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by: Aimee Breitenberg DDS


Aimee Breitenberg DDS
GPA 3.83

Lisa Bain

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Lisa Bain
Class Notes
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This 9 page Class Notes was uploaded by Aimee Breitenberg DDS on Saturday September 26, 2015. The Class Notes belongs to BIOSC 461 at Clemson University taught by Lisa Bain in Fall. Since its upload, it has received 38 views. For similar materials see /class/214217/biosc-461-clemson-university in Biological Sciences at Clemson University.


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Date Created: 09/26/15
Chapter 25 Study Guide Be able to de ne oncogenes tumor suppressor genes and caretaker genes Also de ne and describe the differences between benign malignant and metastatic tumors 0 Oncogenes normally promote cell growth when mutated cell prolif is increased Dominant quot 39 39 39 39 incell Tumor suppressor genes normally involved with cell cycle they restrain all growth recessive need both enzymes to take effe 0 Caretaker genes involvedin repairing DNA enzymes that repair dna 0 Benign localized Heldin place by extracellular attachments 0 Malignant potentially has the ability to spreadto nearby tissue 0 Metastatic implies ability to spreadto distant parts ofbody Makes use of blood supply or lymph Must be able to invade basement membranedigest through to em using sometype of protease to do the digestion Migrates along emdigest or diffuse into capillary Know w 39 39 39 fm tumor growth 39 L r 39 39 39 the growth factors needed 0 Angiogenesis means developing blood supply 0 involving the growth oinew blood vessels from oreexisting vessels 0 Vascular epithelial growth factor VEGF receptors 1 and 2 normally only found on epithelial cells occuring in carcinomonas o Angiopoietins land 2 l recruits pericytes smooth muscle cells 0 2 loosen ecm to beome receptive to vegf including Prcztalysls 7 5cm Mew larw m mum 2 mgmn w hEuMax S a mhtmatan 0 As gets into blood stream vegf2 what is needed to proliferate these endothelial cells get general cell proliferation o l digest the ecm 0 Start by angio 2 to proliferate epithelial cells vegf2 0 When get enough cells that proliferate get tube vegf l o Tumors cannot grow past lme due to lack of oxygen 0 Tumors induce blood vessel growth angiogenesis by secreting various growth factors eg Vascular Endothelial Growth Factor or VEGF Growth factors such as bFGF and VEGF can induce capillary growth into the tumor which some researchers suspect supply required nutrients allowing for tumor expansion 0 angiogenesis is a necessary and required step for transition from a small harmless cluster of cells often said to be about the size ofthe metal ball at the end of a ballpoint pen to a large tumor Angiogenesis is also required for the spread of a tumor or metastasis Single cancer cells can break away from an established solid tumor enter the blood vessel and be carried to a distant site where they can implant and begin the growth of a secondary tumor Understand what the multihit model is and what types of evidence exist that suggests this leads to the formation of cancer age mice colon cancer 0 Need mutations in speci c genes to transform cells into tumor cells 0 Multi hit model more than 1 mutation Initiation promotion and progression Start with single cell and have mutation Initation is mutation in ocogene or suppressor gene That s xed into chromosomes No possibilty of repairing it 0 promotion clonal exposition o Progressionaccumulation of multiple mutations Start to get hetergeneity in tumor all still have original mutation a but not might have mutation now in b c d etc 0 Also supported by human epidemiology studies know this be cancer rates in general increase with age Transgenic mice to test the multihit model 0 Mutation in oncogene tumor suppressor gene 0 Rassignal transduction pathwayscan t exchange gtp for gdp Cant shut ras off 0 If combine myc and ras mutations the tumor free drops signi cantly Successive mutations in colon cancer 0 Loss of adenomatous polyposis coli APC gene 0 Tumor suppressor gene must have two mutation One in each chormosome Leads to polypsprecancerous growth benign Apcsignaling pathway cmycTF9if lose apc than have increase