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A Level Biology Year 2 > 3.8.2 Gene expression and cancer > Flashcards

3.8.2 Gene expression and cancer Flashcards

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1
Q

Totipotent stem cells are able to differentiate into..

A

any type of body cell

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2
Q

multicellular organisms are made up from…

A

many different types of specialised cells

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3
Q

specialised cells originated from..

A

stem cells

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4
Q

unspecialised cells that can develop into other cell types are called

A

stem cells

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5
Q

Two main sources of stem cells can be found..

A

in the embryo, adult tissues

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6
Q

these types of stem cells are only present in mammals in the first few divisions of the embryo

A

totipotent (very early embryo)

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7
Q

these types of stem cells are still found in the embryo but have lost their ability to develop into differentiate into placental cells

A

pluripotent

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8
Q

adult stem cells can be one of two types

A
  1. multipotent stem cells

2. unipotent stem cells

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9
Q

these types of stem cells can differentiate into a limited number of stem cells e.g. bone marrow cells can form RBC and WBC

A

multipotent stem cells

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10
Q

These types of stem cells can only differentiate into ONE type of cell

A

unipotent

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11
Q

Stem cells specialise because…

A

different genes are expressed (turned off and on)

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12
Q

All cells contain the same DNA - true or false?

A

true

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13
Q

Stem cells all contain the same genes - true or false?

A

true

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14
Q

Molecules which regulate the expression of genes are called..

A

transcription factors

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15
Q

Where do transcription factors bind to regulate gene expression?

A

upstream of the gene (promoter region)

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16
Q

What do transcription factors do to regulate gene expression?

A

encourage binding of RNA polymerase (turn on genes) or prevent RNA polymerase binding (turn off genes)

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17
Q

Where are transcription factors found?

A

nucleus

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18
Q

When a cell receives a signal to express a gene what does the transcription factor do?

A

moves from the cytoplasm to the nucleus

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19
Q

Specialised cells all look different - why?

A

they all express different genes and thus proteins - this determines the cells overall structure

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20
Q

Which stem cell can red blood cells originate from?

A

bone marrow stem cells

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21
Q

Transcription is when

A

DNA is copied into mRNA

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22
Q

Translation is when

A

mRNA is translated into a sequence of amino acids

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23
Q

what are cardiomyocytes?

A

heart cells

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24
Q

what can stem cells be used for?

A

treat diseases e.g. paralysis - replace damaged cells/tissues

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25
Q

benefits of using stem cells in medicine?

A

save life and improve quality of life for many people

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26
Q

iPS cells stands for?

A

induced pluripotent stem cells

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27
Q

What are iPS cells?

A

created in the lab - reprogramming adult stem cells to become pluripotent

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28
Q

What are the limitations with adult stem cells?

A

limited differentiation capacity - they are mulitpotent

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29
Q

Where do we source embryonic stem cells from?

A

embryos created in the lab from IVF

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30
Q

Embryonic stem cells are classified as one of twp types

A
  1. totipotent (very early embryo)

2. pluripotent (early embryo)

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31
Q

Issue surrounding embryonic stem cells?

A
  1. ethics surrounding the sourcing of the embryos (embryo will be destroyed)
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32
Q

In all cells which genes will be permanently expressed?

A

genes involved in respiration

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33
Q

All organisms develop from a fertilised egg - what is the scientific name for this?

A

zygote

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34
Q

Zygotes divide by what process?

A

Mitosis

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35
Q

Can specialised cells change into other cell types?

A

animals - no

plants - yes - shoots/roots

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36
Q

Name a hormone that can regulate transcription

A

oestrogen

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37
Q

What type of hormone is oestrogen?

A

steroid hormone

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38
Q

How can oestrogen enter the cell?

A

lipid soluble and diffused through the phospholipid bilayer

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39
Q

What does oestrogen bind to to regulate transcription?

A

a binding site/receptor site on the transcription factor

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40
Q

When oestrogen binds to the receptor on the transcription factor what happens?

A

The DNA binding site on the transcription factor is now able to bind to DNA (transcription activated)

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41
Q

Why is oestrogen able to bind the receptor on transcrption factor?

