Bio Cancer

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  1. Control of the Cell Cycle
    Some genes code for proteins that control movement through the cell cycle

    Mutations to these genes may result in un =restrained cell proliferation (tumor

    Tumor cells continuously divide if nurtured
  2. Types of Cancer (Neoplasm)
    • Beninn
    • Spherical and well encapsulated

    Slow growing

    Unlikely to Spread

    Still can be dangerous

    Ends in -oma

    • Malignant
    • Irregularly shaped and not well encapsulated

    Fast growing

    Likely to spread (metatasize)

    Malignant tumor is Cancer
  3. Classification of Cancer
    Cancers classified based o site of origin

    - Caricoma: epithelial tissue

    - Sarcoma: connective/muscle/nervous tissue

    - Leukemia/Lymphoma: blood cells
  4. Causes of Cancer

    • Carcinogen: agent thought to cause cancer
    • - Mutagen: agent that mutantes DNA
    • Radiation: x-rays, radon, gamma rays, nuclear
    • Chemical: diet, smoking
    • Viruses: HPV, H. Pylori, hepatitis
    • All muturgens are caricinogens, but not all carcinogenes are mutagens

    • - Nonmutagenic: may cause cancer, but not through direct mutation (alcohol)
  5. Cyclin- dependent kinases (Cdks)
    Primary mechanism of cell cycle control

    • Activated by Cyclins
    • Cdks partner with different cyclins at different points in the cell cycle to promote cell division

    • Cdk itself is also controlled by phosphorylation
    • - Pi at one site activates Cdk, & at another site deactivates

    • Cdk- cyclin complex
    • - Also called mitosis- promoting factor (MPF)
  6. Growth factors

    PDGF one of the first growth factors identified

    PDGF receptor is an RTK that initiates a MAP kinase cascade to signal cell division

    Growth factors can overide cellular controls that otherwise inhibt cell division
  7. Cancer
    Unrestrained, uncontrolled growth of cells that have the ability to metastasize

    Failure of cell cycle control

    Two kinds of genes can distrup the cell cycle when they are mutated

    • 1. Tumor- supressor genes
    • 2. Proto- Oncogenes
  8. Proto- oncogenes
    Normal genes involved in signal transduction pathway to signal cell division.

    • Oncogene: mutated proto- oncogene that can cause cancer
    • - Some encode receptors for growth factors
    • if receptor is mutated "on", cell no longer needs growth factors
    • Some encode signal transduction proteins

    Only one copy of a proto-oncogene needed
  9. Tumor- suppressor genes
    Genes that stop cell division

    Prevent Cdk/cyclin binding

    • Oncogenes "step on the gas"
    • Only one copy of a proto-oncogene needed
  10. Tumor-suppressor genes
    Genes that stop cell division

    Prevent Cdk/ cyclin binding

    • Oncogenes "step on the gas"
    • Only one copy of oncogene needed
    • Tumor supressors "apply the breaks"
    • Both coppies of tumor suppressor need mutation
  11. Rb
    E2F: transcription factor that causes cell cycle genes to be expressed

    Rb binds to and inhibits E2F

    • Cdk/ cyclin phosphorylates Rb
    • - Phosphoryylated Rb unable to bind to E2F

    P16 binds to and ihibits Cdk
  12. P53
    P53 monitors integrity of DNA

    • If DNA damaged, p53
    • - Initiate expression of P21
    • Binds to and inhibits cyclin from complexing with Cdk
    • - Intitiates expression of DNA repair genes
    • - Signals apoptosis in damage too extensive

    Prevents dividion of cells with DNA damage
  13. Other DNA changes
    • Methylation of DNA typically inactivated those genes
    • - Many cancer cells have methylated tumor supressor genes

    - Causation or symptom?

    • Nondijunction in cells
    • - Causacion or symptom?
  14. Cancer Treatment
    Surifical Resection


    • Chemotherapy
    • - Traditional
    • - Targeted
  15. Preventing the start
    • Lifestyle
    • - Smoking
    • - Nutrition
    • - Vaccines

    • Early Dtetection
    • - Biochemical tests
    • - Mammograms
    • - Colonoscopy
  16. Her2
    • HER2 is RTK
    • - Growth factor binds and starts transduction

    Overexpressed in over 20% of breast cancer

    • Herception
    • - Antibodies bind to HER2
    • - Target cell for destruction by immune cells
  17. Ras
    Ras is a G protein that signals cell division

    • Mutated in 30 of all cancers
    • - Cannot readily brak down GTP (stuck "on")

    • Farnesyl transferase finishes Ras production
    • -FTI
    • - Does not work well in humans (dead end)
  18. Src
    Src is a signal transduction kinase

    Mutated in 5% of all cancers (hyperactive)

    small RNAs against src
  19. Rb part B
    Rb inhibits E2F

    • Mutated in 40% of all cancers
    • - Defective, cannot bind to E2F

    New inhibitor for E2F
  20. P53
    P53 checks for DNA damage

    • Mutated in more than 50% of all cancers
    • - 70-80% in lung cancer
    • - Defective P53 cannot check DNA

    • Onyx-15
    • -Normal adenovirus uses E1B to blcoks action of P53
    • - Use E1B deficient adenovirus
  21. Telomerase
    • Telomerase adds telomeres to DNA
    • - Normally active in development & germ cells
    • - Inhibited in organism

    Most cancers probably have muated telomerase inhibitor

    New telomerase inhibitor
  22. Angiogenesis
    • The growth of new blood vessels
    • - Tumor requires increasing blood supply

    Tumor cells secrete angiogenesis signals

    • Angiogenesis Inhibits
    • - Angiostatin, endostatin
  23. Metastasis
    • Requires
    • - Breaking away from primary tumor

    - Movement to, into, and out of blood vessel

    - Enzymes to degrade tissues along the way
Card Set
Bio Cancer
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