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BOD > Cancer > Flashcards

Cancer Flashcards

1
Q

What kind of gene changes may cause cancer?

A
  1. Mutations
  2. Epigenetic changes
  3. Tumour viruses
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2
Q

What are malignant tumours?

A

Tumours capable of seeding cells into the circulation to form new colonies of tumour in other parts of the body

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3
Q

What is a metastasis?

A

New colony of cancer cells distinct from site of the primary cancer

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4
Q

What causes most deaths from cancer?

A

Metastasis

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5
Q

What are the distinguishing features of a benign tumour?

A
  1. Confined to original site in body
  2. Clearly defined boundaries
  3. Can be physically separated from surrounding tissue
  4. Surrounded by capsule of connective tissue, which can be peeled away
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6
Q

What are the distinguishing features of a malignant tumour?

A
  1. Ragged edges
  2. Infiltrates into surrounding tissue
  3. Grows into surrounding tissue
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7
Q

What is invasion?

A

Infiltration of malignant tumour into surrounding tissue

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8
Q

When might benign tumours be life-threatening?

A
  1. Menangioma putting pressure on brain

2. Hormone-producing tumours of pituitary or adrenal glands

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9
Q

What is the relationship between benign and malignant tumours?

A

Malignant tumours often progress from benign tumours

Not all benign tumours form malignant tumours

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10
Q

What are the clinically important sites of metastasis?

A
  1. Brain
  2. Liver
  3. Bone marrow
  4. Lung
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11
Q

Where do breast cancers often metastasise to?

A
  1. Lymph nodes

2. Bone

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12
Q

Where do colorectal cancers often metastasise to?

A

Liver

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13
Q

What is the nomenclature for a benign tumour?

A

Tissue name + -oma

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14
Q

What is lipoma?

A

Benign fat tumour

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15
Q

What is leiomyoma?

A

Benign smooth muscle tumour

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16
Q

What is papilloma?

A

Wart

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17
Q

What is adenoma?

A

Benign glandular lump

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18
Q

What is the nomenclature for a malignant tumour from mesenchyme?

A

Tissue name + sarcoma

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19
Q

What is osteosarcoma?

A

Malignant bone tumour

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20
Q

What is leiomyosarcoma?

A

Malignant smooth muscle tumour

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21
Q

What is the nomenclature for a malignant tumour from epithelium?

A

Tissue name + carcinoma

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22
Q

What is a nevus?

A

Benign mole

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23
Q

Give two examples of malignant neural tumours

A
  1. Neuroblastoma

2. Glioblastoma

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24
Q

What is leukaemia?

A

Liquid haemopoietic neoplasms

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25
Q

What is lymphoma?

A

Solid haemopoietic neoplasms

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26
Q

What is a neoplasm?

A
  1. Abnormal growth
  2. Irreversible
  3. Altered architecture
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27
Q

What is hyperplasia?

A

Increased proliferation

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28
Q

What is metaplasia?

A

Changed pattern of growth

Changed differentiation in tissue

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29
Q

What is dysplasia?

A

Abnormal pattern, such as mitoses in the wrong place

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30
Q

What occurs in metaplasia of the cervix?

A

Glandular epithelium of endocervix changes to squamous-like pattern

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31
Q

Where is squamous metaplasia observed?

A
  1. Cervix

2. Lung

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32
Q

What are the mechanisms by which cancer causes disease?

A
  1. Pressure
  2. Erosion/destruction of normal tissue
  3. Epithelial ulceration
  4. Competition with normal tissue
  5. Tumour-specific products
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33
Q

What is cachexia?

A

General, systemic wasting

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34
Q

What are some of the causes of death due to cancer?

A
  1. Failure of bone marrow in leukaemia
  2. Haemorrhage through lack of platelets
  3. Infection due to lack of neutrophils
  4. Liver failure
  5. Pain management
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35
Q

What are the most common types of cancers?

A

Malignant tumours from epithelium

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36
Q

How may a colorectal cancer present?

A
  1. Patient is anaemic due to chronic bleeding of ulcerated tumour
  2. Weight loss
  3. Altered bowel habit
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37
Q

How may a prostate cancer present?

A
  1. Ureter obstruction due to enlarged prostate
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38
Q

How may breast cancer present?

A
  1. Lump in breast

2. Bone pain or pathological fracture due to metastasis to bone

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39
Q

What are the four most common cancers?

