Cancer EOYS1 Flashcards
What are the 3 main groups of genes implicated in cancer? [3]
Oncogenes
Tumour suppressor genes Two types:
* Gatekeepers (regulate cell cycle)
* Care takers (DNA repair)
Which type of genes regulate cell growth? [1]
How? [1]
Proto-oncogenes encode proteins which control cell growth and cell division
Tightly regulated: switched on and off
Name two important cell growth pathways
MAPK pathway
PI3 Kinase pathway
Activation of MAPK pathway causes which cell processes to occur? [2]
PROLIFERATION
APOPTOSIS REGULATION
Activation of PI3 Kinase pathway causes which cell processes to occur? [2]
CELL GROWTH PROLIFERATION
ANGIOGENESIS AND METABOLISM
Describe the consequences of the overexpresson of HER2 [4]
Overexpression growth factor receptors leads to uncontrolled activation of signalling pathways:
- Uncontrolled growth
- Survival of cells containing mutations
- Invasion of tumour cells
- Migration of tumour cells
Why is HER2 receptor particularly oncogenic? [1]
Doesnt require simply GF to cause expression - easily overexpressed
What is role of gate keepers [5] and care taker genes [1]
Gate keepers:
* Directly supresses growth/restricts proliferation
* Cell cycle/cell division regulator genes
* Check point control genes
* Apoptosis - related genes
Care takers:
* Maintains genetic stability: DNA repair proteins
At which stages in cell cycle are checkpoints where cell cycle can be arrested? [2]
G2 / M [1]
G1 / S [1]
In human cancers,[]is the most commonly mutated gene.
In human cancers,TP53is the most commonly mutated gene.
What type of molecule is p53? [1]
Which molecule does it activate? [1]
p53 transcription factor:
Increases expression of p21
(cyclin dependent kinase inhibitors)
Explain how Retinoblastoma occurs (and compare to normal functioning gene) [2]
Unphosphorylated form of Rb: binds to GF E2F - cannot bind the DNA and transcription is blocked
Phosphorylated form of Rb: cannot bind to GF E2F - bind the DNA and transcription goes on uncontrolled growth
Explain how normal proto-oncogenes cause normal cell signalling
- growth factor binds to receptor. two receptors interact (dimerization)
- intracelllar side: phosphorylation of tyrosine
- signalling proteins bind to P-tyrosine
- causes cascade of phosphorylation events
- activates two pathways: MAPK pathway and PI3 Kinase Pathway
- once pathways are activated, activate gene expression and transcription factors occur.
HER2 Receptor is what type of receptor?
GPCR
Enzyme-linked
Nucleus binding
Tyrosine-kinase
HER2 Receptor is what type of receptor?
GPCR
Enzyme-linked
Nucleus binding
Tyrosine-kinase
State whether oncogenes and tumour supressor genes are activated by a single or double mutation [2]
Oncogene: single mutation
Tumour supressor genes: double mutation
What are the five categories of proto-oncogenes? [5]
- Growth factors (signalling proteins)
- Receptors (e.g. tyrosine kinase receptors
- Intracellular signalling proteins e.g. kinases
- Transcription factors
- Anti-apoptotic proteins
Explain the effect of p53 under normal function [4]
- p53 is a transcription factor
- DNA damage activates stimulation of p53 protein
- This activates p21, a cyclin-dependent kinase inhibitor, which leads to cell cycle arrest
- Prevents progession from G1 to S phase
- If damage so severe, p53 can tirgger activation of pro-apoptotic genes
Explain what happens when p53 becomes mutated [2]
- Mutated p53 does not inhibit cyclin B/ CDK1 complex so cell cycle arrest at G2/M does not occur
- Mutated p53 does not inhibit cyclin E/ CDK2 complex so cell cycle arrest at G1/S does not occur