intro to cancer 2 Flashcards
which mutation types will cause cancer?
inactivating tumour suppressors
or
activating proto-oncogenes
how can a mutation activate the photo-oncogenes?
over expression and gaining control of the regulatory regions of the gene.
point mutations
fusions of gene
how can you identify cancer genes ?
although familial cancers are rarer, you study familial cancers to get a lot of important information on sporadic cancer genes.
retinoblastoma - familial cancer or sporadic cancer?
and how likely is it to get it bilaterally?
rare childhood tumour.
in the eye.
but if it is in both eyes it means there is a genetic predisposition for this cancer.
those with retinoblastoma in both eyes also get bone cancer later on so presents as a syndrome.
how is the 2-hit hypothesis possible?
as many loss-of-function mutations as recessive in nature.
if you have not inherited one faulty allele (familial cancer) then you need two separate mutations which are the 2-hits.
how does the two hit hypothesis show that cancer is somatic?
as the mutation is in the somatic cells, if you have familial cancer the offspring only inherit the predisposition and not the second mutation.
why is the second mutation in the 2-hit hypothesis so common?
when you have a predisposition for the cancer or have had 1 mutation, you have 1 bad allele and one good allele.
but the 1 good allele will get LOST or is REPLACED by the bad copy, and you are just left with 1 bad allele. [tumour suppressor genes are associated with LOSS OF HETEROZYGOSITY in tumours]
so the 2nd mutation isn’t random, it is a copying event and happens more often.
in short what does the 2-hit hypothesis explain?
in some way 2 mutations causes the chromosome to lose both copies of the working tumour suppressor
what is the function of the tumour suppressor Rb?
it is in the G1 phase and tells a cell ‘STOP’ don’t divide.
what is the function of P53?
it functions at more than 1 checkpoint.
fixing the cell to continue with the cell cycle
or
says stop and apoptosis of the cell
what are some stresses on the cell P53?
DNA damage
hypoxia
heat/cold chock
mitotic spindle damage
what are some anti-cancer functions the p53 can cause for a cell?
cell cycle arrest ‘stop’
DNA repair
apoptosis
senescence
what are oncogenes mostly involved with?
hyperproliferation of cells
what is more common in familial cancers, oncogene mutations or tumour suppressor mutations?
tumour supressor mutations, as any germ line mutations the oncogenes would disrupt embryonic development, as all the cells would be hyper proliferate.
what is the difference between photo oncogenes and oncogenes?
proto oncogenes are needed normal control of cell division.
mutations the proto oncogene can turn it into an oncogene.
oncogenes cause hyperproliferation and can cause cancer.
