Exam 1 Review Session Notes October 5th 2015 Question Go over Griffith s Experiments Inject S into mouse mouse dies when injected R nothing happens Created back when they were still unsure of the properties of DNA Two living strains S meaning smooth lethal and R strain non lethal Boiling the S cells kills them Weird thing Inject R strain into a mouse with dead S strain mouse dies Tells us that there is something that the R strain is picking up Inject the dead S cells into the mouse and it s fine T Cells How They are Trained to Not Attack Self Body has two circulatory systems red blood cells and lymphatic system white blood cells Innate immunity Always on cells that are not antigen specific Adaptive immunity Turned on in response to specific antigens B and T cells T cells are educated in the thymus and B cells are in the bone marrow T cells are always being bombarded with antigens Not responsive enough nothing will happen If their response is too sensitive it can overattack Central Dogma DNA mRNA Protein DNA is located in nucleus Transcription DNA is read and transformed into mRNA Translation Reading the mRNA and translating it into a protein ATGC mRNA is taken out of the nucleus and into the cytoplasm of the cell DNA polymerase reads the DNA and makes the mRNA Ribosomes translate the mRNA into a protein mRNA is translated by the ribosome by the ribosome reading the codons 3 In mRNA the T is transformed into a U Uracil nucleotide sequences that correspond to specific amino acids What Makes a Cancer Cell a Cancer Cell Apoptosis Programmed cell death Differentiation become specialized They do not reproduce themselves Do not stop reproducing at the right time Do not stick together in the right place Do not self destruct if they are damaged 3 gene families 1 Proto oncogene when is mutated they become an oncogene so they will increase cell replication 2 Tumor suppressor genes they are involved in cell division check points ex Brakes on the car not working DNA repair genes when mutated they will not help repair DNA 1 risk factor of cancer is age Density dependent inhibition of growth of cancer cells normal cells will grow until the flat surface they are on is completely covered They will stop growing once the density is too much Cancer cells are density independent they will continue to just grow on top of each other Anchorage dependent independent Dependent normal cells Need to be anchored to properly grow Independent cancer cells Do not need to be anchored to grow Cancer cells have a lowered need for growth factors normal cells rely on signals from their environment to tell them when to grow Cancer cells are immortal they can just keep dividing and a key to that is the protein telomerase they repair the damaged telomeres so the cell can just keep dividing Telomeres are nonsense sequences on the end of the DNA whenever the cell divides they become a bit more damaged so there is a limit to how many times the cell can divide Tumors need blood in order to grow Angiogenesis Growing of blood vessels from pre existing ones tumors Vasculogenesis Creation of new blood where there were none can only occur early in development Cancer cells are involved in tissue invasion and metastasis Part of cancer screening Indication that cells are replicating faster than they should Mitotic Index Bias Experimenter Preconceptions influence results they think they know the answer so these assumptions may influence the results Detection methods are unequal Selection nonrandom volunteering Recall self reporting errors Publication Relationship publish No relationship no publish 20 studies 19 show no relationship while 1 shows a relationship the misleading story is the one published P Value If statistical value is higher than p value hypothesis is most likely not true If statistical found value is lower than p value but close then your hypothesis is most likely true Blocking Angiogenesis Tumors can only grow so big eventually they will reach a size maximum Can block receptors make growth factors that will bind but they will not activate Ames Test Testing how potent a carcinogen is and whether it could cause cancer Have bacteria mutation in genes so they cannot produce histidine must add it so they can survive Add them to a medium that lacks histidine very few will grow because they divide very fast so mutations eventually will form in a few Add a compound with liver homogenate will process the carcinogen the same as the body would that increases the mutation rate Incubate the mixture then add the bacteria if more colonies of bacteria are prevalent then this chemical is potentially carcinogenic Presentation of Cancer Antigens Antigen is taken up by an antigen presenting cell Antigen is broken up into small fragments inside the cell by antibodies this is how cells learn which antigens are hazardous Antigen fragments are bound to MHC molecules Antigen MHC molecules moves to the cell surface MHC presents the antigen fragment to lymphocytes which are stimulated to attack that antigen
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