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BM 210: Introduction to Biochemistry > Block E Part 3: Stem Cells and Cancer > Flashcards

Block E Part 3: Stem Cells and Cancer Flashcards

1
Q

What type of cells are stem cells?

A

Immortal, unspecialised cells
(Lecture 3, Slide 3)

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2
Q

What 2 eventual cell fates can stem cells pick between?

A

Prolonged self-renewal of identical copies
Differentiation into any tissue type
(Lecture 3, Slide 3)

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3
Q

Rank these 4 terms from most cell types able to be differentiated into, to least cells types able to be differentiated into: Pluripotent, Unipotent, Totipotent and Multipotent

A

Totipotent
Pluripotent
Multipotent
Unipotent
(Lecture 3, Slide 5)

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4
Q

What does totipotent mean?

A

It can generate all of the cells in the adult + placenta
(Lecture 3, Slide 6)

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5
Q

Is the zygote created by fertilisation multipotent, pluripotent, unipotent or totipotent?

A

Totipotent
(Lecture 3, Slide 6)

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6
Q

How can the amount of cells stem cells can become decrease as development proceeds?

A

As cells become committed to one or another specific fate
(Lecture 3, Slide 6)

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7
Q

What can pluripotent steam cells theoretically give rise to?

A

Every cell type in the animal body proper
(Lecture 3, Slide 7)

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8
Q

Do pluripotent stem cells have a limit on how many times they can proliferate?

A

No they can proliferate indefinitely
(Lecture 3, Slide 7)

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9
Q

What 2 processes are stem cells important for?

A

Tissue repair and homeostasis
(Lecture 3, Slide 8)

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10
Q

What are the 5 types of pluripotent stem cell lines?

A

Embryonic stem cells (ES)
Embryonic carcinoma cells (EC)
Embryonic germ cell (EG)
Epiblast stem cells
Induced pluripotent stem cells (iPS)
(Lecture 3, Slide 9)

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11
Q

What is cleavage?

A

The division of cells in the early embryo
(Lecture 3, Slide 11)

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12
Q

Do zygotes undergo rapid cell division with significant or not significant growth?

A

Not significant growth
(Lecture 3, Slide 11)

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13
Q

What does cleavage produce?

A

A cluster of cells the same size as the original zygote
(Lecture 3, Slide 11)

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14
Q

What is a blastocyst?

A

A structure consisting of 128 cells
(Lecture 3, Slide 12)

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15
Q

What 2 cells masses is the blastocyst composed of?

A

An inner cell mass also known as an embryoblast and an outer cell mass also known as a trophoblast
(Lecture 3, Slide 12)

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16
Q

What does the inner cell mass (embryoblast) of the blastocyst go on to form?

A

Embryonic stem cells
(Lecture 3, Slide 12)

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17
Q

What does the outer cell mass (trophoblast) of the blastocyst go on to form?

A

The placenta
(Lecture 3, Slide 12)

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18
Q

How are embryonic stem cells kept in an undifferentiated state when grown in a lab?

A

They are maintained on “feeder layers” and you can then provide the factor(s) that suppress differentiation or promotes self-renewal
(Lecture 3, Slide 16)

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19
Q

What is an example of one factor with differentiation-inhibiting activity for mouse embryonic stem cells?

A

Leukaemia inhibitory factor (LIF)
(Lecture 3, Slide 16)

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20
Q

What occurs in derivation of embryonic stem cell lines in vitro?

A

The inner cell mast from the blastocyst is isolated and cultured on a layer of feeder cells (commonly mouse fibroblasts) the pluripotent stem cells then starts to divide forming colonies
(Lecture 3, Slide 17)

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21
Q

What happens to lab grown embryonic stem cells after cell lines have been formed?

A

They can be differentiated into many cell types
(Lecture 3, Slide 18)

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22
Q

What are 2 things that genetically modified mouse embryonic stem cells can be used for?

A

We can delete a gene to find out what it does or add in a gene mutation to create a “model” of a human genetic disorder
(Lecture 3, Slide 19)

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23
Q

What is “regenerative medicine”?

