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TAMU BIOL 213 - Cancer
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BIOL 213 1st Edition Lecture 25 Outline of Last Lecture I. Eukaryotic cell cyclea. Four phasesb. Regulation was discovered by observing mitosis of Xenopus frog eggsII. Cyclin and Cdks control progression through the cell cyclea. M-cyclin binds to Cdk to create an M-Cdk b. The sharp decrease in levels of M-cyclin after M phase is due to degradation of cyclin by proteasomesIII. S Phase – DNA replicationIV. G1 phase arrest due to DNA damage a. Outline: If DNA damage is detected, p53 will be activated, which will initiate transcription of the p21 gene. The p21 protein (a Cdk) will bind to the active S-Cdk and inactivate it so that S phase cannot be initiatedV. Apoptosis – programmed cell deatha. It’s mediated by an intracellular proteolytic cascade that cuts the cell up into nicelittle piecesb. High stress to the p53 protein causes the p53 to induce apoptosisOutline of Current Lecture I. The hallmarks of cancerII. Discovery of oncogenesIII. Properties of cancer cellsIV. Activate motility pathways to invade tissuesV. Activate telomeraseVI. Genome instabilityVII. Resist apoptosisVIII. Kinds of genes that when they get mutations can cause cancera. Oncogenesb. Tumor suppressor genesIX. Recruit blood vesselsa. Angiogenesis X. Cancer treatmenta. Traditional treatmentsThese 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.b. Developing treatmentsCurrent LectureI. The hallmarks of cancera. Sustained proliferation signalingi. The pathways that initiate proliferation are on even if there’s no proliferation signalb. Evade growth suppressor signalingc. Activate motility pathways to invade tissuesd. Activate telomerasei. To keep the telomeres long so that the cell can keep dividing without worrying whether or not some of the chromosome will be loste. Genome instabilityf. Resist apoptosisg. Recruit blood vesselsh. Deregulated cell energeticsi. Tumor cells usually only go through glycolysis and not the rest of cellular respirationii. Because of this, they use a lot of glucose and essentially starve the other cells around the tumorII. Discovery of oncogenesa. Oncogenes – mutated genes that cause cancerb. A retrovirus was studiedi. This virus normally has three genes: 1. Gag – for the protein coat2. Pol – for reverse transcriptase3. Env – for envelope around the virusii. These genes are transcribed from single-strand RNA to cDNA by reverse transcriptase and inserted into the host’s DNAiii. The virus proteins are synthesized by the cell and the viruses emerge from the host cellc. The Rous Sarcoma virus was found to cause tumor growth in chicken musclesi. They looked at its genome and found that it had an extra gene: SRCii. When they took this gene out of the genome, the virus stopped causing tumor growthiii. When they added this gene to other viruses, these viruses started to cause tumor growthiv. They found that this SRC gene closely resembled an important gene in chicken muscle cellsv. They determined that this gene was the cause of the tumor growthIII. Properties of cancer cellsa. These traits are heritableb. When a cell divides without normal constraints, it becomes a tumori. Benign tumor – just a big mass of fatty tissue that doesn’t invade any other tissueii. Malignant tumor – forms metastases that invade other tissuec. Cancer cells arise from the accumulation of mutationsi. A lot of mutations have to accumulate in the same cell for it to turn into acancer cellii. The chance of cancer increases with age because the cells have had more time to accumulate mutations1. However, there is a higher chance of childhood leukemia at a young agea. When a fetus is growing, there is a gene that causes extremely fast proliferationb. Once the baby is born, this gene is usually turned ofc. Sometimes a really active promoter (like those found in immunoglobulin genes) can be transposed to the proliferation gened. This causes a lot of uncontrolled proliferation, which can lead to leukemiaIV. Activate motility pathways to invade tissuesa. In epithelial cells, cancerous cells start growing on the surfaceb. As they grow and divide, they’ll accumulate more mutations, becoming more cancerous and a tumor arisesc. The growing mass penetrates the surface and grows into the tissue to look for a blood sourcei. They break through the basal laminad. Once they reach a blood vessel, they can metastasize and spread cancerous cells to other tissueV. Activate telomerasea. Some cells like those lining the intestines have active telomerase because they need to frequently divide (because the food is scrapping them away)b. Therefore, there are epithelial stem cellsc. These divide into one stem cell and one other daughter celli. The stem cell is important for future divisions and has active telomerased. The other daughter cell goes through a series of divisions until it’s completely diferentiatede. Its telomerase is then inactivated because it doesn’t need to divide any moref. A mutation can occur in the stem celli. This is bad because the stem cell has active telomerase therefore it will keep dividing and the mutation will spreadg. A mutation can occur in the other daughter celli. This isn’t as bad because its telomerase will be inactivatedii. BUT, if the mutation turns on the telomerase and other hallmarks of cancer, this can lead to cancerVI. Genome instabilitya. Normal cells have nicely packed and organized chromosomesi. All of the DNA that belongs in chromosome 1 is packaged only in chromosome 1b. In cancerous cells, the chromosomes are rearranged so that the DNA of chromosome 1 is spread throughout other chromosomes (the same is true for allthe other chromosomes – they’re not neatly organized)i. This is a result of double-strand DNA breaks and fusion with other DNA strandsii. This is also a result of inactive p531. In a normal cell, if the DNA scanning proteins saw how messed up the DNA was, they would activate p53, and the p53 would cause the cell to either stop dividing until the problem was fixed or go through apoptosisVII. Resist apoptosisa. Mutations in genes can cause the cell to not go through apoptosis like it should when the cell is damagedi. Ex: p53VIII. Kinds of genes that, when they get mutations, can cause cancera. Signaling genes – these mutated proteins are stuck in the on position so that they’re always telling the cell to divide even when there’s no signali. Ex:


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TAMU BIOL 213 - Cancer

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