1. What does the tumour supressor gene do?
- e.g.P35 gene encoded by the TP53 gene on the short arm of chromosome 17 and regulates cell cycle
- Can't induce growth arrest at G1/S regulation point (restriction point)
- The proteins can't initiate apoptosis if DNA damage is irreparable
- They code for proteins that control cell cycle progression/proliferation (many of which are check point genes.
- They code for signalling proteins that codes signalling molecules e.g growth factors, protein kinase and transcription factor
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2. How is proliferation controlled in normal cells
- Activate oncogenes transiently (i.e for a short by mitogens) and INactivate tumour suppressor genes transeintly
- Uncontroled activation of oncogenes and deactivation of tumour supressor genes
3. BCR ABL kinases don't
- Initiate denaturing of checkpoint proteins
- initiate deregulation of signalling network
- initiate abnormal signalling pathways
- transcriptional deregulation of cell
4. What is neoplastic transformation?
- Causes a permanent activation
- cooperation of multiple genetic changes within a cell
- Conversion of a normal cell to a malignant cell
- a gene when mutated or expressed at a high level turns a normal cell into a malignant one
- A gene which encodes signalling molecules that can act as Growth factors, protein kinases and transcription factors that activates gene expression
5. How can Mitotic crossover play a role in cancer?
- It is an event where a cancer causing reccesive allele may be expressed and thus predispose the cell causing development of cancer
- It does not play a role
- It is an event where a cancer causing dominant allele is sometimes expressed and thus predispose the cell causing development of cancer