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BOD > Cancer > Flashcards

Cancer Flashcards

1
Q

How many gene changes are needed to cause cancer?

A

5/10/15

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2
Q

Definition of malignancy?

A

Ability to grow in an alien environment

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3
Q

Where do carcinomas often migrate?

A

Lymphatics

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4
Q

What specific effects are there from lung tumours?

A

ACTH, ADH

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5
Q

What part of the cervix does papilloma virus infect?

A

Columnar to glandular junction

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6
Q

Which molecules receive signals from the basement membrane to tell cells to stop dividing in that plane?

A

Integrins

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7
Q

Why does clonal evolution occur?

A

Neighbouring cells have the same mutations

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8
Q

Which transition does Rb control?

A

G1/S

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9
Q

What inactivates Rb?

A

CDK4 and CyclinD1

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10
Q

What inhibits CDK4 and CyclinD1?

A

p21 and p16

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11
Q

What does E2F control transcription of?

A

S phase genes

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12
Q

Which mutations are dominant?

A

Oncogenes

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13
Q

Which mutations are recessive?

A

Tumour suppressor

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14
Q

How does p53 bind?

A

As a tetramer

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15
Q

Which phase does p53 act in?

A

S

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16
Q

What stabilises p53?

A

Mutant DNA

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17
Q

Which pathway are BRCA1/2 involved in?

A

Homologous repair

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18
Q

Which kind of instability does BRCA1/2 result in?

A

Chromosomal

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19
Q

Which cancer has mutations in DNA polymerase epsilon?

A

Colon

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20
Q

What do microtubule kinetophores monitor?

A

Lagging chromosomes

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21
Q

What do microtubule kinetophores inhibit?

A

APC

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22
Q

What happens when the lagging chromosomes align?

A

Anaphase promoting complex

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23
Q

Which drug selects for resistant cancer?

A

Cis-platin

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24
Q

How do cells reactivate BRCA2?

A

Compensatory frameshift mutation

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25
Q

Why is APC rare?

A

Patients die at reproductive age

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26
Q

What mutation causes Lynch syndrome?

A

Mismatch repair gene

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27
Q

What do patients get if retinoblastoma does not develop?

A

Sarcoma

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28
Q

What do Wnt receptors inhibit?

A

APC degradation complex

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29
Q

What does APC degradation complex activate?

A

Beta catenin

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30
Q

What does beta catenin activate?

A

TCF4

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31
Q

Where is TCF4 located?

A

Nucleus

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32
Q

What does EGF receptor activate?

A

Ras, PI3KCA

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33
Q

What does the TGF beta receptor activate?

A

SMADs

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34
Q

How do SMADs affect proliferation?

A

Inhbiit

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35
Q

What happens to the TGF receptor II in cancer?

A

Inactivated

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36
Q

How is stem cell compartment expanded in APC?

A

Wnt pathway activation or knocking out APC

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37
Q

What does BAX inhibit?

A

BCL2

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38
Q

How does BAX act?

A

Dimerises

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39
Q

What repeats are in telomeres?

A

TTAGGG

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40
Q

How much do telomeres shorten per cell cycle?

A

100bp

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41
Q

What is TERT?

A

The telomerase gene

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42
Q

What is the most mutated gene in human cancer?

A

p53

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43
Q

Which kinases detect DNA damage?

A

ATM/ATR

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44
Q

Which p protein does p53 activate?

A

p21

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45
Q

Which pathway does p21 inhibit?

A

Rb pathway

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46
Q

What mediates p53 degradation?

A

mdm2

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47
Q

What blocks mdm2?

A

p14

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48
Q

How does glycolysis change in cancer cells?

A

Upregulates

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49
Q

Which Krebs cycle enzyme gets point mutations?

A

Isocitrate dehydrogenase

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50
Q

What does the Krebs cycle produce which interferes with DNA methylation?

A

Hydroxyglutarate

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51
Q

Which cancers have isocitate DH mutations?

A

Leukaemias and glioblastomas

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52
Q

How does site on injection affect metastasis of a tumour cell?

