Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Cancer & The Cell Cycle > Lecture 1 - Introduction > Flashcards

Lecture 1 - Introduction Flashcards

1
Q

What is the life cycle of a cancer?

A 
Cell with genetic mutation
Hyperplasia
Dysplasia
in situ cancer
Invasive cancer
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What are the 8 hallmarks of cancer?

A 
Self sufficiency in growth signals
Insensitivity to growth inhibit signals
Tissue invasion and metastatis capability
Limitless replicative potential
Sustained angiogenesis
Evasion of programmed cell death
Reprogram energy metabolism
Evading immune system
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What are the two enabling events?

A

Loss of genome surveillance and checkpoint control

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Why is it so difficult to treat cancers?

A

There is an infinite number of mutations that can cause a tumour

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What does it mean that tumours are often heterogeneous?

A

Often made up of lots of different cell types

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

How do two independent cancers appear nearby seperated by normal tissue?

A

Because a cancer cell is dividing uncontrollably there is a higher chance one of the new cells has another mutation. This can branch off and form another cancer.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What does a mitogenic signal do to a cell?

A

Moves it from a quiescent state (g0) into a proliferative state (s phase)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What kind of molecules can be used in signalling for growth factors?

A

Diffusible growth factors
Extracellular matrix components
Cell to cell adhesion molecules

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Give a short overview of what happens when a diffusible growth factor binds to a cell

A
  1. Ligand binding
  2. tyrosine kinase domains dimerise
  3. Domains phosphorylate other proteins
  4. Signal transduced
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Whatare 3 ways oncogenes can mimic growth signalling?

A

Act at the level of the signal
The receptor
Disrupting signal transduction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What is the difference between oncogenes and tumour suppressor genes?

A

Oncogenes are GOF mutations that promote proliferation.

Tumour suppressor genes are LOFs in genes that restrain proliferation or guard genome.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What kind of mutation is an oncogene usual;y?

A

Dominant

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What kind of mutation are tumour suppresor genes?

A

Recessive (often underlie familial cancers)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What is Her2?

A

A receptor tyrosine kinase of the epidermal growth factor receptor thats overexpressed in 30% of breast cancers

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What happens in Her2 cancers?

A

Receptor is overexpressed making cells hypersensitive to ligand.
Activates intracellular kinases which have effects on apoptosis and proliferation.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What is herceptin?

A

A monoclonal antibody that extends the life of Her2 breast cancer patients

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What is RAS?

A

An intracellular switch that is fixed into the ON position in cancers.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What inactivates RAS?

A

Hydrolysis of GTP to GDP by GAP

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What activates RAS?

A

GDP to GDP triggered by GEF

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What does a mutation is RAS cause?

A

Structural alterations that generate extended firing periods.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

How many cancers involve RAS?

A

25% of human cancers

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What is a viral oncogene?

A

Some viruses have picked up proto-oncogenes and incorporated them into the genome.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What does a viral oncogene do?

A

Host cells harbouring the virus gain a growth advantage (propagating the virus)

24
Q

How is the expansion of cell populations normally controlled?

A

Programmed cell death

25
Q

What is phosphatidyl serine?

A

A label put onto cells that have gone through apoptosis marking it to be cleared by macrophages

26
Q

What can lead to apoptosis?

A

Extrinsic - Responding to signalling imbalances (survival signals, death signals, overexpressed oncogenes)
Intrinsic - Responding to DNA damage or hypoxia

27
Q

What are some pro-apoptotic factors that lead to released cytochrome C in the mitochondria

A

Bax
Bak
Bid
Bim

28
Q

What are some anti-apoptotic factors?

A

Bcl-2
Bcl-XL
Bcl-W

29
Q

How were the Bcl-2 family (anti-apoptotic) first discovered?

A

Identified as half of chromsomal translocation in B-cell lymphoma that up regulates Bcl2 and increases anti-apoptotic activity

30
Q

What is another way to evade apoptosis?

A

Loss of p53 - mutant cells cannot die in response to DNA damage

31
Q

What detemines the maximum size of the tumour?

A

Diffusion from blood - cells must be within 100 microns of a capillary

32
Q

How does a developing tumour encourage blood vessels to grow (angiogenesis)?

A
  1. An endothelial cell is signalled by VEGF released from a tumour nearby.
  2. Endothelial cell moves and develops a capillary sprout
  3. Cells behind replicate and hollow out vacuoles which join creating a tube to the tumour
33
Q

What is VEGF?

A

Angiogenic signal used in normal development and by cancer cells

34
Q

What is HIF?

A

Protein that regulates expression of genes involved in angiogenesis

35
Q

What does HIF do in normal oxygen (normoxic) conditions?

A

One of its prolines is hydroxylated which is recognised by protein complex containing Cul2 (E3 ligase) which destablises the protein.
One of its asparagines is hydroxylated preventing binding of transcriptional coactivators

36
Q

What happens to HIF during hypoxia?

A

Unhydroxylated HIF is stabilised (no Cul2) and can bind to coactivators (p300) leading to transcription

37
Q

Outline metabolism in the presence of oxygen

A

In the presence of O glucose is metabolised by glycolysis in to pyruvate then oxidised to CO2 in the mitochondria by oxidative phosphorylation

38
Q

What are the effects of chemotherapy?

A

Stops any rapidly proliferating cell.

This is why we lose our hair

39
Q

Outline anaerobic glycolysis

A

Glucose broken down to pyruvate then to lactate

40
Q

How do rapidly proliferating cells prefer to metabolise?

A

85% by anarobic glycolysis

41
Q

Why do cancer cells convert glucose to lactate regardless of whether oxygen is present (not an efficient way to generate ATP)?

A

To fuel cell growth and division.
Aerobic glycolysis allows diversion of glycolytic intermediates into biosynthetic pathways required for assembling new cells.

42
Q

How does the immune system deal with cancerous cells?

A

Natural killer (NK) cells target based on aberrant cell surface proteins and secrete cytokines to recruit macrophages to absorb dying cell

43
Q

How can tumour cells inhibit NK cells?

A

Release transforming growth factors beta

44
Q

What is immune privilege?

A

Tumours that have evolved ways to change the immune system

45
Q

How does the FasL system usually work?

A

FasL on surface of cytotoxic T cells triggers trimerisation of Fas receptors on target cell - leads to apoptosis

46
Q

How can cancer cells use immune privilege to avoid the FasL system?

A
  • Down regulate Fas receptor
  • abnormalities of signal transduction proteins
  • downregulation of caspase 1, Bax or Bak
  • Upregulation of Bcl2
  • Express FasL to counterattack
47
Q

Why do transplant patients get cancer easier?

A

Immunosuppressed

48
Q

What is it called when the cell has reached the Hayflick limit?

A

Senescence

49
Q

What happens during crisis?

A

Mass of senescencing cells die

50
Q

How many cells escape crisis?

A

1 in 10^7

51
Q

What is crisis provoked by?

A

Eroded telomeres

52
Q

What is the end replication problem?

A

DNA polymerase can only add nucleotides on 3’ end so lagging strand gets shorter after each cell cycle

53
Q

What does telomerase do?

A

Makes a template on the 3’ end so telomeres do not decrease in length

54
Q

How many cancers have increased telomerase?

A

90%

55
Q

What karyotype of chromosomes is shown in cancers?

A

Fusion and repair by non-homologous end joining affecting expression of other genes (change relationship between genes and promoters)

56
Q

How can you visually show the end joining and juggling of chromosomes in cancers?

A

Put differently coloured tags on each chromosome

Cancer & The Cell Cycle (8 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions