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CMP > Cancer Biology > Flashcards

Cancer Biology Flashcards

1
Q

What proportion of cancers are avoidable?

A

50-80%

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2
Q

Why do stomach and cervical cancer have reduced incidence?

A

Better food storage and cervical cancer screening

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3
Q

What is and why is there an increased incidence of breast cancer each year he to child delay?

A

3% increase, thought to be due to the hormone in flux on giving birth is protective

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4
Q

What are 90% of cancer origins?

A

Epithelial I.e. Lung, bowel, skin

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5
Q

Large bowel cancer is late onset due to

A

Need of cumulative mutations (6-10) in one cell, or immune system failing or epigenetic changes when ageing. Also evidence that the nucleus changes shape as you age which alters gene expression

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6
Q

What cancers have genes that when have mutations or are just inherited lead to increased incidence?

A

Familial adenomatous polyposis coli (APC) 1 mutant allele of APC gene gives 100% risk of owed cancer in 30’s
BRAC1 & BRAC2 gives 60-80% lifetime risk, genes also have pleotropic effect and also cause ovarian and endometrial cancers

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7
Q

What key genes are mutated in colorectal cancer?

A

APC/ beta catenin
Kras and EGFR
p53, 18q LOH/ TGFbeta

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8
Q

What do you give women expressing human epithelial growth factor 2

A

Herceptin to starve the tumour. BUT only in HER2 experts sing breast cancers

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9
Q

What is an anti apoptosis factor that is secreted in the bottom of the crypt

A

Bcl-2

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10
Q

What are pro apoptosis factors secret at the top of the crypt?

A

Bax and TGFbeta

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11
Q

What effect does aspirin have on bowler cancer and why?

A

Aspirin is an anti-inflammatory so reduced risk of bowel cancer. Chronic inflammation is highly linked to cancer

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12
Q

What is retrodifferentiation?

A

Reversion to embryonic phenotype exhibited by tumour cells

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13
Q

What are the 6 hallmarks of cancer?

A
  1. Evade apoptosis 2. Self sufficiency for growth factors 3. Insensitivity to anti growth factors 4. Limitless potential to divide 5. Sustained angiogenesis 6. Tissue invasion and metastasis
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14
Q

Chemical carcinogens include:

A 
Benzo(a)pyrene
Asbestos
Tar, wood, oil
Radon
Wood dust
Aflatoxin B
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15
Q

What in the diet can cause cancer?

A

High fat = increase bile acid = increased bowel cancer
High fibre is protective
Low fibre can lead to cancer.

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16
Q

Proto oncogene (+examples)

A

A normal gene involved in normal growth control and differentiation, oftenr involved in control of the cell cycle. C-Myc and c-ras.

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17
Q

How does c-myc become an oncogene

A

By over expression of the normal protein

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18
Q

How does c-ras become an oncogene?

A

By a single base mutation

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19
Q

Oncogene

A

A gene whose product can act in a dominant fashion to help make a normal cell cancerous. Typically it is a mutant of a normal growth factor gene.

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20
Q

Compete carcinogen

A

Produce tumours on their own without addition of extra chemicals such as tumour promoters

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21
Q

Incomplete carcinogen

A

Sometimes called initiating agents, cannot produce tumours on their own, require subsequent exposure to treated cells or tumour promoting agents

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22
Q

Two stages in cancer developed and what are they exemplified by?

A

Tumour initiation and tumour promotion as shown by the mouse skin model.

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23
Q

What are two initiating agents?

A

B(a)P and DMBA

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24
Q

What is a promoting agent

A

TPA

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25
Q

What happens to the cells after addition of an initiating agent?

A

Mutations but no tumour

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26
Q

How do tumour promoting agents cause cancer

A

By irritation and inflammation, altering gene expression and inhibiting metabolic cooperation

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27
Q

Why are some people at a higher risk of cancer?

A

Genetic variation in activation and detoxification, the enzymes for these have different efficiency dependent on the individual.

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28
Q

C-h-ras has two hotspots what are they and what are the mutations that occur there to cause cancer and what causes the mutation at each hotspot?

