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Cancer Y2 > Genetics Of Cancer > Flashcards

Genetics Of Cancer Flashcards

1
Q

How many hallmarks of cancer are there

A

8

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2
Q

What do the 8 hallmarks of cancer allow

A

Carcinogenesis and malignant growth

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3
Q

8 hallmarks of cancer

A

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

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4
Q

Why are proteases and cytoskeletal proteins upregulated in cancer cells

A

To breakdown Basement membrane and allow migration

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5
Q

Why are mutations in cancer cells not corrected

A

Defective DNA repair proteins

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6
Q

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

A

Autocrine

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7
Q

3 main groups of genes associated with cancer

A

Oncogenes
Gatekeeper and caretaker genes - tumour suppressor genes

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8
Q

How do gatekeeper tumour suppressor genes prevent cancer

A

Regulate and restrict cell cycle
Induce apoptosis in mutated cells

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9
Q

How do caretaker tumour suppressor genes prevent cancer

A

Repair DNA

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10
Q

What is the role of proteins encoded by proto oncogenes

A

Control cell growth and cell division

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11
Q

What is produced when a proto oncogene is mutated

A

Oncogene

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12
Q

What proteins are encoded by proto oncogenes

A

Growth factors
Receptors
Intracellular signalling proteins
Transcription factors
Anti apoptotic proteins

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13
Q

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

A

Kinases

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14
Q

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

A

Gain of function

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15
Q

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

A

Single

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16
Q

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

A

Lamellipodia

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17
Q

How do tyrosine receptors facilitate activation of growth promoting signalling pathways

A

Growth factor binds and tyrosine receptors dimerise activating kinase activity

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18
Q

2 major growth signalling pathways

A

MAPK pathway
Pi3 kinase pathway

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19
Q

Role of MAPK pathway

A

Cel proliferation
Apoptosis regulation

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20
Q

Pi3 kinase pathway role

A

Cell growth
Proliferation
Angiogenesis
metabolism

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21
Q

How do kinases effect proteins

A

Phosphorylate

22
Q

What is constitutive phosphorylation of tyrosine kinase receptors

A

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

23
Q

What does overexpression of HER2 lead to

A

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

24
Q

What is HER2

A

Receptor tyrosine kinase

25
Q

How does increased expression of HER2 cause cancer

A

Increased number of tyrosine kinase receptors causes increased cell growth signalling

26
Q

Why is HER2 more oncogene that other tyrosine kinase receptor genes

A

HER2 receptors don’t need growth factor to be activated

27
Q

Where are HER2 receptors found

A

Cell surface membrane

28
Q

What type of gene are BRCA1 and 2

A

Care taker genes

29
Q

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

A

Loss of function

30
Q

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

A

Both

31
Q

What happens when the cell cycle is not regulated at checkpoints

A

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

32
Q

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

A

P53

33
Q

How does P53 prevent DNA damaged cells continuing through cell cycle

A

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

34
Q

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

A

G1/S checkpoint

35
Q

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

A

G2/M checkpoint

36
Q

What is the most commonly mutated gene in cancer

A

TP53

37
Q

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

A

P53

38
Q

Role of pRb

A

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

39
Q

What type of cancer is caused by pRb mutation

A

Retinoblastoma

40
Q

Main role of BRCA2

A

Regulates RAD51 function to repair DNA damage by homologous recombination

41
Q

Role of BRCA1

A

Involved in Multiple cellular processes in response to DNA damage

42
Q

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

A

Double strand breaks

43
Q

What is caused by loss of BRCA genes

A

Strand breaks and aneuploidy after cell division

44
Q

How do cancer cells avoid apoptosis

A

Upregulates anti apoptotic proteins or down regulate pro apoptotic proteins

45
Q

Are BAX, BAK, and BCL2 pro or anti apoptotic

A

BAX and BAK - pro apoptotic
BCL2 - anti apoptotic

46
Q

What type of protein is BCL2

A

Anti apoptotic

47
Q

How do cancer cells maintain their telomeres to allow unlimited replication

A

Upregulate telomerase reverse transcriptase TERT to produce more telomerase

48
Q

What protein is synthesised by telomerase

A

Telomere

49
Q

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

A

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

50
Q

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

A

Homologous recombination

Cancer Y2 (11 decks)

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