1. Biology ( )
Cancer

2. Genes that control cell division are affected when cancer develops
Proto-oncogenes stimulate cell division
Tumour suppressor genes slow down cell division
The expression of these genes can be affected by:
Heredity (genetic makeup)
Environmental exposure to carcinogens
Personal lifestyle

3. Proto-oncogenes: In a normal cell:
Growth factors attach to receptors on cell membrane
Relay proteins in the cytoplasm ‘switch on’ genes that cause DNA replication
Mitosis follows DNA replication
Mutation changes proto-oncogene into oncogene – cell division is affected by:
Receptor proteins are permanently activated
The gene codes for the production of excessive amounts of growth factors
Cells divide too rapidly, resulting in a tumour.

4. Tumour suppressor genes:
These have been linked with hereditary forms of cancer.
They have the opposite role to proto-oncogenes in normal cells – they cause inhibition of cell division.
In normal cells:
They maintain normal rates of cell division by stopping the process after mitosis is complete
Mutation causes the tumour suppressor gene to become inactive, which leads to:
Cells that divide continuously
Cells that are structurally and functionally different
Most mutant cells die but some may form tumours.

5. Environmental
chemicals and toxins
Tobacco and tobacco smoke carcinogens
Diet and alcohol
Radiation e.g., UV radiation and X-rays
Genetic factors
Viruses

6. Carcinogens in tobacco smoke can cause successive, abnormal changes
Connective tissue
Basement membrane
Ciliated columnar
epithelium
Basal cells
Carcinogens in tobacco smoke can cause successive, abnormal changes
In the normal lung, the epithelial lining of the trachea and bronchi is composed of ciliated cells

7. Normal Lung Tissue
Basal cells multiply
Mutations in basal cell proto-oncogenes and tumour suppressor genes (Ras and p53) accumulate, and these cells lose their ability to stop dividing
These basal cells are now cancerous and penetrate the basement membrane; the spread (metastasis) of these mutated basal cells to other parts of the body is the cause of death (usually within 12 months)

8. Although smoking is by far the major risk factor for lung cancer, certain industrial substances, such as asbestos, and other environmental factors contribute
The cancerous lung illustrated indicates that the patient was a smoker; deposits of tar (black areas) are visible in the tissue
Various lung diseases are caused by environmental irritants. Research the incidence, types, causes and effects of the industrial disease pneumoconiosis

9. Ultraviolet radiation from the sun is a common radiation carcinogen that can lead
to a malignant form
of skin cancer called
melanoma

10. Melanoma develops from cells in the upper epidermis of the skin called melanocytes
Melanocytes produce structures called melanosomes within which the pigment melanin is located
Melanin gives the skin its colour and absorbs ultraviolet light
Absorption of ultraviolet light by melanin protects the DNA of skin cells from damaging radiation

11. Melanocytes in the deeper layers of the epidermis produce the pigment melanin (contained within melanosomes)
magnify
Melanocyte
Melanosomes form a coating above the nuclei of skin cells – this protects the DNA from damaging radiation
Processes carry melanosomes to epidermal cells
Melanin in melanosomes

12. Skin colour is determined genetically and relates to the amount of melanin in the skin
Skin colour is determined through the action of several genes and is therefore an example of polygenic inheritance
Skin colour is a continuously varying trait ranging from very light to very dark
Dark skin differs from fair skin in that the melanosomes (containing melanin) are larger and more evenly spread in the epidermis
Pale skinned individuals are particularly susceptible to developing melanoma, especially if they live in sunny, tropical climates (higher intensities of damaging UV radiation)

13. Malignant skin lesions are usually characterised by rapid growth, an irregular boundary, colour variation, and a tendency to bleed and become crusty

14. Mutation in the CDKN2 gene on What kind of a gene is CDKN2?
Some cases of malignant melanoma are familial – they tend to run in families
Mutation in the CDKN2 gene on
chromosome 9 is responsible for susceptibility to the familial form of melanoma
CDKN2 codes for a protein called p16 that is an important regulator of the cell cycle
p16 stops the cell from synthesising DNA – a precursor step for cell division
When p16 is faulty (due to mutation of the CDKN2 gene), the cell does not have this necessary ‘brake’ and uncontrolled cell division occurs; a skin growth appears
What kind of a gene is CDKN2?

15. Mutation in the CDKN2 gene on CDKN2 is a tumour suppressor gene
Some cases of malignant melanoma are familial – they tend to run in families
Mutation in the CDKN2 gene on
chromosome 9 is responsible for susceptibility to the familial form of melanoma
CDKN2 codes for a protein called p16 that is an important regulator of the cell cycle
p16 stops the cell from synthesising DNA – a precursor step for cell division
When p16 is faulty (due to mutation of the CDKN2 gene), the cell does not have this necessary ‘brake’ and uncontrolled cell division occurs; a skin growth appears
CDKN2 is a tumour suppressor gene

16. Discuss the variation in cancer incidence and types
in different world regions