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Toxicology - genotoxic compounds and cancer

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Flashcards on Toxicology - genotoxic compounds and cancer, created by Tova A on 17/02/2021.
Tova A
Flashcards by Tova A, updated more than 1 year ago
Tova A
Created by Tova A over 3 years ago
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Question Answer
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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