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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
Q

example of low growth fraction tumours

A

breast, colon

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26
Q

low growth fraction tumours production vs. death are simliar? or different?

A

similar. production is 10% greater than loss

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27
Q

doubling time f clinically detectable colon or lung tumours is how long?

A

2-3 months

28
Q

Pten blocks THIS important kinase

A

PI3 kinase (growth pathway)

29
Q

What are proto-oncogenes?

A

normal cell proliferation genes

30
Q

What are oncoproteins?

A

proteins that come from oncogenes

31
Q

In oncogenesis, what happens with growth factors?

A

autocrine loops

32
Q

In oncogenesis, what happens with growth factor receptors?

A

over expression/active

33
Q

In oncogenesis, what happens with cyclins/CDKs

A

uncontroled cell cycle progression

34
Q

RAS Oncogenes (H-Ras & K-Ras), what happens in mutant RAS?

A

the negative feedback(GTP hydrolysis) of active RAS to inactive RAS is broken

35
Q

What are P54 and RB?

A

TSGs that regulate cell cycle directly

36
Q

Pten inhibits what?

A

oncogenic pathway of PI3 kinase

37
Q

How do you get loss of heterozygosity in neoplasm?

A

Both TSG genes lost

38
Q

how are familial predisposition and TSGs involved?

A

inherit one defective gene, lose the other one via mutation, or could lose both on an unlucky fluke

39
Q

What the only cancer that only needs one gene mutation to activate?

A

retinoblastoma

40
Q

prevalance of retinoblastoma?

A

1/20000

41
Q

treatment for retinoblastoma?

A

enucleation

42
Q

Rb causative factor only in eye?

A

Nope, features in many tumour types

43
Q

define loss of heterozygosity (LOH)

A

loss of normal function of one allele where the other one was already inactivated.

44
Q

What is Knudson’s “two hit” hypothesis for LOH?

A

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
Q

What is the guardian of the genome?

A

p53

46
Q

what is p53?

A

transcription factor that can regulate expression of cell cycle factors

47
Q

p53 helps out a lot with what cellular response to damage?

A

apoptosis directing

48
Q

What is miRNA?

A

microRNAs, non-coding single stranded that function as negative regulators of genes

49
Q

about how many nucleotides are miRNA?

A

22

50
Q

How would miRNA affect oncogenes?

A

not enough expressed leads to too much oncoproteins

51
Q

How would miRNA affect TSGs?

A

too many miRNAs leads to too little tumour suppresor proteins

52
Q

What does methylation around TSGs do?

A

inactivated them

53
Q

epigenetic control of TSG expression is heritable?

A

yes

54
Q

pRB checkpoints which part of cell cycle?

A

end of G1

55
Q

p53 checkpoints which part of cell cycle?

A

S-phase

56
Q

6 ways to evade apoptosis

A
  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
Q

What happens with telomeres and cancer?

A

tumour cells reactivate telomerase and achieve immortality

58
Q

4 steps for tumour to become metastatic:

A
  1. detachment of cells from each other
  2. degradation of ECM
  3. attach to novel ECM areas
  4. migration
59
Q

what cellular glues are disrupted in metastasis? 3 of them

A

cadherins
beta-catenin
connexins

60
Q

are adherance molecules affected in cancer signalling pathways?

A

yes

61
Q

What are popular angiogenesis targets for therapeutics?

A

VEGFs

VEGF-Rs

62
Q

Explain tumour heterogeneity.

A

every tumour is different from it’s primary tumour and every region within the same tumour can be different

63
Q

what is a tumour initiating cell?

A

human tumour growing in mouse when transplanted

64
Q

What are cancer stem cells?

A

arise from adult stem cells, intrinsic resistance to conventional therapies

65
Q

Why are cancer stem cells, intrinsic resistance to conventional therapies?

A

conventional therapy doesn’t kill the original cell so it relapses easily

Jason's Respiratory Block (20 decks)

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