A
  1. Breast
  2. Lung
  3. Prostate
  4. Bowel
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40
Q

How do cancers develop?

A

Successive evolution of clones that have a selective advantage over their neighbours

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41
Q

What is clonal expansion?

A
  1. A normal cell acquires a mutation/gene change
  2. Its progeny compete with neighbouring cells
  3. Progeny take up more than normal share of tissue
  4. One of progeny acquires further gene change that confers greater selective advantage

and so on

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42
Q

Why are cells in a tumour heterogeneous?

A

Tumour consists of preceding clones and clones that are dead-ends in the cancer evolutionary tree

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43
Q

What is the first known change in colorectal cancer?

A

Mutation in either APC gene or beta-catenin gene

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44
Q

What is the third change shown in colorectal cancer?

A

Mutation in either KRAS or BRAF

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45
Q

What is an oncogene?

A

Overactivity gain of function mutation

Dominant in cell

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46
Q

What is a tumour suppressor gene?

A

Loss of function mutation

Recessive in cell

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47
Q

What is p53?

A

Tumour suppressor gene

Significant effect seen even when only one copy is mutated as p53 forms a tetramer so most tetramers are faulty

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48
Q

What is Rb1?

A

Retinoblastoma protein

Tumour suppressor gene

Controls cell cycle

Inhibits initiation of DNA replication

Holds cycle at G1/S checkpoint

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49
Q

What is cyclin-dependent kinase 4?

A

Oncogene

Complexes with cyclin D1

Phosphorylates Rb1

Removes Rb1 inhibition

Allows progression through checkpoint

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50
Q

Which proteins inhibit CDK4?

A

p16

INK4A

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51
Q

What is the effect of genetic instability?

A

Cancers are more prone to undergo mutations than normal cells

Have defects in DNA machinery

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52
Q

What are the two types of genetic instability?

A
  1. Chromosomal instability

2. Sequence instability

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53
Q

What is chromosomal instability?

A

Loss of mechanisms that protect cell against chromosomal aberrations

Defects in DNA replication and mitosis

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54
Q

What is sequence instability?

A

Inactivation of DNA mismatch repair

Defects in DNA repair

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55
Q

What kind of mutations directly affect DNA synthesis?

A

Mutations in DNA polymerase proof-reading domain

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56
Q

What kind of mutations affect components in DNA repair mechanisms?

A

Inability to repair chemical damage, strand breaks, cross-links

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57
Q

What are the main categories of DNA repair?

A
  1. Dealing with damaged bases
  2. Mismatch repair
  3. DNA strand break and cross-link repair
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58
Q

How does mismatch repair work?

A

Deals with mismatched bases and small loops

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59
Q

How do mismatches occur?

A

Polymerases slip whilst trying to replicate repeat sequences, adding or deleting a copy of the repeat

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60
Q

What is the effect of persistent mismatches that are not repaired?

A

Shrinkage or expansion of microsatellites

Microsatellite instability

Higher point mutation rate

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61
Q

Which mutations cause defective mismatch repair in colon cancers?

A

Inactivation of MLH1 or MSH2

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62
Q

How is MLH1 inactivated?

A

Epigenetically

DNA methylation of promoter

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63
Q

How are DNA crosslinks repaired?

A

Fanconi anaemia pathway

Shares components with homologous recombination repair

Operates at damaged replication forks

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64
Q

What is the function of the Brca2 gene?

A
  1. Double-strand break repair

2. Cross-link repair

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65
Q

What kind of genetic instability is seen in Brca2-defective breast cancers?

A

Chromosome instability

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66
Q

What is the effect of defects in ATM?

A

ATM is one of damage-signalling proteins

Cells cannot detect damage as easily

Contributes to instability

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67
Q

What causes chromosome instability?

A
  1. Errors in chromosome segregation at anaphase - leads to lagging chromosomes
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68
Q

What is familial adenomatous polyposis?

A

Rare inherited predisposition to colon cancer

Individuals develop polyps in adolescence

High probability of polyps progressing to cancer

Colon usually removed

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69
Q

What is hereditory non-polyposis colon cancer?

A

Mutations in MLH1 or MSH2

AKA Lynch Syndrome

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70
Q

On which chromosome is the retinoblastoma gene located?

A

Chromsome 13

71
Q

What are the proliferation and survival changes seen in cancer cells?

