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MP421 > HALLMARKS OF CANCER > Flashcards

HALLMARKS OF CANCER Flashcards

1
Q

oncogenes

A

refers to genes that contribute to cancer in a gain-of-function manner

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2
Q

proto-oncogenes

A

the genes that normally code for proteins involved in the control of cell division and differentiation

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3
Q

proto-oncogenes into oncogenes

A

proto-oncogenes can be mutated, which disrupts the normal function and the cell can become cancerous (oncogenes)

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4
Q

most common proto-oncogene that mutates into oncogenes and how is it different from its normal function

A

RAS
an abnormal RAS protein loses its ability to regulate itself and is always switched on, always active, which leads to continuous cell division

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5
Q

tumour suppressor genes (anti-oncogenes)

A

genes which code for proteins that are involved in cell processes of checking, repair and suicide

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6
Q

TP53 gene

A
  • tumour suppressor gene (anti-oncogene)
  • codes for the p53 protein
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7
Q

what happens if the TP53 gene is damaged

A

the repair mechanisms become less efficient, defects are carried forward from one cell generation to another, and as the damage increases, the chances of the cell becoming cancerous increase

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8
Q

consequences of genetic defects (hallmarks of cancer)

A
  • abnormal signalling pathways
  • insensitivity to growth-inhibitory factors
  • abnormalities in cell cycle regulation
  • evasion of programmed cell death (apoptosis)
  • limitless cell division (immortality)
  • ability to develop new blood vessels (angiogenesis)
  • tissue invasion and metastasis
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9
Q

growth factors

A
  • hormones
  • extracellular chemical messengers that activate protein kinase receptors in the cell membrane
  • trigger a signal transduction pathway
  • this instructs the transcription of the proteins and enzymes required for cell growth and division
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10
Q

growth signals in cancer

A
  • cancer cells can grow and divide in the absence of external growth factors
  • they do this by producing the growth factors themselves then releasing it such that it stimulates its own receptors, often by autophosphorylation
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11
Q

examples of growth factors that cancer cells can produce

A

platelet-derived growth factor (PDGF)
transforming growth factor a (TGF-alpha)

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12
Q

how can cancer cells grow and divide without growth factors

A
  • receptors can be overexpressed
  • this means that an oncogene is too active and encodes for excessive protein receptor
  • once these receptors are in the cell membrane, the cell becomes super sensitive to low levels of circulating growth factor
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13
Q

growth-inhibitory signals

A

external hormones such as transforming growth factor B (TGF-beta) counteract the effects of stimulatory growth factors and signal the inhibition of cell growth and division

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14
Q

insensitivity to growth-inhibitory signals

A
  • insensitivity to these signals raises the risk of a cell becoming cancerous
  • this can arise from damage to the genes coding for the receptors for these inhibitory hormones - the tumour suppression genes
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15
Q

4 phases of cell growth/multiplication

A

G, S, G2, M
G0 (dormant/resting state)

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16
Q

restriction phase (R)

A
  • during the G1 phase which frequently becomes abnormal in tumour cells
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17
Q

what are checkpoints in cell growth/multiplication

A
  • assess the integrity of the process
  • delays during stages if DNA damage detected
  • this gives sufficient time for damaged DNA to be repaired or for the cell to commit apoptosis
  • these checkpoints can be defective in tumour cells
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18
Q

proteins and enzymes that control the cell cycle

A

proteins > cyclins (~15 types)
enzymes > cyclin-dependent kinases (CDKs) (~9 types)

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19
Q

moving a cell from one phase to another - how is the decision made

A

depends on the balance of stimulatory versus inhibitory signals being received through signal transduction

