What is cancer?

Question 1

Define cancer.

Answer 1

The uncontrolled growth of abnormal cells that is both invasive and metastasising to secondary sites.

Question 2

In what type of tissue do the majority of cancers arise?

Answer 2

Epithelial tissue

Question 3

What is an adenoma?

Answer 3

A benign tumour of the glandular structures in epithelial tissue

Question 4

What is a carcinoma?

Answer 4

Cancer of epithelial cells

Question 5

What is an adenocarcinoma?

Answer 5

A malignant tumour of the glandular structures in epithelial tissue

Question 6

What types of cancers are classified by their effect on haematopoietic and immune cells?

Answer 6

Leukaemia (arise in BM - abnormal WBC)
Lymphoid
Myeloid (Affects all myeloid cells - WBC, platelets, RBC..)

Question 7

Which cells commonly give rise to brain tumours?

Answer 7

Glial cells or neuroblast (embryonic cell)

Question 8

What is the difference between a mutation in germline cells and somatic cells?

Answer 8

Germline mutations PREDISPOSE

Somatic mutations CAUSE

Question 9

How does one mutation result in the development of a many cells with the mutation?

Answer 9

The mutated cell will undergo MONOCLONAL growth

Question 10

Why does cancer not appear to be monoclonal in the late stages?

Answer 10

The cells become heterogeneous as more mutations accumulate and develop.

Question 11

The genes that mutate in cancer usually have a function in control. What functions will this affect?

Answer 11

Growth, Cell cycle, Receptors, Stemness (ability to self renew and differentiate into different types of cells), apoptosis, integrity and repair of DNA

Question 12

Why may a mutation occur?

Answer 12

Due to copying errors in DNA replication.
Exposure - UV, radiation
Spontaneous depurination (chemical damage)

Question 13

What must the mutation provide in order to develop into a malignancy?

Answer 13

Must provide a growth advantage to the cell, allowing it to survive and invade

Question 14

What are the two main types of genes commonly affected in cancer?

Answer 14

TSG

Oncogenes

Question 15

What is the function of a TSG? How is the function lost in cancer?

Answer 15

Negatively regulates growth. Must lose BOTH alleles to lose the suppressor effect.

Question 16

What is an oncogene? How is the function lost in cancer?

Answer 16

Positive regulator of growth. Overexpression and activation may occur with the mutation of only ONE allele.

Question 17

What are the 6 hallmarks of cancer?

Answer 17

The characteristics of a tumour cell that allows it to be malignant and metastasise.

• Self sufficiency in growth signals
• Intensity to anti-growth signals
• Evasion of apoptosis
• Limitless replication potential
• Sustained angiogenesis
• Tissue invasion and metastasis

Question 18

Describe the self sufficiency in growth signals hallmark.

Answer 18

A mutation in a receptor causes continuous signalling through ligand-independent firing, despite the lack of an extracellular signal.
The receptor may also produce its own GF in response to an autocrine signal.

Question 19

Describe the intensity to anti-growth signals hallmark.

Answer 19

Disrupting the TSG pathway of pRB results in loss of control over G1 to S phase progression. Loss of pRB leads to over proliferation.

Question 20

Describe the evasion of apoptosis hallmark.

Answer 20

p53 is pro-apoptotic. It decides if cell damage can be reversed. If a cell is stressed, p53 levels increase for repair or death. If it is lost or mutated, DNA repair will be disrupted and the cell will evade apoptosis.
The cancer will either increase anti-apoptotic and decrease pro-apoptotic.

Question 21

Describe the limitless replication potential hallmark.

Answer 21

When a cell divides its telomere shortens, limiting the number of times it can divide. Once it reaches its limit it will become senescent.
Cancer cells express telomerase so they can proliferate without telomeres.

Question 22

What is the purpose of a telomere?

Answer 22

To limit the number of divisions and to prevent fusion with neighbouring chromosomes.

Question 23

Decribe the sustained angiogenesis halmark.

Answer 23

Tumours are highly metabolic, requiring high blood supply for oxygen and nutrients. Mutations will allow control of transcription of pro-angiogenic inducers and downregulate inhibitors for the sprouting of vessels.
Hypoxia plays a role in this.

Question 24

Describe the tissue invasion and metastasis hallmark.

Answer 24

Epithelial tumours can change there morphology to a mesenchymal cell for migration and metastasis. The cells change the adhesion molecules, cadherins and integrins.
Secondary site preparation occurs through the secretion of cytokines to attract cells and form a microenvironment.
Metastatic spread is determined by the genes of the primary tumour as to where they travel to.

Question 25

What are the two emerging hallmarks?

Answer 25

Deregulating cellular energetics - changes in cellular metabolism and stroma
Avoiding immune destruction

Question 26

What are the two enabling characteristics?

Answer 26

Mutations in genes, maintaining stability and DNA repair give advantage to tumour cells.
Tumour promoting inflammation - Immune cells provide factors to support the tumour, by suppressing the immune system.