Oncogenes and tumor suppressors

Question 1

Whats neoplasia

Answer 1

Dysregulated cellular differentiation, aberrant proliferation and size

Question 2

What are the traits of neoplasia

Answer 2

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

Question 3

Whats selective growth

Answer 3

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

Question 4

Whats dysplasia

Answer 4

Means that youre losing the property the cells normally have

Question 5

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…

Answer 5

Placenta

Question 6

Immune system can kiss (kill) cancer cells?

Answer 6

yes

Question 7

New Hallmarks

Answer 7

Senescence, implication of microbiomes, epigenetic reprogramming

Question 8

T Boveri discovered…(chickens)

Answer 8

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

Question 9

Steve Martin showed…

Answer 9

that V-sarc is an oncogene

Question 10

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

Answer 10

True

Question 11

Oncogene

Answer 11

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

Question 12

Proto-oncogene

Answer 12

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

Question 13

Tumor suppressor

Answer 13

A gene that when activated by mutation increases selective growth

Question 14

Cancer cells, lose… and gain…

Answer 14

lose tumor suppressors
gain oncogenes

Question 15

Oncogens and tumor suppressors are activated and deactivated through…

Answer 15

Mutations

Question 16

Rearrangement

Answer 16

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

Question 17

SBS

Answer 17

Single nucleotide substitution

Question 18

Driver mutation is a mutation that….

Answer 18

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

Question 19

Passenger mutation….

Answer 19

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

Question 20

In most cancers… the mutations are which type?

Answer 20

SBS mutations

Question 21

Whats the 2-hit model (Loss of heterogosity)

Answer 21

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

Question 22

Whats happloinsufficiency?

Answer 22

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

Question 23

Whats an example of a happloinsufficient tumor suppressor

Answer 23

TP53 (P53)

Question 24

Name two tumor suppressors

Answer 24

Not mutated forms of
Ras
P53

Question 25

Whats Ras

Answer 25

GTPAse that is frequently mutated in cancer

Question 26

Ras-GDP is activated by ...and becomes...

Answer 26

SOS1 (GAP) and becomes Ras GTP

Question 27

Ras-GTP is inactivated by ...and becomes...

Answer 27

NF1 (GEF) and becomes Ras GDP

Question 28

What do you need to become neoplasia?

Answer 28

Selective growth advantage

Question 29

P53 is a ....

Answer 29

Transcription factor

Question 30

In cancer, P53 gets...

Answer 30

mutated

Question 31

True or false: P53 is the second most mutated gene

Answer 31

False - its the most mutated gene in cancer

Question 32

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

Answer 32

True

Question 33

Whats oncogene collaboration?

Answer 33

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

Question 34

What is the highest risk factor of getting cancer?

Answer 34

Age

Question 35

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

Answer 35

Oncogene collaboration

Question 36

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

Answer 36

True

Question 37

Myc and Ras activate this protein

Answer 37

P14ARF

Question 38

Mecanisms of apoptosis

Answer 38

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

Question 39

Senescence

Answer 39

To grow old ...

Question 40

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

Answer 40

True

Question 41

What triggers senescence/

Answer 41

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

Question 42

Whats the problem with senescence It makes you….

Answer 42

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

Question 43

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

Answer 43

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

Question 44

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

Answer 44

senescence

Question 45

Hayflick limit numebr of time a cell will divide until ….

Answer 45

numebr of time a cell will divide until cell division stops

Question 46

What can activates senecence Its gtpase but also oncogene…

Answer 46

Ras

Question 47

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

Answer 47

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

Question 48

Whats oncogene addition

Answer 48

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

Question 49

Whats the challenge with Targeted therapy (kinase inhibitor)

Answer 49

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

Question 50

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

Answer 50

Philadelphia 9 & 22

Question 51

Whats horizontal resistance? to resist multiple types of ……

Answer 51

to resist multiple types of treatments

Question 52

Whats vertical resistance resistance that develops against a….

Answer 52

resistance that develops against a specific type of treatment

Question 53

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

Answer 53

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

Question 54

Monoclonal tumors …. gives raise to cancer

Answer 54

One cells that goes off and gives raise to cancer

Question 55

Polyclonal tumors

Answer 55

Solid tumors

Question 56

Tissue organization field Theory how cells …. and become different types

Answer 56

how cells organize and become different types

Question 57

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

Answer 57

c

Question 58

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

Answer 58

1)

Question 59

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

Answer 59

Ras

Question 60

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

Answer 60

3)