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Biology 1002B
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Lecture 18 CancerPresident Nixon declared war on Canada in 1971In Canada men are at higher risk for cancer than womenIn women theres 40 chance of contracting cancer and 27 chance of dying from it The top 4 cancers breast cancer prostate cancer lung cancer and colon cancerRates among young people are risingWe think cancer has something to do with genes and is genetic so how heritable is itHeritability estimates from twin studiesif twin starts smoking theres a chance the other twin will tooBut thing is heritability depends on the kind of cancer but still is on the low endthis could be because cancer rates have high environmental components as compared to other things that have a genetic heritability Embryology rapidly dividing cellsThere is a stage in the life cycle where cells need to divide fastCyclinCDKinase complexes regulate cyclingPay attention to G1S checkpoint which prevents cells from replicating their DNA if its damaged so they cant go through until everythings repairedThis checkpoint is monitored by CDK cyclin dependent kinasekinases transfers phosphate groups it phosphorolatesBut CDKs are only active when theyre bound to other proteins called cyclins Cyclins are called cyclins because theyre production cycles with the cell cycleThis cyclin is produced early in cell cycle It binds onto and activates CDK CDK cyclin complex that phosphorolates a whole bunch of targets downstream andthat releases the G1 checkpoint posttranslational regulation of protein functionThe rest of the diagram is just another rest of cyclin CDKs to get through the next checkpoint and so on EGFR protoonco genesCells need to be responsive to environment and need to know when they should divideEGFR epidermal growth factor receptor does this So when there is EGF in environment it binds onto this receptor and then theres an internal signalling domain in this proteinEGFR is a normal protein and is essential for normal embryonic developmentif EGFR becomes deregulated it can give rise to rapid cell growth oncogenes cancer genes are just embryonic genes that have been deregulatedEGF PathwaysThis picture shows EGFR at the top and the signaling is on the insideThe inside is just a bunch of signals that takes the signals from the surface of the cell where EGFR is present to the nucleus Expression of tumour supressor genes slows cell cycling p 53TP53 is a master tumour supressor gene coding a transcription factor whose activity can result in Genes evolved to shut down that rapid cell growth during embryonic developmentAt some point organisms get large enough and they need to stop this rapid cell division so those genes evolved to be supressors P53 is this transcription factor that can be activated by dna damage invoke repair and block CDKs at the first checkpoint its in charge if that first G1 checkpointOncogenes are mutated forms of certain normal genes of the cell called protooncogenes Protooncogenes are often genes that normally control what kind of cell it is and how often it grows and divides When a protooncogene mutates changes into an oncogene it turns on or activates when it is not supposed to be When this occurs the cell can grow out of control leading to cancerTumor suppressor genes are normal genes that slow down cell division repair DNA mistakes or tell cells when to die a process known as apoptosis or programmed cell death When tumor suppressor genes dont work properly cells can grow out of control which can lead to cancerSporadic CancerSometimes related people are more at risk for cancerBRCA1 is a breast cancer tumour suppressor gene whose normal function is to stop rapid cell division but over life one may have suffered mutations on both those alleles and lost the tumour suppressor activity of BRCA1 and so the cells divide rapidly this is sporadic Sporadic cancer requires new loss function mutations in both allelesHowever familial cancer requires a loss of function mutations in 1 alleleIf you inherit from your dad an already defective tumour suppressor allele than all you have is the functional one from your mom then your at much higher risk of becoming homozygous in a certain cell because now all you need is 1 mutation instead of 2 in order to develop a tumour Even if you were born with healthy genes some of them can become changed mutated over the course of your life These mutations are known as sporadic or somatic meaning they are not inherited Sporadic mutations cause most cases of cancer These mutations may be caused by things that we are exposed to in our environment including cigarette smoke radiation hormones and diet although in many cases there is no obvious cause More gene mutations build up as we get older leading to a higher risk of cancerMicroRNA expression profiles classify human cancersInappropriate expression of miRNA can promote cycling ex OncomirsmiRNA have turned out to be very integral in cell divisionregulationresearchers call them oncomeres but theyre just part of regulationThe miRNAs are diagnosticmiRNA overexpresed where its red normal cell and under expressed where its blue in tumorsEach tumor has its own kind of fingerprint of miRNA expressionIt seems miRNAs are very importantCancer is DeregulationUncontrolled growth can arise from upsetting the balance between the activity of gene products that promote cell cycling vs those products that supress cell cyclingCancer is ProgressiveMost cancers require several changes to occur before you get a tumour Accumulated deregulation gives rise to a tumour Cancer is progressive we knew this but we didnt why and about these genesProbably all your tissues have stem cells that are plurypotentthese stem cells are able to differentiate into a wide range of tissue types Stem cells when they divide to make 2 daughter cells one of them remains a stem cell and the other becomes a progenitor cell which goes on to differentiate into something
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