A

Codon 12: normal to tumour is glycine to valine GGC: GTC
Codon 61: normal to tumour is glutamate to leucine CAA: CTA
Benzo(a)pyrene preferentially binds to guanine causing codon 12 mutations in the tumours. Constitutive signal for proliferation.
DMBA preferentially binds to adenosine causing codon 61 mutations (Change of function mutation)

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29
Q

Why is cancer incidence increasing?

A

Living longer but also lifestyle is getting worse, obesity etc.

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30
Q

How early in papilloma development does c-harvey-ras mutate?

A

the earliest stages

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31
Q

what does the specificity of the tumour mutation depend on?

A

the tumour initiating agent, not the promoter i.e. benzo (a) pyrene not TPA. The promoter makes no difference to the mutation.

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32
Q

Initiation agent benzo(a)pyrene can be replaced by:

A

a retrovirus - harvey murine sarcoma virus and scraping it into the skin

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33
Q

What chromosome is N-ras on and what s it mutated in?

A

chromosome 1, neurblastoma

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34
Q

chromosome cancer mutated in of H-ras

A

chromosome 11 and colon & breast cancers

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35
Q

chromosome and cancer mutation of K-ras

A

chromosome 12, colon and breast cancers

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36
Q

How any human cancers have viral involvement?

A

10-20%

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37
Q

what is a proto-oncogene?

A

a normal gene involved in normal growth control and differentiation that can be converted into a cancer promoting oncogene by mutation.

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38
Q

Over-expression of a proto-onocogene can be due to

A

mutated promoter, chromosome translocation and gene amplification

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39
Q

what is the product of the ras proto-oncogene/

A

p21

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40
Q

The normal ras protein has…

the mutated ras protein has..

A
  1. GTPase activity

2. reduced GTPase activity

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41
Q

how does ras oncogene function?

A

as a G protein involved in signal transduction at the cell membrane

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42
Q

mutations in ras lead to it…

A

being constitutively switched on, to continuously signal for growth

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43
Q

Proto-oncogene mutations are usually…

A

gain of function, dominant acting

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44
Q

Define tumour viruses

A

viruses that are capabe of either alone or in cooperation with other agents of converting normal cells to tumour cells or pushing abnormal cells further along the pathway to cancer. Most viruses are non-oncogenic.

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45
Q

acute transforming viruses include:

A

rous sarcoma virus
avian erythroblastosis virus
simian sarcoma virus
harvey ras virus

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46
Q

what is the oncoprotein in rous sarcoma virus?

A

p60(SRC)

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47
Q

What viral proteins are encoded by RSV?

A

gag, pol, env and p60(SRC)

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48
Q

p60(SRC) has what dominant acting activity?

A

protein kinase activity, phosphorolating tyrosine

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49
Q

What are all the factors of acute transforming viruses?

A
  1. contain oncogenes
  2. insert randomly into the host genome
  3. cause tumours in animals in 2-6 weeks
  4. transform cells in culture
  5. oncogenes are dominant
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50
Q

What is an example of a slow transforming virus?

A

Avian Leukosis virus

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51
Q

How do slow transforming viruses integrate into the host DNA?

A

specifically using the viral LTR promoter which leads to over-expression of the cellular proto-oncogene

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52
Q

Slow transforming viruses: (5)

A
  1. do not have an oncogene
  2. Very low/non-detectable frequency of transformation of cells in culture
  3. After infection takes 3-13 months for tumours to appear
  4. have specific integration sites in cellular DNA leading to viral promoter sequences (LTR) causing overexpression.
  5. “slowness” due to randomness of integration and the time it takes to integrate next to specific proto-oncogene (c-myc)
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53
Q

Is the direct effect of a slow transforming virus encoded in its DNA?

A

No, effect is from insertion, UNLIKE acute transforming viruses.

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54
Q

What does v-sis encode?

A

A viral version of PDGF

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55
Q

What does v-erbB encode?

A

A truncated EGF recptor

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56
Q

Do cancer viruses mutate the host PO’s/TSG’s?

