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ON2 Cancer pathogenesis

Usuario eliminado 11 preguntas Actualizado el 9 oct 2019

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Preguntas del test (11)

  1. 1Oncogenesis is the mechanism by which a tumor arises, involving DNA [blank_start]mutation[blank_end]. If the DNA is not repaired, the cell will
    continue to [blank_start]divide[blank_end] and 'fix' the mutation in place. Successive mutations can build up until the cell division is no longer regulated.
    1. Amutation
    2. Bdivide
  2. 2Oncogenesis:
    • 1 mutation is not enough, need [blank_start]multiple[blank_end] mutations
    • Number of mutations varies – impacts on [blank_start]immunogenicity & prognosis[blank_end]
    • These should generally be picked up at the [blank_start]check[blank_end] points, and the DNA repaired, unless the checkpoint itself is mutated (‘[blank_start]driver[blank_end]’ mutation)…
    1. Amultiple
    2. Bimmunogenicity & prognosis
    3. Ccheck
    4. Ddriver
  3. 3Which of these is not an origin of mutations?
    1. ADNA replication
    2. BInherited
    3. CEnvironmental insult
    4. DInfectious agents
    5. EGMOs
  4. 4DNA replication
    • normal DNA replication introduces 1 mutation /10^7 nucleotides
    • most mutations still [blank_start]won’t[blank_end] cause cancer, however there are some [blank_start]key[blank_end] gene families in which a mutation can lead to oncogenesis:
    - tumor suppressor genes([blank_start]inactive[blank_end] in cancer): [blank_start]growth[blank_end] factors & growth regulators, repair & [blank_start]apoptosis[blank_end] genes, contact inhibition genes
    - activator genes (oncogenes & proto-oncogenes, [blank_start]active[blank_end] in cancer): angiogenic genes – eg [blank_start]vascular endothelial[blank_end] growth factor (VEGF), genes which allow metastasis and escape from [blank_start]immune[blank_end] surveillance
    1. Awon’t
    2. Bkey
    3. Cinactive
    4. Dapoptosis
    5. Egrowth
    6. Factive
    7. Gvascular endothelial
    8. Himmune
  5. 5Inherited mutations
    • some forms of cancer have a higher occurrence in some families
    • they have inherited either:
    - defective [blank_start]tumor suppressor[blank_end] genes
    - activated [blank_start]oncogenes[blank_end]

    BRCA is a tumor [blank_start]suppressor[blank_end] gene involved in repairing DNA [blank_start]damage[blank_end]. BRCA1/2 mutation results is a 56–84% lifetime risk of developing [blank_start]breast[blank_end] cancer and an 36–63% risk for [blank_start]ovarian[blank_end] cancer.
    1. Atumor suppressor
    2. Boncogenes
    3. Csuppressor
    4. Ddamage
    5. Ebreast
    6. Fovarian
  6. 6Environmental Insult:
    • Chemical = carcinogens. Either [blank_start]directly[blank_end] damage DNA or their [blank_start]metabolites[blank_end] damage DNA. Types of damage are strand [blank_start]breakage[blank_end], gene [blank_start]truncation[blank_end], nucleotide deletions & substitutions. Most common chemically induced cancer - lung cancer ([blank_start]30[blank_end]% of all cancer deaths).
    • Physical = radiation – variable toxicity.
    Non-ionizing:
    • UV, microwaves.
    • UV causes [blank_start]melanoma[blank_end]
    Ionizing:
    • X-rays, g-rays, atomic bombs, nuclear reactors
    • [blank_start]Spontaneous[blank_end] tumor development (thyroid, breast, bone marrow)
    1. Adirectly
    2. Bmetabolites
    3. Cbreakage
    4. Dtruncation
    5. E30
    6. Fmelanoma
    7. GSpontaneous
  7. 7Human Papillomavirus Viruses (HPV) is an infectious agent that can cause cancer. HPV is isolated from > 90% of [blank_start]cervical[blank_end] tumors. HPV also causes [blank_start]anogenital and oropharnygeal[blank_end] carcinoma. High risk’ cancer-causing types:
    - HPV-[blank_start]16[blank_end] (55% of tumors)
    - HPV-18 (15%)
    - HPV-45 (10%)
    1. Acervical
    2. Banogenital and oropharnygeal
    3. C16
  8. 8The immune system has pro-tumor effects - chronic inflammation has been associated with oncogenesis, and anti-tumor effects - immune system can kill cancer cells.
    1. AVerdadero
    2. BFalso
  9. 9 CD8 T cells must be activated by a professional [blank_start]antigen presenting cell[blank_end] (APC) to kill cancerous cells. The problem is we need to get activation of the APC, but there is no infection. Hopefully there is enough [blank_start]necrosis[blank_end] and/or cell [blank_start]stress[blank_end] to activate the APC.
    The [blank_start]cytotoxic[blank_end] immune response should kill tumours but tumors are [blank_start]self[blank_end] tissues. CD8 T cells are not allowed to destroy cells expressing self [blank_start]antigens[blank_end]. The solution is an immune response directed against: [blank_start]mutated[blank_end] antigens (new proteins in genetically unstable cells), viral proteins, or [blank_start]inappropriately expressed[blank_end] antigens.
    1. Aantigen presenting cell
    2. Bnecrosis
    3. Cstress
    4. Dcytotoxic
    5. Eself
    6. Fantigens
    7. Gmutated
    8. Hinappropriately expressed
  10. 10Which of these is NOT an immune evasion strategy used by tumours?
    1. Anot make any tumor antigens
    2. Bshut down antigen presentation
    3. Cshut down MHC class I expression
    4. Dshut down expression of co-stimulator or adhesion molecules
    5. Enot make immune cells

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El usuario ha eliminado su información de asignaturas Test sobre ON2 Cancer pathogenesis, creado por Usuario eliminado el 09/10/2019.
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Usuario eliminado
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Creado el 9 oct 2019 · actualizado el 9 oct 2019

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