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BIOL 112 - Cell Structure and Function > week 9 > Flashcards

week 9 Flashcards

1
Q

Why is correct regulation of cell division important?

A

Development - Organs and body parts need to be the correct size/shape, not over/under developed.

Injury - Cells need to divide following injury but stop when damage repaired

Adaptive responses

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2
Q

What is adaptive responses regulation important in cell division?

A

Cells in bone marrow responds to low O2 - produce more RBC - need to stop when O2 returns to normal

Lymphocytes - division triggered in response to antigen - needs to be controlled

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3
Q

What are the consequences of deregulated cell division?

A

If regulation of cell division breaks down in any of the aforementioned processes it results in cancer/tumor formation

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4
Q

What two main ways cell division is regulated?

A

External signals - Diffusable chemical signals produced by other cells which ‘tell the cell how to behave’, eg mitogens (growth factors)

Internal signals - chemical signals produced internally by the cell in order to regulate its own division - eg cyclin dependent kinases

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5
Q

External signals regulating cell cycle processing?

A

Can promote or inhibit cell division,
and are known as Mitogens (growth factors) or anti-mitogens

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6
Q

What happens in the absence of mitogens in external signals that regulate cell cycle?

A

S phase cyclins (i.e. those cyclins which drive the cell into S phase) are not made

Without sustained mitogen stimulation cells will not progress through the G1 checkpoint​

The cells enter G0 instead – quiet phase or quiescence​

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7
Q

How do mitogens promote cell growth?

A

Mitogen binds to specific receptor on plasma membrane - activates - a relay in signal transduction pathway within the cytoplasm - activation of a cellular response as a result

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8
Q

Give an example of an external growth factor?

A

Platelet-derived growth factor (PDGF)

  • Platelets are specialised cells present in blood​
  • Platelets have important roles in blood clotting and wound healing​
  • Release PDGF in response to injury​
  • PDGF binds to receptors on surface of skin cells and causes them to start dividing
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9
Q

What are internal signals that regulate cell cycle?

A

Stimulated by the presence of extracellular factors such as mitogens

M+G2
M+G1 or S
G1+S
G1+G2

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10
Q

How were internal signals of cell division first identified?

A

First identified by fusing cells from different stages of the cell cycle, caused the non-mitotic cell to become mitotic due to a growth factor in the cell

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11
Q

Why do cells need internal signals to control division?

A

Uncontrolled cell division is a hallmark of cancer. ​So, checkpoints enable cells to stop dividing if the correct signals are not present.​

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12
Q

What do checkpoints allow for in cell division (internal signals)?

A

Checkpoints allow cells to review current circumstances and prevent untimely exit from each cell cycle phase. ​

If cell proceeds from one phase of the cycle to the next inappropriately, this can cause genetic instability.​

Genetic instability can cause cancer​

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13
Q

What are the three major checkpoints in cell division?

A

G1,
G2,
Metaphase (spindle assembly checkpoint)

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14
Q

What does G1 checkpoint ensure?

A

Commits cell to DNA replication and cell division

Checks:
Is cell suitable size?
Has it received appropriate external signals?

If no, cell enters non-dividing G0 phase,
If yes, Cell proceeds to S phase

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15
Q

What does G2 checkpoint ensure?

A

Cell makes decision whether or not to enter mitosis​

Checks:​
Is cell a suitable size?​
Is DNA replicated?​
Is environment favourable?​

NO – cell does not proceed
YES – cell proceeds to M phase​

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16
Q

What does metaphase checkpoint ensure?

A

Occurs in metaphase​

Checks:​
Are all the chromosomes attached to spindles?​

NO – cell does not proceed​
YES – cell enters anaphase of mitosis

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17
Q

What are the two internal molecular signals that regulate G1 and G2 checkpoints?

A

Cyclin-dependent kinases (Cdks) and Cyclins

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18
Q

Who discovered Cyclins?

A

Sir Tim Hunt (1982)

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19
Q

What did Sir Tim Hunt observe (internal signals of cell cycle)?

A

Observed that, following fertilisation, cells in sea urchin early embryos divided SYNCHRONOUSLY ​

Whole population of cells at same stage of cell cycle as opposed to a mixed population at different stages​

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20
Q

What did Sir Tim Hunt find (internal signals of cell cycle)?

A

Found a group of proteins levels of which increased and decreased (cycled) between INTERPHASE and MITOTIC PHASE - CYCLINS

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21
Q

What is the basic mechanism of action of Cdk and cyclin proteins?

