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Oncology > Chapter 1- edmead > Flashcards

Chapter 1- edmead Flashcards

1
Q

What is cancer?

A

Cancer is a group of diseases characterised by unregulated cell growth and the invasion and spread of cells from the site of origin (primary site) to other sites in the body

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2
Q

Cancer often occurs as a result of what two things?

A

1) activated growth genes

2) loss of death mechanisms

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3
Q

List 6 characteristics of a cancer cell

A

1) self sufficiency in growth signals
2) insensitivity to antigrowth signals
3) evasion of apoptosis
4) limitless replication potential
5) tissue evasion and metastasis
6) sustained angiogenesis

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4
Q

Give an example of ‘self sufficiency in growth signals’ in tumour cells

A

E.g. In breast cancer they are susceptible to growth by TGFa

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5
Q

Give an example of how tumour cells can be insensitive to antigrowth signals

A

Tumour cells can switch off the pathway that responds to TGFb (this TGFb suppresses cell growth by inducing transcription factors that act as repressors)

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6
Q

Give an example of a pro-survival protein that can be upregylated in a tumour cell to prevent apoptosis

A

BCL-2

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7
Q

Give an example of how tumour cells can have limitless replicative potential?

A

Tumour cells can increase the length of the telomeres

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8
Q

How do tumour cells ‘invade’

A

They don’t have the ability to stop growing when in contact with other cells like normal cells do

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9
Q

Carcinomas arise from what cells

A

Epithelial cells

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10
Q

Adenocarcinomas arise from what cells?

A

Glandular tissues e.g breast

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11
Q

Sarcomas arise from what type of tissues

A

Connective tissue and muscle

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12
Q

What is leukaemia?

A

Blood cell derived sarcomas

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13
Q

Name three ways in which proto-oncogenes can become oncogenic

A

1) point mutation e.g. RAS
2) gene amplification e.g. HER2
3) chromosomal translocation

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14
Q

True or false: tumour suppressor genes are recessive so require to copies of a loss of function

A

TRUE

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15
Q

Is src a tyrosine kinase?

A

YEH

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16
Q

True or false: the active form of src is phosphorylated

A

FALSE the inactive form of src is phosphorylated

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17
Q

How was src permanently active in chickens?

A

Viral DNA inserted and took away src sequence minus the tyrosine kinase so can’t inactivate

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18
Q

What’s the mechanism of action of herceptin

A

Antibody that binds HER2 receptor and causes:

  • decreased signalling pathway
  • induce downregulation of receptor
  • uncouples src
  • increases PTEN activation
  • induces cell cycle arrest increased p27
  • may increase apoptosis and angiogenesis
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19
Q

Name two small molecule inhibitors used to block kinase domain (e.g in cancers with mutated EGFR)

A

Iressa

Tarceva

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20
Q

How can tumour suppressor genes predispose and individual to cancer?

A

They are recessive so if someone inherits one mutated allele they can then acquire another

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21
Q

Give two things that can give you a hereditary predisposition to cancer and what types of cancer are they?

A

APC-> colon cancer

BRCA1-> breast cancer

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22
Q

How does pRb regulate cell cycle?

A

In G1, cyclin D activates kinase (CDK4)
CDK4 then phosphorylates (activates) pRb
pRb then releases E2F
E2F then stimulates genes and proteins that the cell requires for S phase

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23
Q

What does p16 do?

A

Inhibitor of CDK4

Therefore CDK4 free to activate pRb which releases E2F

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24
Q

Why is p16 needed?

A

It inhibits CDK4 in order to halt the cell cycle to repair damaged DNA

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25
Q

What is MDM2

A

Inhibitor protein bound to p53 to block its activity

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26
Q

How is p53 stabilised?

A

Through binding to damaged DNA

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27
Q

How many molecules of p53 do you need to act as a transcription factor?

A

4! It’s a Tetramer

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28
Q

Name a proapoptotic protein

A

BAX

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29
Q

Are mutant p53 proteins more stable?

