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Unformatted text preview: Cancer I. Cell Cycle a. G1 Checkpoint i. Signal to Divide ii. Check size, DNA integrity iii. Move past checkpoint- duplicate DNA b. G2 Checkpoint i. Check cell size ii. Completion of DNA replication integrity c. Metaphase Checkpoint- check chromosomes attached to kinetochore microtubules d. If conditions not correct at any of these checkpoints the cell should i. Fix problem ii. Can’t fix problem- cell suicide pathway (programmed cell death) iii. Problem not fixed and allowed past checkpoint 1. Cancer a. Unregulated cell division b. Cell allowed to go through checkpoint even though it’s wrong II. How and external signals signal a cell to divide- relay molecules in signal transduction pathway a. Reception- molecules binds to receptor (transmembrane protein) and receptor is activated i. Signal molecules- example is growth hormone ii. Signal very specific with receptor iii. Example of a signal- Epidermal growth factor (EGF) would bind to EGF receptor b. Transduction- converting external signal to internal message c. Response- active cell division i. Activation of cellular response ii. Turn on cell cycle control genes iii. Activate cell cycle control proteins III. Receptor- protein (needs genes) a. Gene for receptor – gene for protein A – gene for protein B – gene for protein C (transcription) b. Receptor – protein A – protein B – protein C – activation of cell division (translation) c. Genes that encode signals, receptors, signaling molecules, control proteins = proto- oncogenes i. If these genes mutated – oncogenes = cancer-causing genes IV. How a proto-oncogene becomes an oncogene a. Point Mutation Messense i. Sources 1. Mistakes in DNA replication 2. Exposure to mutogens (cause mutations) 3. Virus inserting DNA into gene ii. Hyperactive (“always thinking active”) iii. Abnormal protein iv. Can’t be degraded always on b. Gene Amplification- normal protein, but too much V. Her2 is a proto-oncogene; a membrane receptor a. When a signal molecule binds Her2, genes are turned on that i. Stimulate cell division ii. Inhibit cells from dying b. Each Her2 gene transcribed/translated- too much Her2 c. 20% breast cancer – amplification of Her2 gene VI. Use of antibodies to shut down excess Her2 a. Antibodies- proteins that recognize and bind specific molecules (block hathogens/receptor) b. Antibody made that can bind to Her2 receptors- Herceptin i. Can get rid of 2/3 of Her2 ii. Stop breast cancer from growing/spreading VII. Tumor suppressor proteins a. Proteins that helps prevents tumors b. Proteins that inhibit cell division c. Normal cell proteins d. Shut down cell division if conditions not favorable i. Some detect and/or repair DNA damage 1. If mutated override check points ii. Some make sure cells are anchored 1. If mutated cells invade other parts of body 2. Needs to be anchored something to divide e. Tumor suppressors to make note of i. BRCA2- helps repair damaged DNA at G2 1. Genes get passes through generations (more likely to have...
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This note was uploaded on 04/06/2009 for the course ZOO 101 taught by Professor Sharon during the Spring '08 term at University of Wisconsin Colleges Online.
- Spring '08