2026 VJC H2 Biology Prelim P3 Ans

2026 H2 Biology Prelim Paper 2 Answer 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] • Tumour suppressor protein; • Cause cell cycle arrest / Trigger apoptosis if the damage is irreparable; (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] • pRb normally binds to and inhibits activity of E2F, preventing transcription; • E7 binding to pRb causes inactivation, allowing E2F to initiate transcription for S-phase; (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] • Missing or extra chromosome; • E6 and E7 prevent DNA repair / apoptosis; • Accumulate mutations that affect spindle formation;

(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 – 2.5 = 2.5; • 2.5 / 5 x 100% = 50% decrease; (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] • National Cervical Screening Programme detects pre-cancerous cells for early intervention; • Improved public health awareness results in more people practising safer sexual behaviours; • Improved treatment for pre-cancerous lesions;

(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] • Antigen-presenting cells ingest VLPs and present the L1 viral antigens on MHC II markers; • Helper T cells activate B cells; • B cells differentiate into plasma cells to secrete antibodies against L1 protein; • Memory B cells are produced to allow a faster antibody response upon future exposure to live HPV; (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] • HPV is not enclosed by membrane, while eukaryotic cells have a cell surface membrane; • HPV lacks cytoplasm, ribosomes, and metabolic organelles; • HPV is significantly smaller than a eukaryotic host cell; (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] • Southern blotting; • DNA in the gel is denatured and transferred to the nitrocellulose filter; • The filter is immersed in a solution containing radioactive probes and viewed over an X-ray film; (ii) Suggest the need for the negative control. [1] • Show that any results come from the actual samples; (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] • It specifically binds to VEGF receptor; • Traditional chemotherapy targets all rapidly dividing cells; • Bevacizumab is more specific to the cancer's blood supply; (ii) HPV can evade the body's immune system. Suggest one mechanism by which a pathogen like HPV could evade the immune response. [1] • HPV can exist in a latent state within cells; • HPV may produce proteins that interfere with antigen processing or presentation; (e) Under hypoxic conditions, cancer cells switch to anaerobic respiration. (i) Identify the process by which anaerobic respiration in human cells produces ATP. [1] • Substrate-level phosphorylation;

(ii) Name the "characteristic waste product" produced by this process. [1] • Lactate; (iii) Explain why the waste product can be used as an indicator of tumour progression, despite it being linked to normal physiological processes. [1] • Lactate is produced in high quantities by the tumour's anaerobic respiration; (f) A healthcare influencer with a large following claimed that HPV infection always results in cervical cancer. Explain whether you agree with the healthcare influencer. [2] • No, HPV infection inactivates only two tumour suppressor proteins pRb and p53; • Ref. to accumulation of gain-of-function mutations of protooncogenes to oncogenes;

2 Routine water quality testing of reservoirs often involves quantifying Escherichia coli (E. coli), a bacterium commonly found in the intestines of humans and many other animals. Most strains of E. coli are harmless, although some can cause intestinal diseases. Following heavy rainfall near a commercial poultry farm, an abnormal increase in bacterial counts was detected during routine testing of a reservoir. Genomic screening of the water sample identified three different strains of E. coli and a particular strain of Salmonella enterica (S. enterica). (a) Explain why E. coli can be used as an indicator of faecal contamination in the reservoir. [2] • E. coli is found in high amount in intestines of animals, then in faeces; • Its presence in water therefore indicates that