A
  1. Independence of growth-stimulating signals
  2. Resistance to growth-inhibitory signals
  3. Differentiation block
  4. Resistance to apoptosis
  5. Immortality
72
Q

Give six examples of pro-proliferation signalling pathways

A
  1. Wnt pathway
  2. KRAS-BRAF-MAPkinase pathway
  3. PI3 kinase-Akt pathway
73
Q

What is the TGF-beta signalling pathway?

A

Growth inhibitory pathway

74
Q

What is the Wnt-signalling pathway?

A

Transmembrane receptor pathway

Mutated in almost all colorectal cancers

Mutation in APC, beta-catenin or Tcf transcription factor

Prevents degradation of beta-catenin by APC complex

75
Q

What is the role of beta-catenin?

A

Acts with Tcf

Interacts with APC

Drives cell proliferation and clonal expansion

76
Q

What are the pro-proliferative defects in Wnt-signalling?

A
  1. Inactivation of APC

2. Activation of beta-catenin

77
Q

Which receptors are included in the ERBB/EGF receptor family?

A
  1. ERBB/EGF receptor

2. ERBB/HER2 receptor

78
Q

What is the target of herceptin?

A

HER2 receptor

79
Q

What are the two downstream signalling pathways for ERBB family signalling?

A
  1. Ras and Raf to MAPkinase

2. PIP3 pathway

80
Q

What is the role of the enzyme PTEN?

A

Dephoshorylates PIP3 to PIP2

Reverse of effect of PI-3-kinase

Tumour suppressor gene

81
Q

What is the role of PIP3?

A

Activates AKT kinases

Inhibits apoptosis

Acts on BAD

82
Q

What is the TGF-beta pathway?

A

Growth inhibitory pathway for epithelial cells

Signal via transmembrane receptor to SMAD family

Mutations in TGFbetaRII, SMAD4 or SMAD2 lead to cancer

Tumour suppressors

83
Q

In which cells can leukaemias arise?

A
  1. Fully differentiated lymphocytes

2. Stem cells

84
Q

How does acute leukaemia develop?

A

From myeloid/lymphoid precursors

Differentiation is blocked

More aggressive

85
Q

How does chronic leukaemia develop?

A

From differentiated myeloid/lymphoid cells

Shows differentiation

Less aggressive

86
Q

What is myeloma?

A

Cancer of fully differentiated B cells

87
Q

How is proliferation limited in lymph nodes?

A

Apoptosis balances proliferation during somatic mutation in the germinal centre of the lymph node

88
Q

What is BAX?

A

Major mediator of apoptosis

Upregulated by p53

Antagonises Bcl2

Mediates permeabilisation of mitochondrial membrane and activation of caspases

89
Q

What is senescence?

A

Cell cycle arrest after a fixed number of cell divisions

Hayflick’s limit

Escaped by tumour cells

90
Q

What controls Hayflick’s limit?

A

Telomere length

91
Q

What are telomeres?

A

Repeat structures at the ends of chromosomes - TTAGGG

Loop

Shortened at each cell division

92
Q

What is telomerase?

A

Reverse transcriptase enzyme that restores telomeres in the germ line

Copies RNA template

Turned on in most cancers

93
Q

How is telomerase activated in tumours?

A
  1. Point mutations in promoter

2. Translocated next to strong promoter following chromosome rearrangement

94
Q

Give some examples of signals that cause cell stress responses

A
  1. Shortening of telomeres
  2. DNA damage
  3. Strong activation of oncogenes
95
Q

What is oncogene-induced senescence?

A

Cells with activated oncogenes become senescent

96
Q

How are stress responses alleviated?

A
  1. Mutation of p53

2. Mutation of RB1

97
Q

How do viruses overcome senescence?

A

Produce proteins that bind and inactivate p53 and RB1

Eg. HPV that causes cervical cancer

98
Q

How does metastasis occur?

A
  1. Escape of cells into vessels
  2. Survival in circulation
  3. Escape out of vessels
  4. Survival and growth of new tumour
99
Q

What is the major barrier to metastasis?

A

Survival and growth at distant site

Very inefficient

100
Q

What is angiogenesis?

A

Sprouting of new blood vessels to provide blood supply to tumour

101
Q

Give two factors that control transcription

A
  1. Transcription factors

2. Chromatin modifiers

102
Q

What is MYC?

A

Oncogene

Transcription factor

Powerfully upregulates genes involved in proliferation

103
Q

What is ERG?