A

Yeh they hang around in cell longer

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30
Q

What is Li Fraumeni syndrome?

A

Inherited disorder - mutated p53

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31
Q

What’s the implications of loss of p53 on function of chemotherapy agents?

A

Chemotherapy relies on inducing apoptosis –> no p53 makes tumours more resistant through lack of functional apoptotic pathway! Need to restore p53 function

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32
Q

List 4 problems with the idea that cancer comes from mature cells

A

1) is a disease of proliferating cells
2) tumours are heterogenous
3) caused by accumulation of mutations so cells need to live long
4) only a small number of tumour cells can recolonise

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33
Q

What are stem cells?

A

Pluripotent cells that can differentiate into many different cell types

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34
Q

Stem cells can keep growing (self renewal) this is a reason why they are of interest in cancer models: true or false?

A

True

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35
Q

When stem cells differentiate they go through intermediate stages .. what are the cells called?

A

Precursor or progenitor cells

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36
Q

True or false: stem cells undergo symmetric cell division

A

False! They undergo asymmetric cell devision

37
Q 
Put the following in order: 
Pluripotent 
Unipotent 
Totipotent 
Multipotent
A

Totipotent
Pluripotent
Multipotent
Unipotent

38
Q

A restricted potential stem cell is on the line to become one of what three things?

A

Endoderm
Mesoderm
Exoderm

39
Q

Give an example of a progenitor cell

A

Haemopoietic cell (precursor to RBC and WBC)

40
Q

What is the purpose of residual adult stem cells in the bone marrow?

A

Required for normal cell turnover

41
Q

What is the purpose of residual adult stem cells in the liver and muscle?

A

Stem cells involved in healing

42
Q

What is Wnt?

A

Protooncogene

43
Q

How is wnt implicated in 90% of colon cancers?

A

In the wnt pathway there is a loss of function in the tumour suppressor gene APC this results in an increase in this growth pathway

44
Q

What is patched?

A

Tumour suppressor gene, LOF in Hh pathway = tumour

45
Q

What makes up the complex that inhibits the release of beta-caterin

A

Axin
APC
CKI
GSK3

46
Q

Explain the wnt pathway

A

Wnt binds frazzled
This takes axin out of inhibitory complex thus releasing APC CKI GSK3 and therefore beta-caterin which causes cell proliferation as beta- caterin is a TF

47
Q

Explain the Hh pathway

A

Hh binds patched which releases smoothened which then releases Gli which is a TF that drives cell growth

48
Q

Why do chromosomes get shorter after each replication?

A

Because telomerase enzymes can’t copy right to the end of DNA

49
Q

What are telomeres?

A

The ends of chromosomes (non coding)

50
Q

What are telomerases?

A

Reverse transcriptase enzymes that add RNA templates to chromosome ends

51
Q

What enzyme do tumour cells express that enable them to repair chromosomes and extend cell life

A

Telomerases

52
Q

Do stem cells have active telomerase enzymes?

A

Yes

53
Q

What is epigenetics

A

The study of changes in organisms caused by modification of gene expression rather than alteration of the genetic code itself

54
Q

What is metastasis

A

The ability of cancer cells to break away from site of origin, travel to and recolonise a distant site

55
Q

Metastasis requires what?

A

Break down in cell-cell adhesion and degradation of basal lamina

56
Q

What is the process of metastasis

A

Mutations in E-cadherins relax cell-cell adhesion, change in expression of integrins allows cell movement through ECM, ability of tumours to induce surrounding stromal cells to produce MMPs to digest ECM, intravasation by degradation of basal lamina, transport through blood vessels, extravasation (E-selectin)

57
Q

Give two theories for the sites of metastasis

A

First pass organ

Pre metastatic niche

58
Q

What is angiogenesis?

A

Growth of new blood vessels

59
Q

Give three examples of when angiogenesis occurs naturally?