in cmyc Gl 9s trasition I People who are born with this mutation already and are born with thousands of polyps Be prepared to give examples of different genes that when mutated cause cancer Examples include Ras HERZ Rb cAbl myc fos and p53 Make sure you can describe the normal function of the gene where the mutation occurs how the mutated gene now functions and howwhy that altered function can lead to tumor formation 0 000 o Ras 0 Where I mutations in the GTP binding siteoncogene intracellular transducer 9active o How functions 0 Howwhy lead to tumor I Switch 1 gtpgdp tend not to see mutation in green part of protein I Glyc 12p loop usually ends up mutated to valine reducers gtpase activity I th stays a lot longer than it should I Amino acid 61 at left side of ploop get decrease in gtpase activity as well 0 Her2 0 Where I Growth promoting and tumor suppressing genes 0 How functions O O o Cabl o Fos O O O O O O O Howwhy lead to tumor I Where Things that are signaling receptors Speci cally receptor 2 ligand independent This mutation from normal receptor into oncogene is caused by single point mutation Have valine that converts to glutamind tyrosines always stay phosphorylated9uncontrolled cell proliferation gl s transistion somatic cell How functions Tumor suppressor gene normally restriction point in late Glirreversibly commits to entering S phase Howwhy lead to tumor Where Going to function by holding a tf called e2f inhibiter of tf When have high enough gcyclin cdk will phosphoylate Rb you can make e2f as much as want and therefore loose the checkpoint of Rb and have proliferation Not bind to e2f or mutation ins Rb so that it continues to phosphorylate chromosomal translocation9 hybrid protein How functions Ablpromotes actin branching helps stabilize shape and movement of protein It is a protein kinase if mutate it will cause it to have P ability constantly On chromo 9 usually swaps with bcr gene unknown func but gene is always be transcribed Howwhy lead to tumor Bcrabl fusion protein kinase activity JaldStatsP no signal needed Cell proliferation occurs TF that bind to dna ex How functions cmyc can undergo point mutation but also translocations Howwhy lead to tumor Where Burkitt s lymphoma T F 39 G S transition Burkitts lymphoma characteristic translocation Cmyc on chrom08 translocates with immunoglobin under immunoglobin is promoting activity then have chimeric protein where have heavy chain Igg icymyc and promoters at begininning of this Mani staton of this in bcells inc division Lymphoma where b cells exist How functions 39 G as transition in cell cycle Normal cells bc involved with transitionfos tends to be very unstable rapidly degraded In general mutation in fos increase the stability and therefore promotes cell to keep going to Sphase o HowWhy lead to tumor P53 0 Where 0 How functions I Loss of p53 abolished the DNA damage checkpoint o HowWhy lead to tumor I r suppresor gene unline I MutatIons9loss of stabihty I 3 inhibition 0 sphase I Mutation in p53 are the most common for cancer cells Will get proliferations TABLE 25 1 Classes of Genes Imp rated the Onset of Cancer NORMAL PROPERTIES FUNCTION EXAMPLES OF GENE EFFECT OF 0F MUTANT OIIIGIN OF OF GENES PRODUCTS MUTATION GENE MUTATIONs Plato Onzogenes Promote ell Annapoptall proteins GEMOFNIICUOII Mutations are Arise by polm s ivalor c mponemsofsignanng and mutationsallow geneIicaIIy mu Iion meiIemiun mIIransdu npaIIIways ume ulaled ell dominam rumosnrllal um result in pmMeminn mewequn i mneIueaIiun lranscdpxian lacmrs val ampll ca on Tumorsuppressor lnhlbkellsurvval Apoptnslspmmntlng Lossenllundhn MumIansare A sehydEIetlun genes Orpmlileralion pmleinsinhibilorsolzell muminns allow 9 Eli IIy point mutation yd progresslon unregulaled cell cesswe mezhyIaxiun checkpnim cunlml proteins meIIeraIIun and thatassess rvival DNAchromosomal damage componentso signal pathways hat restram ell meiIemIon Civetakelgenes Repairarplevenk DNA Iepairenzymss Lnssnf funniun Mumiamm Arisehydaletinn DNA damage mulallonsallow genaIicaIIv paim mulallun mutations a recessive methylaeion accumulate Th 3 e254 MnImlmceIIuInIngys Editinn m zoosw u neemn W and Company De ne the terms carcinogen and mutagen and directacting versus indirectacting Directacting electrophilic compound that reacts With N O