A

No effect

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53
Q

What is the inefficient step in metastasis?

A

Survival after extravasation

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54
Q

Which kind of mutations give cell a selctive advantage?

A

Driver mutations

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55
Q

Which mutations don’t affect cancer development?

A

Passenger mutations

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56
Q

What does ERG control?

A

Differentiation

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57
Q

Which genes does MYC turn on?

A

Cell cycling

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58
Q

What do beta-catenin, TCF4, p53, MYC and ERG all control?

A

Chromatin modification

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59
Q

What is MLL?

A

A histone lysine methyltransferase

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60
Q

Which cancers have MLL?

A

Chromosome translocations in leukaemias

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61
Q

Which protein holds epithelial cells together?

A

E-cadherin

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62
Q

How is E-cadherin inactivated?

A

Methylation of promoter DNA

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63
Q

Which sequencing is used to find small scale mutations?

A

Illumina

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64
Q

Which mutations is Illumina good for?

A

Ras/Raf

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65
Q

Which mutations is illumina not good for?

A

Indels

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66
Q

Which chromosomes are involved in CML?

A

9-22

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67
Q

Which technique is used to see amplifications?

A

FISH

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68
Q

What is amplified in glioblastoma?

A

EGFR

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69
Q

What is deleted in glioblastoma?

A

p16

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70
Q

What is measured to see deletions and amplifications?

A

Copy number

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71
Q

Why is B-RAF duplication activating?

A

Fuses with highly active neighbour gene

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72
Q

What kind of receptor is ABL?

A

Tyrosine kinase

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73
Q

What controls the ABL gene?

A

N-terminal regulatory domain

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74
Q

Which kind of cancers have fusion genes?

A

Epithelial

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75
Q

What forms insertions in some tumours?

A

LINE1 retrotransposons

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76
Q

What does a transformation assay show?

A

Transformation by a transforming oncogene

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77
Q

What can be used to remove the tumour suppressor gene between two “lox” genes?

A

Cre recombinase

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78
Q

What does TPA mimic?

A

DAG

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79
Q

What does DAG activate?

A

PKC

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80
Q

What causes a thymidine dimer?

A

UV light

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81
Q

What is the structure of beta naphthylamine?

A

Aromatic amine

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82
Q

What is the structure of dimethyl nitrosamine?

A

Nitrous acid and amine

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83
Q

Where is dimethyl nitrosamine from?

A

Meat

84
Q

Why does benzopyrene cause cancer if it is inert?

A

It is activated

85
Q

What do hydratases, P450 monoxygenases, and sugar concentration do?

A

Increase solubility to aid excretion

86
Q

Which carcinogen does benzopyrene form?

A

Epoxide

87
Q

Where is beta naphthylamine inactivated?

A

Liver

88
Q

Why does NMU cause mammary tumours in puberty?

A

Dividing cells more susceptible

89
Q

Which Aspergillus toxin causes liver toxicity and cancer?

A

Aflatoxin

90
Q

Which Aristolochiaceae acid causes kidney toxicity, UTUC

A

Aristolochic acid

91
Q

How is aflatoxin activated?

A

Oxidation

92
Q

What is aflatoxin activated to?

A

An epoxide

93
Q

What is the base change in UV light?

A

C to T

94
Q

What is the base change in smoking?

A

C to A

95
Q

What base change does aristolochic acid cause?

A

CT to CA

96
Q

What does the Ames test measure?

A

Histidine biosynthesis defect

97
Q

What does a high LET track show?

A

Alpha particle

98
Q

What does a low LET track show?

A

Gamma wave

99
Q

What is radiation dose measured in?

A

Grays energy absorbed

100
Q

What is the quality factor for x-rays?

A

1

101
Q

What is the quality factor for alpha particles?

A

20

102
Q

How do you work out Sieverts?

A

Gray x quality factor

103
Q

Which cancers does EBV cause?

A

Burkitt’s lymphoma and nasopharyngeal carcinoma

104
Q

Which cancer does HBV cause?

A

Hepatocellular carcinoma

105
Q

Which virus causes Kaposi’s sarcoma?

