Module 8- Cancer Flashcards

1
Q

3 marks

The KRAS gene codes for a protein called K-Ras. The protein relays signals from outside a cell to a cell’s nucleus, stimulating cell division. An alteration in the KRAS gene produces an oncogene which can cause a tumour to develop.
Suggest and explain how an alteration in the KRAS gene can cause a tumour to develop.

A
  1. Mutation in KRAS gene
  2. Change in signalling protein
  3. Results in uncontrollable cell division
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2
Q

3 marks

Describe how alterations to tumour suppressor genes can lead to the development of tumours.

A
  1. Increased methylation of tumour suppressor genes
  2. Mutation in tumour suppressor genes
  3. Tumour suppressor genes are not transcribed/expressed
    OR
    Amino acid sequence/primary structure altered
  4. Results in uncontrollable cell division
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3
Q

Define metastasis

A

Cells can break off these tumours and spread to other parts of the body through the bloodstream or lymphatic system

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4
Q

Define malignant tumour

A

Uncontrolled mitosis, unspecialised cells, metastasis

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5
Q

Define oncogene

A

Could cause expression of excessive growth factor protein or distortion of receptor protein= uncontrolled mitosis

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6
Q

Define tumour suppressor gene

A

Could cause expression of proteins that cause apoptosis (P53)= death of tumour cells

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7
Q

3 marks

Increased methylation of the promoter region of a tumour suppressor gene causes one type of human throat cancer. In this type of throat cancer, cancer cells are able to pass on the increased methylation to daughter cells. The methylation is caused by an enzyme called DNMT. Scientists have found that a chemical in green tea, called EGCG, is a competitive inhibitor of DNMT. EGCG enables daughter cells to produce
mRNA from the tumour suppressor gene. Suggest how EGCG allows the production of mRNA in daughter cells.

A
  1. EGCG binds to active site of DNMT
  2. DNMT cannot methylate promoter region of tumour suppressor gene
  3. Transcription factor can bind to promoter region
  4. RNA polymerase stimulated
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8
Q

3 marks

Sometimes, a mutagenic agent causes DNA to break. A different enzyme called ATM binds to the broken DNA. This leads to the activation of a protein coded for by a tumour suppressor gene. The effect of ATM binding is to stop cell division until DNA is repaired. A mutation could result in a person having non-functional forms of the gene that produces ATM. What can you predict about the possible effects of having a non-functional form of ATM?

A
  1. ATM will not bind to broken DNA
  2. DNA not repaired
  3. Cell division continues
  4. Tumour suppressor gene activated
  5. May have no effect in diploid / heterozygous organism
  6. Which still has a functional ATM
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9
Q

3 marks

Explain how increased methylation could lead to cancer.

A
  1. Methyl groups could be added to both copies of a tumour suppressor gene
  2. The transcription of tumour suppressor genes is inhibited
  3. Leading to uncontrolled cell division
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10
Q

1 mark

Give one way in which benign tumours differ from malignant tumours.

A

Cells of benign tumours cannot metastasise (spread to other parts of the body)

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11
Q

3 marks

Explain how the methylation of tumour suppressor genes can lead to cancer.

A
  1. Methylation prevents transcription of gene
  2. Protein not produced that prevents cell division / apoptosis (cell death)
  3. No control of mitosis
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12
Q

2 marks

The doctors compared median survival times for patients in each group. How would you find the median survival time for a group of patients?

A
  1. Rank all STs in ascending order
  2. Find value with same number of people above and below
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13
Q

MM is caused by a faulty receptor protein in cell-surface membranes. Cells in MM tumours can be destroyed by the immune system. Suggest why they can be destroyed by the immune system.

A
  1. Faulty protein recognised as an antigen (foreign protein)
  2. T cells will bind to faulty protein
  3. T cells will stimulate clonal selection of B cells
  4. Resulting in release of antibodies against faulty protein
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14
Q

1 mark

Some tumours are benign and some are malignant. Give one way in which a benign tumour differs from a malignant tumour.

A

benign does not cause cancer / does not invade other tissues causing damage / with benign cancer, pieces which break off do not start new tumours elsewhere in body / metastasis

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15
Q

Describe two ways in which both types of tumour (benign and malignant) may cause harm to the body.

A
  1. may damage organ concerned
  2. may cause blockages / obstructions
  3. may damage / exert pressure on other organ
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16
Q

2 marks

Explain the link between sunbathing and skin cancer.

A
  1. because sun’s radiation contains ultra violet radiation
  2. This causes mutation of genes which control division
17
Q

1 mark

Suggest why fair-skinned people are at a greater risk of skin cancer than dark-skinned people when sunbathing.

A

because fair skin has little melanin which protects against u.v. radiation

18
Q

1 mark

Suggest why people with a family history of cancer are at a greater risk of cancer than those with no family history of cancer.

A

because cancer has genetic component / may have inherited oncogene / gene which causes cancer

19
Q

3 marks

Treatment with drugs might be able to reverse the epigenetic changes that cause cancers. Suggest and explain how.

A
  1. Drugs could increase methylation of oncogenes
  2. Drugs could decrease methylation of tumour suppressor genes
  3. Increased methylation of DNA/genes inhibits transcription/expression of genes
  4. Decreased acetylation of histones inhibits transcription/expression of genes