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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
Q

Driver mutation

A

have growth advantage and are positively selected during cancer

: few mutations can confer a selective advantage and are recurrently found (in homozygote state)

26
Q

oncogenes

A

cancer genes in which the driver muations are activating or cause new functions

27
Q

tumour suprresors

A

driver mutations are inactiving the functions

28
Q

passenger mutation

A

no great advanteg

many mutations can be tolerated by somatic cells (often in heterozygote state)

29
Q

Drivermutationstend to cause

A

cause clonal expansions

30
Q

do Passenger mutation cause clonal expansion

A

amutationthat 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 drivermutation. This is known as a hitchhiker in evolutionary biology.

31
Q

hitchhiker

A

amutationthat 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 drivermutation

32
Q

Candidate driver mutations may also be distinguished from passengers

A

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
Q

how to identify driver mutation

A

one approach

by assuming driving mutations to be higher in cancer samples that background mutation rate

34
Q

bad

A

too much variabilty in cancer types, samples of cancer, genomes

too mnay false positive calls

35
Q

oncogene

A

gene with potential to cause cancer

36
Q

what are proto oncogenes

A

normal genes involved in cell growth and proliferation or inhibition of apoptosis

37
Q

One mutation is sufficient for role in cancer development

A

(DOMINANT, GAIN OF FUNCTION )

38
Q

what are the 3 mechanism of oncogenes activation

A

gene subsitution
gene amplification
chromosome rearrangemnet

39
Q

where does gene amplification occur

A

redundant part of teh dna
that contain critical dosage
dependent genes

40
Q

example of a dependent gene

A

myc

41
Q

what is myc

A

a potential transcription fator

a proto oncogene

42
Q

a mutation that activate the promoter causes

A

increase proto oncogene expression

43
Q

function of abl gene

A

ABL is activated to stimulate cell proliferation or differentiation, survival or death, retraction, or migration

44
Q

what causes it to do its functoin

A

In response to growth factors, cytokines, cell adhesion, DNA damage, oxidative stress, and other signal

45
Q

what does bcr abl gene cause

A

elevated tyrosine kinase activity

46
Q

function of ras protien

A

control cellular signalling pathway responsible for cell proliferation, cell differentiation, cell adhesion, apoptosis, and cell migration.

47
Q

what family does ras gene belong to

A

GTPase

48
Q

how does ras act

A

on or off switch

49
Q

what does it control normally

A

cell proliferation

50
Q

when mutated

A

cell divides uncontrollably

51
Q

where does the most common mutation take place

A

g12

52
Q

hoe is the activity of rsa governed

A 
binding to gtp (in active state) 
or gdp (in inactive state)
53
Q

how are tumour supressor genes normally caused by loss of function

A

RECESSIVE

54
Q

2 hit hypothesis

A

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
Q

prediction from the hypothesis

A

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
Q

which transcription factor binds does rb bind do

A

e2f

57
Q

function of p53

A

DNA repair, inducing apoptosis, transcription, and regulating the cell cycle

58
Q

what gene encodes p53

A

tp53

59
Q

overall function of p53

A

bind to dna to regulate gene expression and prevent teh accumilation of mutations

60
Q

BRCA1 production role of dna repair

A

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
Q

function

A

BRCA1 binds to BRCA2 which interacts with RAD51 to form a complex which is involved in DNA repair

62
Q

loss of rad51 leads to

A

increased unrepaired dna

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