Oncogenes and tumour suppressor genes

Question 1

The hallmarks of cancer

Answer 1

Sustain proliferative signalling 
Resisting cell death 
Angiogenesis
Replicative immortality 
Invasion and metastases
Evading growth suppressors 
Deregulating cellular energetics 
Genome instability and mutation 
Avoiding immune destruction 
Tumour-promoting inflammation

Question 2

Genetic mutation bladder cancer

Answer 2

KRAS

Question 3

genetic mutation colon cancer

Answer 3

KRAS

Question 4

What are oncogenes?

Answer 4

Genes that, under certain circumstances, transform a normal cell into a cancerous cell

Question 5

How do you activate Ras

Answer 5

GTP- GDP

Question 6

genetic mutation causing lung cancer

Answer 6

EGFR

Question 7

Mutations of c-KIT

Answer 7

In juxtamembrane domain = activation of tyrosine kinase in absence of ligand
Mutation stimulates growth of cancer cells

Question 8

Retinoblastoma o/e

Answer 8

Opacity in eye , present before 8 y/o

Question 9

Hereditary retinoblastoma

Answer 9

Single mutation = all cells in body contain mutation. If there is a second mutation by chance then there will be increased proliferation

Question 10

Non-hereditary retinoblastoma

Answer 10

Two mutations in same cell - often only occurs in one eye

Question 11

Rb gene

Answer 11

• Germline mutation of RB in hereditary retinoblastoma
• Ater restriction point, cell is ‘committed to cell cycle’
• During early G1, RB protein hypo-phosphorylated
• After resurrection, hyperphosphorylation until cytokinesis
• RB binds to E2F transcription factors
• Hyperphosphorylation interferes with binding and releases E2F proteins allowing expression of genes for cell cycle gene
• If both RB mutated, no cell cycle regulation, this removes restriction point

Question 12

Mechanism of p53

Answer 12

Phosphorylated p53 can not bind to MDM2
Phosphorylated p53 acts as transcription factor
Activates Chi p21
Binds cyclin-CDK complexes (cell cycle arrest)
Missense mutations inhibit p53 from binding to target genes