A

No, they normally transform by introducing abnormal virus genes coding for abnormal proteins (not STV’s)

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57
Q

What phase of the cell cycle do PGDF and EGF push the cell into?

A

S phase

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58
Q

How does TGFbeta affect the cell cycle?

A

Causes cell cycle arrest in G1

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59
Q

What is autocrine secretion?

A

Tumour cells responding to their own growth factors

60
Q

Six points of the specificity of grooowth factor action:

A
  1. Often specific growth factor has a specific receptor
  2. Some growth factors are secreted latent and may require activation
  3. Response to one growth factor may be determined by what other growth factors are present
  4. It is possible for two factors to bind to the same receptor (EGF & TGFalpha)
  5. There are positive and negative growth factors
  6. TGFbeta stimulates normal fibroblasts and inhibits normal epithelial cells.
61
Q

What are the growth factor receptor domains

A
  1. outer domain
  2. transmembrane domain
  3. inner domain
62
Q

what is the process of events when a GF binds to a growth factor receptor?

A
  1. activation of intrinsic tyrosine kinase activity associated with the inner cytoplasmic domain of the receptor
  2. this leads to receptor dimerisation
  3. and gives autophosphorylation of the receptor and other cellular proteins, stimulating DNA synthesis.
  4. growth factors activate the mitogen-activated protein kinase cascade (MARKs)
63
Q

Where is PDGF found and what does it support?

A

blood serum (NOT plasma) and supports the growth of serum connective tissue

64
Q

Where PDGF released from?

A

Blood platelets at wounded sites - wound healing

65
Q

What is PDGF a mitogen for?

A

Cells of mesenchymal origin

66
Q

Where are PDGF receptors found?

A

Fibroblasts, smooth muscle cells and glial cells

67
Q

Where are PDGF receptors not found?

A

Epithelial cells, endothelial cells, lymphocytes

68
Q

How was a relationship between viruses and cancer first initiated?

A

due to viral transformed cells having ad reduced growth factor requirement and cancer cells conditioning the medium they are in by secreting growth factors.

69
Q

What was the amino acid sequence of PDGF compared to?

A

the predicted amno acid sequence of p28SIS (of simian sarcoma virus)

70
Q

The PDGF factfile:

A

region of 104 contiguous amino acids showed virtual identity with the predicted sequence of p28SIS, if v-sis is mutated it loses the ability to transform. Simian sarcoma virus has acquired cellular sequence which encode a growth factor identical or very similar to PDGF and the expression of this protein mediated transformation by the virus. V-sis related sequences have been located in the human genome, perhas due to recombination.

71
Q

what viral fusion protein is formed and secreted from the cell to feedback on PDGF receptor?

A

sis-env

72
Q

Processes of simian sarcoma virus exhibiting autocrine growth stimulation:

A

Virus enters cell and transforms it. There is then abnormal expression of PDF through transformation by RNA tumour virus.

73
Q

How does simian sarcoma virus lead to uncontrolled tumour cell growth through autocrine stimulation?

A

Secretes v-sis (PDGFlike protein) stimulates self PDGF receptors and the fact that it has to leave the cell in order to cause an effect is a key interaction. But means reduced requirement for exogenous growth factors.

74
Q

What does EGF consist of?

A

A single polypeptide chain and binds to EGF receptors

75
Q

What receptors re found on all 3 germ layers and are not restricted to epidermis?

A

EGF receptor

76
Q

EGF-receptor has

A

intrinsic tyrosine kinase activity

77
Q

What does the binding of EGF to its receptors trigger?

A

a number of effects that lead to DNA synthesis, presumably as a result of phosphorylating tyrosine kinase activity.

78
Q

Where in mice and rats is EGF produced and why?

A

Salivary glands, to promote wound healing.

79
Q

In human cancers, EGF is usually?

A

Over expressed

80
Q

What does EGF receptor have close structural similarity with?

A

The v-erbB oncogene of avian erythroblastosis virus. However, the virus gives a truncated version of the receptor.

81
Q

What does the v-erbB truncated version of EGF receptor result in?

