2018 Cancer MCQ QP+MS

2018 Cancer MCQ 2018 / H2 / ACJC PRELIM / P1 Q171Elephants have been found to be strangely resistant, though not immune, to cancer. They are four times less likely to develop cancer as compared to humans. Elephants have 40 copies of the p53 gene while humans only have two. In addition, three genes which code for DNA repair proteins have found to be very active.What do these observations suggest?AAll DNA mutations in the elephant are repaired.BWhen elephants develop cancer, it is due to environmental causative factors such as excessive exposure to UV light.CThe occurrence of cancer is due to the p53 oncogene, which stimulates the cell to divide rapidly, bypassing the cell cycle checkpoints.DThere is large amount of p53 proteins in an elephant cell which prevent cells with mutations from moving past the cell cycle checkpoints. 2018 / H2 / AJC PRELIM / P1 Q182mRNA was isolated from a normal individual and a patient suffering from cancer. The mRNA was allowed to hybridise with the p53 DNA gene sequence. The schematic diagram shows the results of the hybridisation process under the electron microscope. Which of the following could be a possible explanation why the patient is suffering from cancer?AA point mutation had occurred in the intron leading to the failure to excise one intron, resulting in a longer dysfunctional protein being produced.BGene amplification had occurred leading to the multiple copies of a trinucleotide repeat in an intron, hence causing splice site to be misread due to frameshift

mutation, resulting in a longer dysfunctional protein being produced.CA point mutation had occurred in the intron leading to the failure to excise one exon, resulting in a hyperactive protein being produced. DA point mutation had occurred leading to the failure of spliceosome to recognise splice sites, causing the excision of the wrong intron, resulting in a degradation-resistant protein being produced.2018 / H2 / DHS PRELIM / P1 Q83Which of the following statements about cancer are TRUE?1.Oncogenes and tumor suppressor genes can both be detected by introducing fragmented DNA from cancer cells into suitable cell lines and isolating colonies that display cancerous properties2.Individuals who inherit one inactive copy of tumour suppressor gene are more likely to develop cancer than individuals with two non-mutant copies3.Viruses and other infectious agents play no role in human cancers4.In the cellular regulatory pathways that control cell growth and proliferation, the products of oncogenes are inhibitory components and the products of tumour suppressor genes are stimulatory components5.When analysed, cancer cells are often found to have only one mutation in a regulatory pathway that controls cell proliferationA1 and 2B2 and 3C3 and 5D1, 2 and 4

2018 / H2 / IJC PRELIM / P1 Q184The diagram below illustrates the development of colorectal cancer. Which of these statements can be inferred from this multistep model of carcinogenesis?1Cells whose APC and β-catenin genes are inactivated have lost density dependent inhibition.2APC and β-catenin genes are most likely tumour suppressor genes.3High levels of Ras protein are produced only when both copies of Ras gene are mutated.4Two copies of normal p53 alleles must be present to inhibit cell division.5Gain-of-function mutation in COX-2 gene is one of the pre-requisites for the formation of carcinoma.A1, 2 and 3B1, 2 and 5C2, 3 and 4D2, 3 and 52018 / H2 / JJC PRELIM / P1 Q165Which feature of the life cycle of some viruses may result in the development of cancer? AViral RNA can integrate into the chromosomes of host cells. BViruses can cause cell lysis and spread to other host cells. CViruses can cause loss of function mutations in proto-oncogenes. DViruses can increase the rate of the cell cycle of host cells.

2018 / H2 / MJC PRELIM / P1 Q16QUESTION 6The ras oncogene is involved in a variety of human cancers. A student extracted DNA isolated from a number of normal and cancerous human tissues and digested the DNA with EcoRI restriction enzyme. A Southern blot was performed and the membrane was probed with radioactive-labelled ras DNA. After exposure to X-ray film, the resulting autoradiograph is shown below. Which of the following could account for the results obtained?ARas gene in normal tissue was mutated. BThere is no ras mutation in cancer tissue 3. CRas mRNA concentration is doubled in cancer tissue 1. DRas DNA is amplified in cancer tissue 2.2018 / H2 / AJC PRELIM / P1 Q147Which event does not increase the chance of cancerous growth?Aamplification of p53 geneBamplification of ras geneCincrease in telomerase activityDloss of immunity

2018 / H2 / NYJC PRELIM / P1 Q178mRNA was isolated from a normal individual and a patient suffering from cancer. The mRNA was allowed to hybridise with the p53 gene. The schematic diagram shows the results of the hybridisation process under the electron microscope Which of the following could be a possible explanation why the patient is suffering from cancer? AA point mutation had occurred in the intron leading to the failure to excise one intron, hence leading to a longer dysfunctional protein being translated.BA point mutation had occurred in the intron leading to an exon being excised, hence leading to a shorter dysfunctional protein being translated. CA point mutation had occurred leading to the failure of spliceosome to recognise splice sites leading to the excision of the wrong intron, leading to a dysfunctional protein being translated.DGene amplification had occurred leading to the multiple copies of a trinucleotide repeat in an intron, hence causing splice site to be misread due to frameshift mutation, leading to a longer dysfunctional protein being translated.2018 / H2 / NYJC PRELIM / P1 Q189Cancer is caused by changes in the genes which control cell division.Which of the following changes would not result in uncontrolled cell division?ATumour suppressor genes become less active.BStimulation of cell division by platelet-derived growth factor.CAbsence of contact inhibition.DInfection by certain viruses, e.g. hepatitis B which carry oncogenes.

2018 / H2 / PJC PRELIM / P1 Q1810Which of the following observations support the development of cancer as a multi-step process?1Cancer involves the accumulation of mutations in at least one proto-oncogene and several tumour suppressor genes in a specific order.2A lag time often separates the exposure to a cancer-causing agent and the development of cancer.3The incidence of cancer increases with age.4The telomerase gene is activated in malignant tumours.A1 and 3 onlyB1, 2 and 4 C2 and 3 onlyD2 and 4 only2018 / H2 / RI PRELIM / P1 Q1311.Which of the following statements describe possible ways by which viruses can cause disease in animals?IThey inhibit normal host cell DNA, RNA or protein synthesis in host cell.IIThey disrupt and inactivate the tumour suppressor genes of the host cell causing uncontrolled cell division.IIIThey disrupt and inactivate the oncogenes of the host cell causing uncontrolled cell division.IVTheir viral proteins and glycoproteins on the surface membrane of host cells cause them to be recognised and destroyed by the body’s immune system.VThey deplete the host cell of cellular materials essential for metabolic functions.AI, II and VBI, II and IVCII, III and VDI, II, IV and V2018 / H2 / SAJC PRELIM / P1 Q1812The diagram below shows the mutli-step model of cancer development in colon cancer. Which of the following contains the most appropriate explanation for the different stages?

ABCAMutation in one copy of a tumor suppressor gene Mutation in other genes such as telomerase geneLoss of anchorage dependence BMutation in one copy of a proto-oncogene Loss of density dependenceLoss of anchorage dependence CMutation in one copy of a proto-oncogeneLoss of anchorage dependenceLoss of density dependenceDMutation in promoter region upstream of a proto-oncogene Mutation in one copy of a tumor suppressor geneLoss of d