A

oestrogen has a complementary shape the the receptor

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42
Q

What property of oestrogen allows it to diffuse through the phospholipid bilayer?

A

lipid soluble

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43
Q

Who proposed the structure of DNA?

A

Watson and Crick

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44
Q

What is meant by epigenetics?

A

heritable changes in gene function without change the base sequence of DNA

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45
Q

What sort of environmental factors might influence phenotype?

A

stress, sunlight, chemical exposure, diet,

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46
Q

How is your DNA organised into chromosomes?

A

DNA wrapped around proteins called histones (forming chromatin)

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47
Q

DNA and histones are covered in chemicals known as ..

A

tags

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48
Q

Tags attached to the DNA and histones form a second layer known as..

A

the epigenome

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49
Q

What determines the shape of the DNA and histone complex?

A

epigenome

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50
Q

DNA that is tightly packed, preventing transcription factors binding leads to

A

gene silencing

51
Q

DNA that is loosely packed, allowing transcription factors to access the DNA leads to…

A

gene activation/expression

52
Q

DNA code is fixed but your epigenome is…

A

flexible

53
Q

What does your epigenome respond to?

A

the environment

54
Q

Tags attached to DNA are knowns as

A

methylation

55
Q

Tags attached to histones are knowns as

A

actylation

56
Q

When the association of DNA and histones is weak what does this mean for gene expression?

A

transcription factors can access the DNA and turn ON a gene

57
Q

Tight association of DNA and histones affects gene expression - how?

A

prevents transcription factors binding to the DNA so turns OFF gene expression

58
Q

tight association of DNA and histones is brought about by..

A

decreased acteylation and increased methylation

59
Q

loose association of DNA and histones is brought about by..

A

increased acteylation and decreased methylation

60
Q

What does decreased acetylation do to the histone proteins?

A

increased + charge so more strongly attracted to phosphate in DNA

61
Q

Why does methylation prevent transcription?

A
  1. prevents transcription factors binding to DNA

2. attracts proteins that would condense DNA

62
Q

increased gene expression is brought about by

A

more acetylation and less methylation

63
Q

reduced gene expression is brought about by

A

less acetylation and more methylation

64
Q

acetyl group binds to

A

histones

65
Q

methyl group binds to

A

DNA

66
Q

more acetylation EQUALS

A

increased gene expression/DNA loosely packed

67
Q

MORE methylation EQUALS

A

reduced gene expression/DNA tightly packed

68
Q

LESS acetylation EQUALS

A

reduced gene expression/DNA tightly packed

69
Q

LESS methylation EQUALS

A

increased gene expression/DNA loosely packed

70
Q

epigenetics has been associated with what type of disease

A

cancer

71
Q

do epigenetic changes alter the DNA base sequence?

A

NO

72
Q

Preventing gene expression can also be done at the level of mRNA - how?

A

mRNA is cut up to prevent it being translated

73
Q

what type of molecule is involved in silencing mRNA?

A

siRNA

74
Q

Once siRNA is formed what does it associate with?

A

an enzyme

75
Q

What is unique about the siRNA and the mRNA it is going to silence?

A

Their base sequences are complementary

76
Q

enzymes can remove acetyl groups - how would this affect transcription?

A

less acetylation - reduced gene expression (mRNA not transcribed)

77
Q

enzymes can remove acetyl groups - how would this affect DNA-histone complex?

A

tightly packed

78
Q

All tumours are cancerous - true or false?

A

false

79
Q

what is a tumour?

A

mass of cell caused by uncontrolled cell division

80
Q

cancer is…?

A

abnormal mass of cells that invades neighbouring tissues or can break away forming secondary tumours

81
Q

two types of tumours are?

A

benign and malignant

82
Q

Which tumour is cancerous?

A

malignant

83
Q

which tumour does not invade neighbouring cells?

A

benign

84
Q

How do cancers spread?

A

blood stream or via lymphatic system

85
Q

name the two genes that control cell division

A

proto-oncogenes and tumour suppressor genes

86
Q

What is the function of a proto-oncogene?