A

Constitutive activation of the mutagenic receptor causing DNA synthesis and proliferation. (Activated the tyrosine kinase activity associated with the inner cytoplasmic domain which leads to autophosphorylation of the receptor)

82
Q

What experiment was used to isolate the first human oncocgene-ras?

A

Transfecting human cancer DNA into mouse 3T3 cells. This was done by:
1. Transfecting DNA from EJ bladder carcinoma into mouse cells (+CaP)
2. Show mouse cell clones are tumourigenic
3. Isolate DNA from several foci and look for human sequences, find human sequences that are common to all they transformed foci.
4. Discovered c-h-ras gene is very similar to viral oncogene (v-ras)
Control: Transfect mouse cells with normal bladder DNA, no transforming ability.

83
Q

What are two carcinoma cell lines with c-h-ras mutations?

A

EJ bladder carcinoma and Hs242.

84
Q

what is the relationship between proto-oncogene, cellular oncogene and viral oncogene?

A

proto-oncogene——>cellular oncogene——>viral oncogene
mutation/ evolution
overexpression

85
Q

How can cancer cells be similar to foetal cells?

A

Cancer cells often show retrodifferentiation and can behave similarly to embryonic cells and express embryonic markers

86
Q

When is a tumour considered malignant?

A

When it is metastatic

87
Q

Can non metastatic tumours cause problems?

A

Yes, they can be carcinomas and cause problems.

88
Q

Differences between benign and malignant tumours

A

Benign: Encapsulated, Non-invasive, highly differentiated, rare mitosis, slow growth, little of mild dysplasia, non metastatic
Malignant: non-encapsulated, invasive, poorly differentiated, mitosis is common, rapid growth, dysplasia, metastatic (90% of patients die).

89
Q

Dysplasia is

A

Tissue becomes disorganised, cells are abnormal, large cytoplasm: nucleus ratio.

90
Q

Neoplasia

A

New growth, benign/malignancy not specified

91
Q

hydatiform mole:

A

A mass of tissue inside the uterus that will not develop into a baby as the result of abnormal conception.

92
Q

Angiogenesis:

A

The process of generating new capillary blood vessels and results in neovasculaisation.

93
Q

When does angiogenesis occur?

A

Embryonic development, ovulation, wound healing, progressive tumour growth.

94
Q

How does a tumour know its hypoxic?

A

Low oxygen levels

95
Q

Neovascularisation can makr what in a tumour

A

The tumours transition from being benign to more rapid growth, local invasion and distant metastasis

96
Q

What state is a solid tumour

A

Prevascular state, most tumours remain this way

97
Q

What are 2 examples of a tumour is revealed due to angiogenesis in a remote location?

A

Neovascularisaton of the eye is associated with neoplasms of the retina.
Neovascularisation of an old mastectomy scar may indicate the recurrence of the breast tumour beneath the scar

98
Q

Metastasis is influenced by angiogenesis, how?

A

Before Vascularisation, tumours are generally unable to shed cells into the circulation. Hence, prevascular tumours have low probability of metastisizing compared to their vascularised counterparts.

99
Q

How can angiogenesis factors be isolated?

A
  1. from endothelial cell cultures

2. implantation in the developing rabbit cornea, induces the production of new vessels

100
Q

Give examples of angiogenesis factors:

A

VEGF, Heparin, Angiogenin, TGFalpha & TGFbeta, acidic and basic fibroblast growth factor

101
Q

The process of angiogenesis is:

A
  1. Endothelial cell will generate new capillary branch
  2. Pseudopodial process guides the development of the capillary sprout as it grows into the surrounding connective tissue.
  3. Capillary sprout hollow out to form tube.
102
Q

What is hypoxia?

A

reduced oxygen levels in the tissues and a hallmark of solid tumours, it has important implications for tumour progression and a hypoxic environment can select for filter varients.

103
Q

What is the cellular response to hypoxia mediated by?

A

HIF-1 transcription factor

104
Q

What is the prognosis of a hypoxic tumour and why is are treatments ineffective?

A

Poor prognosis, radiation is ineffective and drugs often target dividing cells and hypoxic cells are non-dividing. Plus there are no blood vessls fro the drugs to reach the tumour.