A

Using stem cells to replace or repair tissues/organs damaged by disease/injury
(Lecture 3, Slide 20)

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24
Q

What are 5 scenarios that regenerative medicine can be used in?

A

Brain - For stroke
Spinal cord damage after accident
Liver - For cirrhosis
Kidney - For chronic kidney disease
Lung - for cystic fibrosis
(Lecture 3, Slide 20)

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25
Q

What are 3 examples of potential problems of developing transplantation stem cell therapies?

A

Answers include:
Stem cells are high in demand but hard to grow
Must be able to differentiate in a controlled manner
Injecting embryonic stem cells may cause a teratoma or cancer
Are they free from infectious diseases from donor or lab?
(Lecture 3, Slide 21)

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26
Q

What are 3 different stem cell therapy concepts?

A

Direct injection into injury
Differentiate in vitro (in lab) then inject
“Organoid” differentiation in vitro then transplant
(Lecture 3, Slide 23)

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27
Q

What are 2 problems with the “direct injection into injury” stem cell treatment concept?

A

Do they integrate and form part of regenerated tissue?
Do they secrete healing factors in the region?
(Lecture 3, Slide 23)

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28
Q

What is a problem with the “differentiate in vitro, then inject” stem cell treatment concept?

A

Do they integrate and form part of regenerated tissue?
(Lecture 3, Slide 23)

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29
Q

What is a problem with the “organoid differentiation in vitro, then transplant” stem cell treatment concept?

A

Do they carry out normal function of the tissue?
(Lecture 3, Slide 23)

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30
Q

What is the problem with sourcing stem cells?

A

It is technically and ethically difficult
(Lecture 3, Slide 31)

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31
Q

Why do stem cells need to be genetically identical to the patient?

A

To avoid immune rejection
(Lecture 3, Slide 31)

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32
Q

What are 2 options to source stem cells genetically identical to the patient?

A

Somatic cell nuclear transfer
Induced pluripotency
(Lecture 3, Slide 31)

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33
Q

What is a somatic cell?

A

Any cell in the body other than reproductive cells
(Lecture 3, Slide 32)

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34
Q

What is somatic cell nuclear transfer?

A

The nucleus of a somatic cell is transferred into an egg cell which has had its nucleus removed which results in a new organism being created or can sometimes result in embryonic stem cells being created for research or treatment purposes
(Lecture 3, Slide 32)

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35
Q

Why does somatic cell nuclear transfer work?

A

The egg environment wipes all of the programming information from the somatic nucleus, turning it back into its early developmental state and it now acts like a newly fertilised egg which can produce a living animal
(Lecture 3, Slide 33)

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36
Q

What is induced pluripotency (iP)?

A

Somatic cells are “reprogrammed” back into pluripotent cells
(Lecture 3, Slide 34)

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37
Q

How are somatic cells reprogrammed to be pluripotent in induced pluripotency (iP)?

A

Regulatory transcription factors (c-myc, Sox2, Oct4, Klf4) are introduced into the cells; these force somatic cells to become stem cells
(Lecture 3, Slide 34)

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38
Q

What are 2 advantages of induced pluripotent stem cells?

A

They are easier to create
They don’t require human oocytes (eggs) to create
(Lecture 3, Slide 35)

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39
Q

What are 3 disadvantages of induced pluripotent stem cells?

A

Not clear if programming is “complete”
Evidence that cells develop cancer-like mutations due to selection for fast growth - could cause cancer in recipients
Unlikely to be used as therapy - only for research
(Lecture 3, Slide 35)

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40
Q

How can induced pluripotent stem cells be used to study whatever cell type you want?

A

As they can then be artificially differentiated again into the cell type you want
(Lecture 3, Slide 38)

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41
Q

Why are induced pluripotent stem cells particularly good for studying brain disorders?

A

As we don’t normally have access to brain tissue or biopsies
(Lecture 3, Slide 39)

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42
Q

What is a biopsie?

A

An extraction of cells or tissues samples for examination to determine the presence or extent of a disease
(Lecture 3, Slide 39)

43
Q

What are neoplastic cells?