A

Combination of the two proteins known as a ‘promoting factor’​ - control progression of the cell into the next phase of the cell cycle

G1 checkpoint – ​S phase promoting factor (SPF)​

​G2 checkpoint – ​M phase promoting factor​ (MPF) / Maturation promoting factor

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22
Q

How does the G1 checkpoint move to the next phase?

A

Cyclin E and Cdk 2 phosphorylates proteins required for S-phase entry, drives the cell into S phase.

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23
Q

What regulates G1 and G2 checkpoint?

A

G1 = SPF

G2 = MPF

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24
Q

How does cyclin enable cells to pass to the next phase of cell division after checkpoints?

A

Expression levels of Cdk’s remain constant throughout the cell cycle but their activity is enhanced by changes in cyclin levels​

therefore, it is an increase in cyclin expression which enables cells to pass through cell cycle checkpoints​

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25
Q

What is MPF?

A

mitosis-promoting factor (cyclinB + Cdk1)​

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26
Q

MPF and regulation of the cell cycle?

A

MPF = maturation / (mitosis) / M phase promoting factor​ - controls G2 checkpoint and initiation of mitosis​

After mitosis the degradation of cyclin increases (ubiquitination and proteosomal degradation) - MPF activity decreases again

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27
Q

Steps to activation of MPF in G2 phase?

A

Cyclin B accumulates,
Cyclin B and Cdk1 bind to form MPF
MPF triggers mitosis
MPF activates cycling-degrading enzyme
Enzyme degrades cyclin
Loss of cyclin inactivates enzymes
Cdk1 is recycles

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28
Q

Peaks of MPF activity correlate with peaks of cyclin levels - threshold reached - MPF activated. How?

A
  • cyclin expression increases sharply at various stages of the cell cycle
  • cyclin B particularly during G2
  • decrease sharply during M​
    -maximum in early M
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29
Q

When are CDKs present within the cell cycle?

A

At constant levels throughout the cell cycle

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30
Q

What des periodic cycling expression activate?

A

CDKs at defined points in the cell cycle

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31
Q

How does cyclin work?

A

Cyclin binds to CDK and forms the active MPF complex which acts directly by causing the nuclear envelope to fragment, and indirectly by stimulating other kinases​

Cyclin even initiates the process which results in its own destruction - thus switching itself off.​

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32
Q

What is the M checkpoint also known as?

A

Spindle assembly checkpoint

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33
Q

What is the internal regulator for the M checkpoint?

A

a complex of proteins called the ANAPHASE PROMOTING COMPLEX (APC)​

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34
Q

How is anaphase initiated after M checkpoint?

A

Unattached kinetochores – inhibitory pathway active, –> Cohesin –> inactive APC.

However, ‘Wait’ Signal stops when all kinetochores attached. –> Cohesin ubiquitination and breakdown​ –> APC activates anaphase.

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35
Q

Can cell cycle checkpoints be regulated by phosphorylation?

A

Yes

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36
Q

What is the current trend for cancer?

A

1 in 2 people will develop cancer in their lifetime

Its becoming more common in the UK, however mortality rate is decreasing

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37
Q

Cancer has recently over taken what as the leading cause of death in the UK? Why?

A

Heart disease

  1. Better treatment for heart disease; lower mortality
  2. A disease of the aging population
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38
Q

Which is the most common cancer?

A

Lung cancer

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39
Q

What is the second biggest killer in women versus men?

A

Men = prostate cancer

Women = Breast cancer

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40
Q

Cancer definition

A

a serious disease that is caused when cells in the body grow in a way that is uncontrolled and not normal, killing normal cells and often causing death

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41
Q

What are the cancer classifications?

A

Carcinoma
Sarcoma
Myeloma
Lymphoma
Leukemia
Mixed classifications

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42
Q

What is carcinoma?

A

cancers arising from epithelial cells (surface cells - e.g. lining of gut, skin, cells lining airways of the lungs)​

constitute 80-90% of all cancers as these cells are exposed to the environment (carcinogens)

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43
Q

What is sarcoma?

A

cancers of connective and supportive tissues e.g. bone cancer, muscle – rare 1%​

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44
Q

What is myeloma?

A

cancers of the plasma cells of the bone marrow - antibody producing cells - secondary infections (pneumonia and pyelonephritis (urinary tract infection)​

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45
Q

What is lymphoma?

A

solid tumours of the lymphatic system - lymph glands, lymph nodes or in organs - tonsils, spleen, thymus – formed from maturing WBCs​

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46
Q

What is Leukemia?