105
Q

HIF-1alpha is…

A

inducible, it is produced all the time but rapidly degraded

106
Q

HIF-1beta

A

Is found in all cells, produced constitutively.

107
Q

How does hypoxia affect HIF (mechanism)

A

Hypoxia stabilises HIF-1alpha and allows it to bind to HIF-1bta which activates the transcription of angiogenesis factor such as VEGF. This stimulates neovascularisation and makes VEGF a new target for therapy.

108
Q

What are two anti-angiogenesis factors and when are they expressed in normal and tumour cells?

A

Thrombospondin-1
Angiostatin
Expressed in normal cells, overexpressed in tumour cells.

109
Q

Mutations in what genes cause increased angiogenesis factors?

A

proto-oncogenes

110
Q

mutations in what genes decreases anti-angiogenesis factors?

A

TSGs

111
Q

Effects of WT and mutant p53 on TSP-1

A

WT p53 increases TSP-1 and mutated p53 reduces TSP-1

112
Q

Steps for a tumour to become metstatic:

A
  1. Primary tumour size - production of new blood vessels
    a) Tumour is usually >1cm before metastisis
    b) Bigger tumour = more cells = more chance of mutation
    c) 1cm tum = 1 billion cells
  2. Invasion: including EMT
  3. Metastasis - cancer cells spread to other parts of the body, resistance to anoikis
113
Q

In the skin how does the tumour invade the Extracellular Matrix?

A
  1. Attachment to the ECM by cancer cells
  2. Local proteolysis, some cancer cells secrete proteases like collagenases
  3. Tumour cell locomotion into the region of ECM modified by proteolysis.
114
Q

EMT is at what front of the tumour and allows what?

A

the invasive front and allows greater mobility.

115
Q

What is tumour progression EMT characterised by?

A

Loss of E-cadherin

116
Q

Describe EMT:

A

Epithelial to mesenchymal transition plays a major role in cancer invasion and metastasis.
Epithelial has cell-cell adhesion and low motility
The transition to mesenchyme requires: ID of regulatory genes and development of inhibitors.
Mesenchyme cells have cell-matrix interaction, high cell motility and produce high levels of matrix.

117
Q

E-cadherin:

A

Sticks cels together, it is often lost in metastatic tumours. If you knock out E-cadherin, cells become malignant.

118
Q

Anoikis is:

A

A form of programmed cell death with is induced by anchorage-dependent cells detaching from the ECM. Metastatic cells are resistant to anoikis through increased expression of Bcl-2.

119
Q

What experimental model is used to show metastasis?

A

B16 mouse melanoma cell line and shows that metastasis occurs due to a genetic change due to injection of mouse with already metastatic tumour leading to a high frequency of metastatic tumours developing.

120
Q

What gene is expressed in non-metastatic tumours compared to metastatic tumours:

A

NM23 is not expressed in metastatic tumours. Discovered by making cDNA libraries.

121
Q

Only

A

Most are killed by:

  1. Mechanical sheer forces
  2. Loss of attachment and spreading leads to cell death
  3. Oxygen toxicity
  4. Destruction by host NK cells
122
Q

Why will a primary tumour often metastasise to a specific organ?

A

Easy access via circulation from the primary tumour

Some tumours require specific growth factors that are only present in certain tissues.

123
Q

Intravasion is:

A

When a tumour invades the surrounding tissue into the lymphatics or blood supply.

124
Q

Extravasion is:

A

When a tumour travels to a distant site

125
Q

Radiotherapy can target:

A

Only a solid tumour, shrinks primary or secondary tumours pre surgery, Reduces pain by shrinking the tumour. Radiotherapy on brain tumour is a toss up between local damage vs treatment.

126
Q

Chemotherapy:

A

Targets dividing cells in the whole body, hence dangerous side effects because all dividing cells are affected. Some side effects are manageable. Chemo will kill normal cells and is toxic to the bone marrow.

