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Jason's Respiratory Block > Neoplasia 2 > Flashcards

Neoplasia 2 Flashcards

1
Q

What would you target to control cell survival, growth and differentiation?

A

signalling pathways

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2
Q

4 emerging hallmarks in cancer replication?

A

deregulating cellular energetics
immune evasion
tumor-promoting inflammation
genome instability/mutation

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3
Q

4 classes of normal regulatory genes?

A

proto-oncogenes
tumour suppressor genes
apoptosis genes
DNA repair genes

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4
Q

Example of DNA repair genes defective?

A

BRCA1, BRCA2

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5
Q

how would aberrant DNA repair lead to cancer?

A

rapid accumulation of mutations in ‘hotspot’ oncogenes/TSGs

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6
Q

Her2-neu, Ras, Myc are examples of?

A

oncogenes

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7
Q

P53, Rb, APC, PTEN are examples of?

A

TSGs

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8
Q

How many alleles need to be lost to lose TSG function?

A

2

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9
Q

How many alleles of oncogenes need to be activated/mutated?

A

1

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10
Q

Types of gene mutations in cancer? 4 types

A

errors in DNA repair
point mutations in onco/TSGs
amplification of oncogenes
chromosomal rearragements

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11
Q

Difference between mutation and polymorphism?

A

mutation: any change away from what is defined as ‘normal’
polymorphism: variation that is common in population (no sequence is ‘normal’)

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12
Q

Common amplifications/mutation in cancer?

A 
TP53
PIK3CA
PTEN
RB1
KRAS
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13
Q

What is RB gene mutation responsible for?

A

retinoblastoma

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14
Q 
What are?
TP53
PIK3CA
PTEN
RB1
KRAS
A

Common amplifications/mutation in cancer

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15
Q

oncogenes affect 5 categories of growth:

A 
growth factors
growth receptors
protein signal transduction
nuclear-reg proteins
cell-cycle regulators
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16
Q

What is SNP in cancer?

A

single nucleotide polymorphism

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17
Q

polymorphisms in cancer depends how on SNPs?

A

how they are expressed, the alterations could change stability, influence risk

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18
Q

Oncogene amplification and overexpression are synonymous?

A

Nope. Amplification is more copies of a gene

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19
Q

What are double minutes in neoplasia?

A

extra chromosomes containing only oncogenes. holy shit.

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20
Q

Gene translocations and fusions make what?

A

novel hybrid genes that affect signaling pathway

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21
Q

BCR-ABL hybrid gene affects what?

A

tyrosine kinase

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22
Q

What must you consider re: neoplastic growth?

A

rate at which tumor cells are shed or die or differentiate

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23
Q

what happens to the proportion of cells in growth fraction as it grows?

A

growth fraction declines

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24
Q

Example of high growth fraction tumours?

A

leukemias, lmphomas, small-cell carcinoa

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25
example of low growth fraction tumours
breast, colon
26
low growth fraction tumours production vs. death are simliar? or different?
similar. production is 10% greater than loss
27
doubling time f clinically detectable colon or lung tumours is how long?
2-3 months
28
Pten blocks THIS important kinase
PI3 kinase (growth pathway)
29
What are proto-oncogenes?
normal cell proliferation genes
30
What are oncoproteins?
proteins that come from oncogenes
31
In oncogenesis, what happens with growth factors?
autocrine loops
32
In oncogenesis, what happens with growth factor receptors?
over expression/active
33
In oncogenesis, what happens with cyclins/CDKs
uncontroled cell cycle progression
34
RAS Oncogenes (H-Ras & K-Ras), what happens in mutant RAS?
the negative feedback(GTP hydrolysis) of active RAS to inactive RAS is broken
35
What are P54 and RB?
TSGs that regulate cell cycle directly
36
Pten inhibits what?
oncogenic pathway of PI3 kinase
37
How do you get loss of heterozygosity in neoplasm?
Both TSG genes lost
38
how are familial predisposition and TSGs involved?
inherit one defective gene, lose the other one via mutation, or could lose both on an unlucky fluke
39
What the only cancer that only needs one gene mutation to activate?
retinoblastoma
40
prevalance of retinoblastoma?
1/20000
41
treatment for retinoblastoma?
enucleation
42
Rb causative factor only in eye?
Nope, features in many tumour types
43
define loss of heterozygosity (LOH)
loss of normal function of one allele where the other one was already inactivated.
44
What is Knudson's "two hit" hypothesis for LOH?
generation one has one RB allele gone, their kids all have one already gone so all it takes is another one to go before you get tumours
45
What is the guardian of the genome?
p53
46
what is p53?
transcription factor that can regulate expression of cell cycle factors
47
p53 helps out a lot with what cellular response to damage?
apoptosis directing
48
What is miRNA?
microRNAs, non-coding single stranded that function as negative regulators of genes
49
about how many nucleotides are miRNA?
22
50
How would miRNA affect oncogenes?
not enough expressed leads to too much oncoproteins
51
How would miRNA affect TSGs?
too many miRNAs leads to too little tumour suppresor proteins
52
What does methylation around TSGs do?
inactivated them
53
epigenetic control of TSG expression is heritable?
yes
54
pRB checkpoints which part of cell cycle?
end of G1
55
p53 checkpoints which part of cell cycle?
S-phase
56
6 ways to evade apoptosis
1. reduce CD95 2. inactivate death signal via FLICE 3. upregulare BCL2 4. reduce BAX cause of loss of p53 5. loss of APAF-1 6. upregulation of apoptosis inhibitors
57
What happens with telomeres and cancer?
tumour cells reactivate telomerase and achieve immortality
58
4 steps for tumour to become metastatic:
1. detachment of cells from each other 2. degradation of ECM 3. attach to novel ECM areas 4. migration
59
what cellular glues are disrupted in metastasis? 3 of them
cadherins beta-catenin connexins
60
are adherance molecules affected in cancer signalling pathways?
yes
61
What are popular angiogenesis targets for therapeutics?
VEGFs | VEGF-Rs
62
Explain tumour heterogeneity.
every tumour is different from it's primary tumour and every region within the same tumour can be different
63
what is a tumour initiating cell?
human tumour growing in mouse when transplanted
64
What are cancer stem cells?
arise from adult stem cells, intrinsic resistance to conventional therapies
65
Why are cancer stem cells, intrinsic resistance to conventional therapies?
conventional therapy doesn't kill the original cell so it relapses easily

Jason's Respiratory Block (20 decks)

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