A

Embryogenesis
Wound healing
Menstrual cycle

60
Q

Angiogenesis is controlled by endogenous growth factors .. give 4 examples

A

Angiogenin
FGF
VEGF
PDGF

61
Q

Angiogenesis is also controlled by inhibitors, name two

A

Angiostatin

Endostatin

62
Q

Why do tumour cells require angiogenesis

A

New blood vessels are required to bring oxygen and nutrients to the cells in the centre of the tumour

63
Q

Angiogenesis in cancer enables what 3 processes

A

Tumour growth
Invasion
Metastasis

64
Q

What does VEGF stand for

A

Vascular endothelial growth factor

65
Q

How many forms of VEGF are there and which is the best characterised

A

Five

VEGF-A

66
Q

When could you use antisense RNA- bFGF, PDGF in cancer

A

As a way of down regulating growth factors that drive angiogenesis

67
Q

Name 4 approaches to preventing angiogenesis

A

1) antisense RNA (bFGF, PDGF)
2) soluble receptors/monoclonal antibodies (avastin- bevacizumab)
3) enzyme inhibitors e.g VEGFR inhibitors sunitinib & sorafenib
4) activation of tumour suppressor- p53 upregulates anti angiogenic factors (e.g. Thrombospondin, downreg bFGF)

68
Q

Name two ways you can investigate leukaemias

A

1) blood sample

2) bone marrow aspirate (more painful)

69
Q

Patients with leukaemia, their blood looks like what?

A

Milky

70
Q

Name four myeloid cells (cells of the innate immune system)

A

Granulocytes
Neutrophils
Macrophages
Mast cells

71
Q

Name an erythroid cell

A

Red blood cell

72
Q

Name two lymphoid cells (cells of adaptive)

A

T lymphocytes

B lymphocytes

73
Q

Classification of Leukaemia is based on what

A

Based around the origin of the cell

74
Q

What’s different about leukaemia compared to other cancers

A

Starts as chronic phase then goes to serious acute phase

75
Q

How is leukaemia classified

A

1) cell of origin (e.g myeloid or lymphoid leukaemia)

2) acute or chronic phase

76
Q

Name four clinical signs of chronic myeloid leukaemia

A

Fatigue
Anaemia
Splenomegaly
Hepatomegaly

77
Q

How is the spleen and liver involved in chronic myeloid leukaemia

A

Because WBC pass through the spleen and are broken down in the liver so if you have more blood cells you have more activity in these organs (enlargement)

78
Q

Name the three clinical phases of leukaemia

A

1) initial chronic phase
2) accelerated phase
3) acute blast crisis

79
Q

What’s common in the aetiology of leukaemia

A

Chromosomal abnormalities: additions, translocations, deletions and amplification

80
Q

What is chronic myeloid leukaemia due to

A

Genetic alterations in a stem or early progenitor cell

81
Q

95% of CML have reciprocal translocation between what two chromosomes

A

9 and 22

82
Q

What is the function of the c-Abl protooncogene

A

Encodes a cytoplasmic and nuclear protein tyrosine kinase that has been implicated in processes of cell differentiation, division and adhesion

83
Q

What is the drug name of glivec

A

Imatinib

84
Q

What is imatinib and how does it work

A

Small molecule inhibitor - blocks the ATP binding site of tyrosine kinase a including in:

1) Abl (CML)
2) PDGFbR (CMML)
3) c-kit (GIST)

85
Q

Name the first small molecule inhibitor to be released from clinical trials

A

Glivec- imatinib

86
Q

Why was glivec fast tracked by the FDA

A

Good trials- normal white cell count within 4 weeks of one trial

87
Q

Name two ways you can get resistance from glivec

A

1) BCR-ABL amplification

2) point mutation in BCR-ABL changing active site

88
Q

Name two second/ third line treatments for CML cause by BCR-ABL and how are they different to glivec

A

1) dasatinib
2) nilotinib

They bind the active confirmation of BCR-ABL

89
Q

What’s the hypothesis to glivec (imatinib) resistance?

A

You kill off all the cells that are sensitive to glivec and leave behind a population of cells that were resistant from the beginning -> these regrow

Oncology (9 decks)

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