Lecture 3 Flashcards

1
Q

what is neoplasia

A

dysregulated cellular differentiation, aberrant proliferation and size

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

what are the 3 markers of neoplasia

A

-cells proliferate and gro without control
-differenciation is impeded at one or multiple stages aka they don’t
-cells become immortal

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

what are the selective growth advantages of neoplasia

A

-the ratio between birth and death in a cell population in normal adult tissues in the absence of injury is >1

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

what did t boveri say in 1902

A

some chromosomes stimulate cell dicision while others inhibit it

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

what was rous experiment in 1911

A

-HE GAVE saroma to another chicken by extracting the sarcoma from anotyher chicklen
-cell free extract of chicken tumours is oncogenic : RSV first oncogenic retrovirus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

when was the term oncogene coined and when

A

-1969 by robert huebner and george todaro

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

in 1970 what did steve martin show

A

v-src is the oncogene

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

who and when showed that: oncogenes are activated proto-oncogenes aka c-src, found in many organisms incuding humans

A

in 1976 stehelin, bishop and varmus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

what is an oncogene?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

what is a proto-oncogene

A

is a normal genethat can become an oncogene due to mutations or increased expression

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

what is a tumour supressor gene:

A

a gene that when inactivated by mutation, increase the selective growth advantage of the cell in which it resides

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

what does amplification mean

A

a genetic alteration producing a large number of copies of a small segment (less than a few megabases) of the genome

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

what is an indel:

A

a mutation due to a small insertion or deletion of one or a few nucleotides

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

what is a rearrangement

A

a mutation that juxtaposes nucleotides that are normally seperated, such as thpse on 2 different chromosomes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

what is an sbs

A

a single nucleotide substitution like c to t relative to a reference sequence

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

what is a driver gene mutation

A

a muation that directly or inderectly confers a selective growth advantage to the cell in which it occurs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

what is a passenger mutation

A

a mutation that has no direct or indirect effect on the selective growth advantage in which it occured

18
Q

what does LOH mean

A

loss of heterozygosity

19
Q

what happens when tou already have a hit already in RB and then you start having haploinsufficiency

A

the disease gets worse and your last allele can’t work properly

20
Q

what does ras usuallu do

A

it is a gtp binding protein
-aka a gtp ase

21
Q

what does src usualy do

A

it is a non receptor tyrosine kinase

22
Q

true or fa;se: ras ios a gtp ases that is usually mutated in most cancer

23
Q

name viruses that can mutate ras

A

-harvey sarcoma virus
-kirsten sarcoma virus
-neuroblastoma virus

24
Q

this mutation of ras was found in which cancer

A

neuro blastoma

25
gotta explain rtk and ras
ddsdawqerelfgyqwdifhc;saKFcdgvUOpq
26
where does the p53 family come from
The p53 family: evolved from a p63/p73 ancestor gene in invertebrates. -p53 diverged from p63/p73 with a gene duplication in the cartilaginous fish. -p63 and p73 differentiated from each other in bony fish
27
what are the responses/outcomes of fucked up p53
-various like stem cell maintenance and fertility -cell recovery and survival due to the autophagyu of the fucked up cells and transient arrest -cell death or clonal ablation due to senescence, apoptopsis and necrosis
28
what is the highest risk to get cancer
age
29
what does a monolayer of cell means
not cancerous
30
what does it mean when all the cells grow over eachother
cancer
31
what got out of the oncogene collaboration experimenT
that usually you need more than one oncogen for it to get to cancer like ras and myc -they did iy usingh nih 3t3 cells
32
what dioes ras block
apoptosis
33
WHAT DOES myc do
it induces proliferation
34
what is arf
tumour supressor transcribed from an alternate reading frame the INK4a/ARF locus (CDKN2A) encoding p16INK4a.
35
true or false: arf= p14 in humans and p19 in mouse
trie
36
what is mdm2
MDM2 (Mouse double minute 2 homolog): E3 ubiquitin-protein ligase that facilitates degradation of p53
37
what is the hayfloick limit
the number of times a normal human cell population will divide until cell division will stop
38
what does short telomeres lead to
senescence and hihjh INK4a
39
what is oncogene addiction
A cellular condition in which cancer cell requires the activity of a specific oncogene or cellular process for growth and survival.
40
explain tsgs and resistence aka vertical and horizontal resistance
-mutated cells will survive cuz the thing is not affecting tje, -horizontal;: the cancerous cells will strat using another pathways that is not targeted by the drug so that they survive and proliferate
41
true or false: tumours are always monoclonal
nah usually there are multiple mutations
42