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Discuss with reference to specific examples how oncogenes and tumour…

- - - - APC tumour suppressor
        
        1) APC mutation causing frame shift on chr5q21 leads to inherited colorectal cancer by 40.
        
        AP cannot bind and degrades beta cateninin despite no Wnt-receptor binding.
        
        Free beta-catenin increases.
        
        Leading to constitutive activation of Wnt-beta-catenin signalling pathway
        
        Increased B-catenin translocation into nucleus and binding to Tcf/Lef transcription factor
        
        Increased transcription of c-myc and cyclin D1 to increase cell proliferation
        
        3) Wnt-signalling mediated transcription affected.
        
        2) hyper-proliferation of epithelium
        
        4) K-ras oncogene mutation develops early adenoma into intermediate adenoma. leading to propagation of growth factor
        
        6) Most crucial. p53 mutation changes late adenoma to carcinoma
        
        5) DDC mutation leads intermediated adenoma to late adenoma
    - - HNPCC hereditary non-polyposis colorectal cancer / lync syndrome
        
        MMR family with 1 hit awaiting 2nd hit
        
        MSH2 tumour suppressor, MLH1 TSG for mismatch repair, MSH6, PMS2 mutation
        
        microsatellite instability / MSH-H
        
        BAX, PTEN frameshift
    - - Colon epithelium cells
    - - Widespread benign adenomas in population
      - adenomas/polyps from epithelium
    - - malignant adenocarcinoma from adenomas
- - - - DSB repair
      - DNA replication stress response
    - - DSB repair
      - DNA replication stress response
      - Cell cycle checkpoints
    - - Leads to LI Fraumeni syndrome and early onset of breast cancer
- - - - During S and G2 phase
        
        original sister chromatid as template
    - - Error prone