2026 TJC JC2 Prelim H2 Biology P3 (Ans)

1 [TURN OVER READ THESE INSTRUCTIONS FIRST Write your Center number, index number and 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. DO NOT WRITE IN ANY BARCODES. Section A Answer all questions in the spaces provided on the Question Paper. Section B Answer any one question in spaces provided on the Question Paper. The use of an approved scientific calculator is expected, where appropriate. You may lose marks if you do not show any working or if you do not use appropriate units. The number of marks is given in the brackets [ ] at the end of each question or part question. TEMASEK JUNIOR COLLEGE 2026 JC2 PRELIMINARY EXAMINATION Higher 2 CANDIDATE NAME ANSWERS CENTRE NUMBER S INDEX NUMBER BIOLOGY 9477/03 Paper 3 Long Structured and Free Response Questions PART I 16 SEPTEMBER 2026 2 hours Candidates answer on the Question Paper. No Additional Materials are required. For Examiner’s Use 1 / 30 2 / 14 3 / 11 4 / 5 / 20 Total / 75 This document consists of 25 printed pages.

2 Section A Answer all questions in this section. 1 Cancers are caused by disruption of the normal cell cycle, involving proto-oncogenes, tumour suppressor genes and epigenetic factors. Some cancers can be treated using chemotherapy which also kills some of the non-cancerous body cells. After treatment, the tissues can be repopulated using adult stem cells. (a) Define the following terms, (i) proto-oncogene; [1] 1. Proto-oncogenes are normal genes that code for proteins 2. that stimulate normal cell division. (ii) adult stem cell. [1] 1. unspecialized cell with ability to divide and differentiate into specialised cells 2. Multipotent Epigenetic change can be brought about by DNA methylation and histone modification. Fig. 1.1 below shows the effect of DNA methylation on tumour suppressor gene. Fig. 1.1 tumour suppressor gene tumour suppressor gene

3 [TURN OVER (b) With reference to Fig. 1.1, explain how DNA methylation results in tumour growth. [2] 1. Addition of cytosine to CpG sites in the regulator gene promoter, 2. Regulator gene is not transcribed / mRNA from regulator gene not produced and regulator protein is not produced 3. Suppressor gene not expressed/ not switched on/ suppressor gene remains switched off 4. No inhibition of cell cycle, resulting in uncontrolled cell division / mitosis (c) Fig. 1.2 shows histone modification of tumour suppressor genes. Z Fig. 1.2 (i) With reference Fig. 1.2, explain how tumor suppressor genes are switched off in cancer cells. [2] 1. Remove acetyl groups / AC from histones / de-acetylation of histones. 2. DNA becomes tightly coiled. 3. General transcription factors and RNA polymerase cannot access promoter of suppressor gene 4. Transcription initiation complex is not formed, therefore NO transcription (ii) In some humans, tumour suppressor genes can become permanently switched off in all cells in the body. Explain the consequences of such a change. [1] 1. Mutation can be passed onto daughter cells / mutation can accumulate in daughter cells 2. Increased risk of cancer / increased risk of tumour formation Reject: uncontrolled cell division without mentioning chance or risk https://www.ocr.org.uk/Images/621242-question-paper-scientific-literacy-in-biology.pdf

4 (d) Breast cancer is strongly associated with mutations or inactivation of key tumor suppressor genes like BRCA1, BRCA2, and p53. Scientists have identified hundreds of mutations in BRCA2 , but not all of these mutations will increase the risk of cancer. • One specific mutation in BRCA2 gene, known as 999del5, is found in 0.6% of the general global population. • Iceland is an island country in the North Atlantic Ocean. • The ancestors of most of the current population are people who arrived to settle in Iceland in AD 874. • In the Icelandic population, mutation 999del5 is the cause of 7–8% of breast cancer cases in women and 40% of breast cancer cases in men. • This is much higher than the percentage of breast cancer cases in the general global population. (i) Suggest and explain how mutation 999del5 accounts for a very high percentage of breast cancer cases in Iceland compared with the general global population. [3] 1. Mutation in a common ancestor of the current population OR mutation occurred a long time ago OR someone in original population had mutation 2. Due to founder effect 3. This is because the original population was small 4. Small variation in gene pool / low genetic diversity; A inbreeding OR idea that much of the population is closely related 5. The population is geographically isolated 6. caused increase in frequency of mutation 999del5 / mutated BRCA2 allele because the offspring are from the individuals within this island. 7. (AVP) One of the largest global genetic screening programmes for breast cancer involves identifying people with mutations in BRCA2. More people tested results in higher percentage of people with mutation. (ii) Suggest one advantage of genetic screening for mutations in BRCA2. [1] any one from: 1. Early treatment / breast removal / removal of tumor can have frequent checks ; 2. ref. to counselling about informed decision about having children / pre-natal genetic counselling 3. Could lead to lower death rates from breast cancer ;

5 [TURN OVER (e) Women with tumours in their breasts often have biopsies (tissue samples) taken and tested to determine if the tumours are malignant or benign. It was proposed that matrix metalloproteinase (MMP) activity has been linked to the development of cancer and in one study, the total MMP activity was measured in breast biopsies that were classed as either: • benign • malignant grade I (the least malignant) • malignant grade II • malignant grade III (the most malignant) Table 1.1 shows the results of this study. Table 1.1 severity classification MMP activity / a.u. benign 6.58 malignant grade I 1.34 malignant grade II 6.80 malignant grade III 32.29 Use the data in Table 1.1 to evaluate the hypothesis that MMP activity increases the severity of breast cancer. [3] 1. YES / There is a positive relationship / correlation between MMP activity and severity of breast cancer 2. As severity of breast cancer increases from grade I to grade III , the MMP activity increases from 1.34 to 32.29 a.u. OR The MMP activity is the greatest in grade III of 32.29 a.u. compared to grade II of 6.80 a.u. and grade I of 1.34 a.u. Reject : directly proportional 3. NO 4. MMP activity is similar in grade II of 6.80 a.u and benign of 6.58 a.u OR MMP activity is lower in grade I of 1.34a.u. than benign of 6.58 a.u. 5. AVP: Correlation does not imply causation

6 (f) Another cancer, known as metastatic melanoma (MM) is a type of skin cancer caused by a mutated NRAS gene. Suggest what is the main cause of mutation of the NRAS gene. [1]  UV radiation (g) The NRAS gene codes for the NRas protein, a G-protein with a GTPase. The NRas protein is involved in signal transduction that relays signal from the growth factor to the nucleus, regulating cell division. An activated NRas protein only becomes inactivated due to the hydrolysis of GTP to GDP by GTPase. The presence of growth factor at the receptor leads to the changes in the cell as shown in Fig. 1.3. Fig. 1.3 It is obs