A

HHV8

106
Q

Which virus causes T cell leukaemia or lymphoma?

A

HTLV1

107
Q

What is the most important treatment in cancer therapy?

A

Surgery to remove primary tumour

108
Q

What % of testicular cancers does cisplatin cure?

A

70-90%

109
Q

Which pathways do PARP inhibitors target?

A

DNA repair

110
Q

How does PARP recruit repair systems?

A

Binds to strand break and adds ADP-ribose string

111
Q

Why can’t PARP inhibitors work at replication forks?

A

Needs BRCA2

112
Q

What does Glivec bind?

A

ABL kinase

113
Q

What does Vemurafenib inhibit?

A

B-RAF

114
Q

What % of patients does vemurafenib work in?

A

80%

115
Q

How does vemurafenib resistance develop?

A

Ras amplifications or mutations

116
Q

What are the oncolytic adenoviruses and what do they inactivate?

A

Onyx-O15 and H101, Rb1 and p53

117
Q

What does E1A inhibit?

A

RB1

118
Q

What does E1B55k inhibit in engineered adenoviruses?

A

p53

119
Q

If the E1B55k protein is removed, which are the only cells a cytolytic virus can replicate in?

A

p53-mutant

120
Q

How does the acquired immune system affect non-viral cancers?

A

None

121
Q

What could be downregulated to increase cytotoxic T cell killing?

A

CTLA-4 and PD-1

122
Q

What was the survival increase in patients who has peripheral tolerance downregulated?

A

11%

123
Q

Which cancers can be treating by peripheral tolerance downregualtion?

A

Melanoma and lung

124
Q

Which patients have a better response to peripheral tolerance downregulation?

A

Those with more mutations

125
Q

How many Rb-1 copies must be mutated for cancer?

A

Both

126
Q

Which chromosome is Rb-1 on?

A

13

127
Q

Which virus binds and inactivates Rb-1?

A

HPV

128
Q

Which chromosome are APC/beta-catenin found on?

A

5

129
Q

How is APC activated?

A

Preventing degradation by point mutation the domain which degradation machinery bind to

130
Q

What do mutations induce in APC?

A

Stop codon

131
Q

What is the third change in colorectal cancer?

A

KRAS/B-ARF

132
Q

What is the commonest mutation in KRAS/B-RAF?

A

Valine to glutamic acid and position 600

133
Q

What does teh KRAS/B-RAF cause glutamic acid cause activation?

A

Mimics phosphorylation

134
Q

What is the anti-Ras drug?

A

None

135
Q

How many K-RAS copies are usually mutated?

A

Only one

136
Q

How is MLH1 inactivated?

A

Epigenetic methylation

137
Q

What is the usual mutation in PIK3CA?

A

Negatively charged amino acid to positively charged

138
Q

Which positions in PIK3CA are missense mutations?

A

542, 545, 901, 907, 1047

139
Q

What does PTEN reverse the action of?

A

PIK3CA

140
Q

What does herceptin target?

A

EGFR and ERBB2

141
Q

How many new insertions do LINE1 retrotransposons form?

A

10-1000

142
Q

What % of colon cancer have loss of mismatch repair?

A

15%

143
Q

Most common cause of loss of mismatch repair?

A

Methylation

144
Q

What happens to promoters at high doses?

A

Saturates

145
Q

Which protein normally forms dimers or oligomers?

A

BCR

146
Q

Which pathway signals through Smad4?

A

TGFbeta

147
Q

What normally happens to Kras?

A

Point mutation

148
Q

Is p16 oncogene or tumour suppressor?

A

TSG

149
Q

Is SMAD4 an oncogene or tumour suppressor?

A

TSG

150
Q

What is cachexia?

A

Systemic wasting

151
Q

What inhibits CDK4 and CyclinD1?

A

p16/INK4A

152
Q

How many copies of oncogenes must be mutated?

A

1 (dominant)

153
Q

How many copies of TSG must be mutated?

A

Both (recessive)

154
Q

What is a microsatellite?

A

Shrinkage or expansion of short repeats caused by mismatch repair deficiency

155
Q

What is rate of increase of small mutations in colon cancers which are mismatch repair defective?

