Forensic biology - cancer

  • Created by: aarafa11
  • Created on: 02-06-20 02:15
stage 1 (benign tumour) of Tumourigenesis
cell no longer responsive to normal growth controls = cells divide uncontrollably - Hyperplastic
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stage 2 (Malignant tumour) of Tumourigenesis
tumour cells invade neighbouring tissues - express enzymes that break down the extra-cellular matrix proteins such as collagen - Metaplasia
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stage 3 (metastasis) of Tumourigenesis
tumour cells escape into the lymph and blood & travel from the site of the primary tumour to other parts of the body
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types of programmed cell death
apoptosis; cytotoxic T -cell; natural killer cells
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Neoplasia caused by gene mutations in 3 classes of genes
Proto-oncogenes; Tumour Suppressor Genes; DNA repair genes
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Examples of Tumour Suppressor Genes (TSG)
proteins p53, p21 & pRB
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how does tumour mutations create loss-of –function allele
Because the gene product must be absent from the cell to prevent TSG function
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what happens if there is a mutation in the genes responsible for DNA repair
genes causes failure to repair proto-oncogenes; DNA replicated in damaged state – mutation occurs; Proto-oncogene -->Oncogene
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how does ocogene Typically dominant gain-of-function mutation
Allele expressed when it should be inhibited; Or gene is over expressed – too much gene product made
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what are the products of oncogene
Cyclins, CDKs, DNA binding proteins, membrane signal receptor proteins, growth factors, cell adhesion proteins
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where was oncogene originally found
found in viruses that cause cancer
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roles of TP53 – Guardian of the genome
transcription factor; initiates apoptosis; inhibits angiogenesis
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important genes in cancer development
RAS (RAt Sarcoma); E2F; RB1; TP53; APC
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how to treat cancer
Surgery; Hormone therapy ;Chemotherapy; Radiotherapy; Immunotherapy
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Treatment depends on cancer and stage at diagnosis.
Early – surgical removal followed by chemotherapy to destroy any remaining tumour cells; Late – radiotherapy to shrink tumour, then surgery and chemotherapy to ‘mop up’
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Hormone therapy
anti-oestrogen drug, useful against tumours that require oestrogen to grow, e.g. some breast cancers
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example of hormone therpy
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what does tamoxifen do
binds to oestrogen receptor on cell surface, preventing oestrogen binding, but not triggering the receptor
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Chemical agents that normally target actively dividing cells Act on DNA replication; Some agents are mutagens (alkylating agents and base analogues); Others inhibit DNA replication enzymes; Result is DNA damage that triggers apoptosis pathways and
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what does chemotherapy do to normal cells that are nto actively dividing
damage to their DNA is less consequential; But, bone marrow, hair follicles and intestinal lining cells are; Hence, nausea, hair loss and reduce immune system function are side effects of chemotherapy
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when is chemotherapy most effective
young tumours; many of the mechanisms controlling cell growth & apoptosis are still active
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why is it hard to do chemotherapy on large tumours
may cease; Or chemotherapy agents may not be able to penetrate to the centre of the tumour; These tumours can be treated with radiotherapy
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WHat does radiotherapy rely on
relies on causing DNA damage and apoptosis; Relies on TSGs still being in active state, esp. TP53, to trigger apoptosis
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what si the problem with radiotherapy
Tumour becomes resistant to radiotherapy
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what does immunotherapy utililise
adaptive immune system; B cell multiply & mature into Plasma cells, which secrete antibodies; T cytotoxic cells – seek out infected\cancerous cells and destroy them
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in vitro - immunotherapy
preparation of antibodies or immune cells primed against cancer; Very promising, in very early stages; Perhaps hampered by the fact cancer cell evade the immune system
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What does Human Epidermal growth factor Receptor 2 - HER2 do
control growth & over-expressed in some cancers
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how does herceptin work against Human Epidermal growth factor Receptor 2 - HER2
Herceptin antibody binds to extracellular region of HER2 reducing the signal; Anti-body binding may also trigger immune response against tumour cells (NK cells)
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treating cancer using vaccination
Malignant melanoma treated with vaccine based on antibodies that bind to tumour proteins; Can be based on patients own tumour cells
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how does harvesting blood cells form Sipuleucel-T
stimulated with a protein containing prostatic acid phosphatase – a protein produced by prostate cancer cells; Stimulated cell returned to the patient to orchestrate immune response to cancer cell
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Card 2


stage 2 (Malignant tumour) of Tumourigenesis


tumour cells invade neighbouring tissues - express enzymes that break down the extra-cellular matrix proteins such as collagen - Metaplasia

Card 3


stage 3 (metastasis) of Tumourigenesis


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Card 4


types of programmed cell death


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Card 5


Neoplasia caused by gene mutations in 3 classes of genes


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