127
Q

Fluorocil (5FU)

A

Common chemo drug from breast, bowel, stomach, skin and gullet cancers. It is a pyramidine analogue and inhibits DNA synthesis in rapidly growing cells. Administered intravenously over several months and attacks the cell so it cannot become resistant. Rectal cancer treated with 5FU and radiation.

128
Q

Using monoclonal antibodies to treat cancer helps with:

A

Localisation of the tumour and cell type characterisation. Tumour with an undefined origin makes it difficult to treat.

129
Q

Different cell types contain intermediate filaments of distinct composition what are they and what cancer types do they appear in:

A

Intermediate filaments: epithelial cells/carcinomas
Neurofilaments: Neurons, neuroblastoma
Vimentin containing filaments: Fibroblasts, sarcomas + others
Vimentin and desmin: Muscle cells.

130
Q

CEA levels in blood are used for:

A

Monitoring early screening, early detection, response to cancer drugs and cancer recurrence.

131
Q

How do you measure the levels of CEA in serum?

A

Iodine labelled anti-CEA monoclonal antibody.

132
Q

Herceptin is:

A

A drug to treat breast cancers in which HER2 is overexpressed.

133
Q

HER2 has what kind of activity?

A

kinase activity and growth (increased in a subset of breast tumours)

134
Q

What type of drug is Herceptin?

A

A monoclonal antibody that blocks HER2 intrinsic kinase activity.

135
Q

How are oestrogen receptor positive breast cancers treated?

A

Tamoxifen

136
Q

What do OR+ breast cancer cells require?

A

Oestrogen to grow, tumour is “addicted to oestrogen”

137
Q

What does Tamoxifen do?

A

Inhibits oestrogen binding and therefore cancer cells may not survive. It is the standard endocrine therapy for hormone positive early breast cancer. It is also used in male breast cancers.

138
Q

Avastin is:

A

An angiogenesis factor inhibiter. It prevents new blood vessel growth thereby preventing tumour formation by blocking VEGF. It is used in advanced bowel cancer treatment. Has high monetary cost.

139
Q

Ricin Toxin is a natural toxin what is it struction:

A

A polypeptide and B polypeptide joined by a disulphide bond

140
Q

How does the ricin toxin work mechanistically?

A

The B chain binds the A chain to specific receptors on sensitive cells and the A chain then enters the cytoplasm and inhibits protein synthesis, killing cells

141
Q

How can ricin b modified to be a cancer targeting drug?

A

replace the B chain with an antibody specific to cancer cells. I.e. colorectal cancer cells express CEA. To give selective killing.

142
Q

How is toxicity from high dose treatments, to bone marrow removed?

A

Remove bone marrow before treatment and then reinsert it post treatment. But this results in high infection and if there are any cancer cells in the bone marrow then the patient will relapse.

143
Q

Using a high dose cancer treatment kills how many cells?

A

99.99% but this still means quite a few cells survive and need to remember cancer stem cells.

144
Q

How is the bone marrow reconstituted after cancer treatment?

A

Autologous treatment when the BM is removed pre treatment (if leukaemia or lymphoma, it will have infected cells so will need to be cleared of these cells before returning) this means that there is no rejection of the BM.

145
Q

What is the magic bullet process to purge the bone marrow in neuroblastoma?

A
  1. autologous BM transplant
  2. remove neuroblastoma cells from the BM
  3. neuroblastoma is a childhood cancer of specialised nerve cells called neural crest cells which are involved in the development of the nervous system and other tissues.
  4. Tumour cells are isolated and coated with mouse monoclonal anti-NB antibodies and then with a second layer of sheep monoclonal anti-mouse antibodies attached to a polystyrene magnetic microsphere.
  5. Tumour cells are removed by passing the cells through a pair of magnets. This removes 99.9% of the tumour cells from the patient.
146
Q

What is an allogenic bone marrow transplant?

A

Where the patient is given donor bone marrow from another individual to reduce the risk of cancer being reinserted. Host and donor have to histocompatibility antigen matched to prevent GVHD. GVHD occurs even in closely match donors. Use anti-T monoclonal antibodies + rabbit complement to prevent immune system priming by donor T cells.

CMP (5 decks)

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