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Cancer Biology > What is Cancer? > Flashcards

What is Cancer? Flashcards

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AP® Biology flashcards Biology 101 flashcards
1
Q

How many different types of cancer is there?

A

> 200

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2
Q

What is carcinogenesis?

A

The change from a normal cell to a cancerous cell

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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

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4
Q

Define clonal evolution

A

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

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5
Q

Where do cancers originate from?

A

A single cell

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6
Q

What is the role of p53?

A

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

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7
Q

Why do tumour cells undergo clonal evolution?

A

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

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8
Q

Why are blood tumours easier to treat than solid tumours?

A

They are monoclonal, solid tumours are polyclonal

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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

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10
Q

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

A

5-15 years

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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
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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
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13
Q

Give 2 examples of tumour suppressors

A

p53

retinoblastoma (Rb)

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14
Q

How are tumour suppressors inactivated?

A

Mutations

Loss of heterozygosity

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15
Q

Give 3 examples of proto-oncogenes

A

cyclins
Myc
Ras

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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
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17
Q

What is a truncated receptor?

A

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

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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

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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

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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

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21
Q

What factors cause p53 to induce a response?

A
  • Lack of nucleotides
  • UV radiation
  • Ionising radiation
  • Oncogene signalling
  • Hypoxia
  • Blockage of transcription
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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)

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