A

Transcription factor

Controls proliferation

104
Q

What are chromatin modifiers?

A

Proteins that modify histones to turn genes on or off

105
Q

What is MLL?

A

Histone methylase

106
Q

What occurs to E-adhesin in breast cancer?

A

It is inactivated

107
Q

Which TCA enzymes are notably mutated in cancer?

A

Isocitrate dehydrogenase 1

Mutated in glioblastoma and leukaemia

May interfere indirectly with DNA methylation

108
Q

What is chromosome translocation?

A

Pieces of two different chromosomes are joined to each other following breakage of DNA or an accident during DNA replication

109
Q

What are indels?

A

Small insert or deletion

Usually results in frameshifting

110
Q

What is Ras?

A

G-protein

Activated by GTP-binding and inactivated by hydrolysis of GTP to GDP

Mutations block hydrolysis

Some mutations block access to GTPase to active site

111
Q

In which cancers is BRAF notably mutated?

A
  1. Melanoma

2. Colorectal carcinoma

112
Q

What is the commonest BRAF mutation?

A

Val to glu at position 600

Adjacent to activating phosphorylation site

Negative charge of glu mimics phosphorylation so causes activation

113
Q

In which cancers is PI3K catalytic subunit notably mutated?

A

Breast cancers

114
Q

What is a gene fusion?

A

Joining two genes together to create a new gene

Potentially the most powerful kind of cancer mutation

115
Q

Which gene fusion is associated with chronic myeoloid leukaemia?

A

BCR-ABL

Philadelphia chromosome

Chromosomes 9 and 22

116
Q

What is the effect of the BCR-ABL gene fusion?

A

ABL is a tyrosine kinase

N terminus of BCR forms dimers and replaces regulatory N terminus of ABL, activating ABL

BCR has stronger promoter than ABL

117
Q

In which stage of mitosis are cells arrested for karyotyping?

A

Metaphase

118
Q

Which fusion gene is found in 50% of prostate cancers?

A

TMPRSS2-ERG

Formed by deletion between these two genes

119
Q

What is amplification?

A

Cell acquires large numbers of an oncogene after repeated duplication of a segment of the genome

120
Q

Give some examples of amplified genes

A
  1. Cyclin D1

2. ERBB2/HER2

121
Q

Which technique can be used to detect amplification?

A

FISH

Fluorescence in-situ hybridisation

122
Q

Which genes are inactivated by genome modification?

A
  1. MLH1 (mismatch repair)

2. E-cadherin (cell adhesion)

123
Q

What is Bcl2?

A

Oncogene

Anti-apoptosis protein

Upregulated by chromosome translocation in some lymphomas

124
Q

What is BRAF?

A

Oncogene

Downstream of Ras

Found mutated in melanomas

Activated by gene fusion

125
Q

What is cyclin D1?

A

Oncogene

Controls Rb1 with CDK4

Activated by amplification in breast cancer

126
Q

What is the ERBB family of receptors?

A

Family of receptor tyrosine kinases

Includes EGFR and HER2

HER2 is target for herceptin

127
Q

What is ERG?

A

Oncogene

Transcription factor

Involved in gene fusions in prostate cancer

128
Q

What is MLL?

A

Oncogene

Histone methyl transferase

Modifies histones

Fused by translocation in leukaemias

129
Q

What is the MYC family?

A

Oncogenes

Family of transcription factors

Highly amplified

130
Q

What is PI3CA?

A

Catalytic subunit of PI3 kinase

Mutated in breast and colorectal cancers

131
Q

What is the Ras family?

A

Oncogenes

G proteins that carry signals from growth factors to nucleus

Activate MAPkinase pathway

132
Q

What are TCF3 and TCF4?

A

Oncogenes

Downstream of Wnt pathway

Gene fusions occur in colon cancer

133
Q

What is APC?

A

Tumour suppressor gene

Large cytoplasmic protein that interacts with beta-catenin

Inactivated in most colon carcinomas

134
Q

What is BRCA1?

A

Tumour suppressor gene

Component of DNA repair

Mutation associated with hereditary breast cancers

135
Q

What is BRCA2?

A

Tumour suppressor gene

Component of homologous recombination repair

Mutation associated with hereditary breast cancers

136
Q

What is INK4A/p16?

A

Tumour suppressor genes

Inhibitors of CDKs

Often deleted

137
Q

What are MLH1 and MSH2?