A

Abnormal growth of cells, also known as a tumour
(Lecture 4, Slide 4)

44
Q

When is a tumour said to be benign?

A

When the neoplastic (tumour) cells have not yet become invasive
(Lecture 4, Slide 4)

45
Q

How do you usually achieve a complete cure of uncontrolled cell growth when the tumour is benign?

A

Removing or destroying the mass locally
(Lecture 4, Slide 4)

46
Q

When is a tumour considered to be a true cancer?

A

When it is malignant
(Lecture 4, Slide 4)

47
Q

When is a tumour considered to be malignant?

A

When its cells have acquired the ability to invade surrounding tissue
(Lecture 4, Slide 4)

48
Q

What does a tumour developing the ability to invade surrounding tissue allow it to do?

A

Enter blood / lymphatic vessels and be carried to other parts of the body to form secondary tumours
(Lecture 4, Slide 4)

49
Q

What are secondary tumours called?

A

Metastases
(Lecture 4, Slide 4)

50
Q

What generally kills cancer patients?

A

The more widely the cancer spreads, the harder it is to eradicate, therefore it is usually the metastases that kill the patient
(Lecture 4, Slide 4)

51
Q

What do most tumours arise from?

A

A single abnormal cell
(Lecture 4, Slide 5)

52
Q

How long do tumours take to become noticeable (palpable)?

A

It can take years
(Lecture 4, Slide 5)

53
Q

What is the typical doubling time (time taken for the tumour cell population to double) of a tumour?

A

Breast tumour usually takes about 100 days but more virulent tumours may grow much more rapidly
(Lecture 4, Slide 5)

54
Q

Does the chance of developing cancer increase or decrease as age increases?

A

It increases
(Lecture 4, Slide 6)

55
Q

How many independent accidental mutations (hits) is it believed to take to develop cancer?

A

Between 5 and 8 that occur randomly over time
(Lecture 4, Slide 6)

56
Q

What are 2 reasons the chance of developing cancer increase as age increases?

A

As time increases, there is a higher chance that you will have picked up the amount of “hits” to develop cancer and often the chance of mutations occurring increases with age
(Lecture 4, Slide 6)

57
Q

Excluding age, what is another factor that increases an individual’s chance of developing cancer?

A

Smoking cigarettes
(Lecture 4, Slide 7)

58
Q

What is required for a single abnormal cell to give rise to a tumour?

A

It’s aberration (change) must be able to be inherited by its descendant daughter cells
(Lecture 4, Slide 8)

59
Q

As the aberration (change) of an abnormal cell must be able to be inherited by its descendant daughter cells, what does the development of cancer depend on?

A

Genetic changes
(Lecture 4, Slide 8)

60
Q

How do tumour cells contain “somatic mutations”?

A

They have one or more shared detectable abnormalities in their DNA sequence which distinguishes them from normal cells surrounding the tumour
(Lecture 4, Slide 8)

61
Q

How does a tumour develop?

A

Through repeated rounds of mutation and proliferation, where at each step a single cell undergoes a mutation that either enhances cell proliferation or decreases cell death, making its progeny (descendant cells) the dominant clone in the tumour
(Lecture 4, Slide 9)

62
Q

Are cancer cells genetically stable?

A

No
(Lecture 4, Slide 10)

63
Q

Why are cancer cells genetically unstable?

A

As the accumulate genetic changes at an abnormally rapid rate
(Lecture 4, Slide 10)

64
Q

What are 3 abnormalities in the sets of chromosomes that are often present in cancer cells?

A

Duplications, deletions and translocations
(Lecture 4, Slide 10)

65
Q

What are 2 things that can contribute to the genetic instability observed in cancer cells?

A

Defects in the ability to repair DNA damage or to correct replication errors of various kinds
(Lecture 4, Slide 10)

66
Q

How do cancer cells pile up on each other during confluence and why don’t normal cells?

A

Normal cells become inhibited from moving and diving when culture reaches confluence ( where the cells touching each other) but transformed cancer cells continue moving and dividing, and pile up in layers due to lack of space
(Lecture 4, Slide 11)

67
Q

How is the process of metabolising glucose different in tumour cells than normal cells?

