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Pathology & Physiology (Fach) / PIPs (Lektion)
- Rules for naming tumours - word indicating the line of differentiation from a neoplasm + suffix to show whether the tumour is benign/malignant: - OMA - benign - CARCINOMA - malignant epithelial tumour - SARCOMA - malignant non-epithelial tumour
- What are tumours made of? - structure comprises neoplastic cells (parenchyma) and CT (stroma) of which vascular supply is essential for growth 1. Cancer stem cells 2. Cancer cells 3. Immune inflammatory cells 4. Cancer-associated fibroblasts 5. Endothelial cells 6. Pericytes
- Hallmarks of cancer - sustianing proliferative signalling - resisting cell death - evading growth supressors - evading immune system - activating invasion and metastasis - tumour-promoting inflammation - enabling replicative immortality - genome instability and mutation - inducing angiogenesis
- Hallmarks (Autonomous growth, Angiogenesis, Evasion immune system, Invasion and metastasis, stem cells) 1. Autonomous growth - cancer cells don't respond normally to constraints in tissue growth --> e.g. EGFR-KRAS signalling pathway inducing cell proliferation which is constantly active 2. Angiogenesis - physiological process, though which new blood vessels form from pre-existing vessels --> blood vessels in tumours are autonomous, abnormal and often fragile and leaky 3. Evasion immune system - tumour cells coerce immune cells into not recognising them --> e.g. cytotoxic T-cells and NK cells 4. Invasion and metastasis a) Epithelial-mesenchymal transition - reduced cell adhesion --> motility --> digestion of ECM --> Intravasion --> Extravasion b) Mesenchymal-epithelial transition - survival and angiogenesis in secondary tissue 5. Stem cell hypothesis - genetic defects are expected to occur in stem cells or in their immediate progeny --> dangerous because they proliferate more than differentiated cells
- Tumour genetics (Oncogenes & tumour suppressors) 1. Oncogenes - Proto-oncogenes - normal genes which promote cell proliferate --> become oncogenes when expressed abnormally --> e.g. HER-2 in breast cancer 2. Tumour suppressor gene function - Inhibit cell growth or promote apoptosis --> if both copies of them are lost/inactivated the cell with evade apoptosis or divide more rapidly --> e.g. tumour suppressor protein p53 --> normally activated by presence of abnormal DNA, eliciting apoptosis in the cell cysle's "synthesis" phase
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