MicroBio 160 1 st Edition Lecture 6 Outline of Last Lecture I Cancer II How Does Cancer Develop III New Tissue Groups IV Tumor Development Properties 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 Rates Outline of Current Lecture I Maturation of Immune Cells II Cancer begins with Cell Damage III How Cancer Develops IV Cancer Cells V Growth Factors and Cancer VI Density Dependent Inhibition of Growth VII Anchorage Independent Growth VIII Telomeres and Immortality IX Metastasis and Angiogenesis X Cancer Progression These 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 Lecture Mitosis reproduce themselves exactly Cell junctions proteins produced by the cell Maturation of Immune Cells Normal cell Self shrinkage Pieces of membrane bubble off Nuclear collapse continued bubbling off Apoptotic 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 Cell Damage 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 factors How Cancer Develops Cancer mutations are progressive and happen in multiple steps build on top of each other Normal 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 cell begins to reproduce too much but is otherwise normal Third 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 cancerous Cancer 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 apoptosis Can invade nearby tissue and metastasize Normal Cell Dependent on growth factor signals in order to divide Don 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 division In 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 cells Normal 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 inhibition Anchorage 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 growth Cancer cells loose their cell junctions Telomeres 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 divide Because 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 Death Telomerase enzyme that extends telomeres Every time we make a copy of our DNA telomeres are shortened Short telomeres apoptosis Embryos 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 cells The 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 nodes Angiogenesis 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 through Cancer Progression Traveling through the blood stream they can get destroyed Coming in contact with white blood cells if they survive they adhere to blood Cancer cells Evading apoptosis self sufficiency in growth signals insensitivity to antigrowth signals tissue invasion and metastasis limitless replication potential sustained angiogenesis
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