cancer genet Flashcards

1
Q

what are cancer genes

A

changes in the DNA sequence of key genes, which are known as cancer genes. Therefore all cancers are genetic diseases.

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2
Q

factors that cause cancer

A

environmental- chemicals

exogenous factors- Viruses can introduce their own genes into cells

genetics-genes that make a person more susceptible to cancer can be passed to the next generation

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3
Q

Meats cooked at high temperatures

A

temperatures form chemicals that maycausechanges in your DNA, which maylead to cancer. Eating a large amount of well-done, fried or barbecued meats has been linked to an increased risk of colorectal, pancreatic and prostatecancer.

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4
Q

what does poorly diffrentaited mean

A

High grade
This means that the tumor cells don’t look like normal cells. They’re disorganized under the microscope and tend to grow and spread faster

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5
Q

which tumour is well differentiated

A

benign

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6
Q

6 halmarks of cancer

A

self sufficient in growth signals

insensitivity to anti growth signals

evading apoptosis

limitless replicative potential

sustained angoigenisis

tissue invasion and metastasis

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7
Q

define angoigenisis

A

is the growth of new blood vessels that tumors need to grow.

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8
Q

what do germ cells do

A

produce eggs and s

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9
Q

what are teh somatic cells

A

any cell of a living organism other than the reproductive cells.
]only mitosis

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10
Q

are somatic inheritable

A

no as they don’t affect any gametes or mioesis

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11
Q

do germline mutations affect their children

A

heritable
as the mutaions are in gametes
all the cells affected in the offspring

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12
Q

muations is somatic cells

A
Deletions
Duplications
Inversions
Translocations
Single base substitutions (point mutations – silent, nonsense, missense)
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13
Q

cancer genome will always aquire what sort of changes

A

epigenetics

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14
Q

what do they do

A

alter the chromotin structure and gene expression

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15
Q

how are they shown at DNA sequence level

A

methylation of some cytosine

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16
Q

what is Chromosome Instability

A

higher than normal rate of mis segregation of chromosome or part of chromosome

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17
Q

when does it happen and why

A

during mitosis
defective cell cycle
quality control mechansim

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18
Q

3 stages of cancer

A

initiation, promotion, and progression

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19
Q

The firststage of carcinogenesis,

A

initiation, results from an irreversible genetic alteration, most likely one or more simple mutations, transversions, transitions, and/or small deletions in DNA.

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20
Q

Cancer harbours a large number of somatic mutations

A

Cancer harbours a large number of somatic mutations

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21
Q

what does UV radiations do

A

The DNA damage from UV radiation leads to the formation of covalent bonds between two adjacent pyridimines (C and T) in the DNA molecule

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22
Q

what will the dna polymerase do

A

insert 2 adenine opposite teh dimer

if these occur in critical genes leads do aggresisve cell growth

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23
Q

signature of UV radaitaion

A

c to t transition

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24
Q

signature mutation of smoking

A

g to t transition

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25
Driver mutation
have growth advantage and are positively selected during cancer : few mutations can confer a selective advantage and are recurrently found (in homozygote state)
26
oncogenes
cancer genes in which the driver muations are activating or cause new functions
27
tumour suprresors
driver mutations are inactiving the functions
28
passenger mutation
no great advanteg | many mutations can be tolerated by somatic cells (often in heterozygote state)
29
Driver mutations tend to cause
cause clonal expansions
30
do Passenger mutation  cause clonal expansion
a mutation that has no effect on the fitness of a clone but may be associated with a clonal expansion because it occurs in the same genome with a driver mutation. This is known as a hitchhiker in evolutionary biology.
31
hitchhiker
a mutation that has no effect on the fitness of a clone but may be associated with a clonal expansion because it occurs in the same genome with a driver mutation
32
Candidate driver mutations may also be distinguished from passengers
by their tendency to have a greater impact on protein function than passenger mutations do. The functional impact of a mutation may be assessed on the basis of evolutionary conservation
33
how to identify driver mutation
one approach | by assuming driving mutations to be higher in cancer samples that background mutation rate
34
bad
too much variabilty in cancer types, samples of cancer, genomes too mnay false positive calls
35
oncogene
gene with potential to cause cancer
36
what are proto oncogenes
normal genes involved in cell growth and proliferation or inhibition of apoptosis
37
One mutation is sufficient for role in cancer development
(DOMINANT, GAIN OF FUNCTION )
38
what are the 3 mechanism of oncogenes activation
gene subsitution gene amplification chromosome rearrangemnet
39
where does gene amplification occur
redundant part of teh dna that contain critical dosage dependent genes
40
example of a dependent gene
myc
41
what is myc
a potential transcription fator | a proto oncogene
42
a mutation that activate the promoter causes
increase proto oncogene expression
43
function of abl gene
ABL is activated to stimulate cell proliferation or differentiation, survival or death, retraction, or migration
44
what causes it to do its functoin
In response to growth factors, cytokines, cell adhesion, DNA damage, oxidative stress, and other signal
45
what does bcr abl gene cause
elevated tyrosine kinase activity
46
function of ras protien
control cellular signalling pathway responsible for cell proliferation, cell differentiation, cell adhesion, apoptosis, and cell migration.
47
what family does ras gene belong to
GTPase
48
how does ras act
on or off switch
49
what does it control normally
cell proliferation
50
when mutated
cell divides uncontrollably
51
where does the most common mutation take place
g12
52
hoe is the activity of rsa governed
``` binding to gtp (in active state) or gdp (in inactive state) ```
53
how are tumour supressor genes normally caused by loss of function
RECESSIVE
54
2 hit hypothesis
In the first event in the two-hit model is an inherited mutation, however inheriting one germline copy of a damaged gene present in every cell in the body is not sufficient to enable this cancer to develop. A second hit (or loss) to the good copy in the gene pair could occur somatically, producing cancer.
55
prediction from the hypothesis
This hypothesis predicts that the chances for a germline mutation carrier to get a second somatic mutation at any of multiple sites in his/her body cells is much greater than the chances for a non-carrier to get two hits in the same cell.
56
which transcription factor binds does rb bind do
e2f
57
function of p53
DNA repair, inducing apoptosis, transcription, and regulating the cell cycle
58
what gene encodes p53
tp53
59
overall function of p53
bind to dna to regulate gene expression and prevent teh accumilation of mutations
60
BRCA1 production role of dna repair
phosphorylated by ATM and CHK2 in response to double – stranded DNA breaks (i.e. these could be produced due for example by ionizing radiation).
61
function
BRCA1 binds to BRCA2 which interacts with RAD51 to form a complex which is involved in DNA repair
62
loss of rad51 leads to
increased unrepaired dna