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| Pregunta | Respuesta |
| Excision repair | Om en bas har t.ex. reagerat med en elektrofil och förändrat sin struktur kan skadan detekteras av ett "repair-enzyme", som öppnar upp DNA. Andra enzymer tar bort den skadade basen och ersätter med en ny korrekt. |
| Hur repareras DNA om en bas reagerer och ändrar struktur under replikationen? | Den skadade basen kan inte användas som mall och ett glapp uppstår. Information om vilken bas som ska vara där kan fås från andra strängen. |
| Destabilation of DNA bases | Kan vara svårt att reparera |
| Cross-linking of DNA | Mellan två baser Svårt att reparera |
| Intercalation | Flat molecules inserts into the space between the two DNA strands. May not directly lead to mutation but if the intercalator can react with DNA, it can be carcinogenic. |
| 2 mutation classes | 1. Point mutations: - Base pair substitutions - Frame shift mutations 2. Chromosome mutations |
| Baspair substitution | Often a limited damage |
| Frame shift mutation | May cause more damage Can be caused be a failed repair of multiple repitions of the bases if a loop is formed |
| Chromosome mutations | - Deletion of a segment - Duplication of a segment - Inverstion: a segment is reversed (?) - Translocation: a segment has moved - The number of chromosomes has changed |
| Effects of mutations | - decreased function - cell death - no change in function - on inactive genes (silent) - improved survival |
| A classical scenario for the development of cancer | initiation (DNA damage), promotion, transformation |
| Characteristic of cancer cells | Uncontrolled cell division No apoptosis Mutates/"adaptive" Undifferentiated Infiltrating (invasive) Metastasis (translocation) |
| Benign | grow only to a certain size do not spread |
| Malignant | Cancer |
| Carcinogenic | transforms cell into cancer cell |
| Genotoxic carcinogens | Reactive compounds (before or after metabolism) that cause mutations (initiators): • Electrophiles • Radicals or reactive products • Metal ions |
| Epigenetic carcinogens | Chemicals indirectly affecting DNA: • Enzyme inhibitors • Modulates transcription • Immunosuppressive compounds • Hormones • Mitogens • Cocarcinogens or promotors |
| Oncogenes | individual genes that, when introduces in healthy cells, make the cell loose control over cell division |
| Protooncogenes | exact (almost) copies of oncogenes, present in all of our cells. They normally carefully regulate and code for proteins stimulating cell division. |
| Antioncogenes | genes coding for proteins inhibiting cell division |
| Oncogenes’ proteins | Protein kinases: • Enzymes that phosphorylates other proteins (e.g. tyrosine), affecting the proteins’ functions. • Human genome encodes 538 protein kinases, many of which are associated cancer initiation and progression. • Inhibitors of protein kinases as cancer treatment Growth factors • Proteins stimulating cell division (normally expressed e.g. platelets in injured tissue) |
| Cancer can form when | Protooncogenes are activated by: • Activation of the transcription/translation • Point mutations in a protooncogene or in genes involved in their regulation • Chromosome mutations moving a protooncogene from an inactive part to an active part of the genome Antioncogenes are inactivated by: • Point mutations in an antioncogene or in genes regulating it • Chromosome mutations moving an antioncogene from an active to an inactive part of the genome |
| Dominant and recessive mutations | Oncogene: dominant Antioncogene: recessive |
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