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AQA A Level Biology - Mutations and Gene Expression Workbook () £9.50   Add to cart

Exam (elaborations)

AQA A Level Biology - Mutations and Gene Expression Workbook ()

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A useful workbook of past paper questions on Mutations and Gene Expression, preparing students for upcoming exams.

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  • October 4, 2022
  • 12
  • 2021/2022
  • Exam (elaborations)
  • Answers
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kmomoniat
Cardinal Newman College
Name: Teacher:

Mutation and Gene Expression PPQs

Q1.(a) Explain how the structure of DNA is related to its functions.

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Scientists investigated three genes, C, D and E, involved in controlling cell division.
They studied the effect of mutations in these genes on the risk of developing lung cancer.

The scientists analysed genes C, D and E from healthy people and people with lung cancer.

• If a person had a normal allele for a gene, they used the symbol N.
• If a person had two mutant alleles for a gene, they used the symbol M.

They used their data to calculate the risk of developing lung cancer for people with different
combinations of N and M alleles of the genes. A risk value of 1.00 indicates no increased risk.
The following table shows the scientists’ results.

Risk of
Gene C Gene D Gene E developing
lung cancer

N N N 1.00

M N N 1.30

N N M 1.78

N M N 1.45

N = at least one copy of the normal allele is present
M = two copies of the mutant allele are present



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, Cardinal Newman College
(b) What do these data suggest about the relative importance of the mutant alleles of genes
C, D and E on increasing the risk of developing lung cancer? Explain your answer.

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Chemotherapy is the use of a drug to treat cancer. The drug kills dividing cells.
The figure below shows the number of healthy cells and cancer cells in the blood of a patient
receiving chemotherapy. The arrows labelled F to I show when the drug was given to the
patient.




Time / days

(c) Calculate the rate at which healthy cells were killed between days 42 and 46.



.............. cells killed per unit volume of blood per day (1)


(d) Describe similarities and differences in the response of healthy cells and cancer cells to
the drug between times F and G.

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