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The control of gene expression - A Level only (3.8)›Gene expression and cancer - AL only (3.8.2.3)

Gene expression and cancer - AL only (3.8.2.3)

An overview of gene expression and cancer - AL only (3.8.2.3) from AQA A level Biology

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Tumours are abnormal growths that can be either benign (non-cancerous) or malignant (cancerous).

A comparison table titled 'Comparison of Benign and Malignant Tumours.' The table consists of two columns: 'Benign (non-cancerous)' and 'Malignant (cancerous).' Each column contains a diagram and text. The benign diagram shows a cluster of 'Tumor cells' surrounded by 'Normal cells' with a boundary. The malignant diagram shows 'Tumor cells' infiltrating 'Normal cells' without a clear boundary. The text comparisons are as follows: 1. Growth: Benign - 'Slow growing and can grow large in size'; Malignant - 'Fast growing and can grow large in size.' 2. Cell nucleus: Benign - 'Cell nucleus is normal and cells are specialised'; Malignant - 'Cell nucleus is abnormal and usually large, cells become de-differentiated and unspecialised.' 3. Cell adhesion: Benign - 'Cells stick together, often with a capsule surrounding the tumour'; Malignant - 'Cells do not adhere to each other and have no capsule. They can become unattached and produce cancerous tumours elsewhere in the body.' 4. Life-threatening: Benign - 'Unlikely to be life-threatening with only localised effect'; Malignant - 'Often life-threatening with systemic effects.' 5. Removal: Benign - 'Usually removed by surgery'; Malignant - 'Can be removed by surgery. Treatment often involves chemotherapy or radiotherapy too.' 6. Recurrence: Benign - 'Rarely reoccur if fully removed'; Malignant - 'More likely to reoccur after treatment.' The image is © Medify.

Cancer often develops due to a mutation which occurs during mitosis. This can mutate proto-oncogenes, producing oncogenes.

Proto-oncogenes cause the cell to undergo mitosis when a growth factor binds to a cell receptor. A mutated oncogene can disrupt this process, causing a cell to divide rapidly.

Tumour suppressor genes cause any errors in DNA replication to be repaired during mitosis. Tumour suppressor genes slow down the process of mitosis.

Tumour suppressor genes also tell cells when to die, this is called programmed cell death (apoptosis).

If a tumour suppressor gene becomes mutated and is switched off, this leads to increased cell division and a lack of DNA repair, leading to tumour formation.

Hypermethylation is an abnormal increase in methylation, which can lead to cancer. Hypermethylation of a promoter region of a tumour suppressor gene can lead to the tumour suppressor gene being switched off.

Hypomethylation of oncogenes can lead to the oncogenes being expressed more frequently. This leads to increased cell division and can lead to tumour formation.

After menopause, the risk of breast cancer increases due to changes in oestrogen levels.

While systemic oestrogen levels drop, breast tissue produces more oestrogen locally. This causes an increase in oestrogen which can bind to transcription factors, including a gene which controls cell division.

If a tumour begins to form, white blood cells will be attracted to the area. The increase in white blood cells causes more oestrogen to be produced locally. This increases the growth of the tumour.

Diagram titled 'Effect of Oestrogen on Transcription' showing a sequence of three steps. Step 1: A pink circle representing oestrogen passes through the plasma membrane and nuclear membrane into the cell and nucleus, with text 'Oestrogen passes into the cell and nucleus' and labeled 'Plasma membrane' and 'Nuclear membrane'. Step 2: Oestrogen binds to a blue transcription factor, depicted as a blue shape with a concave section, with text 'Oestrogen binds to transcription factor'. Step 3: This leads to 'Increased transcription of DNA occurs', indicated by a downward arrow from the transcription factor complex.