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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
What is MDM2
Inhibitor protein bound to p53 to block its activity
26
How is p53 stabilised?
Through binding to damaged DNA
27
How many molecules of p53 do you need to act as a transcription factor?
4! It's a Tetramer
28
Name a proapoptotic protein
BAX
29
Are mutant p53 proteins more stable?
Yeh they hang around in cell longer
30
What is Li Fraumeni syndrome?
Inherited disorder - mutated p53
31
What's the implications of loss of p53 on function of chemotherapy agents?
Chemotherapy relies on inducing apoptosis --> no p53 makes tumours more resistant through lack of functional apoptotic pathway! Need to restore p53 function
32
List 4 problems with the idea that cancer comes from mature cells
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
33
What are stem cells?
Pluripotent cells that can differentiate into many different cell types
34
Stem cells can keep growing (self renewal) this is a reason why they are of interest in cancer models: true or false?
True
35
When stem cells differentiate they go through intermediate stages .. what are the cells called?
Precursor or progenitor cells
36
True or false: stem cells undergo symmetric cell division
False! They undergo asymmetric cell devision
37
``` Put the following in order: Pluripotent Unipotent Totipotent Multipotent ```
Totipotent Pluripotent Multipotent Unipotent
38
A restricted potential stem cell is on the line to become one of what three things?
Endoderm Mesoderm Exoderm
39
Give an example of a progenitor cell
Haemopoietic cell (precursor to RBC and WBC)
40
What is the purpose of residual adult stem cells in the bone marrow?
Required for normal cell turnover
41
What is the purpose of residual adult stem cells in the liver and muscle?
Stem cells involved in healing
42
What is Wnt?
Protooncogene
43
How is wnt implicated in 90% of colon cancers?
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
What is patched?
Tumour suppressor gene, LOF in Hh pathway = tumour
45
What makes up the complex that inhibits the release of beta-caterin
Axin APC CKI GSK3
46
Explain the wnt pathway
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
Explain the Hh pathway
Hh binds patched which releases smoothened which then releases Gli which is a TF that drives cell growth
48
Why do chromosomes get shorter after each replication?
Because telomerase enzymes can't copy right to the end of DNA
49
What are telomeres?
The ends of chromosomes (non coding)
50
What are telomerases?
Reverse transcriptase enzymes that add RNA templates to chromosome ends
51
What enzyme do tumour cells express that enable them to repair chromosomes and extend cell life
Telomerases
52
Do stem cells have active telomerase enzymes?
Yes
53
What is epigenetics
The study of changes in organisms caused by modification of gene expression rather than alteration of the genetic code itself
54
What is metastasis
The ability of cancer cells to break away from site of origin, travel to and recolonise a distant site
55
Metastasis requires what?
Break down in cell-cell adhesion and degradation of basal lamina
56
What is the process of metastasis
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
Give two theories for the sites of metastasis
First pass organ | Pre metastatic niche
58
What is angiogenesis?
Growth of new blood vessels
59
Give three examples of when angiogenesis occurs naturally?
Embryogenesis Wound healing Menstrual cycle
60
Angiogenesis is controlled by endogenous growth factors .. give 4 examples
Angiogenin FGF VEGF PDGF
61
Angiogenesis is also controlled by inhibitors, name two
Angiostatin | Endostatin
62
Why do tumour cells require angiogenesis
New blood vessels are required to bring oxygen and nutrients to the cells in the centre of the tumour
63
Angiogenesis in cancer enables what 3 processes
Tumour growth Invasion Metastasis
64
What does VEGF stand for
Vascular endothelial growth factor
65
How many forms of VEGF are there and which is the best characterised
Five | VEGF-A
66
When could you use antisense RNA- bFGF, PDGF in cancer
As a way of down regulating growth factors that drive angiogenesis
67
Name 4 approaches to preventing angiogenesis
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
Name two ways you can investigate leukaemias
1) blood sample | 2) bone marrow aspirate (more painful)
69
Patients with leukaemia, their blood looks like what?
Milky
70
Name four myeloid cells (cells of the innate immune system)
Granulocytes Neutrophils Macrophages Mast cells
71
Name an erythroid cell
Red blood cell
72
Name two lymphoid cells (cells of adaptive)
T lymphocytes | B lymphocytes
73
Classification of Leukaemia is based on what
Based around the origin of the cell
74
What's different about leukaemia compared to other cancers
Starts as chronic phase then goes to serious acute phase
75
How is leukaemia classified
1) cell of origin (e.g myeloid or lymphoid leukaemia) | 2) acute or chronic phase
76
Name four clinical signs of chronic myeloid leukaemia
Fatigue Anaemia Splenomegaly Hepatomegaly
77
How is the spleen and liver involved in chronic myeloid leukaemia
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
Name the three clinical phases of leukaemia
1) initial chronic phase 2) accelerated phase 3) acute blast crisis
79
What's common in the aetiology of leukaemia
Chromosomal abnormalities: additions, translocations, deletions and amplification
80
What is chronic myeloid leukaemia due to
Genetic alterations in a stem or early progenitor cell
81
95% of CML have reciprocal translocation between what two chromosomes
9 and 22
82
What is the function of the c-Abl protooncogene
Encodes a cytoplasmic and nuclear protein tyrosine kinase that has been implicated in processes of cell differentiation, division and adhesion
83
What is the drug name of glivec
Imatinib
84
What is imatinib and how does it work
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
Name the first small molecule inhibitor to be released from clinical trials
Glivec- imatinib
86
Why was glivec fast tracked by the FDA
Good trials- normal white cell count within 4 weeks of one trial
87
Name two ways you can get resistance from glivec
1) BCR-ABL amplification | 2) point mutation in BCR-ABL changing active site
88
Name two second/ third line treatments for CML cause by BCR-ABL and how are they different to glivec
1) dasatinib 2) nilotinib They bind the active confirmation of BCR-ABL
89
What's the hypothesis to glivec (imatinib) resistance?
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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