Cellular adaptions Flashcards
cell population controlled by
- Rate of cell proliferation
- Physiological and pathological
- Rate of cell differentiation
- Rate of cell death by apoptosis
Increased numbers=
Decreased=
Increased numbers= proliferation
Decreased= cell death
Control of cell proliferation by
- proto-oncogenes and tumour suppressor genes
- chemical mediators from microenvironemnt
signalling moelcules modulate gene expression by binding to receptors on the :
- cell membrane
- cytoplasm
- nucleus
cell cycle overview
G1
G1 checkpoint
S phase
G2
G2 checkpoint (restriction point)
M and cytokinesis
G1
cellular contents excluding the chromosome are duplicated
G1 checkpoint
- Is the cell big enough
- Is environment favourable
- Is DNA damaged?
S phase
each of the 46 chromosomes are duplicated by the cell
G2
cell doublechecks the duplicated chromosomes for error- makes repairs
G2 checkpoint (restriction point)
- Is all DNA replicated?
- Is the cell big enough?
- Enter M
M and cytokinesis- mitosis
- Division of cell to produce 2 identical sister cells
- Prophase
- Metaphase
- Anaphase
- Telophase and cytokinesis

if there are defects in checkpoints
uncontrolled division
what regulate checkpoints
cyclins
the restriction (R) point is governed by
P53

the majority of cells that pass the R point will
complete cell cycle- point of no return
the R point is the
most commonly altered checkpoint in cancer cells
checkpoint activation at the R point
delays cell cyel and triggers DNA repair mechanisms or apoptosis via P53
P53- the guardian of the genome - activators
- DNA damage
- Oncogene expression
- Hypoxia
- Oxidative stress
- Nutrient deprivation
what occurs as a reuslt of P53
- Senescence
- Cell cycle arrest
- Apoptosis
- DNA repair
all results of P53 activation result in
tumour supression
in 70% of cancers
P53 mutation
P53 pathway
- DNA is damaged
- Increase in activated P53 either induces
- Apoptosis
- Or Increase in p21
- Prevent phosphorylation of cyclins
- Cell cycle arrest
- Allow DNA repair
cyclins and CDK
- Cyclin dependent kinases (CDKs) become activated when cyclins bind
what do CDKs do
- phosphorylate proteins which have downstream effects such as increased transcription of proteins which increase cellular proliferation











