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Midterm 504 > Oncogenes and tumor suppressors > Flashcards

Oncogenes and tumor suppressors Flashcards

1
Q

Whats neoplasia

A

Dysregulated cellular differentiation, aberrant proliferation and size

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2
Q

What are the traits of neoplasia

A

Cells proliferate and grow without control
Differentiation is empeded at one or multiples stages
Cells become immortal

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3
Q

Whats selective growth

A

The ratio between birth and death in cell population
More cells are born,
More cells become immortal,
Less cells die

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4
Q

Whats dysplasia

A

Means that youre losing the property the cells normally have

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5
Q

Tissue that can do all hallmarks is not cancer, what is it? is grows uncontrollably, and most the work done to study agiogenesis in that tissue…

A

Placenta

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6
Q

Immune system can kiss (kill) cancer cells?

A

yes

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7
Q

New Hallmarks

A

Senescence, implication of microbiomes, epigenetic reprogramming

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8
Q

T Boveri discovered…(chickens)

A

Evidence that cancer is a genetic disease, so grow sarcoma in breast muscle, and remove sarcome, grind up, collect and filtrate, inject in other chicken and they develop cancer

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9
Q

Steve Martin showed…

A

that V-sarc is an oncogene

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10
Q

True or false: Throughout evolution, proto-oncogene incorporated our genome and are sitting there

A

True

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11
Q

Oncogene

A

A gene that increases the selective growth advantage of the cell in which it resides

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12
Q

Proto-oncogene

A

normal gene that can become an oncogene due to mutations or increased expression

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13
Q

Tumor suppressor

A

A gene that when activated by mutation increases selective growth

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14
Q

Cancer cells, lose… and gain…

A

lose tumor suppressors
gain oncogenes

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15
Q

Oncogens and tumor suppressors are activated and deactivated through…

A

Mutations

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16
Q

Rearrangement

A

A mutation that juxtaposes nucleotides that are normally seperated such as those on two different chromosomes

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17
Q

SBS

A

Single nucleotide substitution

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18
Q

Driver mutation is a mutation that….

A

directly or indirectly confers a selective growth advantage to the cell in which it occurs

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19
Q

Passenger mutation….

A

has no direct or indirect effect on the selective growth advantage on the cell in which it occured

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20
Q

In most cancers… the mutations are which type?

A

SBS mutations

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21
Q

Whats the 2-hit model (Loss of heterogosity)

A

When you get a somatic mutation in one allele (first-hit) then a second hit on the other allele (second-hit) and cells exhibit malignant property

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22
Q

Whats happloinsufficiency?

A

Even a small loss of a gene allele, less than 50% can cause malignant cancer, disfunction of the tumor suppressor

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23
Q

Whats an example of a happloinsufficient tumor suppressor

A

TP53 (P53)

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24
Q

Name two tumor suppressors

A

Not mutated forms of
Ras
P53

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25
Q

Whats Ras

A

GTPAse that is frequently mutated in cancer

26
Q

Ras-GDP is activated by …and becomes…

A

SOS1 (GAP) and becomes Ras GTP

27
Q

Ras-GTP is inactivated by …and becomes…

A

NF1 (GEF) and becomes Ras GDP

28
Q

What do you need to become neoplasia?

A

Selective growth advantage

29
Q

P53 is a ….

A

Transcription factor

30
Q

In cancer, P53 gets…

A

mutated

31
Q

True or false: P53 is the second most mutated gene

A

False - its the most mutated gene in cancer

32
Q

True or false: Mutant P53 starts activating genes and acts as dominant negative and inhibit the function of P53. P53 loses his function because cant form a tetramer

A

True

33
Q

Whats oncogene collaboration?

A

Carrying one oncogenic even is not enough to cause cancer.. usually you need more oncogene

34
Q

What is the highest risk factor of getting cancer?

A

Age

35
Q

In the experiment done.. they had to put Myc and Ras together to prove….and turned into immortalized fibroids to get malignancy

A

Oncogene collaboration

36
Q

True or false: You need activation of Two oncogenes or action of oncogene and inactivation of tumor suppressors

A

True

37
Q

Myc and Ras activate this protein

A

P14ARF

38
Q

Mecanisms of apoptosis

A

activate P14Arf, inhibits Mdm2, mdm2 inhibits P53, cell cycle arrest and apoptosis

39
Q

Senescence

A

To grow old …

40
Q

True or false: Unlike quiescence, where cells stop proliferating, senescent cells never reenter cell cycle

A

True

41
Q

What triggers senescence/

A

Shortening of telomere (region of repetitive DDNA sequence at the end of a chromosome)

42
Q

Whats the problem with senescence

It makes you….

A

If you want to prevent cancer cells to form you make cells start senescence (look much more older physically)

43
Q

What are the Hayflick factors
(In somatic cells that limit the division and replication) (3)

A

1) shortening of telomere
2) DNA damage
3) Active Arf or INK

44
Q

If you wanna make sure cancer doesnt form… you wanna induce….

A

senescence

45
Q

Hayflick limit

numebr of time a cell will divide until ….

A

numebr of time a cell will divide until cell division stops

46
Q

What can activates senecence

Its gtpase but also oncogene…

A

Ras

47
Q

Senescence mechanism

Activate R…
R… activate A…
A… inhibits mdm2
mdm2 inhibits …
… decides if cells fo through senescence

A

Activate Ras,
Ras activate Arf
Arf inhibits mdm2
mdm2 inhibits P53
P53 decides if cells fo through senescence

48
Q

Whats oncogene addition

A

Oncogene addiction means cancer cells depend heavily on specific mutated genes (oncogenes) for their growth and survival

49
Q

Whats the challenge with Targeted therapy (kinase inhibitor)

A

They all have similar ATP binding pockets, so finding inhibitor to target it

50
Q

philadelphia chromosome was discovered in…. and is a translocation between chromosome … & …

A

Philadelphia
9 & 22

51
Q

Whats horizontal resistance?

to resist multiple types of ……

A

to resist multiple types of treatments

52
Q

Whats vertical resistance

resistance that develops against a….

A

resistance that develops against a specific type of treatment

53
Q

Whats a challenge in treating cancer (tumor complexity and hetegeneity) Clonal expansion

A

If you have an initial mutation, by the time you diagnose, theres going to be a number of different clonal expansion

54
Q

Monoclonal tumors

…. gives raise to cancer

A

One cells that goes off and gives raise to cancer

55
Q

Polyclonal tumors

A

Solid tumors

56
Q

Tissue organization field Theory

how cells …. and become different types

A

how cells organize and become different types

57
Q

Which one of these is not a hallmark?
a) limitless replicative potential
b) tumor-promoting inflamation
c)Exit from cell cucle and differentiation
d)evading growth suppressors

A

c

58
Q

Which of the following is tru regarding to a tumor suppressor gene?
1) when inativated by mutation, inscreases the selective growth advantage of the cell in which it resides
2) when inactivated by mutation, suppresses tumor growth
3) when mutated, has no direct effect on the selective growth advantage of the cell in which occurs
4) is a normal gene that can become oncogenes

A

1)

59
Q

Which of these genes when aberrantly activated or mutated (gtpase)

A

Ras

60
Q

Haploinsuffenciency is … 1) an insuficient immune response to cancer cells
2) a state of irreversible growth arrest due to replpication stress
3) a genetic status where a single wild-type copy of an allelic pair is present but the level of expression of the produc is insufficient to give wild type tumor suppressive function
4) When tumors mutations are eradicated by targeted therapies and only wild type alleles are left

A

3)

Midterm 504 (5 decks)

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