Brainscape's Knowledge GenomeTM

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


See full index

Cancer Biology > What is Cancer? > Flashcards

What is Cancer? Flashcards

1
Q

How many different types of cancer is there?

A

> 200

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

What is carcinogenesis?

A

The change from a normal cell to a cancerous cell

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

Define cancer

A

An accumulation of abnormal cells which multiple through uncontrolled cell division and spread to other parts of the body through invasion and/ or distant metastasis via the blood and lymphatic system

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

Define clonal evolution

A

A series of mutations which accumulate in successive generations of the cell

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

Where do cancers originate from?

A

A single cell

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

What is the role of p53?

A

Monitor cells for signs of damage and cause this to be fixed

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

Why do tumour cells undergo clonal evolution?

A

To increase the cancer cells chances to avoid the hosts defence mechanisms

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

Why are blood tumours easier to treat than solid tumours?

A

They are monoclonal, solid tumours are polyclonal

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

Why are polyclonal tumours harder to tackle?

A

Each of the mutations will have a growth advantage and they will all be different
For chemotherapy, it is hard to find one which will target all of the different tumour cell types at once

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

How long can it take for CRC to turn from an adenoma to a full cancer?

A

5-15 years

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

What are the 6 main hallmarks?

A 
Sustaining proliferative signalling 
Evading growth suppressors
Activating invasion and metastasis 
Enabling Replicative Immortality 
Inducing Angiogenesis 
Resisting Cell Death
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What are the 4 additional hallmarks?

A 
Emerging hallmarks 
- Deregulating cellular energetics 
- Avoiding immune destruction 
Enabling characteristics 
- Genome instability and mutation 
- Tumour-promoting inflammation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Give 2 examples of tumour suppressors

A

p53

retinoblastoma (Rb)

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

How are tumour suppressors inactivated?

A

Mutations

Loss of heterozygosity

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

Give 3 examples of proto-oncogenes

A

cyclins
Myc
Ras

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

How do cancer cells increase cell growth?

A
  • Production of their own extracellular growth factors
  • Overexpression of growth factor receptors - cells become hyper-responsive to growth factors
  • Alterations of the intracellular components of the signalling pathway
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What is a truncated receptor?

A

A receptor which emits signals even in the absence of ligand binding

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

What is the function of Rb in normal cells?

A

Prevents inappropriate transition from the G1 phase of the cell cycle to the synthesis (S) phase

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

What are GAP phases?

A

Points where the cell cycle can be paused to fix any problems/ kill the cell if it is beyond repair by tumour suppressor genes in normal cells

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

How does phosphorylation of Rb effect the cell cycle?

A

Phosphorylation causes the release and activation of E2F family transcription factors and enables cell cycle progression

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

What factors cause p53 to induce a response?

A
  • Lack of nucleotides
  • UV radiation
  • Ionising radiation
  • Oncogene signalling
  • Hypoxia
  • Blockage of transcription
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What does p53 induce when it is activated?

A
  • Cell cycle arrest -> senescence OR return to proliferation
  • DNA repair
  • Block of angiogenesis
  • Apoptosis
23
Q

Where is p53 found?

A

in GAP phases of the cell cycle

24
Q

What is Li-Fraumeni Syndrome?

A

A rare, autosomal dominant, hereditary cancer pre-disposition

25
Q

What mutations are involved in Li-Fraumeni syndrome?

A

Germline p53 mutations

26
Q

What does Li-Fraumeni syndrome cause in terms of cancer?

A

Early onset
Multiple cancers
High frequency of rare cancers, e.g. sarcomas

27
Q

What growth factors are involved in angiogenesis?

A

Vascular endothelial growth factor (VEGF) (main one)
Fibroblast growth factor (FGF)
Platelet-derived growth factor (PDGR)

28
Q

Name an anti-angiogenic factor?

A

thrombospondin (TSP-1)

29
Q

What is an angiogenic switch?

