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ACVIM lectures Flashcards

1
Q

What is the warburg effect?

A

aerobic glycosis

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2
Q

T/F Cancer cells stop using oxidative phosphorylation in favor or glycosis

A

False- they continue to do same amount of oxidative phos AND additionally use glucose for glycolysis

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3
Q

What is another substance that can be used for energy creation?

A

glutamine

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4
Q

What effects dose lactate have on the tumor microenvironment?

A
  • immune suppression/escape (impact APC, increase Tregs)
  • enhance angiogensis (increased VEGF/IL8)
  • enhance tumor cell migration/invasion (ECM/integrins)
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5
Q

What impact does lactate have on patient outcome?

A

high lactate- worse outcome

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6
Q

TKTL1 activity correlates to what activity of glycolysis?

A

increased so higher activity worse outcome (eval in mammary tumors once)

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7
Q

18F-FDG-PETCT is sensitive or specific?

A

sensitive

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8
Q

2-DG (inhibits glycolysis) results in what changes in invasion and metastasis?

A

reduced - possibly due to reduced cathepsin levels (which degrades ECM)

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9
Q

Cancer stem cells can do what actions?

A

initiate and maintain tumor growth and produce heterogenous tumor population

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10
Q

What is symmetric cell division with stem cells?

A

two identical daughter cells

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11
Q

What is asymmetric cell division in stem cells?

A

stem cell and more differentiated progenitor cell (limited self renewal and lead to terminal differentiation)

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12
Q

What are common stem cell markers via flow?

A

CD34, CD133, CD44

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13
Q

T/F There are specific markers that differentiate normal from cancer stem cells

A

false

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14
Q

What therapies are CSC more resistant to?

A

RT and chemo

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15
Q

CSC have dysregulation in DNA repair via what mechaanisms?

A

p53, MDM2, gammaH2AX

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16
Q

Inhibition of EGFR in CSC can lead to what response?

A

increased sensitivity to chemotherapy and radiation

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17
Q

What is dedifferentiation?

A

loss of lineage committment and stem cell feature increase

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18
Q

what is transdifferentiation?

A

change from one lineage (differentiated) to another

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19
Q

Exposure of diff cell to OCT4, cMyc, SOX2, KLF4 results in what?

A

pluripotent stem cell production

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20
Q

Hypoxia and subsequent HIF1 alpha production upregulates ___ and ____ which can promote dedifferentiation

A

Oct4 and Nanog

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21
Q

ZEB, SNAIL, SLUG, TWIST transcription factors help to induce what process?

A

EMT

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22
Q

What metabolic processes do CSC utilize?

A

either! plastic with ox phos and aerobic glycolysis and can switch

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23
Q

what is metformin and how is it used in cancer research/therapy?

A

antidiabetic drug and blocks mitochondrial functon

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24
Q

PGE2 mediates what inflammatory processes and cancer processes?

A

EGFR/VEGFR: proliferation, migration, angiogensis, mets
BCL-2NFkB - apoptosis inhibition
IL12 - immune suppression
MMP2/9 - mets/invasion

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25
Q

T/F PGE2 is a negative regulator of hematopoietic stem cell growth and development

A

False- PGE2 increases it

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26
Q

Rituximab targets what?

A

CD20

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27
Q

Herceptin targets what?

A

HER2

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28
Q

Avastin targets

A

VEGF

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29
Q

what is phenotype drug discovery?

A

look for change in cell/tumor then find target later

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30
Q

What is target based drug discovery?

A

ID target and create drug then test on tumor

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31
Q

T/F high throughput screening typically results in a drug

A

False- then look at hits and look for leads within those to confirm, increase potency/selectivity, reduced tox etc and then lead optimize the drug

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32
Q

what are the 4 types of ab formulations?

A
  • Mouse
  • chimeric
  • caninized
  • fully canine
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33
Q

what are three main methods for creation of monoclonal ab?

A

Hybridoma (using mouse)
phage display
transgenic mouse

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34
Q

What is time to development of animal health drug and how many early phase drugs make it to market?

A

6-8 years

1 in 10 drugs

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35
Q

what is fractional cell kill hypothesis?

A

drug kills constant fraction of cell population (independent # of cells)

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36
Q

overall results of chemo tx depends on what two conditions?

A

drug dose and number/freq of tx cycles

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37
Q

what two drug classes are impacted by rate of cell growth (don’t work as well in tumors with non cycling cells)?

A

antimetabolites and antitumor antibiotics

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38
Q

what are benefits of initial tumor debulking in drug sensitiivty?

A
  • smaller # starting cells (fractional cell kill)
  • improved O2 delivery
  • recruit quiescent cells to cycle
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39
Q

What are most common sites of alkylation for alkylators and end result?

A

N7 and O6 guanine and result in strand breakage when repair attempted

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40
Q

What DNA substitution occurs with alkylation of N7 guanine?

A

C to T (due to modified guanine)

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41
Q

what class of alkylators lead to crosslinks?

A

bifunctional

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42
Q

What are the nitrogen mustards (5)?

A 
cytoxan
ifosfamide
mechlorethamine
chlorambucil
melphalan
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43
Q

What nitrogen mustards must be activated by P450?

A

cyotxan and ifosfamide

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44
Q

how does melphalan enter cells?

A

charged and hydrophilic so requires active uptake via AA transporter - via leucine transporter)

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45
Q

what are nitrosurea?

A

CCNU

BCNU

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46
Q

what are methylating agents?

A

procarb
dacarab
TMZ

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47
Q

what other action does procarbazine have and what is main lesion caused by it?

A

MAO

O6

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48
Q

what is main lesion for methylating aklyators?

A

O6

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49
Q

What alkylators cross BBB?

A

CCNU and TMZ

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50
Q

What is the role of methylguanine methyltransferase?

A

repair O6 alkylation

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51
Q

MMR overexpression or underexpression leads to resistance to alkylators?

A

underexpression

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52
Q

T/F ifosfamdie is given in single fractions because its metabolism can become saturated

A

False - given as multiple doses bc of saturation which reduced efficacy

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53
Q

Is doxorubicin or metabolite doxorubicinol more cardiotoxic?

A

Doxorubicinol

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54
Q

interaction of topo II and doxorubicin leads to what?

A

formation of cleavable complex - so unable to ligate the DS breaks created by topo II

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55
Q

what is MOA of actinomycin D?

A

intercalation DNA (in GC regions) and inhibition of RNA/protein synthesis

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56
Q

What is MOA of bleomycin?

A

binds to Fe intracellularly (Cu extracellularly) and then binds O2 and then cleaves DNA (up to 4/complex)

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57
Q

up or down regulation of TopoII alpha leads to resistance to dox?

A

downregulation

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58
Q

T/F Antimetabolites have high rate of secondary cancer

A

false b/c doesn’t bind to DNA

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59
Q

What MTX form has most activity

A

MTX polyglutamates (also traps inside cell)

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60
Q

What are the cytidine analogs?

A

cytarabine and gemcitabine

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61
Q

what are actions of cytarabine?

A

inhibition DNA polymerase alpha and incorporate into DNA leading to chain elongation

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62
Q

gemcitabine has what actions?

A

inhibits RNR, incorporates into DNA, inhibits DNA polymerase

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63
Q

gemcitabine metabolites increase or decrease kinase enzyme actions?

A

increases - so more active drug made

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64
Q

What are actions of 5-FU?

A

inhibits DNA/RNA synthesis via incorporation and TS inhibition

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65
Q

what enzyme metabolizes 5-FU?

A

DPD

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66
Q

what is metabolism process of Rabacfosadine?

A

hydrolysis
deamination (RL step)
phosphorylation to PMEGpp (analog of dGTP)

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67
Q

what is action of Rabacfosadine?

A

competitive inhibitor DNA polymerase alpha, deta, episolon and incorporated into DNA

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68
Q

Vincas bind to - or + end of microtubules?

A

+ end = prevent assembly

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69
Q

taxanes bind where on microtubule?

A

interior surface

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70
Q

what is main excretion of vincaas?

A

hepatic

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71
Q

T/F alterations in alpha and beta tubulin leads to reduced affinity for vinca binding

A

false-makes tubulin more stable to microtubules are more stable (can lead to increased sensitivity to taxanes

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72
Q

What is most common binding site of platinums?

A

N7 purine (adenine or guanine)

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73
Q

Inter or intrastrand adducts are the main form of platinums?

A

intra, but interstrand is responsible for main cytotoxicity

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74
Q

Regarding “worst drug rule”, which drug is “worst” and when is it used?

A

“worst” = use drug that has least cell kill against cell resistant to other drug
use first

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75
Q

For drugs with similar potency, which drug should be used?

A

more specific agent first and broader action longer

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76
Q

AUC of doxorubicin directly correlates with what in dogs?

A

absolute neutrophil count and outcome

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77
Q

what impacts acute and chronic cardiotoxicity of doxo?

A

max plasma concentration

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78
Q

what is max tolerated AUC for carbo in cats?

A

2.75-2.95mg*min/mL

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79
Q

What is calculation of feline carbo clearance?

A

GFR x 2.60

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80
Q

What are the routes of metastasis?

A

direct extension
lymphatic
hematogenous
permation

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81
Q

T/F E cadherin alone is a better prognostic factor compared to the ratio of type IV collagenases

A

false- ratio is better

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82
Q

metastasis is efficient or ineffecient?

A

inefficient

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83
Q

what can improved survival of tumor cells in circulation (3 things)?

A

homotypic tumor aggregation
heterotypic aggregation with lymphocytes/platelets
plasticity of cell membrane

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84
Q

what are two possible fates of disseminated tumors cells?

A

cell death - (immune recognition or incompatible soil)

survive - (dormancy, recirculation, proliferation)

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85
Q

what is the seed and soil hypothesis?

A

certain organs are more suitable for metastatic growth based on tumor type

86
Q

Does each tumor cell have the same metastatic capability?

87
Q

MDSC are pro or antiangiogenic?

88
Q

What is the foraging hypothesis?

A

less than ideal primary tumor environment (hypoxia, lack of nutrients ect) may drive metastasis

89
Q

what do platelets produce that can activate survival, EMT and invasion pathways in tumor cells?

A

TGF beta (via SMAD in the tumor cell)

90
Q

binding of platelets to tumor cells promotes or downregulates NFkB?

91
Q

platelets release what factor that recruit immune cells that may help to create a niche for tumor metasasis?

A

chemokines

92
Q

T/F circulating tumor cells is proof of metastasis

A

false - can have present w/o overt metastasis - also human with breast cancer in “remission” for 7-22 years can have circulating tumor cells detected w/o illness/progressive disease

93
Q

Is there generally more inflammation in primary or metastatic leisons?

A

metastatic

94
Q

Where are RTK’s located?

A

cell membrane

95
Q

what results after ligand binding to RTK?

A

ATP docks and results in phosphorylation

96
Q

MAPK promotes what genes?

A

Cyclin D, fos/jun, p21

97
Q

What is bound to RAS in active and inactive state?

A

GTP active

GDP inactive

98
Q

Activated RAS has what downstream effects?

A

RAF
PI3K
and several more

99
Q

what main things does the PI3K signaling pathway impact?

A

cellular anabolism anad catabolism

100
Q

Who many classes of PI3K are there?

101
Q

which class of PI3K mainly activates AKT?

102
Q

what is a critical downregulator of PI3K?

103
Q

what molecules are inhibited by AKT

A

MDM2, caspase 9, Ink4, BAD

104
Q

What molecules are activated by AKT?

A

mTOR, GSK3B (inhibits cyclin D1 and alters cell proliferation)

105
Q

What results in JAK activation?

A

cytokines binding to receptor resulting in dimerization/phosphorylation

106
Q

TGF beta results in what phosphorylation?

A

serine/theronine

107
Q

What are HSP90 responsible for?

A

folds new proteins to active form

108
Q

If HSP90 is not active, what occurs to proteins?

A

protein is tagged for ubiquination and degraded

109
Q

What is the role of XPO1?

A

exports tumor suppressor proteins from nucleus

110
Q

what are 3 ways cell signaling is turned off?

A
  • reduced growth factors/chemokines (internalization/degraded)
  • intracellular phosphatases
  • proteasome mediated degradation
111
Q

what are 4 mechanisms of dysregulation of cell signaling?

A
  • overexpression
  • mutation
  • chr. translocation
  • autocrine loop activation
112
Q

what are methods to inhibit RTK cell signaling?

A
  • block ATP binding

- mAb bind extracellular domain (result in endocytosis/ADCC to reduce signaling)

113
Q

T/F aberrant expression of a protein indicates the tumor is relying on the protein for survival

114
Q

What are the main steps to drug development for targeted therapies?

A
  • ID target
  • Drug lead generation
  • optimize the lead compound
  • clinical trials
115
Q

type 1 small molecule inhibitors bind when?

A

when kinase is in DFG-IN (ATP bound state) - turned on

116
Q

What other area on the target do small molecular inhibitors bind to?

A

gatekeeper amino acid (near the ATP binding pocket)

117
Q

type 2 small molecular inhibitor bind when?

A

DFG- out (inactive state)

118
Q

where do type 3 and 4 small molecular inhibitors bind?

A

allosteric site -outside ATP binding site but block ATP binding (more unique binding sites vs type 1-2)

119
Q

What are irreversible small molecule inhibitors?

120
Q

what is most common tumor response to small molecular inhibitors?

121
Q

Are basket or umbrella trials more common for small molecular inhibitors?

122
Q

what are 3 types of resistance to small molecular inhibitors?

