2026 RI H2 Biology Prelims P3 Answers

© RI 2026 Preliminary Examination 9477/03 [Turn over RAFFLES INSTITUTION 2026 Year 6 Preliminary Examination Higher 2 BIOLOGY 9477/03 Paper 3 Long Structured and Free-response Questions 18th Sept 2026 2 hours Candidates answer on the Question Paper. Additional Materials: Writing paper. READ THESE INSTRUCTIONS FIRST Write your index number, CT group & name 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 either question 4 or 5 on the writing papers. The 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. At the end of the examination, hand in Section A and B separately. The number of marks is given in brackets [ ] at the end of each question or part question. This document consists of 16 printed pages. CIVICS GROUP CANDIDATE NAME INDEX NUMBER 6 S 0 3 2 Raffles Institution Internal Examination For Examiner’s Use Section A 1 / 32 2 / 12 3 / 11 Section B 4 or 5 / 20 Total / 75 2 6

2 © RI 2026 Preliminary Examination 9477/03 For Examiner’s Use Section A Answer all the questions in this section 1 Cancer stem cells (CSCs) possess characteristics associated with normal stem cells, including the ability to give rise to different cell types found in a tumour. CSCs persist in tumours as a distinct population and have been found to be responsible for relapse and metastasis. In different environments, the type of cells that make up the tumours are different. Fig. 1.1 shows one model of how CSCs give rise to different cells. Fig. 1.1 (a) With reference to Fig. 1.1, and using your understanding of characteristics of stem cell, describe the similarities in characteristics between CSCs and a named multipotent stem cell. [3] 1. myeloid/ lymphoid/ blood* stem cell; 2. have ability to self-renew* and proliferate; 3. to maintain a constant pool of stem cells; 4. unspecialised cells* capable of undergoing differentiation* to form different cells (I: related cell types); 5. Symmetrical and asymmetrical cell division; As CSCs develop to form cells of different shapes, their cell surface membrane will have certain glycoproteins, known as biomarkers, embedded in them. Biomarkers are potential tools to classify different types of cancers as each type of cancer has its own unique set of biomarkers.

3 © RI 2026 Preliminary Examination 9477/03 [Turn over For Examiner’s Use Table 1.1 shows a list of biomarkers associated with some cancer types. Table 1.1 type of cancer biomarkers breast cancer CD24, CD44, CD29, CD133, CD200 pancreatic cancer CD24, CD44, ESA, CD133, CXCR4 bone cancer CD44, CD105, Stro-1 colorectal cancer CD44, EpCAM, CD166, CD133 (b) With reference to Table 1.1, (i) identify one biomarker that can be found in the four types of cancer that is likely to be coded for by an oncogene, and suggest the role of this biomarker. [2] 1. CD44*; 2. Receptor* for ligand/ growth factors to bind , resulting in cell signalling that stimulates excessive proliferation/ causes uncontrolled cell division; (ii) suggest why each cancer cell type found in their respective location in the human body has its own set of unique biomarkers. [2] [Any 2] 1. Random mutations in the CSCs resulting in some CSCs responding to molecular signals/activate cell signalling; OR Epigenetic changes (A: named example – histone acetylation/ DNA methylation) resulting in some CSCs responding to molecular signals/activate cell signalling; 2. Each location has its own specific growth factors/ molecular signals; 3. resulting in switching of different set of genes/ changes in gene expression in the cancer stem cell; (c) A benign tumour can become metastatic after a while. Explain how these changes happen. [2] Any two] 1. DNA damage and accumulation of mutations* in a single cell; 2. Mutations resulting in angiogenesis* occurring within the tumour so that blood vessels formed can transport oxygen and nutrients for its growth 3. loss of anchorage dependence/ loss of cell adhesion/ break through basal lamina to spread to other parts of the body through the bloodstream; (d) The comet assay is used to detect DNA strand breaks in individual cancer cells. Single cells are mixed in an agarose gel on a glass slide. Chemicals are added to dissolve the cell surface membrane and nuclear envelope, leaving behind a tight ball of DNA. The DNA is then subjected to agarose gel electrophoresis as shown in Fig. 1.2.

4 © RI 2026 Preliminary Examination 9477/03 For Examiner’s Use Fig. 1.2 The slide was then stained to visualise the DNA which appears in the form of a “comet”. Cells with greater DNA damage exhibit a longer "comet tail" during electrophoresis. Fig. 1.3 shows an example of how a comet assay may be studied for one cell. Fig. 1.3 (i) Explain how a named property allows the chemicals to dissolve the cell surface membrane and the nuclear envelope. [2] 1. Amphipathic*; 2. Chemicals disrupt the hydrophobic interactions between the non- polar hydrophobic hydrocarbon tails of phospholipids; (ii) Explain why cells with more DNA damage exhibit a longer “comet tail”. [3] 1. Negatively charged DNA migrates towards the positive electrode; 2. More damage results in more strand breaks; 3. Smaller DNA fragments are formed which travel faster/ further distances resulting in a longer tail; (iii) Determine the tail moment length in Fig. 1.3. Show your working. Tail moment length = 250 x 3.2/1.4 = 571 µm …………………………….[1] (e) Drug M targets colon cancer cells, and causes DNA breaks. - current + tail length head tail moment length 250 µm

5 © RI 2026 Preliminary Examination 9477/03 [Turn over For Examiner’s Use Fig. 1.4 shows the photos of colon cancer cells taken in the first three hours after drug M was administered. A comet assay was carried out. first hour second hour third hour Fig. 1.4 (i) With reference to Fig. 1.4, explain whether drug M is effective. [2] 1. Tail moment length increases significantly from 1st to 3rd hour; 2. Effective because there are more DNA strand breaks as time passes; (ii) Suggest two limitations of the comet assay. [2] Any two: 1. The size of the slide limits the number of cells that can be studied at any one time; 2. The cells must be analysed individually, so time-consuming; 3. Difficulty in determining the length of the tail (due to the diffused nature); 4. False positive results as necrosis/ apoptosis can also result in tails; 5. Overlapping comet tails; 6. Each assay is only for one cell at one particular time, and so effect of DNA damage cannot be assessed for tha