest -> senescence or return to proliferation

2 - DNA repair

3 - Block of angiogenesis

4 - Apoptosis

18
Q

Describe a mechanism that enables limitless replicative potential.

A

Increased expression & activity of telomerase leading to circumvention of senescence & crisis

19
Q

What is the angiogenic switch?

A

The point at which the balance between pro- and anti-angiogenic factors tilts towards a pro-angiogenic outcome, resulting in the transition from dormant avascularised hyperplasia to outgrowing vascularised tumour and eventually to malignant tumour progression

20
Q

List 2 emerging hallmarks of cancer.

A

1 - Deregulation of cellular energetics

2 - Avoidance of immune destruction

21
Q

List 2 enabling characteristics of cancer.

A

1 - Genome instability & mutations in genes for stability & DNA repair

2 - Promotion of inflammation