20
Q

p53 protein

A
  • protein that monitors the health of the cell and the integrity of DNA
  • controls the inhibitory protein p21
21
Q

extrinsic route for apoptosis

A
  • lack of growth factors or hormones
  • proteins called death activator proteins which can bind to cell membrane proteins called tumour necrosis factor receptors (TNFR) triggering apoptosis
  • the immune system produces T-lymphocytes which perforate the cell membrane of damaged cells and inject an enzyme called granzyme, which initiates apoptosis
22
Q

intrinsic pathway of apoptosis

A
  • can arise from factors such as DNA damage arising from exposure to chemicals, drugs or oxidative stress
  • the cell has mechanisms that detect damage and lead to the increased production of the tumour suppressor gene p53
  • this gene will trigger apoptosis
23
Q

cytochrome c

A
  • released from mitochondria
  • results in the assembly of a large oligomeric protein complex - apoptosome
24
Q

apoptosome

A
  • made up of a scaffolding protein called Apaf-1
  • the apoptosome then recruits and activates an enzyme - procaspase 9, which in turn activates caspases
25
Q

caspases

A
  • protease enzymes containing a cysteine residue in the active site which is important to the catalytic mechanism
  • as proteases they destroy the cell’s proteins, which destroys the cell
26
Q

proteins that promote apoptosis

A

Bad
Bax

27
Q

proteins that suppress apoptosis

A

Bcl-2
Bcl-x

28
Q

telomeres

A
  • repeated DNA sequences at the ends of chromosomes
  • get shorter with age and every cell division
29
Q

telomerase

A
  • enzyme that can add hexanucleotide repeats on the end of telomeric DNA and thus maintain its length
  • absent from normal cells
  • cancer cells up-regulate this enzyme
30
Q

how do cancer cells go into a state of hypoxia

A

as a tumour grows in size its cells become increasingly remote from the blood supply and become starved of these resources

31
Q

hypoxia-inducible factors

A
  • such as HIF-1
  • start to build up within the tumour cells, and up-regulate genes that promote survival in oxygen-starved environments
32
Q

vascular endothelial growth factor (VEGF) and fibroblast growth factor (FGF-2)

A
  • interact with receptors of the endothelial cells of nearby blood vessels and stimulate these cells to divide, leading to the branching and extension of existing capillaries
  • angiogenesis
33
Q

angiogenesis inhibitors

A

angiostatin
thrombospondin

34
Q

what do blood vessels in tumours lack

A

cells display molecules called integrins on their surface which are absent from mature vessels and which protect the new cells from apoptosis

35
Q

E-cadherin

A

cell adhesion molecule

36
Q

how can cancer cells metastasise without going through apoptosis

A
  • cell adhesion molecules are absent in metastasised cancer cells, allowing them to break away from the primary tumour
  • oncogenes in cells that code for proteins send false messages back to the nucleus implying that the cell is still attached
37
Q

4 phases of metastasis

A
  1. emigration from original organ
  2. dispersal and survival in transportation fluid
  3. invasion of new organ
  4. colonisation
38
Q

neovasculature

A

excessive formation of blood vessels in tumours from the constant production of VEGF

39
Q

epithelial-mesenchymal transition (EMT)

A

process which cells delaminate from epithelium and take on appearance/properties of fibroblasts

40
Q

delamination

A

tumour cells lose adhesion and migrate

41
Q

metabolic reprogramming

A

the ability of cancer cells to alter their metabolism in order to support the increased energy request due to continuous growth

42
Q

T-cell exhaustion

A

progressive loss of effector function due to prolonged antigen stimulation
induced by cancer cells to evade immune response

43
Q

CTLA4

A

inhibits T-cell activation

44
Q

RAS protein operates in 2 pathways:

A

mitogen-activated protein kinases (MAPK)
phosphoinositide-3 kinase (PI3K)

45
Q

retinoblastoma protein (Rb)

A
  • protein that regulates antigrowth signals
  • key inhibitor of entry into S-phase of the cell cycle, thereby regulating cell proliferation
  • Rb pathway also regulates apoptosis via transcriptional regulation of pro-apoptotic factors - E2F1 overexpression
  • Rb pathway functionally inactivated in cancers
46
Q
A

MP421 (12 decks)

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