A

The balance of pro-angiogenic factors and anti-angiogenic factors

30
Q

What does the tumour cells intake via the blood vessels?

A

Nutrients and oxygen

31
Q

What do tumour cells remove via blood vessels?

A

Waste products and carbon dioxide

32
Q

How many deaths are caused by metastasis in solid tumours?

A

90%

33
Q

How does increased number of blood vessels promote metastasis?

A

The more there are, the better the cells are able to move around the body

34
Q

What is the relationship between growth factors, angiogenesis and metastasis?

A

Increase growth factor production -> angiogenesis -> metastasis

35
Q

What is intravasation?

A

Movement of the cancer cells into the blood vessels

36
Q

What is extravasation?

A

Movement of the cancer cell from the blood vessels into the tissue

37
Q

What is an epithelial phenotype?

A
  • Cell polarity
  • Cell adhesion
  • Stationary
  • High level of E-Cadherin
  • Low level of N-Cadherin
38
Q

What is an mesenchymal phenotype?

A
  • No cell polarity
  • Loss of cell adhesion
  • Ability to migrate and invade
  • Low level of E-Cadherin
  • High level of N-Cadherin
39
Q

How do melanoma cells induce an EMT?

A

They are no longer bound to keratinocytes (epithelial) and bind to endothelial cells (mesenchymal) and fibroblasts (mesenchymal)

40
Q

What cellular changes are lost when undergoing an EMT?

A
  • Cytokeratin expression
  • Tight junctions and epithelial adherens junctions involving E-Cadherin
  • Epithelial cell polarity
  • Epithelial gene expression program
41
Q

What cellular changes are gained when undergoing an EMT?

A
  • Fibroblast-like shape
  • Motility
  • Invasiveness
  • Increased resistance to apoptosis
  • Mesenchymal gene expression program including EMT-inducing transcription factors
  • Mesenchymal adherens junction proteins (N-Cadherin)
  • Protease secretion
  • Vimentin expression
  • Fibronectin secretion
  • PDGF receptor expression
  • alphavbeta6 integrin expression
  • Stem cell-like traits
42
Q

What sets the boundaries for how many times a cell can divide?

A

Telomeres

43
Q

What are telomeres?

A

The ends of chromosomes

44
Q

How do telomeres regulate the number of cell divisions in normal cells?

A

Each division causes them to get shorter and shorter until they are so short that they can no longer divide

45
Q

How do cancer cells divide an unlimited number of times?

A

Their telomeres are maintained through upregulation of the protein telomerase which adds a few bps onto the chromosome every time a few are removed by cell division

46
Q

What is hayflick limit?

A

~40-60 cell divisions before senescence

47
Q

What is the process of apoptosis?

A

Normal cell -> cell shrinkage/ chromatin condensation -> membrane blebbing -> nuclear collapse/ continued blebbing -> Apoptotic body formation -> Lysis of apoptotic bodies -> Phagocytosis

48
Q

Describe genomic instability

A

Increased mutation rates:

  • compromised cell surveillance mechanisms e.g. p53 mutation/loss
  • altered DNA damage detection and repair capability
  • altered apoptotic abilities
49
Q

What does immune surveillance do?

A

remove early stages of cancer and small metastasis

50
Q

What is the association between SCC and the immune system

A

Patients who are immune-compromised, e.g. transplant patients - have increased risk of developing SCC

51
Q

How does hypoxia effect tumour cellular energetics?

A

Leads to increased expression of HIF-1alpha, which orchestrates an adaptive survival mechanism - including the promotion of glycolysis

52
Q

Why do tumour cells use aerobic glycolysis?

A

It produces extra nucleotides, amino acids and lipids - the building blocks for cancer formation

53
Q

How do tumour cells compensate for only producing 2 ATP molecules instead of 32 in normal respiration?

A

they upregulate GLUT1

54
Q

What is the basis of PET scans?

A

Use radiolabelled glucose as a tracer dye to look for metabolically active cells

Cancer Biology (13 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions