MicroBio 160 1st EditionLecture 6Outline of Last LectureI. CancerII. How Does Cancer DevelopIII. New Tissue GroupsIV. Tumor DevelopmentProperties of Tumors V. Tumor Grade and Cancer Survival VI. Tumor Stage VII. Different Kinds of Cancer VIII.Cancer Cases and Cancer Deaths IX. Five Year Survival Rates X. Factors Influencing Survival RatesOutline of Current LectureI. Maturation of Immune CellsII. Cancer begins with Cell DamageIII. How Cancer DevelopsIV. Cancer CellsV. Growth Factors and CancerVI. Density Dependent Inhibition of GrowthVII. Anchorage Independent GrowthVIII.Telomeres and ImmortalityIX. Metastasis and AngiogenesisX. Cancer ProgressionThese notes represent a detailed interpretation of the professor’s lecture. GradeBuddy is best used as a supplement to your own notes, not as a substitute.Current LectureMitosis: reproduce themselves exactlyCell junctions: proteins produced by the cellMaturation of Immune Cells:•Normal cell•Self shrinkage•Pieces of membrane bubble off•Nuclear collapse, continued bubbling offApoptotic body formation: self destruct if they are damaged (self suicide), Necrosis: outside forces acting on the source, the cell doesn’t want to die Lysis of Apoptotic Bodies Cancer begins with CellDamage:•As you get older, not much of a risk— spike between 60 and 80 (older and more prone to sickness)•Weakened immune system— can't fight off cancers as they develop• They have been exposed to more environmental and hormonal factorsHow Cancer Develops: Cancer mutations are progressive and happen in multiple steps— build on top of each otherNormal cell: one of the daughter cells gain a mutation— can gain a mutation once it has divided and been exposed to something in the environment First Mutation: Cell seems normal but is predisposed to reproduce excessively Second Mutation: Mutations randomly occur and have different genes— cellbegins to reproduce too much but is otherwise normalThird Mutation: Dysplasia (abnormality of growth, development, or differentiation) Cell reproduces more rapidly; it also undergoes structural changes Fourth or Later Mutation: Cell grows uncontrollably and looks obviously deranged Transformation between noncancerous to cancerousCancer Cells:Become independent of external growth factors Loose density dependent growth inhibition Gain anchorage independent growth Have limitless replicative potential (immortality) Stimulate sustained angiogenesis (developing blood vessels) Able to escape apoptosisCan invade nearby tissue and metastasize Normal Cell:• Dependent on growth factor signals in order to divideDon’t adhere to each other (don’t make proteins)— independent growth Can divide about 20 times then then go through apoptosis (cancer cells divide indefinitely) Growth Factors Signals and Cancer:Growth factors= proteins that stimulate cell growth and divisionIn normal cells, a growth receptor can’t start a growth pathway until it is turned on by a growth factor Binds to a receptor, signal cascade, ends up in nucleus, produce proteins, cell stats to divide In cancer cells, growth receptors can be mutated so that they are ALWAYS on Constantly telling the cell to divide and cell checkpoints are ignored Growth factor independence Density Dependent Inhibition of Growth:Experiment: Normal cells in a flask in liquid medium—cells only grow to a certain density if they are normal cellsNormal and cancer cells will attach to the surface Both will start dividing•Normal cells stop diving when they reach the bottom and come in contact with their neighbor because they signal each other “Don’t grow over me” (organized)•Cancer cells do not stop— they continue dividing and ignore the signals from other cells (disorganized)•Cancer has lost its density dependent growth inhibitionAnchorage Independent Growth:•Cells need to be attached to a surface in order to grow well— if they cant make attachments to a surface or other cells, they undergo apoptosis-Cancer cells don’t need to attach to a surface or to neighbors-Cancer cells have achieved anchorage independent growthCancer cells loose their cell junctionsTelomeres and Immortality:•Telomeres: short pieces of DNA that protect chromosome ends•Do not code for protein•Are responsible for limiting the number of times a cell can divideBecause of this a cell can only divide about 20 times then their telomeres become too short Telomeres shrink as you age; 0—8,000 65—1,500 ; once you run out that cell stops dividing (cell starts to lose genes) Cancer cells gain the ability to keep dividing constantly Telomerase and Cell DeathTelomerase: enzyme that extends telomeres Every time we make a copy of our DNA, telomeres are shortened Short telomeres— apoptosisEmbryos: reaches certain points then turns off telomerase (cancer cells gain the ability to turn it back on) Cancer cells add to telomeres A step in the process of differentiation is to stop telomerase Telomerase= Cell Immortality:•Telomerase can make its own copy of DNA-If you remove blocks, cells become immortal-The more they divide, the more they move back to a stem cell like state•Telomerase activity is blocked by inhibitors in adult cellsThe presence of telomerase allows cancer cells to continue to divide and grow indefinitely— becoming “immortal” Metastasis and Angiogenesis:Metastasis: last stage (most dangerous/deadly)— process where cancer spreads to other parts of the body (cancer growth process— not normal process)•Can spread through the blood or lymph nodesAngiogenesis:the process of new blood vessel formation (normal process)•Used by tumors to survive and grow bigger•If you get a cut, cut far enough that you’re bleeding the body has a way of repairing those blood vessels to get more blood vessels throughCancer Progression:•Traveling through the blood stream— they can get destroyed•Coming in contact with white blood cells— if they survive they adhere to bloodCancer cells:Evading apoptosis, self sufficiency in growth signals, insensitivity to anti-growth signals, tissue invasion and metastasis, limitless replication potential, sustained
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