Cells of the immune system have cell surface receptors that detect molecules made by pathogens. One of these cell surface receptors is known as TLR8. The gene TLR8 is found on the X chromosome in humans. Fig. 4.1 shows the production of messenger RNA (mRNA) formed from the gene TLR8 in the nucleus of a macrophage. The nucleotide sequence TTAGGG is repeated in the direction 5' to 3' in the telomeres of human chromosomes. Melanoma is a type of tumour that develops from pigment-producing skin cells known as melanocytes. A melanoma tumour is cancerous and may spread to other parts of the body. T-vec is a new drug that has been developed to treat melanoma that has spread to other parts of the body, including lymph nodes. T-vec contains a virus that infects some of the melanoma cells, causing the cells to burst and release their contents. Some of the contents of the melanoma cells act as cytokines and others act as antigens. [Figure 4.1]

Mark scheme

Marking points from the official mark scheme (May/June 2025). The mark or mark type is shown in brackets.

1. [1] (a)(i) RNA polymerase ;
2. [1] (a)(ii) 1 protects mRNA from being, broken down / degraded / damaged, by enzymes ; A protects mRNA from enzyme action
3. [1] (a)(ii) 2 prevents mRNA molecules joining together ; A prevents ends of a mRNA molecule joining
4. [1] (a)(ii) 3 helps to, direct / move, mRNA, through nuclear pores / to ribosome(s) / to leave nucleus / to cytoplasm ;
5. [1] (a)(ii) 4 required to start, translation / assembly of amino acids at ribosome; A helps / allows / AW, (mRNA) attachment to ribosome(s) R refs to start and stop codons
6. [1] (a)(ii) 5, 6 AVP ;; e.g. makes sure 5' end enters ribosome first / AW
7. [1] (a)(iii) 1 gene / RNA, splicing; A primary transcript splicing R DNA splicing / mRNA splicing / genetic splicing
8. [1] (a)(iii) 2 introns removed ;
9. [1] (a)(iii) 3 exons, attached together / joined up; R extrons
10. [1] (a)(iii) 4 shortens / AW, the RNA molecule ;
11. [1] (a)(iii) 5 removal of non-coding sequences / only keeping the coding sequences ; A non-coding regions / AW A non-coding introns R non-coding / coding, genes
12. [1] (a)(iii) 6 AVP; e.g. rearranging exons / alternative splicing I annealing ref. to phosphodiester bonds forming between RNA nucleotides / AW ref to spliceosome
13. [1] (b)(i) (at the) ends / AW ; A at the ends of, DNA / chromatids I sides / edges
14. [1] (b)(ii) 1 allows DNA replication to, occur many times ;
15. [1] (b)(ii) 2 allows (some) cells to carry out, many / continuous / repeated, mitoses / cell cycles / cell divisions ; I cell replication
16. [1] (b)(ii) 3 prevents the loss of, genes / genetic information; A prevents loss of coding sequences I loss of DNA I prevents loss of genetic material
17. [1] (b)(ii) 4 AVP; e.g. prevents fusion of chromosome ends prevents ends of chromosomes being recognised as damaged
18. [1] (c) 1 mutation in a gene;
19. [1] (c) 2 leads to uncontrolled / unregulated, mitosis / cell division ;
20. [1] (c) 3 proto-oncogene to oncogene; A ref. to oncogene in correct context (without the proto-)
21. [1] (c) 4 ref. to tumour suppressor gene(s); A in context of 'switched off'
22. [1] (c) 5 idea that normal (named) checkpoints do not function; A not checked during (named) stage of cell cycle A bypass checkpoints / checkpoints not used
23. [1] (c) 6 mass of, abnormal / non-functional / damaged, cells formed; A irregular / abnormal, mass of cells I undifferentiated
24. [1] (c) 7 AVP; e.g. supplied with blood vessels cells do not carry out, apoptosis / programmed cell death cancer cells ignore stop signals from other cells / no contact inhibition
25. [1] (d) 1 cytokines stimulate, clonal expansion / division (by mitosis), of, T-lymphocytes / B-lymphocytes; A T-cells / B-cells A T-helper cells / T-killer cells
26. [1] (d) 2 cytokines stimulate (action of), macrophages / phagocytes ; A form angry macrophages
27. [1] (d) 3 cytokines act as cell-signalling molecules ;
28. [1] (d) 4 antigens stimulate, clonal selection of (specific) B-lymphocytes / T-lymphocytes ; A B-/T-, lymphocytes (with receptors / immunoglobulins / antibody) that are complementary to antigen A T-cells / B-cells A T-helper cells / T-killer cells
29. [1] (d) 5 antigens, stimulate / AW, B-lymphocytes to divide (by mitosis) to form plasma cells ; A clonal expansion of B-lymphocytes to form plasma cells A if cytokines stated instead of antigens
30. [1] (d) 6 plasma cells, secrete / release / produce, antibodies ;
31. [1] (d) 7 antibodies mark cancer cells for destruction by, T-killer cells / macrophages / phagocytosis;
32. [1] (d) 8 killer cells, release / AW, perforin / granzymes / toxins / hydrogen peroxide / hydrolytic enzymes, to kill / destroy, (cancer) cells; A description of how cell is killed e.g. breaks open / makes holes, in cell surface membrane
33. [1] (d) 9 AVP; e.g. proteins released from melanoma cell act as non-self antigens