A

‘blood’ cancers - more specifically precursor blood cells in bone marrow – circulating white or red blood cells. Excess of immature cells - don’t function - anaemia - suppressed immunity​

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47
Q

What is mixed classifications of cancer?

A

cancers originating in germ cells and stem cells – therefore encompasses a range of cancers (as they have the capacity to form different types of cells during differentiation) – testicular, ovarian, even placental​

e.g. teratocarcinoma

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48
Q

How do the growth characteristics of a cancerous cell differ from those of a normal cell?

A

Normal cells:
1. Anchorage dependent growth - no attachment no growth​
2. Density dependent growth - stop growing when confluent - signals from other cells​ - will re-grow to fill gaps but then stop again​

Cancerous cells:
1. No anchorage dependence - seldom anchor to base of flasks but grow anyway - generally have rounded appearance​
2. No density dependence - growth not controlled by other cells - instead of a monolayer they just continue growing on top of each other​
3. Can form ‘foci’

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49
Q

What is ‘foci’?

A

Where cancer cells are cultured at high density they grow in multilayered, dense clumps of cells which is known as ‘foci’

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50
Q

Cell immortality - cancerous versus healthy?

A

Normal cells have a limited life expectancy eg 50-60 doublings, however cancerous cells have an indefinite number of population doublings.

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51
Q

Why are cancerous cells immortal but healthy cells are not?

A

Normal cell life expectancy is related to shortening of chromosomal telomeres. Cancerous cells are able to maintain telomere length by the protein telomerase

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52
Q

Other factors contributing to abnormal proliferation of cancer cells?

A

Reduced reliance on growth factors produced by other cells

Increased production of growth factors. (Cancerous cells may overproduce growth factors in order to promote growth - increased expression/shedding of growth factors)

Changes in cell membrane structure

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53
Q

Example of how reduced reliance on growth factors produced by other cells could cause cancer?

A

External growth factors required for progression through G1 cell cycle checkpoint​

​

e.g. 3T3 fibroblasts - normal cells only grow in culture media containing certain growth factors. Transform these cells (turn them into cancerous cells) by viral infection (e.g. SV40, Rous sarcoma virus) - grow happily on a basal media lacking the same growth factors​

​

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54
Q

How can changes in cell membrane structure and function cause cancer?

A

Cell surface / plasma membrane is a strong determinant of cellular ‘social’ behaviour; e.g. communication, cell movement, adherence, access to nutrients, recognition by the immune system​

​

- glycolipids, glycoproteins, proteoglycans, mucins
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55
Q

What are the basic stages of cancer disease progression?

A

Initiation​

Clonal expansion​

Primary tumour​

Secondary mutations​

Malignancy ​

Invasion​

Metastasis ​

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56
Q

Step 1 of cancer disease progression?

A

Initiation

Single cell undergoes a single mutation - confers a growth advantage which causes it to lose some of its growth control

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57
Q

Step 2 of cancer disease progression?

A

Clonal expansion

Proliferation begins - mutated cell divides quicker than surrounding cells to form a cluster of ‘clones’ - disease is monoclonal

58
Q

Step 3 of cancer disease progression?

A

Primary tumour

The cancer remains in situ (ie not moved from site of original mutation). Tumour benign - not invaded surrounding tissues - surgery possible

59
Q

Step 4 of cancer disease progression?

A

Secondary mutation

Secondary mutations provide a new phenotype with a selective advantage

60
Q

Step 5 of cancer disease progression?

A

Following the secondary mutation, the cells lose contacts with their neighbours - become invasive - secrete proteases to breakdown the extracellular matrix holding cells in place - risk of metastasis

61
Q

Step 6 of cancer disease progression?

A

Invasion of lymph or/and blood vessels

First stages of metastasis - cancer cells have low adherence - easy to break off main tumour and enter vessels

62
Q

Step 7 of cancer disease progression?

A

Metastatic tumour

Cell from original tumour in organ/tissue has now entered a vessel/lymph node and emerge at the other end to form a new tumour in another organ/tissue

63
Q

What are the characteristics of malignant tumour cells?

A
  • Show excessive proliferation
  • Unusual number of chromosomes (aneuploidy)
  • ‘Deranged’ metabolism (eg Warburg Effect)
  • Reduced attachments to neighbouring cells, enables spread to other tissues
  • Invasive phenotype: detaches from original tumour and enter blood stream and lymph system
  • Proliferate in other parts of the body - Metastasis
64
Q

What is metastasis?