A

In normal cells, after glycolysis, they will start the process of oxidative phosphorylation, provided they have the oxygen needed to do this

In tumour cells they will undergo and fermentation and produce abundant amounts of lactate even in the presence of oxygen
(Lecture 4, Slide 12)

68
Q

What causes tumour cells to undergo fermentation even when in conditions where oxygen is present?

A

It results from a greatly increased rate of glycolysis resulting from a very large increase of the rate of glucose import
(Lecture 4, Slide 12)

69
Q

Why do tumour cells undergo fermentation even when in conditions when oxygen is present?

A

It fulfils their requirement for biosynthesis of a large supply of the small-molecule building blocks that can be produced from glucose to sustain their rapid growth
(Lecture 4, Slide 12)

70
Q

Excluding increased cell division, what in another way in which cancer can develop?

A

Inhibition of apoptosis
(Lecture 4, Slide 13)

71
Q

What 2 categories can cancer-critical mutations fall into?

A

Dominant and recessive
(Lecture 4, Slide 15)

72
Q

What is the difference between dominant and recessive cancer-critical mutations?

A

A dominant mutation (AKA an overactivity mutation) results in a gain in function and creates an oncogene which enables the oncogene to promote cell transformation (into malignant cells)

A recessive mutation (AKA an underactivity mutation) results in a loss in function (e.g inactivating tumour suppressor gene) but it has no effect until a second mutation event inactivates the second gene copy which effectively eliminates the tumour suppressor gene, promoting cell transformation
(Lecture 4, Slide 15)

73
Q

What happens when Rous sarcoma virus infects a cell?

A

Its RNA genome is copied into DNA by reverse transcription (Retrovirus) and the DNA is inserted into the host’s genome where it can be inherited by subsequent generations of cells, but in the process something makes the host cell cancerous
(Lecture 4, Slide 20)

74
Q

Why does the Rous sarcoma virus make host cells cancerous?

A

When infecting a previous cell the virus had accidentally picked up a gene called c-Src which is present in the normal vertebrate genome and it had undergone mutation to become an oncogene called (v-Src)
(Lecture 4, Slide 20)

75
Q

What is an oncogene?

A

A mutated gene which has the potential to cause cancer
(Lecture 4, Slide 20)

76
Q

What is an oncogene called before it becomes mutated?

A

A proto-oncogene
(Lecture 4, Slide 20)

77
Q

What does a proto-oncogene play a role in regulating?

A

Normal cell division
(Lecture 4, Slide 20)

78
Q

What does a deletion or point mutation in a proto-oncogene lead to?

A

A hyperactive protein made in normal amounts
(Lecture 4, Slide 21)

79
Q

What does a regulatory mutation (deactivating a regulator) in a proto-oncogene lead to?

A

A normal protein which is greatly overproduced
(Lecture 4, Slide 21)

80
Q

What does a gene amplification mutation in a proto-oncogene lead to?

A

A normal protein which is greatly overproduced
(Lecture 4, Slide 21)

81
Q

What 2 things can as chromosome rearrangement mutation in a proto-oncogene lead to?

A

A nearby regulatory DNA sequence causing a normal protein to be overproduced

Fusion to actively transcribed gene produces hyperactive fusion protein
(Lecture 4, Slide 21)

82
Q

What mutation do Ras (from lecture 1) oncogenes in human and animal tumours contain and what does this result in?

A

Point mutations that create a hyperactive Ras protein that cannot shut itself off by hydrolysing its bound GTP to GDP
(Lecture 4, Slide 22)

83
Q

Are Ras oncogene point mutations dominant or recessive?

A

Dominant
(Lecture 4, Slide 22)

84
Q

Why are Ras genes one of the most important cancer-critical genes?

A

As one of the 3 human Ras family members are mutated in ~30% of all human cancers
(Lecture 4, Slide 22)

85
Q

How can the epidermal growth factor (EGF) receptor become oncogenic?

A

It can mutate to become active in the absence of EGF
(Lecture 4, Slide 24)

86
Q

How was the first tumour suppressor discovered?