A

100x

156
Q

Which kind of mutations do TGFbetaRII and Bax get?

A

Frameshifts

157
Q

What is genetic cause of HNPCC/Lynch syndrome?

A

Mismatch repair defect

158
Q

Which phase does HR operate in?

A

G2

159
Q

What does BRCA1 do?

A

Switches on HR

160
Q

What does BRCA2 do?

A

Prepares single strand ends for base pairing to the other helix

161
Q

Are inherited mutations normally oncogene or TSG?

A

TSG

162
Q

How many women have a BRCA mutation?

A

1 in 500

163
Q

What % of spontaneous colon cancer patients have a APC mutation?

A

80%

164
Q

What is lifetime cancer risk in BRCA1/2?

A

40-80%

165
Q

What do the Wnts signal by?

A

Beta-catenin

166
Q

What do AKt kinases act on to inhibit apoptosis?

A

BAD

167
Q

What is the effect of the TGFbeta pathway on growth?

A

Inhibitory

168
Q

Which TGFbetaRII components are mutated in colon cancer?

A

SMAD4 and SMAD2

169
Q

Which kinases does PIP3 activate?

A

Akt

170
Q

Which cell type does myeloma arise from?

A

Plasma cells

171
Q

What happens to the crypt region in APC?

A

Expands

172
Q

How many divisions are usually permitted?

A

50-100

173
Q

Which viruses inhibit p53?

A

HPV and adenovirus

174
Q

What mediates oncogene activation of p53?

A

p14

175
Q

How many cancers have p53 mutation?

A

1/3

176
Q

Is there a special metastatic subpopulation?

A

No

177
Q

Two kinds of translocations?

A

Unbalanced or reciprocal

178
Q

What does CGH hybridisation look for?

A

Deletion and amplification

179
Q

What kind of protein is RAS?

A

G protein

180
Q

Which kindof cancers have BRAF mutations?

A

Melanomas

181
Q

What is the most frequent mutation found in breast cancer?

A

PIK3CA

182
Q

Which kind of mutations are many APC mutations?

A

INDELS

183
Q

WHich tumour suppressirs are often deleted?

A

PTEN and p16/INK4

184
Q

WHich gene is amplified in lung cancer?

A

MYC

185
Q

What can BRAF be fused to in pediatric brain tumours?

A

KIAA1549

186
Q

What does the BCR do to the ABL kinase?

A

N terminus removed to holds it activated in dimers or oligomers

187
Q

Which gene encodes Cyclin D1 and which cancer is it amplidied in?

A

CCND1, breast

188
Q

What do promoters behave like?

A

Drugs

189
Q

What does chronic inflammatiom behave like?

A

A drug

190
Q

Do promoters work alone?

A

No - only after initiation which causes DNA damage

191
Q

Is cigarette smoke a promoter or initiator?

A

Both

192
Q

What do people with xeroderma pigmentosum lack?

A

Excision repair

193
Q

How is beta-napthylamine activated?

A

Hydroxylation

194
Q

What is added to beta-naohthylamine to make is harmless?

A

Glucuronic acid

195
Q

What is the most powerful promoter known?

A

TPA

196
Q

What cannot be tested for in animals?

A

Promoters

197
Q

Which PV proteins inactivate p53 and/or Rb?

A

E6 and E7

198
Q

In which areas do people get Burkitt’s lymphoma?

A

Malaria endemic

199
Q

Which enzym does single strand repair require?

A

PARP

200
Q

What does imatinib bind to?

A

ATP bindign region in the inactive conformation

201
Q

What is the mutation for imatinib resistance?

A

Removes hydrogen bonding site for the drug

202
Q

What domain does vemurafenib target?

A

ATP binding

203
Q

What kind of cancer is vemurafenib used in?

A

Melanomas

204
Q

How does CTLA-4 downregulate T cells?

A

Compete with CD28 by binding B7

205
Q

What are the first cancers to respond to immune checkpoint inhibitors?

A

Most mutations so the highest number of alien peptides

BOD (7 decks)

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