A

Cancerous cells proliferate in other parts of the body by using lymph system or blood vessels to move

65
Q

Examples of carcinogens that cause cancer?

A

Cigarette smoke
- Mutagenic chemicals

Sunlight
- UV radiation

Viruses
- Insert DNA into genome, eg human papillomavirus (HPV) causing cervical cancer

66
Q

Example of a virus that causes cancer?

A

HPV (human papillomavirus) causes cervical cancer

67
Q

Give an example of an inherited predisposition that can cause cancer?

A

retinoblastoma

68
Q

DNA mutations that can cause cancer?

A

Mutations in genes encoding proteins which regulate cell division: eg proto-oncogenes and tumour suppressor genes

69
Q

In what ways can a proto-oncogene become oncogenes?

A

Increase Translocation or transposition efficiency of a new promotor gene

Gene replicated

Mutation in existing promotor, enabling more efficient transcription

Point mutation within the gene (changes the protein itself)

70
Q

How are oncogenes found? [1]

A

Extract DNA from human tumor cells - contains mutated oncogene​

71
Q

How are oncogenes found? [2]

A

Tumour DNA ‘transfected’ (introduced) into mouse cells (3T3). Cells which have taken up the oncogene proliferate and form dense foci​

72
Q

How are oncogenes found? [3]

A

Cells in the foci may have taken up other bits of the human DNA in addition to the oncogene. ​

73
Q

How are oncogenes found [4]?

A

DNA from ‘focus’ is reintroduced into fresh mouse (3T3) cells to dilute out human DNA other than the oncogene

74
Q

How are oncogenes found [5]?

A

Extract mouse genomic DNA from cells - now contains the human oncogene​

Fragment DNA (restriction digest) & introduce into bacterial virus - PHAGE LIBRARY​

75
Q

( How are oncogenes found [6]? )

How do we know which phage contains the oncogene?

A

Add phages to a plate of bacteria - at the right dilution each single phage will kill the bacteria - empty spot on plate

‘Blot’ plate onto filter paper. Human DNA contains Alu sequences (mouse does not) - detect the human oncogene DNA using a probe against Alu

76
Q

How was The Ras oncogene discovered??

A

When DNA from a bladder tumour was used to transform mouse 3T3 cells

77
Q

How does the Ras oncogene differ from the proto-oncogene?

A

The oncogene differs from the proto-gene by only a single nucleotide - different amino acid in protein (G12V) - causes Ras to remain permanently bound to GTP – permanently active!​

​Stimulatory signal to nucleus never switched off - excessive production of cyclins - uncontrollable growth!​

​This therefore explains why cancer cells don’t require external growth factors like normal cells​

78
Q

How many oncogene mutations are needed to cause cancer?

A

One copy in diploid cells, the mutations are dominant

79
Q

Are tumour suppressor gene mutations dominant or recessive?

A

recessive and inactivate proteins.

Two copies are needed, and one functional copy is enough to maintain tumour suppressor function

80
Q

How can cancer develop by tumour suppressor genes?

A

For cancer to develop both copies need to be mutated - cancer causing mutations in tumour suppressors are, therefore, recessive​

81
Q

What does mutations in tumour suppressor genes reduce?

A

Inhibition of cell division - therefore stimulating cell proliferation

One good (functional) copy of the gene is enough to inhibit cell division – so both copies must be mutated for cancer to result (recessive)​

82
Q

What are the two forms of retinoblastoma?

A

Familial (10%) - occurs in young children retinal tumours in both eyes​

  1. ‘Sporadic’ (90%) - occurs later in life - affects just ​
    one eye in most (2/3s) cases​
83
Q

Retinoblastoma gene is recessive, what does this mean?

A

For cancer to arise both copies are inactivated by mutation (one is enough for normal function)​

​Only 1 in million cells becomes cancerous (recessive at cellular level) - average of 4 tumours per eye​

84
Q

What is retinoblastoma?

A

Tumour of the retina

85
Q

What was the first tumour suppressor gene identified?

A

Retinoblastoma

86
Q

The patters of inheritance of retinoblastoma is dominant, how can this be when the gene is recessive?

A

Retinoblastoma is caused by a mixture of inheritance and somatic mutation

87
Q

What is retinoblastoma caused by?

A

Mitotic recombination

88
Q

What is mitotic recombination (causing cancer)?

