Cancer Summary (Core 4)

Intro to Cancer: 

Clinically, cancer is defined as a family of a large number of different complex diseases.
• Cancers vary in their ages of onset, growth rates, prognoses and responsiveness to treatments.
• Despite their differences, all cancers exhibit common characteristics at the molecular level that
unite them as a family.
• Cancers are a result of uncontrolled cell division (mitosis).

TUMOURS
• When a cell loses genetic control over cell growth
(due to mutations), it can result in a tumour.
• Tumour = a mass or lump of cells, with an inherited
capacity for autonomous, uncontrolled growth, resulting
from uncontrolled cell division.

• 2 types of tumours:
ƒ Benign tumours
o Surrounded by a connective tissue capsule
and thus isolated (eg, moles, warts).

o Cells are not cancerous but conversion to
cancerous cells is possible.


o Benign tumours can be removed surgically or
killed by radiation, usually eliminating any
further cancer development at that site.

o More typical compared to malignant tumours.

ƒ Malignant tumour
o Made up of cancer cells
o Connective tissue capsule breaks down and cancer cells send out signals for the
production of a new blood vessels (angiogenesis) at the tumour site.
ƒ This is because blood supply allows removal of metabolic waste and supply of
nutrients which allow for rapid growth.
ƒ Angiogenesis is also required for the spread of cancer.

o These cells can also:
ƒ (i) invade and damage surrounding tissues (invasion);
ƒ (ii) separate from the original tumour and penetrate blood and lymph vessels
of the circulatory system, thus spreading to other parts of the body and
proliferate to form new tumours (metastasis).
ƒ
ƒ Metastasis is the spreading of cancer cells to locations distant from their original site. Usually
surgery is performed to remove the tumour, followed by radiation and chemotherapy.

Cell Cycle Control

G1 Checkpoint




Assess cell growth
Go ahead  G1, S, G2 and M phase
Or exit the cycle  G0 phase
G0 phase: Forever (Muscle & Nerve) or Enter into cell cycle (during injury)

G2 Checkpoint


Assess success of DNA replication
Go ahead to begin mitosis.

M Checkpoint

Assess mitosis.
Exit from mitosis and cytokinesis and beginning of G1.


2 Mechanisms of Cell Cycle Control

Cyclins and Cyclin-dependent protein kinase (Cdk)

Interact at checkpoints to trigger the next events in the cell cycle.

(2) External Physical Factors

A growth factor is a protein  stimulates other cells to divide.
Binding of a growth factor leads to a cascade of intracellular signaling pathway  triggers cell division.
No need to memorize Figure 15. It is only for illustration purpose!

Normal cells

Show density-dependent inhibition
Show anchorage dependence

CANCER

Failure to Regulate Checkpoints of Cell Cycle
 Uncontrolled cell growth

Cancer cells do not:
Exhibit density-dependent inhibition
Exhibit anchorage dependence
Stop dividing when growth factors are depleted
Stop cell division to repair DNA

(1) Proto-oncogenes

GAIN OF FUNCTION MUTATION

Proto-oncogene Oncogene

Promote excessive cell division  cancer

(1) Proto-oncogenes

LOSS OF FUNCTION MUTATION

Tumour suppressor gene

Example
of
Tumour
suppressor
gene:
p53 gene

Mutation

Cannot inhibit abnormal cell division  cancer