What is Cancer?

Question 1

What is the most common type of cancer?

What proportion of all cancers are represented by this type of cancer?

Answer 1

• Carcinomas.

- 85%.

Question 2

List 4 types of cancer.

For each cancer, state the name of the tissue from which they arise.

Answer 2

1 - Carcinoma (epithelium).

2 - Sarcomas (mesenchymal cells).

3 - Leukaemias (haematopoietic tissue and immune cells).

4 - Neuroectodermal tumours (CNS and PNS).

Question 3

List 5 examples of carcinomas.

Answer 3

1 - Adenocarcinoma.

2 - Squamous cell carcinoma.

3 - Small-cell lung carcinoma.

4 - Large-cell lung carcinoma.

5 - Transitional cell carcinoma.

Question 4

List 5 examples of sarcomas.

State the cell lineage from which each sarcoma is derived.

Answer 4

1 - Osteosarcoma (osteoblasts).

2 - Liposarcoma (adipocytes).

3 - Leiomyosarcoma (smooth muscle).

4 - Rhabdomyosarcoma (striated and skeletal muscle).

5 - Malignant fibrous histiocytoma (adipocytes and muscle cells).

Question 5

List 4 examples of leukaemias.

Answer 5

1 - Acute / chronic lymphocytic leukaemia.

2 - Multiple myeloma.

3 - Non-Hodgkin’s lymphoma.

4 - Hodgkin’s lymphoma.

Question 6

List 5 examples of neuroectodermal tumours.

State the cell lineage from which each neuroectodermal tumour is derived.

Answer 6

1 - Astrocytoma (astrocytes).

2 - Glioblastoma multiforme (astrocytes - a more highly progressed tumour).

3 - Meningioma (arachnoidal cells of meninges).

4 - Schwannoma (Schwann cells).

5 - Retinoblastoma (cone cells of the retinae).

Question 7

List 3 mechanisms that cause mutations in DNA.

Answer 7

1 - Copying errors during DNA replication.

2 - Spontaneous depurination.

3 - Exposure to carcinogenic agents.

Question 8

What is the function of tumour suppressor genes?

Answer 8

To prevent cell growth.

Question 9

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

Why?

Answer 9

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.

Question 10

What is the function of oncogenes?

Answer 10

To promote cell growth.

Question 11

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

Why?

Answer 11

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.

Question 12

List the stages of development of a carcinoma.

Give an example of a protein involved in each stage.

What is this sequence known as?

Answer 12

1 - Normal cells become early adenomas (APC protein).

2 - Early adenomas become late adenomas (k-ras protein).

3 - Late adenomas become carcinomas (p53).

• Known as the adenoma-carcinoma sequence.

Question 13

List 6 hallmarks of cancer.

Answer 13

1 - Sustaining proliferative signalling.

2 - Evading growth suppressors.

3 - Evasion of apoptosis.

4 - Enabling replicative immortality.

5 - Inducing angiogenesis.

6 - Activating invasion and metastasis.

*The rest of this deck goes into more depth on these points.

Question 14

List the processes involved in sustaining proliferative signalling.

Answer 14

1 - Alterations of extracellular growth signals.

2 - Alterations of transmembrane transducers of growth signals.

3 - Alterations of intracellular circuits that translate growth signals.

Question 15

How might alterations of transmembrane transducers produce sustained proliferative signalling?

Answer 15

Mutations to growth factor receptors might enable ligand-independent firing.

Question 16

What type of receptor are growth factor receptors?

Answer 16

Tyrosine kinase receptors.

Question 17

List the pathways initiated by ras protein.

Answer 17

1 - Ral-GEF pathway.

2 - MAPK-ERK pathway.

3 - PI3k-Akt pathway.

Question 18

Describe a mechanism that enables evasion of growth suppressors.

Answer 18

Disruption of the pRb pathway causes loss of control over progression from G1 into S phase.

Question 19

What is the function of pRb?

Answer 19

To inhibit cell proliferation.

Question 20

List 5 factors that contribute to the ‘cell cycle clock’.

Answer 20

1 - Tyrosine kinase receptor activity.

2 - GPCR activity.

3 - TGF-beta receptor activity.

4 - Integrin activity.

5 - Nutrient status.

Question 21

List the phases of the cell cycle in order.

Answer 21

1 - G1.

2 - S.

3 - G2.

4 - M.

Question 22

Describe a mechanism that enables evasion of apoptosis.

Answer 22

Loss of p53 function (a proapoptotic regulator).

Question 23

List 5 p53-activating signals.

Answer 23

1 - Lack of nucleotides for DNA production.

2 - UV radiation.

3 - Ionising radiation.

4 - Oncogene signaling.

5 - Hypoxia.

Question 24

List 4 effects of p53.

Answer 24

1 - Apoptosis.

2 - Blockage of angiogenesis.

3 - DNA repair.

4 - Cell cycle arrest leading to senescence or return to proliferation.

Question 25

Describe a mechanism that enables replicative immortality.

Answer 25

Increased expression of telomerase (a protein that extends the telomere).

Question 26

How does telomere length affect replicative potential?

Answer 26

Decreased telomere length is interpreted as DNA damage, halting the cell cycle.

Question 27

List 2 angiogenic activators.

Answer 27

1 - VEGF-A, B and C.

2 - FGF1 and 2.

Question 28

List 5 angiogenic inhibitors.

Answer 28

1 - Thrombospondin-1 and 2.

2 - Interferon-alpha and beta.

3 - Angiostatin.

4 - Endostatin.

5 - Collagen IV fragments.

Question 29

Define angiogenic switch.

Answer 29

An alteration in the balance of pro-angiogenic and anti-angiogenic molecules that leads to tumor neovascularization.

Question 30

Describe the mechanism by which cancerous cells invade other tissues.

Answer 30

1 - Changes in expression of adhesion receptors such as cadherins and integrins.

2 - Activation of extracellular proteases such as with epithelial-mesenchymal transition.

Question 31

Define glycolytic switch.

Answer 31

The switch from oxidative phosphorylation to glycolysis as seen in cancerous tissue.

Question 32

What is a philadelphia chromosome?

In which type of cancer is this particularly common?

Answer 32

• A genetic abnormality in chromosome 22 of leukaemia cancer cells.
• Particularly common in chronic myeloid leukaemias.

Question 33

Give an example of a non-hodgkin lymphoma.

From which cell lineage is this cancer derived?

Give an example of a gene involved in the formation of this cancer.

Answer 33

• Burkitt lymphoma.
• B cells.
• The MYC gene is involved in the formation of this cancer.