Lecture 3 Flashcards
what is neoplasia
dysregulated cellular differentiation, aberrant proliferation and size
what are the 3 markers of neoplasia
-cells proliferate and gro without control
-differenciation is impeded at one or multiple stages aka they don’t
-cells become immortal
what are the selective growth advantages of neoplasia
-the ratio between birth and death in a cell population in normal adult tissues in the absence of injury is >1
what did t boveri say in 1902
some chromosomes stimulate cell dicision while others inhibit it
what was rous experiment in 1911
-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
when was the term oncogene coined and when
-1969 by robert huebner and george todaro
in 1970 what did steve martin show
v-src is the oncogene
who and when showed that: oncogenes are activated proto-oncogenes aka c-src, found in many organisms incuding humans
in 1976 stehelin, bishop and varmus
what is an oncogene?
a gene that increases the selective growth advantage of the cell in which it resides
what is a proto-oncogene
is a normal genethat can become an oncogene due to mutations or increased expression
what is a tumour supressor gene:
a gene that when inactivated by mutation, increase the selective growth advantage of the cell in which it resides
what does amplification mean
a genetic alteration producing a large number of copies of a small segment (less than a few megabases) of the genome
what is an indel:
a mutation due to a small insertion or deletion of one or a few nucleotides
what is a rearrangement
a mutation that juxtaposes nucleotides that are normally seperated, such as thpse on 2 different chromosomes
what is an sbs
a single nucleotide substitution like c to t relative to a reference sequence
what is a driver gene mutation
a muation that directly or inderectly confers a selective growth advantage to the cell in which it occurs
what is a passenger mutation
a mutation that has no direct or indirect effect on the selective growth advantage in which it occured
what does LOH mean
loss of heterozygosity
what happens when tou already have a hit already in RB and then you start having haploinsufficiency
the disease gets worse and your last allele can’t work properly
what does ras usuallu do
it is a gtp binding protein
-aka a gtp ase
what does src usualy do
it is a non receptor tyrosine kinase
true or fa;se: ras ios a gtp ases that is usually mutated in most cancer
true
name viruses that can mutate ras
-harvey sarcoma virus
-kirsten sarcoma virus
-neuroblastoma virus
this mutation of ras was found in which cancer
neuro blastoma
gotta explain rtk and ras
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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
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
what is the highest risk to get cancer
age
what does a monolayer of cell means
not cancerous
what does it mean when all the cells grow over eachother
cancer
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
what dioes ras block
apoptosis
WHAT DOES myc do
it induces proliferation
what is arf
tumour supressor transcribed from an alternate reading frame the INK4a/ARF locus
(CDKN2A) encoding p16INK4a.
true or false: arf= p14 in humans and p19 in mouse
trie
what is mdm2
MDM2 (Mouse double minute 2 homolog): E3 ubiquitin-protein ligase that facilitates degradation of p53
what is the hayfloick limit
the number of times a normal human cell population will divide until cell division will stop
what does short telomeres lead to
senescence and hihjh INK4a
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.
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
true or false: tumours are always monoclonal
nah usually there are multiple mutations