A
  1. Normal cell (one good gene enough to inhibit cell division)
  2. Normal DNA replication; result duplicated normal and mutant chromatids
  3. Rare complications; simple exchange of genetic material between normal and mutant chromatids
  4. Subsequent mitotic segregation of chromatids and cytokinesis - one cell homozygous normal, other mutant
89
Q

How does retinoblastoma mutate the cell to cause cancer?

A

Inhibits the G1-S transition checkpoint, so the cell bypasses this, allowing it to regulate and divide

90
Q

What is p53?

A

Tumour suppressor gene

Main role is to protect the cell against damaged DNA. It arrests the cell cycle giving DNA repair machinery more time to fix DNA before mitosis and passing on of the damaged DNA to daughter cells

91
Q

In the absence of p53….?

A

Mutations are able to pass on at a higher frequency

92
Q

p53 is stabilised when?

A

In presence of genetic damage or cellular stress.

It’s constitutively expressed but constantly degraded in absence of genetic damage

93
Q

If DNA damage is too severe, what does p53 gene stimulate?

A

Cells enter permanently non-replicative state called senescence or under go apoptosis

94
Q

How does p53 respond to DNA damage?

A
  1. DNA damaged in nucleus by, eg UV light
  2. Signal is passed to p53 via a cascade of protein kinases each phosphorylating and activating each other.
  3. Activated p53 is a transcription factor - triggers expression of proteins which inhibit cell cycle
95
Q

What is the function of p53?

A

Cell cycle checkpoint in G1 and in G2.

Upregulation of DNA damage repair enzymes:
- Repaired: cell cycle re-entry
- Unrepaired: Senescence, apoptosis. (Prevent transmission of incorrect coding / mutation to the next generation)

96
Q

p53 alters gene expression: CDK inhibitor of p21? (1)

A

p21 expression is up regulated by p53​

p21 is an inhibitor of Cyclin E-Cdk2​

Prevents G1 exit causing cell cycle to arrest​

Preventing duplication of damaged DNA and passing on of DNA to daughter cells

97
Q

p53 alters gene expression: DNA repair proteins are transcriptionally regulated by p53? (2)

A

Expression up regulated by p53​

Allows cell to repair DNA during cell cycle arrest​

If DNA damage is unrepaired cells enter senescence or apoptosis. These pathways are regulated by p53​

98
Q

p53 alters gene expression: Genes involved in apoptosis (3)?

A

If the DNA is damaged so badly that it cannot be repaired p53 activates genes which cause the cell to commit suicide

Apoptosis

99
Q

What is apoptosis?

A

A form of cell death in which a programmed sequence of events leads to the elimination of cells without releasing harmful substances into the surrounding area

100
Q

Step one: apoptosis?

A

Normal cell ‘realises’ that its DNA is beyond repair and so p53 activates apoptosis

101
Q

Step two: apoptosis?

A

Cell begins to shrink and invaginations form at the cell surface

102
Q

Step three: apoptosis?

A

Organelles become enclosed in vesicles. DNA in nucleus is dissolved by enzymes, cellular material is engulfed and degraded by phagocytes

103
Q

What proteins regulate the activation of apoptosis?

A

Caspases

p53 gene

104
Q

What are the two types of apoptosis?

A

Intrinsic apoptosis,

Extrinsic apoptosis

Both regulated by p53

105
Q

How is intrinsic apoptosis induced?

A

by factors within the cell

106
Q

How is extrinsic apoptosis induced?

A

by specialised cells by activation of the FAS death receptor

107
Q

How does Intrinsic apoptosis occur?

A

When DNA is damaged p53 induces Bid expression​

Activated Bid induces Bax to form a pore in the mitochondrial membrane​

Release of cytochrome c activates caspases present in cytoplasm of the cell leading to cell death (apoptosis)​

108
Q

How does extrinsic apoptosis occur?

A

Activation of p53 induces expression of Death receptors.​

Fas ligand binding activates the Fas death receptor and recruits the Fas associated death domain (FADD) ​

Formation of the DISC, activates caspases that regulate cellular disintegration - apoptosis
​

109
Q

What is a death receptor?

A

Death receptors are activated by cells expressing Fas ligand e.g. Lymphocytes​

(Induced by p53 in response to genetic damage)

110
Q

Upregulation of p21 expression does what?

A

Halts cell by binding to Cdks allowing time for the cell to repair damage

111
Q

Summary of p53, tumour suppressor?

A

a transcription factor that controls responses to DNA damage. It does this by:
Upregulation of p21 expression
Upregulation of genes
p53 activates genes promoting apoptosis if not repaired

112
Q

Mutations in p53 gene can cause what?

