biology of cancer Flashcards
what is sporadic cancer?
cancer that is NOT caused by an INHERITED gene
how is cancer somatic?
there mutation occurs after conception
what is familial cancer?
cancer occurring in families more than expected by chance.
this would happen due to a combination of genetic and environmental factors.
what is telomere shortening?
acts as a tumour suppressor.
it limits the proliferation of a cell to only a few rounds of mitosis.
what is angiogenesis?
the formation of new blood vessels
what are the 5 characteristics of cancer cells?
- excessive proliferation
- avoids telomere shortening/senescence
- angiogenesis is needed
- metastasizes
- can’t be stopped by apoptosis
why are there multiple different driver mutations in multiple different key genes to make a malignant tumour?
as there are more than one key tumour suppressors to overcome to form a malignant tumour.
why do carcinogens increase the chance of cancer?
it increases the random rate of mutations
what is the difference between driver and passenger mutations?
driver mutations- ones that affect genes that control proliferation, apoptosis, immortality and can actually lead to cancer.
passenger mutations-these mutations are in genes that will not promote cancer.
what are proto-oncogenes?
if a gene mutation switches this on- it increases cancer risk by increasing excessive proliferation
what happens if there is a mutation in tumour suppressor genes?
TS genes are meant to inhibit events leading to cancer, if there is a loss of their function cancers can arise
what are some activities of tumour suppressor genes?
- stop excessive proliferation
- promote cell death
how does the excessive proliferation in cancer tumours take place?
normally the cell cycle is controlled by 4 checkpoints.
these are deregulated in cancer cells.
what is senescence?
cell can’t proliferate or re-enter the cell cycle.
altered cell function.
cancer cells need to avoid this to become immortal
what are telomeres?
the repeat sequences at the end of chromosomes.
how does telomere shortening work?
ever time the cell divides, the chromosome loses a telomere.
if all the telomeres are lost the chromosome reaches CRISIS which is bad.
so instead when the number of telomeres get short the P53 tumour suppressor starts senescence of that cell.
what happens if the chromosome reaches crisis?
there are no telomeres, so it is just broken, naked DNA ends.
these two ends get fused to form a loop.
the loops complicates during anaphase of mitosis and causes chromosome instability and mutations.
apoptosis needs to destroy this, to avoid destroying the genome.
how does inactive telomere shortening lead to cancer?
if P53 is inactive the chromosomes get rearranged (this is fine as they will rearrange until the cell dies) but in some cancer cells the TERT enzyme is activated by another mutation.
it adds telomeres to the damaged chromosomes so they can eep proliferating. and leads to cance.
what is the Rb enzyme?
Rb is important at the restriction point at the G1 checkpoint.
how do cancer tumours induce angiogenesis?
the release VEGF which induces new vessel growth
how do the secondary tumours form from the primary ones?
the tumour cells move in the blood vessels, when leading to the capillary beds the vessel lumen gets too small for the enlarged cancer cells. the cancer cells get stuck in the capillary and metastasise.
