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57 Cards in this Set
- Front
- Back
Transformation
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The process by which a cell loses its ability to remain constrained in its growth properties
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Tumor
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Neoplasm; "New Growth"
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Metastasis
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The spreading of malignant tumor cells throughout the body
- "Change of State" |
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Oncogenesis
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Initiation of tumors in an organism
- onco- "mass/bulk"; -genesis "birth" |
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Cell Cycle Checkpoints
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Different points in the cell cycle that are control points at which the cell cycle is arrested if there is damage to the genome or cell cycle machinery
- Prevents cells from becoming cancerous |
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Cyclins and Cyclin-dependent kinases
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Key components of the regulatory events that occur at checkpoints
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Cyclins
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Proteins that regulate events that occur at checkpoints
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Cyclin-dependent kinases
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Enzymes that regulate events that occur at checkpoints
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2 main ways our cells regulate cell growth
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Cell cycle & growth factors
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Growth Factors
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Molecules that stimulates cell division of a target cell by binding to specific receptors on their target cells
-- Signal is relayed via a serious of proteins, eventually activating nuclear genes that encode proteins for stimulating cell growth and divisions |
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Growth-inhibitory factors
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Lead to inhibition of cell growth and division
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Signal Transduction
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The process of relaying a growth-stimulatory or growth-inhibitory signal after a growth factor binds to a cell
-- proteins involved are called signal transducers |
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Neoplastic cell
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Cancer cell; lost control of cell division and reproduces without constraints
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5 ways we know cancer is genetically linked
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1.) Cancer has been known to be passed down through generations
2.) Some viruses cause cancer 3.) Descendents of cancerous cells are all cancerous 4.) Exposures to mutagens increases the chances of cancer 5.) Certain chromosomal mutations are associated with particular forms of cancer (Ex. Burketts Lymphoma, Chronic Myelogenous Leukemia) |
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3 Classes of Genes Mutated in Cancer
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1.) Proto-Oncogenes
2.) Tumor Suppressors 3.) Mutator Genes |
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Proto-Oncogenes
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Normally: Stimulate cell growth/reproduction
Mutant: more active than normal or active at inappropriate times |
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Tumor Suppressors
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Normally: Inhibit tumors
Mutant: lost their inhibitory function |
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Mutator Genes
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Normally: ensure loyalty of replication and maintenance of genome integrity
Mutant: lost their normal function and make cell prone to accumulate mutational errors in gene - include proto-oncogenes and tumor suppressor genes |
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Tumor Virus
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Induce the cells they infect to proliferate in an uncontrolled fashion and produce a tumor
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Oncogene
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A gene whose action stimulates unregulated cell proliferation
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Two types of Tumor Viruses
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1.) RNA Tumor Virus
2.) DNA Tumor Virus |
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RNA Tumor Virus
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All RNA Tumor Viruses are retroviruses, but not all retroviruses are tumor viruses
- When an RNA Tumor Virus infects the cell, the RNA genome is released from the viral particle, and via reverse transcriptase, a cDNA copy of the genome - called the proviral DNA - is synthesized. The proviral DNA integrates into the genome of the host cell. Then, using host transcriptional machinery, viral genes are transcribed, and full length viral RNA's are produced. Progeny viruses assembled within the cell then exit and can infect other cells. |
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Example of an RNA Tumor Virus
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Rous Sarcoma Rivus (RSV)
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Proto-oncogenes
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These genes, when introduced into other cells growing in culture, transformed those cells into cancer cells
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What is the role of proto-oncogenes?
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Regulating the cell cycle
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oncogenes (oncs)
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when proto-oncogenes become mutated or translocated so that they contribute to inducing tumor formation
-- this mutation is sufficient enough to caused complete loss of the cell cycle control |
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v-oncs
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oncogenes carried by a virus
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cellular oncogenes (c-oncs)
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oncogenes that reside in the host chromosome
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Main difference between cellular proto-oncogene and viral oncogene
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most proto-oncogenes contain introns that are not present in v-oncs. This is because of splicing that occurs in the transcription event that generates rival RNA genomes from proviral DNA
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Examples of Proto-oncogenes
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1.) Growth Factors
2.) Protein Kinases 3.) Membrane Associated G Proteins |
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Membrane Associated G Proteins
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Normally involved in the signalling cascade; the steps from the growth factor receptor to the nucleus
-- Example includes RAS that is involved in the activation of transcription of a cell cycle-specific target gene. When Ras binds to GTP, it becomes Ras-GTP. Ras-GTP recruits Raf-1 and activates it. Normal: Turning the Ras signal off in normal genes involves GAP making Ras hydrolyze the GTP bound to it back to GDP. This inactivates Ras and cancels the cell cycle stimulatory signal |
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How does Ras become an oncogene?