atoms in DNA this is RARE Indirectacting more common must be metabolized to an electrophile When get metabolized are bound With cytochrome p450 Which are a family of enzymes that metabolize cmpds to indirect Carcinogen chemical that cause cancer 0 utagen chemical that causes a mutation e e acting carcinogens Understand hoW chemicals can actually cause a DNA mutation Benzoaoyrene 7 found in smoke coal tar charbroiled meats 0 p53 mutations at codons I75 248 and273 o Cytochormoes p450 adds on epoxide can do this in couple of different places on particular chem Some can be hydrolyzed and some can t o Epoxide electrophilicreactive Natoms in guanine Nucleotide that has some other chemical hanging off of it o Adduct chemical that covalently bonded to nucelotide o g triple to c g t 9 point mutation o A atoxin 7 mutations in p53 grains and nuts 0 Need this to be modi ed by enzyme of p450s to convert it to electrophliic compound This is going to bind to your nitrogen atoms of guanine 0 Base mispoairing and a point mutation o Adduct cuases g to mispair with t loss of ability to correctly basepair Cha ter 22 Stud Guide m 5 o Genomic imprintingthe 2 pronuclei do not have equal capacity to activate genes 0 Dna methylation blocks transcription of genes 0 Generally done on cytosomes o CpG ch3 comes off C 0 however in a small subset one copy is turned off in a parentof origin dependent manner These genes are called 39imprinted39 because one copy of the gene was epigenetically marked or imprinted in either the egg or the sperm Thus the allelic expression of an imprinted gene depends upon whether it resided in a male or female the previous generation 0 Recent research shows that maternal methyl deficient diets during pregnancy can alter the expression of imprinted genes in the offspring Know what polarity means with respect to development 0 In epithelial cells the differentiation of apical and basal specialisations In many epithelia the apical and baso lateral regions of plasma membrane differ in lipid and protein composition and are isolated from one another by tight junctions The apical membrane may for example be the only region where secretory vesicles fuse or have a particular ionic pumping system 0 migration axis formation and asymmetric cell division 0 Wherever this begins to set up will form the posteriorbottom of organism o Anteriortop o Dorsalback o Ventralfront Describe early vertebrate embryo differentiation from the zygote to gastrulation What occurs during each step in terms of how the embryo is growing and undergoing differentiation 0 Each cell in this embryo at 8 cell stage can still create a complete organism 0 One you hit 16 cells they have started differentiation 50 have a morula In this phase increase affinity for one another and they become compact and compressed into one anoter 0 At 32 cell stage you have a small cavity inside the mass where fliud begins to flow Called blastocoel 0 When get to bloastocyst 64 cells 0 Started to get compaction rudimentary flow 0 Extra embryonic structure 0 Inner cell mass embryo o Depends on localization outsideTE Trophectoderm and insidelCMinner cell mass 0 During implantation the ICM cells separate into 2 layers 0 Hypoblast truly forms embryo o Epiblast forms extra embryonic structure 0 3 germ cell layers 0 Do this by forming the primitive streak 0 1st cells that migrate endoderm o 2quotd cell mesoderm 0 Don t move ectoderm o Gastrulation first time we start seeing germ layers 0 Once 3 germ layers are formed see something called primitive streak assume posterior cell fates o Posterior end fibroblast growth factors bone morphogenic protein Bmpwnt antagonists block signals 0 0 Signal strength how much a concentration is given the development of the zygote into an embryo proceeds through specific recognizable stages of blastula gastrula and organogenesis The blastula stage typically features a fluidfilled cavity the blastocoel surrounded by a sphere or sheet of cells also called blastomeres During gastrulation the cells of the blastula undergo coordinated processes of cell division invasion andor migration to form two diploblastic or three triploblastic tissue layers In triploblastic organisms the three germ layers are called endoderm ectoderm and mesoderm However the position and arrangement of