2018 Cancer STQ MS

2018 Cancer STQ MS2018 / H2 / AJC PRELIM / P2 Q51Skin cancer cells may be grown in culture and examined using the technique of immunofluorescence in which antibodies are used to attach fluorescent dyes to specific molecules within the cells. Fig. 5.1 is an immunofluorescent light micrograph of skin cancer cells. A particular type of protein is stained with the dye and appears as pale regions in the skin cancer cells. Fig. 5.1 (a)(i)Before the skin cancer cells could be stained with antibodies, the cells had to be fixed and treated with a mild detergent to increase the permeability of the cell surface membranes.Explain the purpose of this step.Membrane has a hydrophobic core; Antibodies that is polar in nature are unable to pass thru the membrane.Accept: too large to pass through the membrane[2](ii)There are two cells in the process of dividing. Each of these cells has two areas stained heavily, labelled A on Fig. 5.1.Suggest the identity of these two areas and outline their functions in these cells.spindle apparatus / spindle fibresaccept: spindle / microtubules / tubulin / centrioles / microtubule organising centres / MTOCs Attach to centromere/kinetochore protein of the chromosomes; Can elongate/shorten to move chromosomes during mitosis[3]

(accept if students describe function of spindle fibre in prophase/anaphase); Accept if centrioles given as identityforms poles of the cell ;organises the spindle ;(iii)Suggest why the proteins stained in the cytoplasm of the non-dividing cells in Fig. 5.1 are not evenly distributed.forming cytoskeleton/actin filaments in the cells. to maintain shape of cells.to help to support/anchor organelles in different parts of the cells. For movement of transport vesicles/secretory vesicles[1](b)Explain two ways in which the behaviour of chromosomes in prophase of meiosis I differ from prophase of mitosis. During prophase I, homologous chromosomes pair up. However, in prophase of mitosis, homologous chromosome doses not pair up; During prophase I, chiasmata formed and crossing over between non-homologous sister chromatids occurs. However, in mitosis, no crossing over occurs. [2](c)Some chemicals known to inhibit the cell cycle are used as drugs for the treatment of cancer. A particular drug was found to be most effective when applied to cancer cells in the G2 phase of the cell cycle. Suggest the possible mechanism of this drug. Inhibit the condensation of chromosomes; Inhibit the replication of centrioles/centrosome; Inhibit the organisation of spindle fibres within the cells; Reject: “inhibit protein synthesis” unless specifically mention that inhibition of synthesis of proteins required for chromosome condensation; Compulsory point: Induced a G2 check point and prevent the cells from entering mitosis; [3] [Total: 11]

2018 / H2 / MJC PRELIM / P2 Q5QUESTION 2Fig. 5.1 shows the stages involved in the synthesis of a p53 protein in a eukaryotic cell. Fig. 5.1(a)Name the structure H. [1]Promoter (R: deoxyribonucleic acid)(b)Outline the events that occur in the nucleus of the cell to produce a functional molecule of mRNA encoding a p53 protein. [4]RNA polymerase reads the template strand from 3’ to 5’ to form pre-mRNA / adds complementary ribonucleotides to the 3’OH end of the pre-mRNA strand 7-methylguanose / modified guanine cap added to the 5’ end of the pre-mRNA strandIntrons are excised and exons are spliced3’ poly(A) tail added

(c)In a particular defective cell, all the pre-mRNA encoding the p53 protein were not cut.(i)Explain how this would affect the function of the p53 protein. [4]Introns which are non-coding would be translated (along with the exons)If the number of nucleotides in introns are not in multiples of three, there would be a shift in the reading frame by the ribosomeOR There may be a premature stop codon which produces a truncated proteinOR There may also be a longer protein produced if the stop codon is removed These will lead to a change in the sequence of amino acids / primary structure of p53 proteinAnd thus different folding to give a different 3D conformation of the p53 protein, which may give rise to a non-functional p53 protein(ii)Explain why this may not lead to cancer. [2]Cancer is a multi-step process The cell would need additional gain-of-function mutations to the proto-oncogenes / accumulation of mutations to a single cell line2018 / H2 / NYJC PRELIM / P2 Q2123Fig. 2.1 shows some Allium sp. plant cells in various stages of the mitotic cell cycle. Fig. 2.1

(a)(i) Identify the three stages shown by the labelled cells.A InterphaseB AnaphaseC Prophase [3](ii)Identify the stage of mitosis that follows that shown in cell C.Metaphase [credit will be given as long as the stated answer follows their answer in a(i)C] [1](iii)In the cell outline below, draw and label the structures visible in a cell that is in the stage you have named in (ii). 2n for this plant is 6. Drawing within cell outline; label chromosomes; 2n=6;® asters / centrioles which are absent in plants [3](b)Uncontrolled cell division can result in cancer. Some types of cancer can be treated by chemotherapy, which involves the injection of chemicals into the bloodstream.One chemical used for chemotherapy is called Methotrexate. This is a reversible competitive inhibitors of one of the enzymes in the metabolic pathway that results in the formation of purines.Explain how the use of Methotrexate will slow down the mitotic cell cycle. (Due to competition, less purines formed) so less nucleotides synthesised ;Leading to less DNA replication ; (slowing down mitotic cell cycle) cell wallcell surface membrane

[2](c)Prokaryotic organisms such as Escherichia coli divide by simple cell splitting (binary fission), not mitosis.Apart from ribosomes, prokaryotes have no organelles comparable to those found in eukaryotes and have a circular ‘chromosome’ with no centromere. With reference to the information above and your knowledge of mitosis, suggest why mitosis does not occur in prokaryotes.Lack of centrioles / microtubules to separate the chromosomes during anaphase ;Circular chromosomes does not allow for separation unlike linear chromosomes ; [2][Total: 11]2018 / H2 / PJC PRELIM / P2 Q54Cancer cells do not heed the normal signals that regulate cell cycle.(a)Describe the development of cancer as a multi-step process. [3]a.Accumulation of somatic mutations is needed to produce all the changes characteristic of a full-fledged cancer cell;b.gain of function mutations in proto-oncogenes, where only one allele needs to be mutated into an oncogene, and loss of function mutations in tumour suppressor genes (TSGs), where mutations must be in both alleles;;c.gene for telomerase is activated, expression of telomerase in cancer cells removes a natural limit on the number of times the cells can divide;;d.cancer cells escape normal confines of epithelial layer and invade tissue immediately around it, blood vessels formed via angiogenesis to bring oxygen and nutrients to the cancer cells; e.cancer cells enter bloodstream or lymphatic systems, and travel to other tissues / organs, at these new locations, when cancer cells cross epithelium barriers, metastasis has occurred;;max. 3Fig. 5.1. shows a cell cycle-inhibiting pathway involving the p53 protein in a normal cell.

Fig. 5.1(b)With reference to Fig. 5.1, explain how a missense mutation in p53 protein increases the likelihood of a cell becoming cancerous. [2]a.p53 is a specific transcription factor / activator, in its active form, it binds to DNA to activate the transcription of genes of proteins that inhibit the cell cycle;;b.Missense mutation results in a change in amino acid sequence, resulting in a change in the 3D conformation of the p53 protein, so mutant p53 protein cannot be activated by the protein kinases / cannot bind to the DNA to activate transcription;;c.Protein that inhibits the cell cycle is not synthesized, cell cycle is not inhibited even