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Via mutation
-- Abolishes its ability to hydrolize GTP to GDP. -- Even with GAP, the Ras-GTP complex remains and the signal is continuously on. |
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3 ways a proto-oncogene can turn into an oncogene
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1.) Point mutation; via base-pair substitutions
2.) Deletions 3.) Gene amplifications; increased number of copies of a gene |
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Point Mutation of Proto-oncogene
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- Base-pair substitution
- in the coding region or in the controlling sequences - cause an increase in either the activity of the gene product, or the expression of the gene |
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Deletion mutation of a Proto-Oncogene
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occur on part of the coding region or part of the regulatory regions
- cause changes in the amount of growth stimulatory protein, resulting in unprogrammed proliferation of the cell |
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Gene Amplification of Proto-Oncogenes
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- Over replication of small segments of DNA make extra copies of genes
- Extra copies of genes result in extra gene expression |
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Transducing Retrovirus
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Retrovirus carrying an oncogene
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Normal Cellular Genes that are similar to those of viral oncogenes and encode proteins that stimulate cell growht and division
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Proto-oncogenes
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Retroviral Oncogenes
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modified copies of the cellular proto-oncogenes that have been picked up by the retrovirus
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2 Hit Model for Cancer
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explains the difference between familial and sproradic cancers
-- In familial cancers, one mutation is inherited. A second mutation occurs later in somatic cells, and cancer may then develop. - In sporadic cancers, both mutations occur in somatic cells. |
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DNA Tumor Viruses
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Transform host cells into cancerous cells through action of genes within the viral genome
-- ex.: papovavirus, hepatitis B, herpes, adenovirus, pox virus |
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How do DNA Tumor Viruses Work?
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1.) Virus activates viral protein
2.) Protein results in excess replication of viral DNA 3.) Viral progeny lyse cell and infect other cells |
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normal p53
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Tumor suppressor protein.
Normal cell: unphosphorylated, and binds with the unphosphorylated Mdm2, which degrades p53. Cell w/ DNA damage: Mdm2 and p53 are phosphorylated, and cannot bind. p53 accumulates, and WAF1 is activated by p53 which encodes for p21 protein that binds to the G1-S checkpoint. Cdk3-cyclin D complexes, and inhibits their activity. As a result pRB in the pRB-E2F complex doesn't become phosphorylated and E2F is kept inhibited. Entry into S is blocked, and the cell arrests in G1 of the cell cycle |
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TP53
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Tumor suppressor that encodes for p53
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p53 causing cancer
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When both alleles of TP53 carry loss of function mutations, no active p53 can be produces. Through the cascade of events, the cell is unable to arrest in G1 and the cell can proceed into S phase of the cell cycle.
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Carcinogens
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Natural and artificial agents that increase the frequency with which cells become cancerous.
-- mostly chemicals and types of radiation -- cause genomic changes in the cell -- act directly on the genome or indirectly on the genome -- typically point mutations |
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Direct-acting carcinogens
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chemicals that bind to DNA and act as mutagens
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Procarcinogens/Indirect carcinogens
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must be converted metabolically to become active carcinogens called ultimate carcinogens most of which bind to DNA and act as mutagens
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Gene pool
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Genes shared by the individuals of a Mendelian population
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Mendelian population
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a group of interbreeding individuals who share a common set of genes
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Goal of population genetics
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Understand the genetics of evolution
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Questions frequently studied by population geneticists
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1.) How much genetic variation is found in natural opulations and what processes control the amount of variation observed
2.) What processes are responsible for producing genetic divergence among populations 3.) How do biological characteristics of a population, such as mating system, fecundity, and age structure, influence the genetic structure of the population |
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Hardy-Weinberg law
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Set of equations that describe the influence of random mating on the allele and genotype frequencies of an infinitely large population
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5 assumptions of Hardy-Weinberg
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1.) Large population
2.) No mutation 3.) No natural selection 4.) No migration 5.) Random Mating |
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Hardy-Weinberg Results (2)
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1.) The frequencies of the alleles do not change over time, where p is the allele frequency of A and q is the allele frequency of a
2.) Genotypic frequencies remain in the proportions p^2, 2pq, and q^2. The sum of the genotype frequencies equals 1 -- 1 = p^2 + 2pq + q^2 |
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Discontinuous Traits
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Traits that show an exact phenotype
-- Ex.: Seed color, pea shape, pod color, etc. |
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Continuous traits
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Traits which show great variation in phenotype
-- Ex.: body weight or height |