eBook Chapter 4 - Oncogenes Flashcards

1
Q

-

A
  • retrovirus acquisition

- somatic mutation (most human cancers)

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2
Q

What two groups can retroviruses by divided into? What are the characteristics of each?

A
  • slowly transforming retroviruses - cause tumours after many months of viraemia. Mechanism = insertional activation of cellular oncogenes (c-onc)
  • acutely transforming retroviruses - cause tumours rapidly due to a viral oncogene (v-onc). The v-onc genes of acutley transforming retroviruses are homologous to genes in cellular DNA of the host species. But v-onc typically have mutational changes that deregulate the function of the encoded oncoprotein. It is expressed at high level under control of a viral promoter.
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3
Q

Give a summary of the lifecycle of a retrovirus

A
  • structure = lipid envelope contains RNA genome
  • attaches to host cell membrane via receptor ligand interactions
  • reverse transcription makes DNA
  • provirus integrates at random into host genome
  • this is transcribed by local machinery
  • makes RNA and protein for new virus particles
  • virus leave cell with cell membrane coating
    NB - virus doesn’t kill the host cell
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4
Q

What are the three mechanisms by which c-myc oncogenes can arise?

A
  • deregulation of chromosomal translocation (Burkitt’s lymphoma)
  • gene amplification and increased expression of c-myc (early relapse in breast cancer)
  • amplification of related N-myc gene (childhood neuroblastoma)
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5
Q

Below is the summery of types of alteration affecting cellular oncogenes that contribute to human cancer
x6

A
  1. affecting the function of the encoded oncoprotein
  2. point mutations at specific sites
  3. chimeric fusion proteins resulting from chromosomal translations
  4. affecting the expression of the oncoprotein
  5. chromosomal translocations that place the oncogene under control of alternative, strong regulatory sequences (enhancers)
  6. gene amplification
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