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45 Cards in this Set
- Front
- Back
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What is a diverse set of genetic diseases? |
Cancer |
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What gene accelerates or stops cell division |
Cancer genes |
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What causes cancer cells to divide rapidly and uncontrollably |
Mutations |
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What type of cells becomes cancer cells? |
Somatic cells |
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What are 3 ways cells becomes cancer cells |
•Produce cell division signals (autocrine signaling) •Lose contact inhibition •Avoid programmed death |
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What feature of chromosomes mains length of chromosomes ends? |
Telomerase |
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What is it called when cancer cells produce to encourage blood vessel growth? |
Angiogenesis |
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What is it called when blood vessels provide nutrients to tumors? |
Metastasis |
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When cancer mutations distrupt DNA repair they create? |
Permanent mutation after replication |
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Mistakes in DNA replication cause? |
Genomic instability |
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Successive mutations become? |
Malignant |
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Are cancer cells clones of normal cells (T/F) |
True |
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Does the rate of cancer increase or decrease with age? |
Increase |
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What kind of cancer mutation increase cell mutation rate? |
Passenger mutations |
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What mutation causes phenotypic changes and needs several of them to result in cancer? |
Rare driver mutations |
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What are 3 cancer like properties |
Growth Division Genomic instability |
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What growth factor stimulates cell proliferation? |
Mitogens |
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What are the steps for dignal transduction |
•Receptor bound to cell surface •Blind growth factor initiate signal transduction cascade •Synthesis of transcription factors activated |
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What regulates genes whose protein products cause cells to divide or stop dividing? |
Transcription factors |
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What signal initiates cell division over long/short distances |
Extracellular signals |
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What are examples of extracellular signals? |
Hormones, steroids peptides or protein, Thyroid hormone |
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The Thyroid hormone is produced where? |
Pituitary gland |
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What type of factors transmit signaled into cells through transmembrane receptors? |
Growth factors |
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Growth factor receptor binding |
Growth factor binds to signal binding site Inside cell signal transducers relay information Ras binds to gtp and becomes active |
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Ras binds to gtp and becomes active |
Map kinase cascade 》 Transcription factor》 Proliferation |
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Ras binds to gtp and becomes active |
Map kinase cascade 》 Transcription factor》 Proliferation |
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Cdk-cylin complex does what? |
Phosphorylate proteins |
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What provides structural support to the nucleus? |
Lamins |
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Cdk-cylin complexs |
Cyclin D- G1/ anaphase Cyclin E- S Cyclin A- G2 Cyclin B- metaphase |
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What happens when p53 producing cells when damage is great |
They arrest in G1 Commit to apoptosis - DNA degraded, nucleus condense, phagocytic cells destroy cell |
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What are 3 kinds of genetics instability |
Point mutation Translocations Gene amplification |
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What has HSRs |
Tumor cells |
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What type of gene dominantly promotes cancer? |
Oncogenes |
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What type of alle is proto- oncogene ? |
Nonmutant allele |
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proto- oncogenes encode proteins needed for? |
Cell cycle progression |
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Gain of function mutation results in? |
Increase proliferation |
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What acts to recessively promote cancer? |
Tumor suppressors |
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Normal alleles of tumor suppressor genes encode proteins that |
Slow down the cell cycle |
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Loss of function mutations result in |
Increased proliferation |
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Gain of function oncogenes |
Ras -active when bound to growth factor c-AbI - Her2 Found over expressed in Breast cancer |
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Retinoblastoma (Tumor suppressor) |
-Dominant genetic cancer - a recessive trait -Mutation in RB gene -Increased cell proliferation |
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Loss of Heterozygosity mechanisms |
Nondisjunction Uniparental disomy Mitotic recombination Gene conversion Deletion Point mutation |
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Tumor suppressors |
Rb- delays S phase P53- g1-S BRCA1&2 repairs double strand breaks in DNA |
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Oncogenes targeting drugs: Gleevec |
Gleevec binds to ATP binding site inactivatibg enzyme |
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Oncogenes targeting drugs: herceptin |
Binds to her2 preventing activation |