A
  • mutation in target (can be gatekeeper)
  • overexpression of target molecule
  • additional mutations in other parts of pathway or other pathways
123
Q

T/F - when resistance forms to small molecule inhibitors, additional drugs, even cytotoxic therapy may then be more effective

124
Q

What are 3 methods to prevent resistance to small molecular inhibitors?

A
  • combination therapy (RT, chemo, mAbs)
  • combine w/ checkpoint inhibitors
  • treat microscopic disease
125
Q

What two main tumor types in pets express KIT mutations?

A

MCT, GIST, AML

126
Q

What main tumor in pets has BRAF mutations?

A

TCC (>80%)

127
Q

what are the targets of imatinib?

A

BCR-ABL, Kit, PDGFR

128
Q

What are targets of toceranib?

A

KIT, PDGFR, VEGFR1 and 2, FLT3, CSF1 (at very high concentrations, VEGFR3, RET, ALK, AXL)

129
Q

What are the targets of masitinib?

A

Kit and PDGFR (more selective than imatinib) and also Lyn and FGFR3

130
Q

what is ORR of canine MCT to toceranib?

A

43% (70% if KIT mutation- early study)

131
Q

In a retro eval, what other tumor types does toceranib have activity (outcome MCT)

A

head/neck carcinomas
agasaca
nasal tumor
thyroid carcinoma

132
Q

what can act as a surrogate marker for toceranib activity vs taking a biopsy?

A

serum VEGF increase w/ inhibition of VEGFR2 pathway

133
Q

An unpublished study of palladia vs RT vs combination for nasal carcinoma had what results?

A

RT alone MST 12mn
combination 20mn
palladia 8mn

134
Q

What is impact of toceranib with microscopic met dz after SOC in OSA and HSA?

135
Q

what has been shown to increase and decrease with toceranib treatment?

A

reduced Tregs and increased IFNgamma

136
Q

RV1001 targets what?

137
Q

What is main toxicity noted with RV1001?

A

hepatotox gr 3-4 in all patients after 2-3 weeks

138
Q

what was ORR to RV1001 in canine LSA?

A

77% (phase 2 study)

139
Q

what is target of KPT335?

A

SINE (XPO1)

140
Q

What is duration of benefit in canine LSA to KPT335?

141
Q

What is target of Acalabrutinib?

A

BTK (covalent)

142
Q

phase 1 study of acalabrutinib in DLBCL what was response?

A

no CR, some PR and more SD (ORR 25%- with PFS 22.5d)

143
Q

Where is most common DNA methylation location?

A

Cytosine (5 position) followed by guanine

144
Q

What occurs routinely to cytosine in DNA?

A

deaminated to uracil that is corrected

145
Q

Is C followed by G common?

A

No - rare, but densely packed in CpG islands

146
Q

Is methylation heritable?

147
Q

In cancer, what is the methylation status of promoters of TSG?

A

hypermethylation

148
Q

MGMT expression induces resistance to what drug in dogs/cats in LSA?

149
Q

Open active chromatin has what histone modification?

A

hyperacetylation

150
Q

T/F microRNAs code for a protein

A

false - silence protein expression

151
Q

long non-coding RNA have what functions

A
  • collect mRNA (prevent expression)
  • form scaffolding for DNA
  • mRNA stability to enhancing
  • contribute to splicing mRNA
  • impact translation mRNA
152
Q

Canyons in DNA regions are hyper or hypomethylated?

A

hypomethylated

153
Q

What genes are have been ID to have hypermethylation in cancers in dogs?

A

DAPK
p16
DLC1
TFPI1

154
Q

What is bisulfite sequencing used for?

A

ID methylated CpG dinucleotides

155
Q

what is digital restriction enzyme analysis of methylation?

A

Way to evaluate methylated regions of DNA (leaves only methylated sequences)

156
Q

Methylation patterns may act as a biomarker of what?

A

predisposition ot cancer development

157
Q

What are demethylating drugs evaluated in dog cell lines?

A

6-TG and Zeb

158
Q

Valproic acid acts as what agent?

159
Q

T/F miRNAs are overexpressed only in cancer

A

False- can be over and underexpressed

160
Q

What damage molecule represents steady state oxidative DNA damage?

A

8 -oxo-7- hdyrodeoxyguanosine

161
Q

what is the p and q arm of a chromosome?

A

q long arm

p short term

162
Q

Myc-IgH translocation occurs in what disease?

A

Burkitt lymphoma

163
Q

what is lost in CLL in humans and dogs?

164
Q

what causes AML4-ALK mutation

165
Q

What is the MC tumor type with ITD noted in dogs?

