Cheatography
https://cheatography.com
Personal exam revision use hehe
This is a draft cheat sheet. It is a work in progress and is not finished yet.
Nomenclature
Sacromas |
Mesenchymal tumors |
Carcinomas |
Epithelial tumors |
Epidemiology (Acquired predisposing conditions)
1. Chronic inflammation |
2. Immunodeficiency states |
3. Precursor lesion |
Clinical aspects
1. Local effects of tumor encroachment of tissues/ organs |
2a. Functional activity e.g. Hormone synthesis |
2b. Paraneoplastic syndromes -> Ectopic hormone secretion |
3. Bleeding & infections when tumor ulcerates thru adjacent surface |
4. Rupture/ infarction |
5. Cachexia (Weakness, e.g. weight loss) |
Molecular basis of cancer
Nonlethal genetic damage |
Hallmark: Genetic alteration |
Cancer genes (Target of genetic damage) |
1. Oncogene (Mutated gene) |
- Mutation from proto-oncogenes |
2. Tumor suppressor genes |
- Prevent uncontrolled growth |
3. Apoptosis-regulating gene |
- Overexpressed in cancer cell-> Protect against apoptosis |
4. Regulate interactions between tumor and host cells |
- Change recognition of tumor by host immune system |
2. Insensitivity to Tumor suppressor signals
Retinoblastoma Gene |
- Active hypophosphorylated state: Halts cell cycle |
- Inactive hyperphosphorylated state |
-Heterozygosity: X Affect cell function |
- Both to be inactivated to affect function |
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p53 |
1. Cell cycle arrest |
2. DNA repair |
3. Apoptosis |
4. Evasion of cell death
- Overexpression of BCL-2 protein -> Long life |
8. Evasion of immune surveillance
Host defence against tumor -- Tumor immune |
Tumor antigens |
Antitumor effectors |
- Overexpressed cellular proteins, Oncogenic viral products, Differentiation antigens |
- CD8+ |
- Oncogenic viral products |
- NK lymphocytes |
- Differentiation antigens |
- Macrophages |
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- Humoral immunity |
Immune evasion |
- Immunosuppression |
- Selective outgrowth |
- Antigen masking |
- X MHC expression |
- Apoptosis of CD8+ |
- X Costimulation |
10. Tumor-promoting inflammation
- Interaction between inflammatory cell& tumor |
1. Proliferation-promoting factor release |
2. Growth suppressor removal |
3. Cell death resistance |
4. Angiogenesis |
5. Invasion & Metastasis |
6. Immune evasion |
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Benign Malignant differentiation
Benign |
Malignant |
Differentiation & anaplasia |
1. Well differentiated |
1. Well to undifferentiated (Anaplasia: Functional& structural differentiation loss) |
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- Dysplasia (Disordered growth) |
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- Carcinoma in situ (Non-invasive malignant tumor) |
Rate of growth |
- Correlates w./ level of differentiation |
2. Progressive & slow |
2. Erratic (Unpredictable) |
Local invasion |
3. No, expansion w./ clear boundaries |
4. Yes, infiltrate & destroy |
Metastasis |
(1)Seeding of body cavities (2) Lymphatic spread (3) Hematogenous spread |
4. Absent |
4. Frequently present |
1. Self-sufficiency in growth signals
Proto-oncogenes |
-Normal genes, promote proliferation |
Oncogenes |
-Mutant version, function anonymously w./o growth-promoting signals |
Oncoproteins |
-Proteins encoded |
Self-sufficient in: |
1. Growth factors & receptors |
3. Transcription factors |
2. Signal transduction proteins |
4. Cyclins & CDKs |
3. Altered cellular metabolism
Warbug effect |
- Aerobic situation: Distinct form of cellular metabolism |
- High levels of glucose uptake |
- Increased conversion of glucose to lactose via glycoyitic pathway |
5. Limitless replicative potential: Telomerase
- Telomerase shorten with each cell division |
- Cancer cell have enzyme that regenerate telomerase |
6. Sustained angiogenesis
- Controlled by balance between angiogenesis promoter (VEGF) and inhibitors (bFGF) |
7. Invasion & Metastasis
- Invasion of extracellular matrix |
a. Loosening of intracellular junctions |
b. Degradation |
c. Attatchment |
d. Migration |
- Embolus: Evade WBC killing |
9. Genetic instability
- Both copies of DNA repair proteins are lost |
1. Hereditary Nonpolyposis Cancer Syndrome |
2. BRCA-1 & BRCA-2 (80% familial breast cancer, not sporadic-associated) |
Carcinogenic Agents
1. Chemical Carcinogenesis |
Initiation |
- Carcinogen exposure -> permanent DNA |
Promotion |
- Promoter induce tumor in initiated cell (Nontumorigenic) |
- Promoting agent enhance proliferation & results in cancer |
2. Radiation Carcinogenesis |
- UV rays (UVB, 280-320nm) |
- Ionizing radiation (X-ray, gamma ray, particles) |
3. Oncogenic DNA viruses |
1. Papillomaviruses (HPV) |
2. Epstein-Barr virus (EBV) |
3. Hep B virus (HBV) |
4. Kaposi sacroma herpes virus (KSHV) |
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