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10 Cards in this Set
- Front
- Back
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Example of a Proto-Oncogene
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The cell cycle is highly regulated by cyclin-CDK complexes
CDK: Cyclin Dependent Kinase CDK is only active when it is bound to cyclin CDK expression is constitutive (made all the time) but the production of cyclin in cycle (goes up and down) CDK2 binds to cyclin to make an active complex The active CDK releases the G1 S checkpoint, and cells then proceed into S phase |
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EGFR
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Epidermal growth factor receptor
A typical transmembrane protein with an active site outside of the cell that binds a protein called the EGF EGF stimulates cell division by binding on the outside of the cell and signals the inside of the cell EGFR detects EGF from outside the cell and transduces that message to the nucleus *It never goes inside the cell, just the presence of it is signaled This is a VERY complex pathway.. A cascade of "telephone game" to transmit the signal from the cell surface to the nucleus to get certain genes expressed Any step along the pathway could be expressed too little or too much Proto-oncogenes can be activated to become oncogenes, causing cancer |
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Protooncogenes
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Protooncogenes are good genes and are needed by eukaryotes, essential for growth and normal development
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Upregulation of Proto-oncogenes
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Uncontrolled Growth 1
Normal EGFR is a proto-oncogene but when it is upregulated it becomes an oncogene How? 1) Translocation: Moved to a new place? 2) Point mutation: Coding regions? The promoter of the oncogene that makes the promoter more attractive to polymerase, therefor getting more expression? 3) Regulation problems with repressors or enhancers... not operons |
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Example of a Tumor Suppressor Gene
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Uncontrolled Growth 2
Down regulation of tumor suppressor genes, put the brakes on cell division and work against the activity of proto-oncogenes Cells that go under genotoxic stress can induce TP53 TP53 is a tumor suppressor gene, a transcription factor that binds the promoters of target genes Leads to DNA repair, apoptosis or G1 arrest |
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Particular Mechanisms of Inactivation of the Tumor Suppressor Gene
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If the mutation is in the tumor suppressor gene itself, the whole gene may be inactivated
If something is methylated by mistake the promoter may be turned off |
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The Role of Micro RNA in Cancer
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A mutation in the micro RNA will mistakenly shut off the tumor suppressor genes
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Sporadic Cancer vs. Familial Cancer
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Activated oncogenes that are passed along in families are NOT the cause of cancer because oncogenes destroy embryos
It is more likely that the families are inheriting inactivated tumor suppressor genes -Through mutation or epigenetic marking an individual is inheriting one defective ALLELE, then at a point through their life and cell division, at ONE time that defective allele gets replicated OR They arent inheriting cancer, they are inheriting an increased risk of cancer because they only have one copy of the tumor suppressor gene that is functional |
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HPV
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NOT a retrovirus
A DNA virus that messes with the cell cycle that is sexually transmitted Causes increased growth, which may result in warts, in different tissues of men and women Strains 16 and 18 are oncongenic and associated with cervical cancer |
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How does HPV cause cancer when it is not mutagenic?
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ON EXAM!
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