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- 27. In the context of 6-mercaptopurine (6-MP) therapy for leukemia, which statement about thiopurine methyltransferase (TPMT) levels is correct? A) High TPMT levels are associated with increased sensitivity to 6-MP and higher risk of adverse reactions. B) Low TPMT levels are associated with increased sensitivity to 6-MP and higher risk of adverse reactions C) High TPMT levels result in reduced metabolism of 6-MP, leading to decreased therapeutic efficacy D) Low TPMT levels result in increased metabolism of 6-MP, leading to excessive drug accumulation and toxicity.34. Explain the mechanism of action of tamoxifen in the treatment of breast cancer.Mrs. Anderson, a 45-year-old woman with a history of chronic back pain, has been taking X as prescribed by her rheumatologist for the past eight months. During a routine check-up, her liver function tests revealed significantly elevated liver enzymes. She has not experienced any noticeable symptoms but is now being closely monitored for potential liver-related issues. 2. Propose a pharmacoepidemiological study design to confirm or refute the signal of hepatotoxicity associated with X. Consider factors such as study population, exposure definition, and outcome measures. Discuss the strengths and limitations of your chosen study design? Outline the methods and data sources that could be used to collect information on hepatotoxicity in patients using X.? Discuss how the findings of the study could have regulatory implications. If a significant association is identified, explore how regulatory agencies might implement other measures to ensure patient safety.? Develop communication…
- Distinguish between What is known of CD105 (endoglin) as an hepatcellular carcinoma marker and it’s potential as a drug target. Discuss: - Is anything known about its biology? E.g does it have known ligands and normal functions? - if you were to target it would you just use it to get growth inhibiting compound into the new blood vessels or is CD105 required for neovascularization?explain and analyse each gene mutaition in the CIN, MSI, CIMP pathways and what are the causes of these mutations in regards to adenocarcinoma tumours colorectal cancer. Provide detailed analysis with examples1. (a) Define placebo (b) Suppose there is a new drug targeting a type of cancer and the clinical trials are to be done with cancer patients, outline and explain the potential set-up of the evaluation for effect of the new drug. (Hint: The set-up should not jeopardize the patients receiving a placebo.)
- why is LDHA an attractive target for a cancer therapeutic? https://www.nature.com/articles/s41598-019-40617-3#Tab11. Describe & explain the pathophysiology of cancer based on the diagram. Reference: https://www.onlinebiologynotes.com/cancer-etiology-pathophysiology-types-diagnosis-and- treatment/ Acquired (environmental) DNA damaging agents: • chemical • radiation viruses Activation of growth- promoting oncogenes NORMAL CELL DNA Damage Failure of DNA repair Mutations in the genome of somatic cells Alteration of genes that regulate apoptosis Malignant neoplasm / Successful DNA repair CANCER Inherited mutations: • Genes affecting DNA repair • Genes affecting cell growth Expression of altered gene products and loss of regulatory gene products Inactivation of cancer suppresor genes Clonal expansion Additional mutations (progression) T HeterogeneityDiscuss the challenges to producing anticancer drugsthat counteract the effects of mutations in tumorsuppressor genes