Lecture 3

Question 1

what is neoplasia

Answer 1

dysregulated cellular differentiation, aberrant proliferation and size

Question 2

what are the 3 markers of neoplasia

Answer 2

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

Question 3

what are the selective growth advantages of neoplasia

Answer 3

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

Question 4

what did t boveri say in 1902

Answer 4

some chromosomes stimulate cell dicision while others inhibit it

Question 5

what was rous experiment in 1911

Answer 5

-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

Question 6

when was the term oncogene coined and when

Answer 6

-1969 by robert huebner and george todaro

Question 7

in 1970 what did steve martin show

Answer 7

v-src is the oncogene

Question 8

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

Answer 8

in 1976 stehelin, bishop and varmus

Question 9

what is an oncogene?

Answer 9

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

Question 10

what is a proto-oncogene

Answer 10

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

Question 11

what is a tumour supressor gene:

Answer 11

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

Question 12

what does amplification mean

Answer 12

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

Question 13

what is an indel:

Answer 13

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

Question 14

what is a rearrangement

Answer 14

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

Question 15

what is an sbs

Answer 15

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

Question 16

what is a driver gene mutation

Answer 16

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

Question 17

what is a passenger mutation

Answer 17

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

Question 18

what does LOH mean

Answer 18

loss of heterozygosity

Question 19

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

Answer 19

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

Question 20

what does ras usuallu do

Answer 20

it is a gtp binding protein
-aka a gtp ase

Question 21

what does src usualy do

Answer 21

it is a non receptor tyrosine kinase

Question 22

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

Answer 22

true

Question 23

name viruses that can mutate ras

Answer 23

-harvey sarcoma virus
-kirsten sarcoma virus
-neuroblastoma virus

Question 24

this mutation of ras was found in which cancer

Answer 24

neuro blastoma

Question 25

gotta explain rtk and ras

Answer 25

ddsdawqerelfgyqwdifhc;saKFcdgvUOpq

Question 26

where does the p53 family come from

Answer 26

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

Question 27

what are the responses/outcomes of fucked up p53

Answer 27

-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

Question 28

what is the highest risk to get cancer

Answer 28

age

Question 29

what does a monolayer of cell means

Answer 29

not cancerous

Question 30

what does it mean when all the cells grow over eachother

Answer 30

cancer

Question 31

what got out of the oncogene collaboration experimenT

Answer 31

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

Question 32

what dioes ras block

Answer 32

apoptosis

Question 33

WHAT DOES myc do

Answer 33

it induces proliferation

Question 34

what is arf

Answer 34

tumour supressor transcribed from an alternate reading frame the INK4a/ARF locus
(CDKN2A) encoding p16INK4a.

Question 35

true or false: arf= p14 in humans and p19 in mouse

Answer 35

trie

Question 36

what is mdm2

Answer 36

MDM2 (Mouse double minute 2 homolog): E3 ubiquitin-protein ligase that facilitates degradation of p53

Question 37

what is the hayfloick limit

Answer 37

the number of times a normal human cell population will divide until cell division will stop

Question 38

what does short telomeres lead to

Answer 38

senescence and hihjh INK4a

Question 39

what is oncogene addiction

Answer 39

A cellular condition in which cancer cell requires the activity of a specific oncogene or cellular process for growth and survival.

Question 40

explain tsgs and resistence aka vertical and horizontal resistance

Answer 40

-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

Question 41

true or false: tumours are always monoclonal

Answer 41

nah usually there are multiple mutations