Sample/practice exam, questions and answers biomedical science year 3 PDF

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Past and sample exam questions with planned answers...

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BI3325 - Cancer Biology Choice will be 2 questions from 5 to be completed in 3 hours Q1. Evaluate the evidence for commencing a national screening programme for childhood leukaemia. Answer should include and expand on the following: Most common cancer in childhood • Strong epidemiological evidence • In utero initiation • Some forms rarely accompanied by other genetic events • Secondary genetic event most commonly required, these can be varied and numerous • Direct evidence of link between in utero event and leukaemia event from Guthrie card studies • Majority of translocation identified at birth to do not lead to cancer. Q2. With reference to existing and potential anti-cancer agents, discuss how our understanding of the intrinsic (stress induced) apoptotic pathway has contributed to the development of anti-cancer therapies. Outline answer: • Describe the intrinsic apoptosis pathway: BH3 sentinels, Bcl2 family of proteins; mitochondrial membrane permeabilisation; cytochrome C; caspases and the proteolytic degradation of cellular organelles. • Apoptosis is a key tumour surveillance mechanism, and increased understanding of its regulatory components (including aberrations in cancer cells) provides new targets for pharmacological intervention. • For example, inducers of intrinsic cell death: DNA damage, hypoxia, growth factor deprivation, cytoskeletal changes etc. can be targeted with DNA damaging agents, inducers of reactive oxygen species, growth factor receptor antagonists and spindle/cytoskeletal poisons respectively. Synthetic lethality targets a combination of DNA repair mechanisms. Combinatorial therapies often take advantage of lowering apoptosis thresholds to cellular stress. • Suppressors of apoptosis eg IAPs can be targeted with SMAC mimetics, Bcl2 can be targeted with BH3 mimetics. • Inclusion of specific examples of agents and therapeutics will warrant additional marks. Q3. Discuss the anticancer properties of tyrosine kinase inhibitors designed to inhibit cell surface receptors. Answer should contain and expand upon the following points: Explanation of what is a tyrosine kinase: Found in intracellular portion of growth factor receptors (could mention briefly that tyrosine kinases are also part of non-receptor cytoplasmic molecules e.g. src but question specifically says ‘cell surface receptors’ so no detail in this area is required) Uses ATP as substrate to phosphorylate target proteins Using a specific growth factor receptor as an example (could be EGFR): Explain how a growth factor receptor such as EGFR initiates and relays signalling events to influence cell proliferation (Ras/Raf/ERK) and cell survival (PI3kinase/AKT) Role of this growth factor signalling in cancer : mechanisms promoting oncogenesis Explanation of how tyrosine kinase inhibitors (TKIs) work i.e. ATP analogues Examples of EGFR TKIs i.e. Tarceva, Iressa (activity enhanced in patients with activating mutations in cytoplasmic domain) Can expand to discuss other growth factor receptors: VEGFR: Role in angiogenesis; TKIs in preventing angiogenesis e.g. sorafenib, sunitinib and axitinib Should also include TKIs for PDGFR; importance of PDGFR signalling in pericyte attachment for angiogenesis Opportunities to discuss other receptors or additional information on TKIs for receptors mentioned above from independent reading Answer should not contain any information on inhibitors for AKT or Raf for example, as they are serine/threonine kinases (also MEK as dual kinase) and of course, not cell surface receptors.

Q4. Discuss the relevance of the metastatic cascade with respect to cancer progression and evaluate the therapeutic opportunities presented by different target molecules. Answer should contain and expand upon the following points: Explanation of the elements of the cascade and how they support tumour spread and influence the clinical outcome for the patient. In your answer, you should provide details of the role of CDH1 and cMet in this process. Your answer should point to the fact that trying to enhance expression of CDH1 would be harder than inhibit the activity of cMet, particularly as CDH1 is likely mutated and more difficult to therapeutically target. There is excellent opportunity to include other attractive targets from independent reading or integration from other content in the module. BI3211 - Eukaryotic Gene Expression Two questions from a choice of five -

Discuss the structure of transcription factors Discuss the significance and mechanism of RNA editing and alternative splicing in the generation of protein diversity. Explain the link between RNA splicing and nonsense mediated decay. Discuss the physical organisation of RNA polymerase-II-mediated gene transcription Evaluate the techniques used to determine the epigenetic status of a promoter in mammalian cells Discuss the regulation of the Wnt signalling pathway

BI3216 - Genetic Models of Disease Three questions from a choice of six -

Discuss the experimental evidence that suggests insulin-like growth factor 2 is an imprinted gene Evaluate the different transgenic approaches used to generate animal models of Huntington disease Discuss how you would attempt to demonstrate the suitability of a known pro-apoptotic gene as a therapeutic target for breast cancer

BI3331 - Mechanisms of Human Disease Two questions from a choice of five -

Discuss the pathophysiology of asthma and relate this to current and new/proposed treatments Consider the usefulness of acuity tests in the early diagnosis of common disorders of vision in adults and children Discuss the roles of macrophages in the pathogenesis of atherosclerosis...