A

By studying retinoblastoma cancer
(Lecture 4, Slide 26)

87
Q

How does retinoblastoma cancer arise?

A

Cells in the retina of the eye being converted to a cancerous state
(Lecture 4, Slide 26)

88
Q

What is odd about retinoblastoma cancer?

A

Cells are converted to cancerous in an unusually small amount of mutations
(Lecture 4, Slide 26)

89
Q

What mutation is present in every somatic cell of all patients who suffer from retinoblastoma cancer?

A

A deletion or loss of function mutation in the Rb gene
(Lecture 4, Slide 26)

90
Q

What does a deletion or loss of function mutation in the Rb gene present in all patients with retinoblastoma cancer result in?

A

Rb protein can be turned off, allowing cells to enter the cell cycle inappropriately
(Lecture 4, Slide 26)

91
Q

What are the 2 forms of retinoblastoma?

A

Hereditary and non-hereditary
(Lecture 4, Slide 27)

92
Q

What is the difference between the hereditary and non-hereditary forms of retinoblastoma cancer?

A

In the hereditary form, all cells in the body lack 1 of the normal 2 functional copies of the Rb tumour suppressor gene meaning for a tumour to occur only 1 somatic mutation needs to occur to disable the other functional copy.

In the non-hereditary form all cells contain 2 functional copies of the Rb tumour suppressor gene, meaning that for a tumour to occur 2 somatic mutations disabled both genes needs to occur in a single line of cells
(Lecture 4, Slide 27)

93
Q

What are 4 possible ways for a cell with 1 healthy Rb gene copy and 1 unhealthy Rb gene copy to lose its remaining good copy?

A

Answers Include:

Nondisjunction - causing chromosome loss
Chromosome loss , then chromosome duplication
Mitotic recombination event
Gene conversion during mitotic recombination
Deletion
Point mutation
Epigenetic change
(Lecture 4, Slide 28)

94
Q

What gene do over 50% of human cancers carry loss of function mutations for?

A

p53 gene
(Lecture 4, Slide 29)

95
Q

What are 5 things which cause p53 levels to rise?

A

Hyperproliferative signals, DNA damage, hypoxia (not enough oxygen available), telomer shortening and other things which stress cells
(Lecture 4, Slide 31)

96
Q

What are 3 things that p53 can do to a cell in response to cell stress signals?

A

It can either arrest cell cycling in a way that allows the cell to adjust and survive, trigger cell suicide by apoptosis or cause cell “senescence” - an irreversible cell-cycle arrest
(Lecture 4, Slide 31)

97
Q

What is the most favourable organism for cancer studies?

A

Mice
(Lecture 4, Slide 32)

98
Q

How can we use mice to explore the function of a candidate oncogene or tumour suppressor gene?

A

By creating a transgenic mouse (inducting a gene from another organism into a mouse) that overexposes it or a knockout mouse that lacks it
(Lecture 4, Slide 32)

99
Q

What do transgenic mouse studies prove?

A

That a single oncogene is usually not enough to turn a normal cell into a cancer cell
(Lecture 4, Slide 32)

100
Q

What tissue do colorectal cancers arise?

A

The epithelium lining the colon
(Lecture 4, Slide 33)

101
Q

What did clinical analysis in colorectal cancer identify?

A

A benign tumour (called an adenoma) which are thought to be the precursor of more colorectal cancer - as removing them reduces cancer rates
(Lecture 4, Slide 33)

102
Q

What does adenomatous polyps screening identify and remove?

A

Adenoma benign tumours
(Lecture 4, Slide 33)

103
Q

Is progression to colorectal cancer fast or slow?

A

Slow
(Lecture 4, Slide 33)

104
Q

What happens in the later stages of colorectal cancer?

A

Some tumour cells become invasive in a small fraction of polyps (growth of tissue sticking out of colon) and they first break through the epithelial blast lamina, before spreading through the layer of muscle that surrounds the gut and then finally to the lymph nodes via lymphatic vessels and to the liver, lung and other organs through blood cells
(Lecture 4, Slide 33)

BM 210: Introduction to Biochemistry (12 decks)

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