A

exon 11 of ckit in dogs

166
Q

What is aneupolidy?

A

abnormla # chr (loss or gain)

167
Q

what is polypoidy?

A

more than 2 complete sets of chr

168
Q

In canine HS - what genes have losses?

A

Rb1 (more common in flat coats vs BMD), CDK2NA and PTEN

169
Q

what are possible mechanisms of aneuploidy?

A

merotelic attachment, supranumerary centrosome, spindle assembly checkpoint defect and chromosome cohesion defects

170
Q

microsatellite instability is whaat type of nucelotide instability?

A

insertion/deletion

171
Q

what type of mutation occurs in adult tissue and doesn’t pass to progeny?

172
Q

what type of mutation occurs in germinal tissue and present in every cell?

173
Q

what are different types of DNA damage stx changes?

A

DSB
SSB
adduct
base pairing abnormalities

174
Q

MRE11, RAD50, NBS1 respond to SS or DS breaks?

175
Q

ATR kinase is activated in what DNA damage?

A

SSB and alkylation/adducts

176
Q

AMT kinase is activated in what type of DNA damage?

177
Q

ATM and ATR phosphorylate what substances

A

H2AX (histone)

p53

178
Q

which DNA repair pathway is active in G1 phase?

179
Q

what DNA repair pathways are active in S and G2 phases?

180
Q

When is HR vs NHEJ repair used?

A

S and G2 for HR and all phase G1

HR requires template strand

181
Q

which DNA repair mechanisms is slower and most accurate?

182
Q

what activates NHEJ?

A

DNA-PKcs (with Ku70 and Ku80 interaction)

183
Q

what is needed for RAD51 to bind appropriately for ATM?

184
Q

PARP assist with which type of DNA breaks?

185
Q

what repair process is activated when fanconi proteins identify interstrand crosslinks?

A

HR and NER

186
Q

oxidized bases are repaired by what method?

187
Q

UV lesions and alkyl adducts are repaired by what method?

188
Q

MMR deficiency have increases in what?

A

microsatellite instabilities

189
Q

hypoxia increase or reduced effects of genomic instability?

190
Q

Knockout of ATM or ATR will result in fatal changes?

191
Q

what is the only genetic driver of human and canine LSA is conserved?

192
Q

What are main components of the TME across most tumors?

A 
CSC 
ECM
stromal fibroblasts
blood vessels networks
lymph vessel networks
stromal adipocytes
inflammatory macs
immunosuppressive cells 
innate immune cells
adaptive immune cells
193
Q

what is an important event that initiates TME?

A

changes in normal stromal cells due to interactions w/ CSC

194
Q

T/F normal ECM promotes spread of tumor cells

A

false! usually inhibits

195
Q

The following are characteristics what

  • increased stiffness
  • fragmented hyaluronic acid
  • increased Tenascin C
  • increased IL6 and pro inflammatory cytokines
A

tumor associated ECM

196
Q

decreased CAV-1, increased SMA, vimentin, FAP and MCT4 are markers on what cells?

197
Q

what does MCT4 do?

A

export lactate

198
Q

what immunomodulatory factors do CAFs release?

A

IDO
TGFbeta
Arg

199
Q

under normoxic condition how do VHL and HIF interact?

A

VHL degrades HIFalpha

200
Q

what is the most potent stimulator of angiogenesis?

201
Q

Which VEGFR is more responsible for tumor associated neoangiogensis

202
Q

What is role of Tie 2 when bound to Ang1 and Ang2?

A

Ang1 binding maintains current state

Ang2 binding results in new vasculature (less stable though)

203
Q

what are methods to target angiogensis pathway?

A

blocked VEGFA
block VEGF R or other RTKs (PDGFR, EGFR, MET R)
target downstream pathways (MAPK pathway ex)

204
Q

what is the goal of anti-angiogentic tx?

A

normalize tumor associated vasculature

205
Q

what factors control lymphangiogenesis?

A

VEGFC and D (bind VEGFR3)

206
Q

what do adipocytes provide to TME?

A

support angiogenesis
provide energy for tumor cells
encourages pro-inflammatory state

207
Q

TAMs that are M1 and M2 have what role?

A

M1: pro immune
M2: pro tumor

208
Q

Is state of TAM static/discrete?

209
Q

Adenovirus FASL overcomes what tumor feature?

A

immunosuppressive barrier

210
Q

what is eBAT?

A

EGF and uPA targeted carrier of pseudomonas exotoxin

211
Q

what are the main effects of eBAT?

A

EGFR/uPAR+ tumor cells
uPAR+ stromal environment
uPAR+ macs

Oncology Boards (4 decks)

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