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31 Cards in this Set
- Front
- Back
knudson hypothesis
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a cell can initiate a tumor only when it contains two mutant alleles or a heterozygous individual must mutate the good allele
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challeneges
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tumorigenesis is a multistep process involving activation of oncogenes and inactivation of tumor suppressor genes
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haploinsufficiency
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inactivation of one allele is sufficient to inactivate a genes activity
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oncogenes
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erb2/her2/neu, src, able, bcr-abl, ras, bcl2, fos, jun, myc
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growth factor receptors
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erb2/her2.neu
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signaling molecules
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src, abl, bcr-abl, ras, bcl2
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transcirption factors
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fos, jun ,myc
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erb2/her2/neu
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receptor tyrosine kinase, activated through heterodimerization with other erbB proteins
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where is it found
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breast cancers
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what does it do
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mediates gene transcription and cell proliferation through the ras signaling pathway, promotes cell survival and inhibits apoptosis through the PI2 kinase pathway
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abl and src
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non receptor tyrosine kinases,
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bcr-abl
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encoded on the philadelphia chromosome, CML, potent tyrosine kinase activity
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ras
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gtp bound protein,
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bc2
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b cell lymphoma, govern mitochondria outer membrane permeabiliazation
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tumor suppressor gene
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restran cell growth, involved in cell cycle regulation dna repair or apoptosis
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name them
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rb, p16, p53, smads, apc, brca1/2, pten
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rb
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regulates cell cycle progression by binding to e2f
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e6
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inactivate p53
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e7
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inactivates rb
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p53
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encodes a transcription factor, tumor suppressor,
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p21
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cell cycle arrest
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bax
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apoptosis
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gadd45
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dna repair
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mdm2
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degrade p53
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tgf beta
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activages smad transcription factors
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smad4
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tumor suppressor in pancreatic cancer
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wnt/b catenin
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transcritption factor, in its absenceits phosphorylated and degraded. When its on it inactivates destruction complex
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apc
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tumor suppressor, when mutated results in abberant stabilization of b catenin and short non functional protein
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brca
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tumor suppressor protects against genome instability, mediate dna repair, heriditary breast and ovarian cancers
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src
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oncogenic virus, protooncogene is a non receptor tyrosine kinase
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pten
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a phosphatase that opposes the pi2k-akt oncogenic paathway
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