gene expression and cancer Flashcards

1
Q

what is cancer?

A

a group of diseases caused by damage to genes that regulate mitosis and the cell cycle leading to unrestrained growth of cells. Consequently, a group of abnormal cells, a tumour, develops and constantly expands in size

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2
Q

not all tumours are cancerous, those that are cancerous are called

A

malignant

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3
Q

tumours that are not cancerous are called

A

benign

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4
Q

what are some key differences between malignant and benign tumours?

A
  • benign grow very slowly whereas malignant grow rapidly
  • cell nucleus of benign has a relatively normal appearance whereas the cell nucleus of malignant often appear darker and larger due to an abundance of DNA
  • benign tumour cells produce adhesion molecules that makes them stick together and so they remain in tissue from which they arise= PRIMARY TUMOURS whereas malignant tumour cells do not produce adhesion molecules so they spread to other regions of the body, a process called metastasis= SECONDARY TUMOURS
  • benign tend to have localised effects on the body whereas malignant often have whole-body effects like weight loss and fatigue
  • benign can usually be removed by surgery alone whereas malignant removal usually involves radio and or chemotherapy along with surgery
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5
Q

in general, cancer cells are derived from a single mutant cell- explain how

A
  • the initial mutation causes uncontrolled mitosis in this cell
  • later, a further mutation in one of the descendant cells leads to other changes that causes subsequent cells to be different from normal in growth and appearance
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6
Q

what are the 2 main types of gene that play a role in cancer?

A
  • oncogenes

- tumour suppressor genes

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7
Q

what are oncogenes?

A

mutations of proto oncogenes

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8
Q

what is the role of proto oncogenes?

A

stimulate a cell to divide when growth factors attach to a protein receptor on its cell-surface membrane
- this then activates genes that cause DNA to replicate and cell to divide

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9
Q

if a proto oncogene mutates into an oncogene genes that cause DNA to be replicated can be permanently activated (switched on) for 2 reasons:

A

1- the receptor protein on the cell-surface membrane can be permanently activated so cell division is switched on in even in the absence of growth factors
2- the oncogene may code for a growth factor that is then produced in excessive amounts, again stimulating excessive cell division

result is that cells divide too rapidly and out of control= a tumour, or cancer develops

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10
Q

a few cancers are caused by inherited mutations of proto-oncogenes that cause the oncogene to be activated but most cancer-causing mutations oncogenes are

A

acquired not inherited

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11
Q

explian how a proto oncogene’s role in cell division is like the accelerator pedal of a car

A
  • it simply controls how fast it goes
  • when it mutates into an oncogene it is as if the accelerator pedal has become stuck down and so cell division occurs at a very rapid and uncontrolled rate
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12
Q

what is the role of tumour suppressor genes?

A

slow down cell division, repair mistakes in DNA and ‘tell’ cells when to die- apoptosis (programmed cell death) so therefore have the opposite role to oncogenes

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13
Q

what happens if a tumour suppressor gene become mutated?

A
  • it is inactivated (switched off)
  • as a result, it stops inhibiting cell division and cells can grow out of control
  • the mutated cells formed are usually structurally and functionally different from normal cells
  • while most of these die, those that survive can make clones of themselves and form tumours
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14
Q

give an example of a tumour suppressor gene

A

BRAC1

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15
Q

what’s an important difference between oncogenes and tumour suppressor genes?

A
  • oncogenes can cause cancer as a consequence of activation of proto oncogenes
  • tumour suppressor genes cause cancer when inactivated
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16
Q

explain how hypermethylation can silence tumour suppressor genes

A
  • hypermethylation (increased methylation) occurs in a specific region (promoter region) of tumour suppressor genes
  • this leads to tumour suppressor gene becoming inactivated
  • so transcription of the promoter region of tumour suppressor gene is inhibited
  • tumour suppressor gene therefore silenced leading to increased cell division and thus tumour formation
17
Q

explain how increased levels of oestrogen in post-menopausal women can lead to increased risk of breast cancer?

A
  • oestrogen effectively activates a gene by binding to a receptor which promotes transcription
  • if the gene that oestrogen acts on is one that controls cell division and growth, then it will be activated and its continued division could cause a tumour
  • also known that oestrogen causes proto oncogenes of cells in breast tissues to develop into oncogenes= development of tumour and thus breast cancer