A

stimulate cell division

87
Q

what is the function of a tumour suppressor gene?

A

slow down cell division

88
Q

what would happen if there was a mutation in a proto-oncogene?

A

turn into oncogene - uncontrolled cell division

89
Q

what would happen if there was a mutation in a tumour suppressor gene?

A

uncontrolled cell division

90
Q

Mutations in genes that control cell division cause…

A

cancer

91
Q

Which type of tumour grows more slowly?

A

benign

92
Q

How might tumour cells look compared to normal cells?

A

different shape
larger/darker nucleus
divide more rapidly

93
Q

what does methylation do to the DNA?

A

adds a methyl group to it

94
Q

In a proto-oncogene what happens to the methylation of the DNA to turn it into a oncogene?

A

hypomethylation (reduced methylation)

95
Q

In a tumour suppressor gene what happens to the methylation of the DNA to cause cells to divide out of control?

A

hypermethylation (increase methylation) - turn gene off

96
Q

which type of tumour grows rapidly?

A

malignant

97
Q

which type of tumour involves using radiotherapy as well as surgery?

A

malignant

98
Q

Which type of tumour remains compact

A

benign

99
Q

which type of tumour grows finger like projections into surrounding tissue?

A

malignant

100
Q

which type of tumour has a capsule?

A

benign

101
Q

what are oncogenes?

A

mutated pro-oncogenes

102
Q

How to proto-oncogenes stimulate cell growth?

A

growth factor binds to receptor stimulating cell division

103
Q

An oncogene can become permanently activated for one of two reasons?

A
  1. oncogene codes for a receptor that is permanently activated
  2. oncogene codes for excessive growth factor
104
Q

How do tumour suppressor genes work?

A

they slow down cell division, repair DNA or tell cells to die

105
Q

what does apoptosis mean?

A

programmed cell death

106
Q

Which gene regulates cell division and prevents formation of tumours?

A

TSG

107
Q

if a TSG is mutated what is the consequence?

A

stops inhibiting cell division and cells divide out of control

108
Q

some cancers are inherited others are…

A

aquired

109
Q

what does the TP53 gene code for?

A

p53 protein

110
Q

why is p53 important?

A

p53 protein is important in apoptosis

111
Q

A mutation in the TP53 will lead to…?

A

inactive p53 protein and no apoptosis, damaged cells continue to divide

112
Q

mutation in a proto-oncogene leads to

A

oncogenes being activated - uncontrolled cell division

113
Q

mutation in a TSG leads to

A

TSG being inactivated - uncontrolled cell division

114
Q

abnormal methylation is common in many tumours - what effect can this have on a TSG?

A

hypermethylation of a TSG - inactivity - uncontrolled cell division (p53 not made)

115
Q

what is hypermethylation?

A

addition on methyl groups on DNA - switching off gene expression

116
Q

transcription of genes is controlled by protein molecules called?

A

transcription factors

117
Q

How do transcription factors move?

A

from the cytoplasm to the nucleus

118
Q

Expression of genes can be affected by other molecules e.g. hormones e.g. ….

A

oestrogen

119
Q

can epigenetic changes be inherited?

A

yes!

120
Q

How would methylation of a TSG lead to cancer?

A
  1. Methylation prevents transcription of gene;turns off gene expression
  2. Protein (p53) not produced that prevents cell division/ causes cell death/apoptosis;
  3. No control of mitosis; uncontrolled cell growth due to mitosis
121
Q

Which cancer gene would be inhibited due to increased methylation?

A

tumour suppressor gene (TSG) - gene not transcribed!

122
Q

give one way benign tumours differ from malignant tumours

A

Cells of benign tumours cannot spread to other parts of the body/metastasise
OR
Cells of benign tumours cannot invade neighbouring tissues;

123
Q

Describe how alterations to TSG can lead to development of tumours

A
  1. increased methylation of TSG
  2. mutations in TSG
  3. TSG not expressed
  4. Leading to rapid uncontrolled cell division

A Level Biology Year 2 (25 decks)

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