2026 VJC H2 Biology Prelim P3 QP

1 VICTORIA JUNIOR COLLEGE JC 2 PRELIMINARY EXAMINATION 2026 HIGHER 2 NAME : ……………………………………………………….………………. CT CLASS: ………………..……… BIOLOGY Paper 3 Long Structured and Free-response Questions 9477 / 03 01/09/2026 2 hour Candidates answer on the Question Paper. No Additional Materials are required. READ THESE INSTRUCTIONS FIRST Write your name and CT class in the spaces at the top of this page. Write in dark blue or black pen. You may use an HB pencil for any diagrams or graphs. Do not use staples, paper clips, glue or correction fluid. Section A Answer all questions in the spaces provided on the Question Paper. Section B Answer any one question in the space provided on the Question Paper. Use of an approved scientific calculator is expected, where appropriate. You may lose marks if you do not show your working or if you do not use appropriate units. The number of marks is given in bracket [ ] at the end of each question or part question. Question Marks Section A 1 2 3 Section B Total This document consists of 20 printed pages. [Turn over]

2 Section A Answer all the questions in this section. 1 Cervical cancer is the fourth most common cancer in women globally. In the vast majority of cases, it is caused by persistent infection with high- risk types of the human papillomavirus (HPV), most notably HPV-16 and HPV-18 variants. The virus, which is sexually transmitted, encodes two key oncoproteins, E6 and E7, which are critical for viral replication but also drive the transformation of the infected host cells. E7 binds to and inactivates the retinoblastoma protein (pRb), a crucial tumour suppressor. This inactivation releases the cell cycle brake, forcing the cell into the S-phase. Concurrently, E6 binds to the p53 protein, targeting it for degradation. These can result in the development of cervical intraepithelial neoplasia (CIN), a pre-cancerous condition. (a) (i) Describe the role of the p53 protein in a normal, healthy cell when DNA damage is detected. ………………………………………………………………………………………………... ………………………………………………………………………………………………... ………………………………………………………………………………………………... ………………………………………………………………………………………………... …………………………………………………………………………………………….. [2] (ii) Fig. 1.1 shows the mode of action of E7 oncoprotein. Fig. 1.1 Explain how E7 contributes to the development of cervical intraepithelial neoplasia. ………………………………………………………………………………………………... ………………………………………………………………………………………………... ………………………………………………………………………………………………... ………………………………………………………………………………………………... …………………………………………………………………………………………….. [2]

3 (iii) The actions of E6 and E7 oncoproteins results in a chromosomal aberration known as aneuploidy. Define what is meant by aneuploidy and describe one way the actions of E6 and E7 oncoproteins could lead to this condition. ………………………………………………………………………………………………... ………………………………………………………………………………………………... ………………………………………………………………………………………………... ………………………………………………………………………………………………... ………………………………………………………………………………………………... ………………………………………………………………………………………………... …………………………………………………………………………………………….. [3]

4 (b) Over the past two decades, incidence of cervical cancer in the United Kingdom has been in decline, largely due to the success of the National Cervical Screening Programme and, more recently, the introduction of the HPV vaccination programme for adolescent girls. The graph below shows the age -standardised incidence rates of cervical cancer in the United Kingdom per 100,000 women. Fig. 1.2 (i) Using the data in Fig 1.2, calculate the percentage decrease in the incidence rate of cervical cancer between 1995 and 2020. Show your working. [2]

5 (ii) Suggest two reasons, other than the HPV vaccination programme, for the general decline in cervical cancer incidence rates shown in the Fig. 1.2. ………………………………………………………………………………………………... ………………………………………………………………………………………………... ………………………………………………………………………………………………... ………………………………………………………………………………………………... …………………………………………………………………………………………….. [2] (iii) Current preventive HPV vaccines contain recombinant virus -like particles (VLPs) composed of the viral L1 protein. These particles contain no viral genomic materials. Explain how the administration of this vaccine leads to long- term active immunity against high-risk HPV strains. ………………………………………………………………………………………………... ………………………………………………………………………………………………... ………………………………………………………………………………………………... ………………………………………………………………………………………………... ………………………………………………………………………………………………... ………………………………………………………………………………………………... ………………………………………………………………………………………………... …………………………………………………………………………………………….. [4] (iv) Upon closer examination, it is found that HPV is a non-enveloped double-stranded DNA virus, which is also associated with skin lesions and several forms of epithelial cancer, besides cervical cancer. Describe two structural features of HPV that differ from that of a host eukaryotic epithelial cell. ………………………………………………………………………………………………... ………………………………………………………………………………………………... ………………………………………………………………………………………………... ………………………………………………………………………………………………... …………………………………………………………………………………………….. [2]

6 (c) Infection with HPV can be detected using polymerase chain reaction (PCR) and gel electrophoresis. Fig. 1.3 shows a typical gel run that shows the possible genetic markers for HPV. Fig. 1.3 The electrophoretic pattern of the HPV PCR products lane 1 – actual sample from patient lane 2 – negative control lane 3 – positive control (i) Using your knowledge of molecular techniques, explain how the band in lane 1 was detected and identified. ………………………………………………………………………………………………... ………………………………………………………………………………………………... ………………………………………………………………………………………………... ………………………………………………………………………………………………... ………………………………………………………………………………………………... ………………………………………………………………………………………………... …………………………………………………………………………………………….. [3] (ii) Suggest the need for the negative control. ………………………………………………………………………………………………... …………………………………………………………………………………………….. [1]

7 (d) Current treatments for invasive cervical cancer include surgery, radiotherapy, as well as chemotherapy. Traditional chemotherapy involves the use of strong cytotoxic drugs that travel throughout the body via the bloodstream, killing rapidly dividing cells. However, for recurrent or metastatic disease, the prognosis has been poor. This has led to the development of targeted therapies, such as Bevacizumab. Bevacizumab is a monoclonal antibody that binds to the receptor for vascular endothelial growth factor (VEGF), preventing it from being activated by its ligand. This prevents the formation of new blood vessels, effectively starving the tumour of nutrients and oxygen. Under these hypoxic conditions, tumour cells adapt by switching to anaerobic respiration, allowing them to survive despite the lack of oxygen, and producing a characteristic waste product that was previously linked to muscle fatigue. (i) Bevacizumab is a monoclonal antibody that targets the VEGF receptor. Explain why this treatment is described as "targeted" and suggest why it may have fewer side effects than traditional chemotherapy. ………………………………………………………………………………………………... ………………………………………………………………………………………………... ………………………………………………………………………………………………... ………………………………………………………………………………………………... ………………………………………………………………………………………………... ………………………………………………………………………………………………... …………………………………………………………………………………………….. [3] (ii) HPV can evade the body's immune system. Suggest one mechanism by which a pathogen like HPV could