A

Cancer by allowing cells with damaged DNA to survive.

Accumulation of mutations drives cancer formation

113
Q
A
114
Q

Identify that stages that are associated with transformation of a normal cell into a malignant tumour that can move to a new area in the body:

A

Initiation
Clonal expansion
Primary tumour
Secondary mutations
Malignancy
Invasion
Metastasis

115
Q

Identify the steps in MPF regulation and activation

A

Cyclin B accumulates
Cyclin B and Cdk1 bind to form MPF
MPF tiggers mitosis
MPF activated Cyclin-degrading enzyme
Degrades Cyclin
Loss of Cyclin inactivated enzyme
Cdk1 is recycled

116
Q

What regulates the cell cycle checkpoints

A

SPF - Checkpoint G1
MPF - Checkpoint G2
APC/C - Checkpoint Metaphase

117
Q

Which genes are transcriptionally regulated by P53 activity?

A

DNA damage repair enzymes and CDK inhibitor proteins

118
Q

What stimulates apoptosis

A

When BAX interacts with BID it forms a pore in the membranes surface which results in apoptosis

119
Q

What cell can regulate / trigger extrinsic apoptosis

A

Cytotoxic t-cells

(Casphases regulate internal apoptosis)

120
Q

What happens to the cell membrane during apoptosis?

A

Blebbing or invaginations of the cell membrane

121
Q

On the outer surface of the plasma membrane there are marker molecules that identify the cell-type. Often these molecules are…

A

Carbohydrate chains

122
Q

The part of a membrane protein that extends through the phospholipid bilayer is primarily composed of amino acids that are ….

A

Non-polar

123
Q

The fluid nature of the membranes is attributed to a lateral movement of what?

A

The entire lipid bilayer

The non-covalent interactions between the lipid bilayer give the membrane fluidity

124
Q

The process often thought of as “cell eating” is…

A

Phagocytosis

This method is used by special white blood cells called phagocytes to ‘eat’ bactetia

125
Q

Are collagen fibres found in the cytoskeleton?

A

No

126
Q

In the digestive tract adjacent cells develop connections to form a sheet that prevents leakage of small molecules. These connections between cells are called

A

Tight junctions

127
Q

True or false

In the mito tic spindle, microtubule dare responsible for pulling the chromosomes apart as well as pushing the poles away from each other

A

True

microtubule motors are believed to anchor kinetochore to the shortening microtubule

128
Q

Junctions in which the cytoskeleton is attached to that of the other cells or the extracellular matrix are called

A

Anchoring junctions

Desmond ones are the commonest type of anchoring junction

129
Q

The electron transport chain, a series of membrane-associated electron carriers, loses most of the energy by driving several transmembrane …..

A

Proton pumps

130
Q

The energy release in the mitochondrial electron transport chain is used to transport protons into the …..

A

Inter membrane space of mitochondria

131
Q

The enzymes of the krebs cycle are located in the….

A

Matrix of the mitochondrja

132
Q

The reaction, C6H6O6 = 6 CO2 + 6 H2O, when it occurs in living cells is known as what

A

Cellular respiration

133
Q

….. are enzymes that regulate cell division by phosphorylation proteins

A

Cyclin-dependent kinases

134
Q

…. Are external factors capable of governing passage through the G1 checkpoint (restriction point)

A

Growth factors

135
Q

True or false

Cyclin is maintained for use in the subsequent cell cycle

A

False

136
Q

One way cancer cells differ from normal cells is that they demonstrate anchorage-……. of growth

A

Independence

Cancer cells also demonstrate loss of contact inhibition of growth

137
Q

The retinoblastoma protein is what ?

A

A tumour suppressor

138
Q

Which of the following is not a change associated with proto-oncogenes becoming oncogenes?

Movement to a new location
Amplification
A point mutation causing loss of protein function
A mutation in a controlling element causing over-expression
A point mutation leading to a hyperactive protein

A

A point mutation causing loss of protein function

139
Q

Which if the following statements are true regarding the Ras oncogene

It codes for a molecular switch
It codes for a protein kinase
It is found in bladder cancers
It will transform mouse 3T3 cells
It suppresses cell division

A

It codes for a molecular switch
It is found in the bladder cells
It will transform mouse 3T3 cells

140
Q

Who first described cells?

A

Hooke

141
Q

Who first looked at tiny living cells and called them as ‘animalecule’

A

Leeuwenhoek

BIOL 112 - Cell Structure and Function (4 decks)

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