SA Med 1

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SA Med 1
2011-09-20 17:26:44
SA Med

exam 1
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  1. What is the cause of cancer?
    • clonal overgrowths of cells bearing multiple genetic injuries caused by multiple factors
    • there is no one cause of cancer
  2. tumor clonality
    • dev of a tumor from a single cell that begins to proliferate
    • multi step process in which cells gradually become malignant thru a series of alterations
  3. one gram tumor
    • one billion cancer cells
    • takes months to years to get this size
  4. Multistep dev of cancer
    • 1) tumor initiation or hereditary mutation
    • 2) tumor progression
    • 3) clonal selection
  5. aquired mutation
    • exposure to viruses, radiation, or toxins
    • starts in one cell and found only in the offspring of that cell
  6. somatic mutation
    old age no known cause
  7. inherited mutation
    • found in many cells
    • young age
  8. tumor progression
    • gain a selective advantage (survival, invasion, metastisis, rapid growth)
    • clonal selection allows these cells to dominate
  9. clonal selection
    • throughout tumor dev becomes more rapidly growing and increasingly malignant
    • becomes more resistant to therapy
  10. chromothripsis
    • shattering of chromosomes- usually dies bc no checkpoints
    • cell tries to repair itself and may amplify cancer genes or delete cancer suppressor genes
  11. growth fraction
    • percent of cells synthesizing nucleic acid at any given time
    • how many cells are actively dividing and how fast are the cells making it thru the cell cycle
  12. Ki-67
    • monoclonal antibody that stains proliferating cells to determine growth fraction
    • present during G1, S, G2, M (absent fro G0)
    • prognostic marker
    • measure of cycling cells
  13. argyrophilic NORs (AgNORs)
    • black dots in interphase nucleus
    • transcriptional activity/mitotic index
    • prognostic marker
    • measures speed of cell proliferation
  14. benign tumor growth
    • stable genome
    • slowly expand
    • stable in size
    • number of cells dividing is marginally higher than those dying
  15. contact inhibition
    • when normal cells touch they stop dividing and adhere to each other
    • tumor cells continue growth after touching and become multilayered
  16. E-cadherin
    tumor cells lose this and do not adhere- exfoliate easy and become malignant
  17. coagulase and protease in tumor cells
    • malignant tumor cells produce these to digect extracellular matrix components allowing cancer cells to invade
    • ex- MCT
  18. angiogenesis
    • formation of new blood vessels
    • cancer cells secrete this
    • ex- vascular endothelial growth factor (VEGF) or endothelial precursor cells (EPCs)
  19. vascular endothelial growth factor (VEGF)
    form of angiogensis in which there is a proliferation and sprouting of existing blood vessels close to the tumor
  20. endothelial precursor cells (EPCs)
    for of angiogenesis in which cells come from the bone marrow and differentiate into blood vessels
  21. fibroblast growth factor (FGF) and transforming growth factor alph (TGFa)
    stimulate angiogenesis after tumor cells degrade the basal lamina that surrounds nearby capillaries
  22. antagonists of VEGF receptor
    • tx cancer
    • Bevacizumab
    • TKI- interfer with cell signaling to block VEGF
  23. primary tumors and angiogenesis
    • some primary tumors can secrete a substance that inhibits angiogenesis around secondary metastases
    • once primary tumor is taken out then all others are allowed to grow
  24. termial differintiation
    • normal cells mature and go thru apoptosis
    • tumor cells arrest before final stage so keep proliferating and never undergo apoptosis (not even when DNA is damaged)
  25. apoptosis
    • programmed cell death
    • cancer cells fail to undergo bc can live without growth factors and not affected by DNA damage
  26. oncogenes
    • activated/altered versions of anormal genes
    • activated by point mutation, translocation, or inc copy number
    • tells cell to divide even when it should not
    • v- viral oncogene
    • c- cellular oncogene
  27. proto-oncogenes
    • normal genes
    • control normal cell proliferation
    • c-kit causes growth of mast cells and GI stromal cells- mutation to oncogene causes malignancy (use TKI to block)
  28. c-kit
    • proto-oncogene
    • causes proliferation of mast cells and GI stromal cells
    • mutation causes malignancy
    • TKI block c-kit mutation to oncogene
  29. tumor suppressor genes (TSGs)
    • "anti-onco genes"
    • tells cells when not to divide
    • both copies of the gene are damaged or missing= more chance of cancer
    • mosty common alteration leading to cancer
    • ex- p53 (50% of mutations), molecular chaperones
  30. p53
    • tumor suppressing gene
    • tells cells when not to divide so they will apoptose
    • mutations account for 50% of cancers
    • mediates cell cycle and causes apoptosis if DNA damage
    • hereditary cancer syndrome- possible on golden retrievers
  31. molecular chaperones
    • tumor suppressor gene
    • molecular housekeeper
    • DNA repair
  32. tumor viruses
    • DNA tumor causing virus- papillomavirus/warts/equine sarcoid (self limiting)- degeneration of p53 tumor suppressing gene
    • TRN tumor causeing virus- feline leukemia virus- uses reverse transciptase and joins host DNA
  33. carcinogens
    • substances that cause cancer
    • chemical radiation
    • ultraviolet radiation
    • tumor promoters
  34. chemical carcinogens
    • damage DNA and induce mutations
    • initiating agents
    • chemotherapy
    • Cyclophosphamide leads to TCC
    • benzene leads to leukemia
    • aflotoxin- affects liver, made my moldsasbestos- causes mesothelioma
  35. radiation carcinogens
    • radiation exposure
    • radium use
    • atomic radiation- leukemic effect
  36. ultraviolet radiation carcinagen
    • skin cancer- SCC
    • UVA and UVB
    • UVB- immunosuppressive
  37. tumor promoters in carcinogens
    hormones- estrogen, progesterone