1. What does the tumour supressor gene do?
- The proteins can't initiate apoptosis if DNA damage is irreparable
- They code for signalling proteins that codes signalling molecules e.g growth factors, protein kinase and transcription factor
- e.g.P35 gene encoded by the TP53 gene on the short arm of chromosome 17 and regulates cell cycle
- They code for proteins that control cell cycle progression/proliferation (many of which are check point genes.
- Can't induce growth arrest at G1/S regulation point (restriction point)
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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
- transcriptional deregulation of cell
- Initiate denaturing of checkpoint proteins
- initiate abnormal signalling pathways
- initiate deregulation of signalling network
4. Which of these is correct for a normal cell?
- Loss of differentiation
- Continue cell proliferation
- balance process disrupted
- By reducing the immune barrier
- balance between the growth promoting and restriction factors
- Apoptosis doesn't occur
5. What is neoplastic transformation?
- Causes a permanent activation
- cooperation of multiple genetic changes within a cell
- A gene which encodes signalling molecules that can act as Growth factors, protein kinases and transcription factors that activates gene expression
- 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