A

Recognition proteins of mismatch repair complex

Mutation in some colon cancers

138
Q

What is p53?

A

Nuclear protein that arrests cell cycle in cases of DNA damage and other insults

139
Q

What is PTEN?

A

Phosphatase that antagonises PI3KCA

140
Q

What is SMAD4?

A

Carries inhibitory signals in the TGF-beta signalling pathway

Mutated in some colon cancers and other cancers

141
Q

What is the TGF-beta family?

A

Inhibitory growth factors that regulate the differentiation of cells

142
Q

What are mutagens?

A

Agents that directly damage DNA

Eg. chemicals and radiation

143
Q

What are promoters?

A

Non-mutagenic agents that increase the effects of mutagens

144
Q

What is the best known promoter?

A

TPA

145
Q

What is aflatoxin?

A

Most potent mutagenic carcinogen

146
Q

What is TPA?

A

Promoter

Comes from seeds of tropical plant Croton tiglium

Mimics DAG, agonist for PKC

147
Q

What is a risk factor for breast cancer?

A

Risk proportional to interval between menarche and first pregnancy for childbearing women

148
Q

What are the causes of cancer?

A
  1. Mutagens
  2. Promoters
  3. Tumour viruses and other infections
  4. Chronic irritation
  5. Spontaneous error
149
Q

What is the principal effect of UV radiation?

A

Photoactivation of pyrimidine residues

Form dimers where two thymines or one thymine and one cytosine occur sequentially

Disrupts base pairing

150
Q

How is UV damage repaired?

A

Base excision repair

151
Q

Which condition is at particular risk from UV damage?

A

Xeroderma pigmentosa

Lack base excision repair machinery

152
Q

How are carcinogens activated in the body?

A

By metabolism

Enzymes that detoxify lipid-solube molecules for excretion by the body

153
Q

How is β – napthylamine activated?

A

Hydroxylation

154
Q

How is β – napthylamine made harmless?

A

Made soluble

Conjugated with glucuronic acid

155
Q

Where does β – napthylamine act?

A

Bladder tissue in man

Where glucuronic acid conjugate is removed by glucuronidase

Only a carcinogen in species that express glucuronidase in the bladder

156
Q

Where does aflatoxin come from?

A

Produced by Aspergillus flavus

Grows on peanuts in warm, humid conditions

157
Q

What are aristolochic acids?

A

From aristolochia plant

Carcinogens

Cause kidney toxicity and kidney and liver cancer

158
Q

What is the effect of asbestos inhalation?

A

Small fibres penetrate deep into lung

Cause chronic inflammation and affect cell turnover

Cause mesothelioma in lining of pleural cavity

159
Q

What is ionising radiation?

A
  1. X-rays
  2. γ rays
  3. β particles
  4. α particles
160
Q

How does ionising radiation damage DNA?

A

Produces free radicals and ions as it passes through tissue

These are highly reactive and subsequently alter the structure of bases or cause strand breaks

161
Q

What kind of damage do alpha particles cause?

A

Double strand breaks

Multiple chemical changes

Due to larger size

162
Q

What kind of damage do gamma rays cause?

A

Leave scattered ions and radicals

Only damage one residue on one strand of DNA molecule

Usually repairable

163
Q

How do infections cause cancer?

A
  1. Viruses bring oncogenes into genome

2. Chronic inflammation

164
Q

How does HPV cause cancer?

A

Produces E6 and E7 proteins

Inactivate p53 and Rb1

165
Q

Which virus causes cervical cancer?

A

High risk HPV

166
Q

Which virus causes nasopharyngeal carcinoma and Burkitt’s lymphoma?

A

Epstein-Barr virus

167
Q

Which virus causes hepatocellular carcinoma?

A

Hepatitis B virus

168
Q

Which virus causes Kaposi’s sarcoma?

A

Human herpesvirus 8

169
Q

Which virus causes T-cell leukaemia and lymphoma?

A

Human T-cell lymph trophic virus type 1 (HTLV1)

170
Q

What is HTLV1?

A

T-cell tropic retrovirus

171
Q

What kind of cancer is associated with schistosome infection?

A

Bladder

172
Q

What kind of cancer is associated with H. pylori infection?

A
  1. Gastric adenocarcinoma

2. MALT lymphoma

173
Q

When do promoter molecules cause cancer?

A

After exposure to initiator mutagen, not before

BOD (8 decks)

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