Lecture 24 Flashcards
Intestinal epithelial cells: replaced every –
few days
Skin cells: replaced every –
2-4 weeks
Hepatocytes, heart muscle cells, neurons: replaced only during –
healing processes
Cancer occurs when the mechanisms that maintain these normal growth rates malfunction to cause –
excess cell division
A cell with impaired abilities to control its proliferation and tissue characteristics.
transformed cell
CANCER IS A – DISEASE
GENETIC
Cancer results from multiple genetic changes in a –
single cell
Cancer = Accumulation of mutations over lifetime:
late life disease
proto-oncogenes → oncogenes (gain-of-function)
promote cell growth
tumor suppressor→loss of function
restrain cell growth
care-taker genes→loss of function
protect genome integrity (repair)
Encode proteins that stabilize the genome
Tumors arise from both increase in point mutations and chromosome instability
care taker genes
Tumor cells frequently show – (i.e. highly aberrant chromosome compliments).
aneuploidy
Something in M phase cytoplasm causing G1 nuclei to enter mitosis. (induces mitosis)
Maturation Promoting Factor (MPF)
MPF is a –
Cdk and a cyclin.
Cells divide when cycling band decays. Cycling band called a –
cyclin.
T/F: The Cdk is only active when it is bound to cyclin.
true
The – of cyclin goes up and down with the cell cycle, therefore the kinase activity of Cdk also goes up and down with the cell cycle.
concentration
Cdc2 kinase is a –. In yeast there are two cyclins, a G1 cyclin and a mitotic cyclin.
Cdk
In yeast, a – in mitotic cyclin required to enter G1.
Decrease
Retinoblastoma encodes a protein that inhibits –, required for activation of DNA synthesis machinery
transcription factor E2F
Rb is a – of Cdk
target
Cyclins and CDKs are –
proto-oncogenes
Mutation of cyclins can lead to – expression of cyclins, resulting in kinases that are always active
constant
Other mutations can lead to CDKs that are active –
without cyclin
Mutations of – can stimulate constant DNA synthesis and mitosis
proto-oncogenes
Growth factors are – that stimulate cells to divide
mitogens
RAS is a G-protein that kinase cascade so RAS is a –
proto-oncogene
All cancer cells acquire same six characteristics
Ability to proliferate without –
external signal
All cancer cells acquire same six characteristics
Fail to sense signals that – cell division
restrict
All cancer cells acquire same six characteristics
– replicative potential
limitless
All cancer cells acquire same six characteristics
change their - to other cells
attachment
All cancer cells acquire same six characteristics
obtain a – as they grow larger
blood supply
All cancer cells acquire same six characteristics
tissue invasion and –
metastasis
T/F: there are various pathways to cancer
true
Some cancers are inherited
Heterozygous for mutant allele
Good allele is –, leading down the road to cancer
lost
familial retinoblastoma – eye tumors
many
sporadic retinoblastoma – eye tumors
one
loss of heterozygosity through – and –
nondisjunction and mitotic recombination
Effectors that can Inhibit Cell Cycle Machinery
– (induces DNA damage in a cell)
Ionizing irradiation
Inhibits the kinase activity of the G1 cdk and prevents cells from entering into S.
p21
mutations can be found in 50% of human cancers.
p53
X-ray damages DNA → P53 is stabilized when DNA is damaged by phosphorylation = active p53 –>
production of p21
Retinoblastoma is a – gene
tumor-suppressor
pass if cell size is adequate and chromosome replication is successfully completed
G2 checkpoint
pass if all chromosomes are attached to mitotic spindle
metaphase checkpoint
pass if cell size is adequate, nutrient availability is sufficient, and growth factors (signals from other cells) are present
G1 checkpoint
pass if DNA replication is complete and has been screened to remove base-pair mismatch or error
S-phase checkpoint