the germ layers are highly speciesspecific depending on the type of embryo produced In vertebrates a special population of embryonic cells called the neural crest has been proposed as a quotfourth germ layerquot and is thought to have been an important novelty in the evolution of head structures Zygotefertilized ovum Weekl Fertilization Egg activation Zygote Cleavage Momla Blastula Elastornere Blastocyst Inner cell mass Bilgn tf Hypoblast Epiblast Week 3 Trilaminar39l Germ layers ArchenteronPrimitive streak Primitive pit Primitive Primitive groove 39 GastmlaGastmlation Reg39onal speci cation Ectoderm Surface ectoderm Neuroectoderrn Somatopleure Neumlation Neural crest Endoderm Splanchnopleure Mesoderm Chorda Pamxial 39 39 Wermztnmel Intermediate Lateral plate Intraernbggonic coelorn SplanchnopleureSomatopleure Describe how signaling molecule gradients can be used during differentiation to determine what type of cell develops Signals set up the patterns and determine a cell s fate pr0gressive restriction Early on cell can become anything later can only progress down 1 or 2 paths progressive restriction Signaling is important in setting up fates Relay same concentration gradient occurs through out the cells Gradient what typically happens Cell is seeing a concentration gradient 0 Cell a sends out strong signal that dictates what happens down the line As goes downstream the signal becomes weaker Bmpwnt antagonists block signals Signal strength how much a concentration is given Understand how somites develop including where somites are located the types of signaling molecules that are used the genes involved and what somites eventually become How developed 0 Somites are forming pairs either side of midlinestart out with somites forming at anterior and have a wave forming towards posterior end 0 Only get somite formation with fgf is in very high concentration and in close contact to cells Where located 0 Presomitic mesoderm in embryo Types of signal molecules used 0 Retinoic acidanterior end 0 Fgf8 posterior end Genes involved 0 What do they eventually become 0 Somites will eventually become ribs vertebrae limbs muscle of dermis Wnt and notch 0 Need to turn proliferation on and then have them shut off 0 Length of transcription is the same time it takes to form a somite or one pair of somites Example activation of hes7notch signaling pathway Wnt and notch thought to work the same way 0 Coming from posterior end You get expression of large amts of fng and that s going to activate hes7 Essentially get proliferation signal Increase in cell prolif in area of somite 0 Once amt of hes 7 gets high enough hes7 will shut off its own mrna production 0 Autoregulatory feedback loop to what will ultimately be cell proliferation To form somites undergo transcription in cycles Know how early development of the nervous system occurs starting with the formation of the neural tube What types of signals and genes are involved in this process End of gastrulation Ushaped structure ectoderm folds in Which eventually seals up and is what forms neural tube spinal cord nvagination of tissuealso get formation of neural crest cellsbecome part of heart and peripheral nervous system Shhventral Dmpdorsal Shh glialfloor plate Shh floor plates now bc they are part of neural tube are rest of fate of neural tube is not dpendent of presecene or absencelike floor plates but on gradients Shh at high numbers motor neurons Shh at decreasing numbers neurons Extremely low conc of shh sensory neurons BMP sensory neurons at right side of trianglewith shh levels corresponding to bmp Describe how the patterning of the limbs occurs during development What types of signals and genes are involved in this process Control other signals that actually grow limb bud Once limb bud has grown out enough you start forming fine structures like fingers FG F10 going to initiate that outgrowth of limb bud Fgf10 starts growth sets up formation of aer apical ectodermal ridge Aersets up signal at distalfingers Zpa zone of polarizing activity posterior end little finger Needs these two areas In aer have fgf 10 that starts proliferation s going to induce fng Fng induces shh Shh induces fgf4 FgflO 8 4 shh proliferation Hox genes digit formation


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