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UNT BIOL 3451 - Cancer and Regulation of the Cycle
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BIOL 3451 1st Edition Lecture 24 Outline of Last Lecture I. 17.7 Gene Regulation in a Model Organism: Transcription of the GAL genes of Yeast II. 17.8 Posttranscriptional Gene Regulation Occurs at All the Steps from RNA Processing to Protein ModificationIII. 17.9 RNA Silencing Controls Gene Expression in Several WaysIV. 19.1 Cancer is a Genetic Disease That Arises at the Level of Somatic CellsV. 19.2 Cancer Cells Contain Genetic Defects Affecting Genomic Stability, DNA Repair, and Chromatin ModificationsOutline of Current Lecture I. 19.2 Cancer Cells Contain Genetic Defects Affecting Genomic Stability, DNA Repair, and Chromatin ModificationsII. 19.3 Cancer Cells Contain Genetic Defects Affecting Cell-Cycle RegulationIII. 19.4 Proto-oncogenes and Tumor-Suppressor Genes Are Altered in Cancer CellsIV. 19.5 Cancer Cells Metastasize and Invade Other TissuesV. 19.6 Predisposition to Some Cancers Can Be InheritedVI. 19.7 Viruses Contribute to Cancer in Both Humans and AnimalsVII. 19.8 Environmental Agents Contribute to Human Cancers Current LectureI. 19.2 Cancer Cells Contain Genetic Defects Affecting Genomic Stability, DNA Repair, and Chromatin Modificationso Cancers show chromosomal defects that we use to diagnose the type and stage of cancer- Chronic myelogenous leukemia (CML): involving translocation of the C-ABL gene on chromosome 9 into the BCR gene on chromosome 221. Figure 19.42. this structure known as the Philadelphia chromosome Xeroderma pigmentosumo Number of cancers caused by defects in genes that control DNA repair- Xeroderma pigmentosum (XP)1. Defective nucleotide excision repair leading to skin cancer- Hereditary nonpolyposis colorectal cancer1. Autosomal dominant syndromeThese 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.2. Increased risk (check a box off) of colon, ovary, uterine, and kidney cancers3. 8 genes implicated, with four involved in DNA mismatch repaira. Could be just one of these, or several b. Alleles (oncogenes) can be dominant or recessive to the wild typei. Increases risko Epigenetics: study of factors that affect gene expression but do not alter the nucleotide sequence of the DNA- DNA methylation (Barr bodies)1. Responsible for gene silencing associated with parental imprinting, heterochromatin gene expression, X chromosome inactivation- Histone acetylation and acetylation (histone modification of histone code)1. Genes that encode histone acetylases, deacetylases, methyltransferases, and demethylases are often mutated or aberrantly expressed in cancer cells- Genomic patterns and locations of these modifications can affect gene expression and be passed on from generation to generationII. 19.3 Cancer Cells Contain Genetic Defects Affecting Cell-Cycle Regulationo Growth and differentiation of cells are strictly regulated- Involves multiple processes with multiple steps- This allows for lots of opportunity for regulation- In cancer cells, these are mutated or aberrantly expressed, leading to uncontrolled cell proliferation1. Lock one part of the step into the mutationo Interphase of cell cycle is when cell grows and replicates its DNA (most cells are in G1 stage)- Cells that stop proliferating enter G0, where they do not grow or divide but are metabolically active1. Neurons- Cancer cells are unable to enter G0 and cycle continuouslyo Signal transduction: initiates a program of gene expression that propels the cells out of G0 and back into the cell cycle - Cancer cells often have defects in signal transduction pathwayso Checkpoints- G1S: do I replicate DNA? - G2/M: did I replicate correctly?- M: monitors spindle formation and attachment to kinetochores- These all decided whether to move on to next cell cycle (Fig 19.5)o Regulation of checkpoints mediated by - Cyclins- Cyclin-dependent kinases (CDKs)- Regulate synthesis and destruction of cyclin proteins- Fig 19.6 and 19.7 o Cells halt progress through cell cycle if DNA replication, repair, or chromosome assembly is aberranto If DNA damage is so severe that repair is impossible, the cell may initiate apoptosis, or programmed cell death- Prevents cancer by having defective cells that could kill you, kill themselves1. BAX homodimer promotes apoptosis- Also eliminated cell not contributing the final adult organism- Most cancer patients have P53 problems (controls apoptosis and DNA repair)o Steps in apoptosis are:- Fragmentation of nuclear envelope- Disruption of internal cellular structures- Dissolution of cell into small, spherical apoptotic bodies (called vesicles)- Engulfing of the apoptotic bodies by phagocytic cells- A series of proteases (cascade) called caspases 1. Responsible for initiating apoptosis and digesting intracellular componentsIII. 19.4 Proto-oncogenes and Tumor-Suppressor Genes are Altered in Cancer Cellso Proto-oncogenes: normal genes whose products promote cell growth and division- Encode: 1. Transcription factors: stimulate expression of other genes2. Signal transduction molecules that stimulate cell division3. Cell-cycle regulators that move through the cell cycleo In cancer cells, one or more proto-oncogenes are altered in such a way (turned on in improper way) that their activities cannot be controlled normally- Table 19.1 show some proto-oncogenes and tumor-suppressors that have been discoveredo Oncogene is proto-oncogene that is mutated or aberrantly expressed and contributes to the development of cancer- only one allele o tumor-suppressor genes: products of these that normally regulate cell-cycle checkpoints and initiate the process of apoptosis (says don’t divide)- when mutated, cells unable to respond normally t cell-cycle checkpoints or are unable to undergo apoptosis if DNA damage is extensive (leads to more mutations and development of cancer)o Ras genes: encode for signal transduction molecules that are associated with the cell membrane and regulate cell growth and division- Fig. 19.9- Mutations to convert the ras proto-oncogene to an oncogene freeze the ras protein into its active conformation, constantly stimulating the cell to divideo p53 tumor-suppressor gene: encodes a nuclear protein that acts as a transcription factor that represses or stimulates transcription of more than 50 different genes- It is continuously synthesized but rapidly degraded, thus present low levels- Increased levels result from increases in protein phosphorylation, acetylation,and other


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UNT BIOL 3451 - Cancer and Regulation of the Cycle

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