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Department
Biology
Course
Biology 1002B
Professor
Tom Haffie
Semester
Winter

Description
Lecture 18 CancerFour most common types of cancer in Canada Breast cancer Prostate cancer Lung cancer Colon cancer 40 of women 45 of men can expect to contract some kind of cancer in their livesJust less than 25 of women can expect to die from cancer more than 25 of men can expect to die from cancerLikely factors contributing to cancer incidence in Canada older you are the more likely you are at developing cancer Second most likely nonaccidental cause of death heart disease is the first Risk factors exposure to dietary risk factors exposure to environment Lung and colon cancer suggest environmental risk factors Breast and prostate cancer suggest internal risk factors Balance of and interactions or internal and external factors that contribute to cancerRole of cyclinCDK complexes in cell cycle regulation Embryogenesis is rapidly diving cells Cells may actively cycle sit in G0 or undergo apoptosis In the cell cycle there is a G1s checkpoint that prevents cells from replicating their DNA if it is damaged This is monitored by CDK Cyclin Dependent KinaseCDK is a protein It works by phosphorylating but only when it is bound to cyclinCDKCyclin phosphorylates it target proteins together to release the G1s checkpoint and cells proceed into S phase This is an example of posttranslational regulation Constitutive expression a gene that is transcribed continually compared to a facultative gene which is only transcribed as needed Production of cyclin is cyclic Another CDKcyclin complex regulates movement from S phase into M phasestUncontrolled Growth 1 reason Role of protooncogenes and oncomirs in caner ProtoOncogenes are essential for normal growth and developmentEGFR Epidermal Growth Factor Receptor It is a typical transmembrane proteinActive site outside the cell that binds protein hormone EGF EGF stimulates the cell to divideEGFR signals on the outside of the cellphosphorylation cascade signals presence of EGF on the outside of the cellcauses the expression or no expression of certain genes in the nucleus Any step along the pathway could be expressed inappropriately causing it to become cancerous When deregulated protooncogenes become cancerous and people call them oncogenes Mutation is EGFR causing it to signal even when EGF is not present will lead to the cell dividing all the timeupregulation How might protooncogenes be activatedTranslocation issues mutation in promoter causes the promoter to be more attractive to polymerase resulting in more expression regulation problem with enhancers or repressors enhancers become more effective than usual ndUncontrolled Growth 2 reason Tumor suppressor genes and role of p53 gene Suppressor gene work against protooncogenes to ensure that cell division occurs at a regular pace genes that evolved to shut down rapid cell division TP53 is a master tumor suppressor gene it codes a transcription factor that binds to the promoters of many target genes When it binds to the target genes it can result in i Increased DNA repairii G1 arrest cell cycle arrest by blocking cyclinCDKiii ApoptosisA tumor suppressor gene may be inactivated throughmutation in the gene itself high methylation shutting off promoter mutation in microRNAs mistakenly shuts off tumor suppressor gene miRNAs highly important in gene expression and for diagnostic particularly in cancer oncomirs oncomicroRNAsExplanation for why increased cancer risk can be inherited Most cancer in this country is sporadic not due to family However for families that is at higher risk Some sort of gene thats damaged or possessed certain epigenetic marks is being inherited through the family People DO NOT inherit activated oncogene more likely that they are inheriting an inactivated TS genemutation epigenetic marking inherit one defective allele for the gene at some point in their life the other allele in one of their cells becomes inactivated too leading to development of tumors Relatedness does affect cancer Example of BRCA1 which is a normal tumor suppressor and brca1 is the defected tumor suppressorExplanation for why cancer incidence tends to increase with age Cancer is PROGRESSIVE Age is a big factor as you get older you have more time to accumulate mutationsRole of stem cells in tumor growth Cancer may begin as alterations to gene expression in stem cells Most of your tissues have stem cellsThey know how to be every kind of cell pluripotent Stem cells divide differently than normal cells stem cells make two daughter cells one is a progenitor cell and one is a stem cell Progenitor cell becomes differentiated cell can be anything BUT all three stem cells progenitor cells and differentiated cells can suffer mutations and become CANCER STEM CELLS Thus tumors may be driven by cancer stem cellsEvidence that epigenetic regulation may be relevant in cancer Cancer is DEREGULATION Uncontrolled growth can arise from upsetting the balance between the activities of gene products that promote cell cycling vs those gene products that suppress cell cyclingIrregular deregulation versions of promoting cell cycling and suppressing cell cyclingLecture 19 Molecular Homology Strategies for determining if features are homologous Comparative genomics Sequence genomesGenome annotationProtein predictionAlign sequences
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