Genetics Of Cancer

Question 1

How many hallmarks of cancer are there

Answer 1

8

Question 2

What do the 8 hallmarks of cancer allow

Answer 2

Carcinogenesis and malignant growth

Question 3

8 hallmarks of cancer

Answer 3

Self sufficiency in growth signals
Insensitivity to anti growth signals
Evade apoptosis
Militless reproductive potential
Sustained angiogenesis
Tissue invasion and metastasis
Deregulated cellular energetic
Avoid immune detection

Question 4

Why are proteases and cytoskeletal proteins upregulated in cancer cells

Answer 4

To breakdown Basement membrane and allow migration

Question 5

Why are mutations in cancer cells not corrected

Answer 5

Defective DNA repair proteins

Question 6

What type of signalling is used by cancer cells to enhance cell division

Answer 6

Autocrine

Question 7

3 main groups of genes associated with cancer

Answer 7

Oncogenes
Gatekeeper and caretaker genes - tumour suppressor genes

Question 8

How do gatekeeper tumour suppressor genes prevent cancer

Answer 8

Regulate and restrict cell cycle
Induce apoptosis in mutated cells

Question 9

How do caretaker tumour suppressor genes prevent cancer

Answer 9

Repair DNA

Question 10

What is the role of proteins encoded by proto oncogenes

Answer 10

Control cell growth and cell division

Question 11

What is produced when a proto oncogene is mutated

Answer 11

Oncogene

Question 12

What proteins are encoded by proto oncogenes

Answer 12

Growth factors
Receptors
Intracellular signalling proteins
Transcription factors
Anti apoptotic proteins

Question 13

Increased activity of what type of protein leads to excess cell division and uncontrolled cell growth

Answer 13

Kinases

Question 14

Do proto oncogenes become oncogenes by a gain of function or loss of function mutation

Answer 14

Gain of function

Question 15

Does activation of an oncogene from a proto oncogene require a single or double mutation

Answer 15

Single

Question 16

What cell structures on cancer cells are highly active and play a role in cancer cell motility

Answer 16

Lamellipodia

Question 17

How do tyrosine receptors facilitate activation of growth promoting signalling pathways

Answer 17

Growth factor binds and tyrosine receptors dimerise activating kinase activity

Question 18

2 major growth signalling pathways

Answer 18

MAPK pathway
Pi3 kinase pathway

Question 19

Role of MAPK pathway

Answer 19

Cel proliferation
Apoptosis regulation

Question 20

Pi3 kinase pathway role

Answer 20

Cell growth
Proliferation
Angiogenesis
metabolism

Question 21

How do kinases effect proteins

Answer 21

Phosphorylate

Question 22

What is constitutive phosphorylation of tyrosine kinase receptors

Answer 22

Mutation in ATP binding site means receptor remains phosphorylated so signalling transduction cannot be switched off leading to excess growth via MAPK/Pi3

Question 23

What does overexpression of HER2 lead to

Answer 23

Uncontrolled growth
Survival of mutated cells
Invasion of tumour cells
Migration of tumour cells

Question 24

What is HER2

Answer 24

Receptor tyrosine kinase

Question 25

How does increased expression of HER2 cause cancer

Answer 25

Increased number of tyrosine kinase receptors causes increased cell growth signalling

Question 26

Why is HER2 more oncogene that other tyrosine kinase receptor genes

Answer 26

HER2 receptors don’t need growth factor to be activated

Question 27

Where are HER2 receptors found

Answer 27

Cell surface membrane

Question 28

What type of gene are BRCA1 and 2

Answer 28

Care taker genes

Question 29

Do tumour suppressor genes undergo a loss of function or gain of function mutation to cause cancer

Answer 29

Loss of function

Question 30

Do tumour suppressor genes need 1 or both genes to be mutated to cause cancer

Answer 30

Both

Question 31

What happens when the cell cycle is not regulated at checkpoints

Answer 31

DNA damaged cells not repaired or apoptosed so continue through cell cycle causing cancer

Question 32

What transcription factor is activated when DNA damage is detected at cell cycle checkpoints

Answer 32

P53

Question 33

How does P53 prevent DNA damaged cells continuing through cell cycle

Answer 33

Activates P21 which inhibits cyclin dependent kinase arresting the cell cycle Activates pro apoptotic genes

Question 34

Where in the cell cycle does Inhibition of the cyclin E/CDK2 complex cause arrest

Answer 34

G1/S checkpoint

Question 35

Where in the cell cycle does cyclin B/CDK1 complex inhibition cause cycle arrest

Answer 35

G2/M checkpoint

Question 36

What is the most commonly mutated gene in cancer

Answer 36

TP53

Question 37

What causes Inhibition of cyclin B/CDK1 and cyclin E/CDK2 complexes

Answer 37

P53

Question 38

Role of pRb

Answer 38

Inhibits S phase gene expression to prevent cell cycle progression past G1

Question 39

What type of cancer is caused by pRb mutation

Answer 39

Retinoblastoma

Question 40

Main role of BRCA2

Answer 40

Regulates RAD51 function to repair DNA damage by homologous recombination

Question 41

Role of BRCA1

Answer 41

Involved in Multiple cellular processes in response to DNA damage

Question 42

What type of DNA damage are BRCA genes most important in repair of

Answer 42

Double strand breaks

Question 43

What is caused by loss of BRCA genes

Answer 43

Strand breaks and aneuploidy after cell division

Question 44

How do cancer cells avoid apoptosis

Answer 44

Upregulates anti apoptotic proteins or down regulate pro apoptotic proteins

Question 45

Are BAX, BAK, and BCL2 pro or anti apoptotic

Answer 45

BAX and BAK - pro apoptotic BCL2 - anti apoptotic

Question 46

What type of protein is BCL2

Answer 46

Anti apoptotic

Question 47

How do cancer cells maintain their telomeres to allow unlimited replication

Answer 47

Upregulate telomerase reverse transcriptase TERT to produce more telomerase

Question 48

What protein is synthesised by telomerase

Answer 48

Telomere

Question 49

What repair mechanisms fix single strand breaks, bulky adducts , nucleotide mutation/substitutions/deletions/insertions, and double strand breaks (from clinical trial workshop)

Answer 49

Single strand break - base excision repair Bulky adducts- nucleotide excision repair nucleotide mutation/substitutions/deletions/insertions - mismatch repair Double strand breaks - homologous recombination, non homologous end joining, microhomology mediated end joining

Question 50

Is homologous recombination, non homologous end joining, or microhomology mediated end joining of double strand breaks least mutagenic (from clinical trial workshop)

Answer 50

Homologous recombination