eBook Chapter 4 - Oncogenes Flashcards
1
Q
-
A
- retrovirus acquisition
- somatic mutation (most human cancers)
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.
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
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)
5
Q
Below is the summery of types of alteration affecting cellular oncogenes that contribute to human cancer
x6
A
- affecting the function of the encoded oncoprotein
- point mutations at specific sites
- chimeric fusion proteins resulting from chromosomal translations
- affecting the expression of the oncoprotein
- chromosomal translocations that place the oncogene under control of alternative, strong regulatory sequences (enhancers)
- gene amplification