Biochemistry
Oncogenesis and Immunity
Oncogenesis and immunity for MBBS: oncogenes, tumour suppressors and tumour markers, innate and adaptive immunity, antibody structure and vaccines, mapped to NMC codes BI10.1 to BI10.5.
MedNext Academy | 3 min read
Oncogenesis and Immunity
Oncogenesis and immunity for MBBS: oncogenes, tumour suppressors and tumour markers, innate and adaptive immunity, antibody structure and vaccines, mapped to NMC codes BI10.1 to BI10.5.
This chapter connects molecular biology to cancer and immunology. It covers oncogenes and tumour suppressor genes, the multistep origin of cancer and its biochemical markers, and the innate and adaptive immune systems, including antibody structure, the role of T-helper cells and the basis of vaccination.
High-yield: Oncogenesis and Immunity
- Carcinogenesis is a multistep process of initiation, promotion and progression driven by accumulating genetic changes.
- Proto-oncogenes promote normal growth; when activated by mutation, amplification or translocation they become oncogenes.
- Tumour suppressor genes such as TP53 and RB normally restrain the cell cycle, and their loss removes that brake.
- TP53, the guardian of the genome, halts the cycle for repair or triggers apoptosis, and is the most commonly mutated gene in cancer.
- The RAS oncogene, mutated in many cancers, drives continuous growth signalling.
- The Philadelphia chromosome, a BCR-ABL fusion from a 9;22 translocation, causes chronic myeloid leukaemia.
- Tumour markers aid monitoring: alpha-fetoprotein in liver and germ cell tumours, PSA in prostate cancer, CA-125 in ovarian cancer and CEA in colorectal cancer.
- Tumour markers are used mainly for monitoring and follow-up rather than for screening, since they lack specificity.
- Innate immunity is rapid and non-specific, using barriers, phagocytes, complement and natural killer cells.
- Adaptive immunity is specific and has memory, with B cells making antibodies and T cells providing cellular immunity.
- Antibodies have a Y shape of two heavy and two light chains, with the Fab region binding antigen and the Fc region mediating effector function.
- IgG is the most abundant antibody and the only one that crosses the placenta; IgM is the first made in a response.
- IgA guards mucosal surfaces, IgE mediates allergy and parasite defence, and IgD sits on naive B cells.
- T-helper cells orchestrate the immune response, and their depletion in HIV infection causes immunodeficiency.
- Vaccines create protective immunity by presenting antigens so the adaptive system forms memory without natural infection.
Cancer genes and markers
- **Oncogenes:** Activated proto-oncogenes, such as RAS and BCR-ABL. Gain-of-function drives growth.
- **Tumour suppressors:** TP53 and RB restrain the cycle. Loss of function removes the brake.
- **Tumour markers:** AFP, PSA, CA-125, CEA. Mainly for monitoring, not screening.
- **Antibody isotypes:** IgG crosses placenta, IgM first response, IgA mucosal, IgE allergy.
NMC competencies in this chapter
- **BI10.1:** Cancer initiation and promotion, oncogenes and their activation
- **BI10.2:** Biochemical tumour markers and the basis of cancer therapy
- **BI10.3:** Cellular and humoral components of the immune system and antibody structure
- **BI10.4:** Innate and adaptive immunity and the central role of T-helper cells
- **BI10.5:** Antigens and concepts in vaccine development
Frequently Asked Questions
What is the difference between an oncogene and a tumour suppressor gene?
An oncogene is an activated growth-promoting gene that drives cancer through a gain of function, while a tumour suppressor gene normally restrains growth, so cancer arises when it loses function.
Why is TP53 so important in cancer?
TP53 arrests the cell cycle to allow DNA repair or triggers apoptosis if damage is severe. Because it protects the genome, its loss allows mutations to accumulate, and it is the most commonly mutated gene in human cancer.
How do tumour markers help clinically?
They are used chiefly to monitor treatment response and detect recurrence rather than to screen, since raised levels are not specific to cancer and can occur in benign conditions.
How do innate and adaptive immunity differ?
Innate immunity acts quickly and non-specifically through barriers, phagocytes and complement. Adaptive immunity is slower but specific and remembers past antigens through B and T lymphocytes.
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