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BI13.1-5 | Miscellaneous — Summary & Reflection
REFLECT
Take a moment to connect what you've learned to real life:
- Cancer and p53: Next time you hear about a cancer diagnosis, think about which of the two "accelerator/brake" systems failed. Can you recall the three ways an oncogene can be activated?
- Alcohol metabolism: Have you or anyone you know noticed that some people flush red after even a small amount of alcohol? This is due to acetaldehyde accumulation (often from a genetic variant of aldehyde dehydrogenase common in East Asian populations). How does this connect to the disulfiram reaction?
- HIV: Antiretroviral therapy targets multiple enzymes in the HIV life cycle. Can you name at least three drug targets from the life cycle you learned?
- AI in the lab: The next time you get a blood test result, consider: was an AI algorithm involved in validating that result before it reached your doctor?
KEY TAKEAWAYS
Key Takeaways — Your Study Checklist:
- Oncogenesis is the transformation of normal cells to cancer cells, driven by oncogenes (stuck accelerators like RAS, MYC) and loss of tumour suppressors (failed brakes like p53) — BI13.1
- Tumour markers (AFP, CEA, CA-125, PSA, HCG) are proteins used for cancer screening, diagnosis, and monitoring — but none is 100% specific. Cancer therapy targets oncogene products (imatinib, trastuzumab) and metabolic pathways (antimetabolites) — BI13.2
- HIV is a retrovirus that uses reverse transcriptase to convert RNA → DNA, targets CD4+ cells via gp120, and causes metabolic derangements (wasting, dyslipidaemia, oxidative stress) as it progresses to AIDS — BI13.3
- Alcohol is metabolised by ADH (main), MEOS, and catalase, producing toxic acetaldehyde and flooding the liver with NADH. Chronic alcoholism causes fatty liver → hepatitis → cirrhosis. Remember:
FALL-HUG— BI13.4
- AI in biochemistry labs enables autoverification, quality control, pattern recognition, predictive analytics, and reference range optimisation — always with human oversight — BI13.5